WikiVet English - User contributions [en]

User:Lizzies

2010-08-27T20:09:04Z

Lizzies: /* Hours Worked */

==About Me==

[[File:lizzieslack.jpg|200px|thumb|right|Copyright Lizzie Slack 2010]]

I graduated from the University of Edinburgh's BVM&S course in 2010, and also have an intercalated BSc in Veterinary Pathology from the [[Royal Veterinary College, London, UK|Royal Veterinary College]]. I have two [[Feline Clinical Section|cats]] and a cockatiel and currently live in Berkshire.

==What I Hope To Get Out of This Project==

This summer, I am hoping that authoring WikiVet pages will help me to consolidate my veterinary knowledge before starting practice. I am looking forward to becoming more familiar with what WikiVet now has to offer and getting to know others involved with the project.

==Pages I Am Working On==
[[:Category:To Do - Lizzie|My pages]]

==Hours Worked==

{| class="wikitable collapsible"
|Day
| <center> '''Week 1''' (2-8th August) </center>
| <center>'''Week 2''' (9-15th August) </center>
|<center>'''Week 3''' (16-22nd August) </center>
|<center>'''Week 4''' (23-29 Aug) </center>
|-
|Monday
| /
| 2
| /
| 14
|-
|Tuesday
| /
| 8
| /
| 14
|-
|Wednesday
| 7
| 9
| /
| 14
|-
|Thursday
| 5
| 8
| 7
| 14
|-
|Friday
| 8
| 8
| 8
| 12
|-
|Saturday
| /
| /
| /
| /
|-
|Sunday
| /
| /
| 2
| /
|-
|'''Total hours'''
| 20
| 35
| 17
| 68
|-
|}

Porcine Reproductive and Respiratory Syndrome

2010-08-27T20:07:23Z

Lizzies: /* References */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteritis and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is reduced as temperature rises.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virus then secondarily replicates in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acquire PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. The tropism for macrophages impairs the cellular immune response, and mucosal surfaces are also damaged. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistence of infection occurs despite this.

==Diagnosis==

In the field, suspicion of PRRS is based on clinical signs of reproductive failure and high levels of neonatal mortality. Farm records may provide useful information for confirming reproductive failure.

The differential diagnoses for PRRS include those of respiratory and reproductive signs. Respiratory differentials include swine influenza, enzootic pneumonia, ''Haemophilus parasuis'' infection, porcine respiratory coronavirus and porcine circovirus-associated disease. Reproductive differentials include porcine parvovirus, porcine enterovirus, and Aujesky's disease.

===Clinical Signs===
[[Image:Blue Eared Pig.jpg|thumb|righ|200px|A pig with PRRS, showing blue ears. Source: Wikimedia Commons; Author: Dingar (2007)]]
There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. Occasionally, the snout, ears and vulva can appear blue. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. In order for meaningful results to be generated, serum should be collected from around 20 exposed animals in the herds. Both of the ELISA and the IFAT tests measure antibodies against PRRS virus. Anti-PRRS specific IgM can be detected within 7 days of infection, and IgG can be detected within 14 days. Titres peak about 5–6 weeks after infection, and can persist for up to 144 days while circulating virus is present. Once virus ceases to circulate, antibody levels quickly drop. If titres are particularly high, exposure may be recent exposure and the sampled population could currently be shedding virus.

Tests for the PRRS virus itself also exist. These include RT-PCR and virus isolation. For virus isolation, buffy coat, serum, lung, lymph nodes, spleen and tonsils are the specimens of choice. The virus is incubated with swine pulmonary alveolar macrophages, and cytopathic effect are seen in around four days. RT-PCR can be performed on whole blood, buffy coat and clarified homogenates of the tissues appropriate for virus isolation. The test is particularly useful for examination of mummified or aborted litters. Immunohistochemistry is also possible, and nucleic acid sequencing of the 5' end of the virus has recently become commercially available. This is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

===Pathology===

Although PRRS virus is capable of infection many organs of the pig, but gross lesions are usually only observed in the respiratory and lymphoid tissues. Both gross and microscopic lesions are most marked in neonatal and young weaned pigs.

After an uncomplicated PRRS infection in finishing pigs, gross lesions can vary from unremarkable to severe. In severe disease, lungs are mottled red and tan, and fail to collapse properly. The cranioventral lobes are worst affected. Lymph nodes appear moderately to severely enlarged, tan in colour and may be haemorrhagic with some strains of virus. Most PRRS virus-infected pigs are co-infected with one or more secondary pathogens, so pathology can vary quite widely depending on these. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn foetuses, but histopathology inconsistently reveals interstitial pneumonia, myocarditis and pulmonary arteritis. However, these changes are neither specific nor diagnostic for PRRS.

==Treatment and Control==

There is currently no known effective treatment for PRRS. Non-steoidal anti-inflammatory drugs have been used in an attempt to reduce fever, and appetite stimulants to counteract inappetance and poor weight gain. However, these appear to have minimal benefit. Antibiotics may be used to counteract secondary bacterial infections.

As treatment for PRRS is ineffective, prevention is very important. In herds where PRRS is not present, bought-in stock and semen should be PRRS-free, and any animals joining the herd should be quantined on-site before being introduced to the cohort. Pigs should be tested on arrival to the unit, and again 45-60 days later before they join the main herd. In herds where PRRS is endemic, breeding gilts may be exposed to adult sows before they becomre pregnant in order to induce immunity. Existing infection can also be elimitated by multisite production and segregated early weaning, but the long-term risk of reinfection is high. Complete depopulationn, disinfection and repopulation can also be successful, as can test-and-removal strategies.

Both modified live and killed vaccines are available. These are effective in controlling outbreaks and preventing economic losses.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]
*[http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/54100.htm The Merck Veterinary Manual - Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) [http://www.oie.int/downld/Doc_OIE/PRRS_guide_web_bulletin.pdf PRRS: the disease, its diagnosis, prevention and control.] ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W (2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:To_Do_-_Review]][[Category:Respiratory_Viral_Infections]]

File:Blue Eared Pig.jpg

2010-08-27T20:05:37Z

Lizzies: {{Information |Description=A pig with PRRS showing blue ears. |Source=Wikimedia Commons |Date=Orginally uploaded to Wikimedia Commons 31st December 2007. Uploaded to WikiVet 27th August 2010. |Author=Dingar |Permission=See below }}

== Summary ==
{{Information
|Description=A pig with PRRS showing blue ears.
|Source=Wikimedia Commons
|Date=Orginally uploaded to Wikimedia Commons 31st December 2007. Uploaded to WikiVet 27th August 2010.
|Author=Dingar
|Permission=See below
}}

== Licensing ==
{{cc-att-2.0}}

Porcine Reproductive and Respiratory Syndrome

2010-08-27T20:02:34Z

Lizzies: /* Clinical Signs */

Blue Eared Pig Disease

2010-08-27T19:59:55Z

Lizzies: Redirected page to Porcine Reproductive and Respiratory Syndrome

#REDIRECT[[Porcine Reproductive and Respiratory Syndrome]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:58:51Z

Lizzies: /* References */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteritis and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is reduced as temperature rises.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virus then secondarily replicates in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acquire PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. The tropism for macrophages impairs the cellular immune response, and mucosal surfaces are also damaged. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistence of infection occurs despite this.

==Diagnosis==

In the field, suspicion of PRRS is based on clinical signs of reproductive failure and high levels of neonatal mortality. Farm records may provide useful information for confirming reproductive failure.

The differential diagnoses for PRRS include those of respiratory and reproductive signs. Respiratory differentials include swine influenza, enzootic pneumonia, ''Haemophilus parasuis'' infection, porcine respiratory coronavirus and porcine circovirus-associated disease. Reproductive differentials include porcine parvovirus, porcine enterovirus, and Aujesky's disease.

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. In order for meaningful results to be generated, serum should be collected from around 20 exposed animals in the herds. Both of the ELISA and the IFAT tests measure antibodies against PRRS virus. Anti-PRRS specific IgM can be detected within 7 days of infection, and IgG can be detected within 14 days. Titres peak about 5–6 weeks after infection, and can persist for up to 144 days while circulating virus is present. Once virus ceases to circulate, antibody levels quickly drop. If titres are particularly high, exposure may be recent exposure and the sampled population could currently be shedding virus.

Tests for the PRRS virus itself also exist. These include RT-PCR and virus isolation. For virus isolation, buffy coat, serum, lung, lymph nodes, spleen and tonsils are the specimens of choice. The virus is incubated with swine pulmonary alveolar macrophages, and cytopathic effect are seen in around four days. RT-PCR can be performed on whole blood, buffy coat and clarified homogenates of the tissues appropriate for virus isolation. The test is particularly useful for examination of mummified or aborted litters. Immunohistochemistry is also possible, and nucleic acid sequencing of the 5' end of the virus has recently become commercially available. This is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

===Pathology===

Although PRRS virus is capable of infection many organs of the pig, but gross lesions are usually only observed in the respiratory and lymphoid tissues. Both gross and microscopic lesions are most marked in neonatal and young weaned pigs.

After an uncomplicated PRRS infection in finishing pigs, gross lesions can vary from unremarkable to severe. In severe disease, lungs are mottled red and tan, and fail to collapse properly. The cranioventral lobes are worst affected. Lymph nodes appear moderately to severely enlarged, tan in colour and may be haemorrhagic with some strains of virus. Most PRRS virus-infected pigs are co-infected with one or more secondary pathogens, so pathology can vary quite widely depending on these. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn foetuses, but histopathology inconsistently reveals interstitial pneumonia, myocarditis and pulmonary arteritis. However, these changes are neither specific nor diagnostic for PRRS.

==Treatment and Control==

There is currently no known effective treatment for PRRS. Non-steoidal anti-inflammatory drugs have been used in an attempt to reduce fever, and appetite stimulants to counteract inappetance and poor weight gain. However, these appear to have minimal benefit. Antibiotics may be used to counteract secondary bacterial infections.

As treatment for PRRS is ineffective, prevention is very important. In herds where PRRS is not present, bought-in stock and semen should be PRRS-free, and any animals joining the herd should be quantined on-site before being introduced to the cohort. Pigs should be tested on arrival to the unit, and again 45-60 days later before they join the main herd. In herds where PRRS is endemic, breeding gilts may be exposed to adult sows before they becomre pregnant in order to induce immunity. Existing infection can also be elimitated by multisite production and segregated early weaning, but the long-term risk of reinfection is high. Complete depopulationn, disinfection and repopulation can also be successful, as can test-and-removal strategies.

Both modified live and killed vaccines are available. These are effective in controlling outbreaks and preventing economic losses.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]
*[http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/54100.htm The Merck Veterinary Manual - Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) [http://www.oie.int/downld/Doc_OIE/PRRS_guide_web_bulletin.pdf PRRS: the disease, its diagnosis, prevention and control.] ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W (2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:58:26Z

Lizzies: /* Links */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteritis and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is reduced as temperature rises.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virus then secondarily replicates in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acquire PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. The tropism for macrophages impairs the cellular immune response, and mucosal surfaces are also damaged. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistence of infection occurs despite this.

==Diagnosis==

In the field, suspicion of PRRS is based on clinical signs of reproductive failure and high levels of neonatal mortality. Farm records may provide useful information for confirming reproductive failure.

The differential diagnoses for PRRS include those of respiratory and reproductive signs. Respiratory differentials include swine influenza, enzootic pneumonia, ''Haemophilus parasuis'' infection, porcine respiratory coronavirus and porcine circovirus-associated disease. Reproductive differentials include porcine parvovirus, porcine enterovirus, and Aujesky's disease.

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. In order for meaningful results to be generated, serum should be collected from around 20 exposed animals in the herds. Both of the ELISA and the IFAT tests measure antibodies against PRRS virus. Anti-PRRS specific IgM can be detected within 7 days of infection, and IgG can be detected within 14 days. Titres peak about 5–6 weeks after infection, and can persist for up to 144 days while circulating virus is present. Once virus ceases to circulate, antibody levels quickly drop. If titres are particularly high, exposure may be recent exposure and the sampled population could currently be shedding virus.

Tests for the PRRS virus itself also exist. These include RT-PCR and virus isolation. For virus isolation, buffy coat, serum, lung, lymph nodes, spleen and tonsils are the specimens of choice. The virus is incubated with swine pulmonary alveolar macrophages, and cytopathic effect are seen in around four days. RT-PCR can be performed on whole blood, buffy coat and clarified homogenates of the tissues appropriate for virus isolation. The test is particularly useful for examination of mummified or aborted litters. Immunohistochemistry is also possible, and nucleic acid sequencing of the 5' end of the virus has recently become commercially available. This is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

===Pathology===

Although PRRS virus is capable of infection many organs of the pig, but gross lesions are usually only observed in the respiratory and lymphoid tissues. Both gross and microscopic lesions are most marked in neonatal and young weaned pigs.

After an uncomplicated PRRS infection in finishing pigs, gross lesions can vary from unremarkable to severe. In severe disease, lungs are mottled red and tan, and fail to collapse properly. The cranioventral lobes are worst affected. Lymph nodes appear moderately to severely enlarged, tan in colour and may be haemorrhagic with some strains of virus. Most PRRS virus-infected pigs are co-infected with one or more secondary pathogens, so pathology can vary quite widely depending on these. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn foetuses, but histopathology inconsistently reveals interstitial pneumonia, myocarditis and pulmonary arteritis. However, these changes are neither specific nor diagnostic for PRRS.

==Treatment and Control==

There is currently no known effective treatment for PRRS. Non-steoidal anti-inflammatory drugs have been used in an attempt to reduce fever, and appetite stimulants to counteract inappetance and poor weight gain. However, these appear to have minimal benefit. Antibiotics may be used to counteract secondary bacterial infections.

As treatment for PRRS is ineffective, prevention is very important. In herds where PRRS is not present, bought-in stock and semen should be PRRS-free, and any animals joining the herd should be quantined on-site before being introduced to the cohort. Pigs should be tested on arrival to the unit, and again 45-60 days later before they join the main herd. In herds where PRRS is endemic, breeding gilts may be exposed to adult sows before they becomre pregnant in order to induce immunity. Existing infection can also be elimitated by multisite production and segregated early weaning, but the long-term risk of reinfection is high. Complete depopulationn, disinfection and repopulation can also be successful, as can test-and-removal strategies.

Both modified live and killed vaccines are available. These are effective in controlling outbreaks and preventing economic losses.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]
*[http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/54100.htm The Merck Veterinary Manual - Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:58:14Z

Lizzies: /* Links */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteritis and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is reduced as temperature rises.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virus then secondarily replicates in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acquire PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. The tropism for macrophages impairs the cellular immune response, and mucosal surfaces are also damaged. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistence of infection occurs despite this.

==Diagnosis==

In the field, suspicion of PRRS is based on clinical signs of reproductive failure and high levels of neonatal mortality. Farm records may provide useful information for confirming reproductive failure.

The differential diagnoses for PRRS include those of respiratory and reproductive signs. Respiratory differentials include swine influenza, enzootic pneumonia, ''Haemophilus parasuis'' infection, porcine respiratory coronavirus and porcine circovirus-associated disease. Reproductive differentials include porcine parvovirus, porcine enterovirus, and Aujesky's disease.

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. In order for meaningful results to be generated, serum should be collected from around 20 exposed animals in the herds. Both of the ELISA and the IFAT tests measure antibodies against PRRS virus. Anti-PRRS specific IgM can be detected within 7 days of infection, and IgG can be detected within 14 days. Titres peak about 5–6 weeks after infection, and can persist for up to 144 days while circulating virus is present. Once virus ceases to circulate, antibody levels quickly drop. If titres are particularly high, exposure may be recent exposure and the sampled population could currently be shedding virus.

Tests for the PRRS virus itself also exist. These include RT-PCR and virus isolation. For virus isolation, buffy coat, serum, lung, lymph nodes, spleen and tonsils are the specimens of choice. The virus is incubated with swine pulmonary alveolar macrophages, and cytopathic effect are seen in around four days. RT-PCR can be performed on whole blood, buffy coat and clarified homogenates of the tissues appropriate for virus isolation. The test is particularly useful for examination of mummified or aborted litters. Immunohistochemistry is also possible, and nucleic acid sequencing of the 5' end of the virus has recently become commercially available. This is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

===Pathology===

Although PRRS virus is capable of infection many organs of the pig, but gross lesions are usually only observed in the respiratory and lymphoid tissues. Both gross and microscopic lesions are most marked in neonatal and young weaned pigs.

After an uncomplicated PRRS infection in finishing pigs, gross lesions can vary from unremarkable to severe. In severe disease, lungs are mottled red and tan, and fail to collapse properly. The cranioventral lobes are worst affected. Lymph nodes appear moderately to severely enlarged, tan in colour and may be haemorrhagic with some strains of virus. Most PRRS virus-infected pigs are co-infected with one or more secondary pathogens, so pathology can vary quite widely depending on these. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn foetuses, but histopathology inconsistently reveals interstitial pneumonia, myocarditis and pulmonary arteritis. However, these changes are neither specific nor diagnostic for PRRS.

==Treatment and Control==

There is currently no known effective treatment for PRRS. Non-steoidal anti-inflammatory drugs have been used in an attempt to reduce fever, and appetite stimulants to counteract inappetance and poor weight gain. However, these appear to have minimal benefit. Antibiotics may be used to counteract secondary bacterial infections.

As treatment for PRRS is ineffective, prevention is very important. In herds where PRRS is not present, bought-in stock and semen should be PRRS-free, and any animals joining the herd should be quantined on-site before being introduced to the cohort. Pigs should be tested on arrival to the unit, and again 45-60 days later before they join the main herd. In herds where PRRS is endemic, breeding gilts may be exposed to adult sows before they becomre pregnant in order to induce immunity. Existing infection can also be elimitated by multisite production and segregated early weaning, but the long-term risk of reinfection is high. Complete depopulationn, disinfection and repopulation can also be successful, as can test-and-removal strategies.

Both modified live and killed vaccines are available. These are effective in controlling outbreaks and preventing economic losses.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]
*[http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/54100.htm The Merck Veterinary Manual - Porcine Reproductive and Respiratory Syndrome}

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:56:53Z

Lizzies: /* Pathology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteritis and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is reduced as temperature rises.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virus then secondarily replicates in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acquire PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. The tropism for macrophages impairs the cellular immune response, and mucosal surfaces are also damaged. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistence of infection occurs despite this.

==Diagnosis==

In the field, suspicion of PRRS is based on clinical signs of reproductive failure and high levels of neonatal mortality. Farm records may provide useful information for confirming reproductive failure.

The differential diagnoses for PRRS include those of respiratory and reproductive signs. Respiratory differentials include swine influenza, enzootic pneumonia, ''Haemophilus parasuis'' infection, porcine respiratory coronavirus and porcine circovirus-associated disease. Reproductive differentials include porcine parvovirus, porcine enterovirus, and Aujesky's disease.

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. In order for meaningful results to be generated, serum should be collected from around 20 exposed animals in the herds. Both of the ELISA and the IFAT tests measure antibodies against PRRS virus. Anti-PRRS specific IgM can be detected within 7 days of infection, and IgG can be detected within 14 days. Titres peak about 5–6 weeks after infection, and can persist for up to 144 days while circulating virus is present. Once virus ceases to circulate, antibody levels quickly drop. If titres are particularly high, exposure may be recent exposure and the sampled population could currently be shedding virus.

Tests for the PRRS virus itself also exist. These include RT-PCR and virus isolation. For virus isolation, buffy coat, serum, lung, lymph nodes, spleen and tonsils are the specimens of choice. The virus is incubated with swine pulmonary alveolar macrophages, and cytopathic effect are seen in around four days. RT-PCR can be performed on whole blood, buffy coat and clarified homogenates of the tissues appropriate for virus isolation. The test is particularly useful for examination of mummified or aborted litters. Immunohistochemistry is also possible, and nucleic acid sequencing of the 5' end of the virus has recently become commercially available. This is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

===Pathology===

Although PRRS virus is capable of infection many organs of the pig, but gross lesions are usually only observed in the respiratory and lymphoid tissues. Both gross and microscopic lesions are most marked in neonatal and young weaned pigs.

After an uncomplicated PRRS infection in finishing pigs, gross lesions can vary from unremarkable to severe. In severe disease, lungs are mottled red and tan, and fail to collapse properly. The cranioventral lobes are worst affected. Lymph nodes appear moderately to severely enlarged, tan in colour and may be haemorrhagic with some strains of virus. Most PRRS virus-infected pigs are co-infected with one or more secondary pathogens, so pathology can vary quite widely depending on these. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn foetuses, but histopathology inconsistently reveals interstitial pneumonia, myocarditis and pulmonary arteritis. However, these changes are neither specific nor diagnostic for PRRS.

==Treatment and Control==

There is currently no known effective treatment for PRRS. Non-steoidal anti-inflammatory drugs have been used in an attempt to reduce fever, and appetite stimulants to counteract inappetance and poor weight gain. However, these appear to have minimal benefit. Antibiotics may be used to counteract secondary bacterial infections.

As treatment for PRRS is ineffective, prevention is very important. In herds where PRRS is not present, bought-in stock and semen should be PRRS-free, and any animals joining the herd should be quantined on-site before being introduced to the cohort. Pigs should be tested on arrival to the unit, and again 45-60 days later before they join the main herd. In herds where PRRS is endemic, breeding gilts may be exposed to adult sows before they becomre pregnant in order to induce immunity. Existing infection can also be elimitated by multisite production and segregated early weaning, but the long-term risk of reinfection is high. Complete depopulationn, disinfection and repopulation can also be successful, as can test-and-removal strategies.

Both modified live and killed vaccines are available. These are effective in controlling outbreaks and preventing economic losses.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:56:40Z

Lizzies: /* Pathology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteritis and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is reduced as temperature rises.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virus then secondarily replicates in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acquire PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. The tropism for macrophages impairs the cellular immune response, and mucosal surfaces are also damaged. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistence of infection occurs despite this.

==Diagnosis==

In the field, suspicion of PRRS is based on clinical signs of reproductive failure and high levels of neonatal mortality. Farm records may provide useful information for confirming reproductive failure.

The differential diagnoses for PRRS include those of respiratory and reproductive signs. Respiratory differentials include swine influenza, enzootic pneumonia, ''Haemophilus parasuis'' infection, porcine respiratory coronavirus and porcine circovirus-associated disease. Reproductive differentials include porcine parvovirus, porcine enterovirus, and Aujesky's disease.

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. In order for meaningful results to be generated, serum should be collected from around 20 exposed animals in the herds. Both of the ELISA and the IFAT tests measure antibodies against PRRS virus. Anti-PRRS specific IgM can be detected within 7 days of infection, and IgG can be detected within 14 days. Titres peak about 5–6 weeks after infection, and can persist for up to 144 days while circulating virus is present. Once virus ceases to circulate, antibody levels quickly drop. If titres are particularly high, exposure may be recent exposure and the sampled population could currently be shedding virus.

Tests for the PRRS virus itself also exist. These include RT-PCR and virus isolation. For virus isolation, buffy coat, serum, lung, lymph nodes, spleen and tonsils are the specimens of choice. The virus is incubated with swine pulmonary alveolar macrophages, and cytopathic effect are seen in around four days. RT-PCR can be performed on whole blood, buffy coat and clarified homogenates of the tissues appropriate for virus isolation. The test is particularly useful for examination of mummified or aborted litters. Immunohistochemistry is also possible, and nucleic acid sequencing of the 5' end of the virus has recently become commercially available. This is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

==Pathology==

Although PRRS virus is capable of infection many organs of the pig, but gross lesions are usually only observed in the respiratory and lymphoid tissues. Both gross and microscopic lesions are most marked in neonatal and young weaned pigs.

After an uncomplicated PRRS infection in finishing pigs, gross lesions can vary from unremarkable to severe. In severe disease, lungs are mottled red and tan, and fail to collapse properly. The cranioventral lobes are worst affected. Lymph nodes appear moderately to severely enlarged, tan in colour and may be haemorrhagic with some strains of virus. Most PRRS virus-infected pigs are co-infected with one or more secondary pathogens, so pathology can vary quite widely depending on these. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn foetuses, but histopathology inconsistently reveals interstitial pneumonia, myocarditis and pulmonary arteritis. However, these changes are neither specific nor diagnostic for PRRS.

==Treatment and Control==

There is currently no known effective treatment for PRRS. Non-steoidal anti-inflammatory drugs have been used in an attempt to reduce fever, and appetite stimulants to counteract inappetance and poor weight gain. However, these appear to have minimal benefit. Antibiotics may be used to counteract secondary bacterial infections.

As treatment for PRRS is ineffective, prevention is very important. In herds where PRRS is not present, bought-in stock and semen should be PRRS-free, and any animals joining the herd should be quantined on-site before being introduced to the cohort. Pigs should be tested on arrival to the unit, and again 45-60 days later before they join the main herd. In herds where PRRS is endemic, breeding gilts may be exposed to adult sows before they becomre pregnant in order to induce immunity. Existing infection can also be elimitated by multisite production and segregated early weaning, but the long-term risk of reinfection is high. Complete depopulationn, disinfection and repopulation can also be successful, as can test-and-removal strategies.

Both modified live and killed vaccines are available. These are effective in controlling outbreaks and preventing economic losses.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:56:17Z

Lizzies: /* Treatment and Control */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteritis and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is reduced as temperature rises.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virus then secondarily replicates in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acquire PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. The tropism for macrophages impairs the cellular immune response, and mucosal surfaces are also damaged. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistence of infection occurs despite this.

==Diagnosis==

In the field, suspicion of PRRS is based on clinical signs of reproductive failure and high levels of neonatal mortality. Farm records may provide useful information for confirming reproductive failure.

The differential diagnoses for PRRS include those of respiratory and reproductive signs. Respiratory differentials include swine influenza, enzootic pneumonia, ''Haemophilus parasuis'' infection, porcine respiratory coronavirus and porcine circovirus-associated disease. Reproductive differentials include porcine parvovirus, porcine enterovirus, and Aujesky's disease.

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. In order for meaningful results to be generated, serum should be collected from around 20 exposed animals in the herds. Both of the ELISA and the IFAT tests measure antibodies against PRRS virus. Anti-PRRS specific IgM can be detected within 7 days of infection, and IgG can be detected within 14 days. Titres peak about 5–6 weeks after infection, and can persist for up to 144 days while circulating virus is present. Once virus ceases to circulate, antibody levels quickly drop. If titres are particularly high, exposure may be recent exposure and the sampled population could currently be shedding virus.

Tests for the PRRS virus itself also exist. These include RT-PCR and virus isolation. For virus isolation, buffy coat, serum, lung, lymph nodes, spleen and tonsils are the specimens of choice. The virus is incubated with swine pulmonary alveolar macrophages, and cytopathic effect are seen in around four days. RT-PCR can be performed on whole blood, buffy coat and clarified homogenates of the tissues appropriate for virus isolation. The test is particularly useful for examination of mummified or aborted litters. Immunohistochemistry is also possible, and nucleic acid sequencing of the 5' end of the virus has recently become commercially available. This is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

==Pathology==

Although PRRS virus is capable of infection many organs of the pig, but gross lesions are usually only observed in the respiratory and lymphoid tissues. Both gross and microscopic lesions are most marked in neonatal and young weaned pigs.

After an uncomplicated PRRS infection in finishing pigs, gross lesions can vary from unremarkable to severe. In severe disease, lungs are mottled red and tan, and fail to collapse properly. The cranioventral lobes are worst affected. Lymph nodes appear moderately to severely enlarged, tan in colour and may be haemorrhagic with some strains of virus. Most PRRS virus-infected pigs are co-infected with one or more secondary pathogens, so pathology can vary quite widely depending on these. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn fetuses, but histopathology inconsistently reveals interstitial pneumonia, myocarditis and pulmonary arteritis. However, these changes are neither specific nor diagnostic for PRRS.

==Treatment and Control==

There is currently no known effective treatment for PRRS. Non-steoidal anti-inflammatory drugs have been used in an attempt to reduce fever, and appetite stimulants to counteract inappetance and poor weight gain. However, these appear to have minimal benefit. Antibiotics may be used to counteract secondary bacterial infections.

As treatment for PRRS is ineffective, prevention is very important. In herds where PRRS is not present, bought-in stock and semen should be PRRS-free, and any animals joining the herd should be quantined on-site before being introduced to the cohort. Pigs should be tested on arrival to the unit, and again 45-60 days later before they join the main herd. In herds where PRRS is endemic, breeding gilts may be exposed to adult sows before they becomre pregnant in order to induce immunity. Existing infection can also be elimitated by multisite production and segregated early weaning, but the long-term risk of reinfection is high. Complete depopulationn, disinfection and repopulation can also be successful, as can test-and-removal strategies.

Both modified live and killed vaccines are available. These are effective in controlling outbreaks and preventing economic losses.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:51:50Z

Lizzies: /* Control */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteritis and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is reduced as temperature rises.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virus then secondarily replicates in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acquire PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. The tropism for macrophages impairs the cellular immune response, and mucosal surfaces are also damaged. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistence of infection occurs despite this.

==Diagnosis==

In the field, suspicion of PRRS is based on clinical signs of reproductive failure and high levels of neonatal mortality. Farm records may provide useful information for confirming reproductive failure.

The differential diagnoses for PRRS include those of respiratory and reproductive signs. Respiratory differentials include swine influenza, enzootic pneumonia, ''Haemophilus parasuis'' infection, porcine respiratory coronavirus and porcine circovirus-associated disease. Reproductive differentials include porcine parvovirus, porcine enterovirus, and Aujesky's disease.

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. In order for meaningful results to be generated, serum should be collected from around 20 exposed animals in the herds. Both of the ELISA and the IFAT tests measure antibodies against PRRS virus. Anti-PRRS specific IgM can be detected within 7 days of infection, and IgG can be detected within 14 days. Titres peak about 5–6 weeks after infection, and can persist for up to 144 days while circulating virus is present. Once virus ceases to circulate, antibody levels quickly drop. If titres are particularly high, exposure may be recent exposure and the sampled population could currently be shedding virus.

Tests for the PRRS virus itself also exist. These include RT-PCR and virus isolation. For virus isolation, buffy coat, serum, lung, lymph nodes, spleen and tonsils are the specimens of choice. The virus is incubated with swine pulmonary alveolar macrophages, and cytopathic effect are seen in around four days. RT-PCR can be performed on whole blood, buffy coat and clarified homogenates of the tissues appropriate for virus isolation. The test is particularly useful for examination of mummified or aborted litters. Immunohistochemistry is also possible, and nucleic acid sequencing of the 5' end of the virus has recently become commercially available. This is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

==Pathology==

Although PRRS virus is capable of infection many organs of the pig, but gross lesions are usually only observed in the respiratory and lymphoid tissues. Both gross and microscopic lesions are most marked in neonatal and young weaned pigs.

After an uncomplicated PRRS infection in finishing pigs, gross lesions can vary from unremarkable to severe. In severe disease, lungs are mottled red and tan, and fail to collapse properly. The cranioventral lobes are worst affected. Lymph nodes appear moderately to severely enlarged, tan in colour and may be haemorrhagic with some strains of virus. Most PRRS virus-infected pigs are co-infected with one or more secondary pathogens, so pathology can vary quite widely depending on these. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn fetuses, but histopathology inconsistently reveals interstitial pneumonia, myocarditis and pulmonary arteritis. However, these changes are neither specific nor diagnostic for PRRS.

==Treatment and Control==

There is currently no known effective treatment for PRRS. Non-steoidal anti-inflammatory drugs have been used in an attempt to reduce fever, and appetite stimulants to counteract inappetance and poor weight gain. However, these appear to have minimal benefit. Antibiotics may be used to counteract secondary bacterial infections.

As treatment for PRRS is ineffective, prevention is very important. Bought-in stock and semen should be PRRS-free, and any animals joining the herd should be quantined on-site before being introduced to the cohort. Pigs should be tested on arrival to the unit, and again 45-60 days later before they join the main herd.
Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:47:01Z

Lizzies: /* Pathology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteritis and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is reduced as temperature rises.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virus then secondarily replicates in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acquire PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. The tropism for macrophages impairs the cellular immune response, and mucosal surfaces are also damaged. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistence of infection occurs despite this.

==Diagnosis==

In the field, suspicion of PRRS is based on clinical signs of reproductive failure and high levels of neonatal mortality. Farm records may provide useful information for confirming reproductive failure.

The differential diagnoses for PRRS include those of respiratory and reproductive signs. Respiratory differentials include swine influenza, enzootic pneumonia, ''Haemophilus parasuis'' infection, porcine respiratory coronavirus and porcine circovirus-associated disease. Reproductive differentials include porcine parvovirus, porcine enterovirus, and Aujesky's disease.

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. In order for meaningful results to be generated, serum should be collected from around 20 exposed animals in the herds. Both of the ELISA and the IFAT tests measure antibodies against PRRS virus. Anti-PRRS specific IgM can be detected within 7 days of infection, and IgG can be detected within 14 days. Titres peak about 5–6 weeks after infection, and can persist for up to 144 days while circulating virus is present. Once virus ceases to circulate, antibody levels quickly drop. If titres are particularly high, exposure may be recent exposure and the sampled population could currently be shedding virus.

Tests for the PRRS virus itself also exist. These include RT-PCR and virus isolation. For virus isolation, buffy coat, serum, lung, lymph nodes, spleen and tonsils are the specimens of choice. The virus is incubated with swine pulmonary alveolar macrophages, and cytopathic effect are seen in around four days. RT-PCR can be performed on whole blood, buffy coat and clarified homogenates of the tissues appropriate for virus isolation. The test is particularly useful for examination of mummified or aborted litters. Immunohistochemistry is also possible, and nucleic acid sequencing of the 5' end of the virus has recently become commercially available. This is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

==Pathology==

Although PRRS virus is capable of infection many organs of the pig, but gross lesions are usually only observed in the respiratory and lymphoid tissues. Both gross and microscopic lesions are most marked in neonatal and young weaned pigs.

After an uncomplicated PRRS infection in finishing pigs, gross lesions can vary from unremarkable to severe. In severe disease, lungs are mottled red and tan, and fail to collapse properly. The cranioventral lobes are worst affected. Lymph nodes appear moderately to severely enlarged, tan in colour and may be haemorrhagic with some strains of virus. Most PRRS virus-infected pigs are co-infected with one or more secondary pathogens, so pathology can vary quite widely depending on these. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn fetuses, but histopathology inconsistently reveals interstitial pneumonia, myocarditis and pulmonary arteritis. However, these changes are neither specific nor diagnostic for PRRS.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:42:46Z

Lizzies: /* Laboratory Tests */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteritis and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is reduced as temperature rises.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virus then secondarily replicates in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acquire PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. The tropism for macrophages impairs the cellular immune response, and mucosal surfaces are also damaged. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistence of infection occurs despite this.

==Diagnosis==

In the field, suspicion of PRRS is based on clinical signs of reproductive failure and high levels of neonatal mortality. Farm records may provide useful information for confirming reproductive failure.

The differential diagnoses for PRRS include those of respiratory and reproductive signs. Respiratory differentials include swine influenza, enzootic pneumonia, ''Haemophilus parasuis'' infection, porcine respiratory coronavirus and porcine circovirus-associated disease. Reproductive differentials include porcine parvovirus, porcine enterovirus, and Aujesky's disease.

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. In order for meaningful results to be generated, serum should be collected from around 20 exposed animals in the herds. Both of the ELISA and the IFAT tests measure antibodies against PRRS virus. Anti-PRRS specific IgM can be detected within 7 days of infection, and IgG can be detected within 14 days. Titres peak about 5–6 weeks after infection, and can persist for up to 144 days while circulating virus is present. Once virus ceases to circulate, antibody levels quickly drop. If titres are particularly high, exposure may be recent exposure and the sampled population could currently be shedding virus.

Tests for the PRRS virus itself also exist. These include RT-PCR and virus isolation. For virus isolation, buffy coat, serum, lung, lymph nodes, spleen and tonsils are the specimens of choice. The virus is incubated with swine pulmonary alveolar macrophages, and cytopathic effect are seen in around four days. RT-PCR can be performed on whole blood, buffy coat and clarified homogenates of the tissues appropriate for virus isolation. The test is particularly useful for examination of mummified or aborted litters. Immunohistochemistry is also possible, and nucleic acid sequencing of the 5' end of the virus has recently become commercially available. This is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

==Pathology==

PRRS virus produces a multisystemic infection in pigs, but gross lesions are usually only observed in
respiratory and lymphoid tissues. Both gross and microscopic lesions are most marked in neonatal and young
weaned pigs. The gross pathology observed after uncomplicated infection of PRRS virus in finishing pigs may
be anything from severe to unremarkable.
In severe disease, lungs are mottled, tan and red, and fail to collapse; the cranioventral lobes are most affected.
Lymph nodes are moderately to severely enlarged and tan in colour and, for some strains of virus, may be
haemorrhagic. Under field conditions, most PRRS virus infected pigs are co-infected with one or more
pathogens, which complicates the diagnosis of PRRS based on pathology.

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn fetuses, but histopathology inconsistently interstitial pneumonia, myocarditis anr pulmonary arteritis. However, these changes are not specific or diagnostic for PRRS.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:38:39Z

Lizzies: /* Laboratory Tests */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteritis and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is reduced as temperature rises.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virus then secondarily replicates in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acquire PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. The tropism for macrophages impairs the cellular immune response, and mucosal surfaces are also damaged. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistence of infection occurs despite this.

==Diagnosis==

In the field, suspicion of PRRS is based on clinical signs of reproductive failure and high levels of neonatal mortality. Farm records may provide useful information for confirming reproductive failure.

The differential diagnoses for PRRS include those of respiratory and reproductive signs. Respiratory differentials include swine influenza, enzootic pneumonia, ''Haemophilus parasuis'' infection, porcine respiratory coronavirus and porcine circovirus-associated disease. Reproductive differentials include porcine parvovirus, porcine enterovirus, and Aujesky's disease.

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. In order for meaningful results to be generated, serum should be collected from around 20 exposed animals in the herds. Both of the ELISA and the IFAT tests measure antibodies against PRRS virus. Anti-PRRS specific IgM can be detected within 7 days of infection, and IgG can be detected within 14 days. Titres peak about 5–6 weeks after infection, and can persist for up to 144 days while circulating virus is present. Once virus ceases to circulate, antibody levels quickly drop. If titres are particularly high, exposure may be recent exposure and the sampled population could currently be shedding virus.

Tests for the PRRS virus itself also exist. These include PCR and virus isolation on clinical samples, and immunohistochemistry on tissues. Nucleic acid sequencing of the 5' end of the virus is commercially availabe ans is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

The following specimens should be collected.
– For virus isolation and RT-PCR — whole blood (EDTA) and also serum, lung, respiratory tract, spleen
and tonsils of affected animals. Samples from mummified or aborted litters are unlikely to yield virus, but can
still be useful for RT-PCR.
􀂃 Virus isolation
Buffy coat, serum, lung, lymph nodes, spleen and tonsils are the specimens of choice. The virus
replicates well on swine pulmonary alveolar macrophages and some strains, particularly those of
genotype 2, on Marc 145 cells. Cytopathic effects are evident in 1–4 days. Perform two 7-day
passages for maximum sensitivity.
􀂃 RT-PCR
Whole blood (EDTA), buffy coat and clarified homogenates of the above tissues are best. At this
time, there is no fully validated PCR that has international acceptability. Please consult the OIE
Manual for suggested methods.

==Pathology==

PRRS virus produces a multisystemic infection in pigs, but gross lesions are usually only observed in
respiratory and lymphoid tissues. Both gross and microscopic lesions are most marked in neonatal and young
weaned pigs. The gross pathology observed after uncomplicated infection of PRRS virus in finishing pigs may
be anything from severe to unremarkable.
In severe disease, lungs are mottled, tan and red, and fail to collapse; the cranioventral lobes are most affected.
Lymph nodes are moderately to severely enlarged and tan in colour and, for some strains of virus, may be
haemorrhagic. Under field conditions, most PRRS virus infected pigs are co-infected with one or more
pathogens, which complicates the diagnosis of PRRS based on pathology.

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn fetuses, but histopathology inconsistently interstitial pneumonia, myocarditis anr pulmonary arteritis. However, these changes are not specific or diagnostic for PRRS.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:34:03Z

Lizzies: /* Aetiology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteritis and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is reduced as temperature rises.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virus then secondarily replicates in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acquire PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. The tropism for macrophages impairs the cellular immune response, and mucosal surfaces are also damaged. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistence of infection occurs despite this.

==Diagnosis==

In the field, suspicion of PRRS is based on clinical signs of reproductive failure and high levels of neonatal mortality. Farm records may provide useful information for confirming reproductive failure.

The differential diagnoses for PRRS include those of respiratory and reproductive signs. Respiratory differentials include swine influenza, enzootic pneumonia, ''Haemophilus parasuis'' infection, porcine respiratory coronavirus and porcine circovirus-associated disease. Reproductive differentials include porcine parvovirus, porcine enterovirus, and Aujesky's disease.

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. Both of these tests measure IgG antibodies against PRRS virus, which can be detected from 7-10 days post-infection. Titres persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population.

Tests for the PRRS virus itself also exist. These include PCR and virus isolation on clinical samples, and immunohistochemistry on tissues. Nucleic acid sequencing of the 5' end of the virus is commercially availabe ans is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

The following specimens should be collected.
– For virus isolation and RT-PCR — whole blood (EDTA) and also serum, lung, respiratory tract, spleen
and tonsils of affected animals. Samples from mummified or aborted litters are unlikely to yield virus, but can
still be useful for RT-PCR.
– For antibody testing (serology) — serum from up to 20 exposed animals in the herd.
Specimens should be chilled and forwarded unfrozen on water ice or with frozen gel packs.
􀂃 Virus isolation
Buffy coat, serum, lung, lymph nodes, spleen and tonsils are the specimens of choice. The virus
replicates well on swine pulmonary alveolar macrophages and some strains, particularly those of
genotype 2, on Marc 145 cells. Cytopathic effects are evident in 1–4 days. Perform two 7-day
passages for maximum sensitivity.
􀂃 RT-PCR
Whole blood (EDTA), buffy coat and clarified homogenates of the above tissues are best. At this
time, there is no fully validated PCR that has international acceptability. Please consult the OIE
Manual for suggested methods.
􀂃 Serological tests
IgM can be detected within 7 days of infection and IgG can be detected within 14 days. Humoral
antibody titres reach a maximum about 5–6 weeks after infection. Antibody can be detected by ELISA
and by the indirect staining of pre-prepared monolayers of infected cells (IPMA and IFA). Antibody
levels can drop quite quickly in the absence of circulating virus.

==Pathology==

PRRS virus produces a multisystemic infection in pigs, but gross lesions are usually only observed in
respiratory and lymphoid tissues. Both gross and microscopic lesions are most marked in neonatal and young
weaned pigs. The gross pathology observed after uncomplicated infection of PRRS virus in finishing pigs may
be anything from severe to unremarkable.
In severe disease, lungs are mottled, tan and red, and fail to collapse; the cranioventral lobes are most affected.
Lymph nodes are moderately to severely enlarged and tan in colour and, for some strains of virus, may be
haemorrhagic. Under field conditions, most PRRS virus infected pigs are co-infected with one or more
pathogens, which complicates the diagnosis of PRRS based on pathology.

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn fetuses, but histopathology inconsistently interstitial pneumonia, myocarditis anr pulmonary arteritis. However, these changes are not specific or diagnostic for PRRS.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:32:15Z

Lizzies: /* Pathogenesis */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virus then secondarily replicates in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acquire PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. The tropism for macrophages impairs the cellular immune response, and mucosal surfaces are also damaged. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistence of infection occurs despite this.

==Diagnosis==

In the field, suspicion of PRRS is based on clinical signs of reproductive failure and high levels of neonatal mortality. Farm records may provide useful information for confirming reproductive failure.

The differential diagnoses for PRRS include those of respiratory and reproductive signs. Respiratory differentials include swine influenza, enzootic pneumonia, ''Haemophilus parasuis'' infection, porcine respiratory coronavirus and porcine circovirus-associated disease. Reproductive differentials include porcine parvovirus, porcine enterovirus, and Aujesky's disease.

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. Both of these tests measure IgG antibodies against PRRS virus, which can be detected from 7-10 days post-infection. Titres persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population.

Tests for the PRRS virus itself also exist. These include PCR and virus isolation on clinical samples, and immunohistochemistry on tissues. Nucleic acid sequencing of the 5' end of the virus is commercially availabe ans is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

The following specimens should be collected.
– For virus isolation and RT-PCR — whole blood (EDTA) and also serum, lung, respiratory tract, spleen
and tonsils of affected animals. Samples from mummified or aborted litters are unlikely to yield virus, but can
still be useful for RT-PCR.
– For antibody testing (serology) — serum from up to 20 exposed animals in the herd.
Specimens should be chilled and forwarded unfrozen on water ice or with frozen gel packs.
􀂃 Virus isolation
Buffy coat, serum, lung, lymph nodes, spleen and tonsils are the specimens of choice. The virus
replicates well on swine pulmonary alveolar macrophages and some strains, particularly those of
genotype 2, on Marc 145 cells. Cytopathic effects are evident in 1–4 days. Perform two 7-day
passages for maximum sensitivity.
􀂃 RT-PCR
Whole blood (EDTA), buffy coat and clarified homogenates of the above tissues are best. At this
time, there is no fully validated PCR that has international acceptability. Please consult the OIE
Manual for suggested methods.
􀂃 Serological tests
IgM can be detected within 7 days of infection and IgG can be detected within 14 days. Humoral
antibody titres reach a maximum about 5–6 weeks after infection. Antibody can be detected by ELISA
and by the indirect staining of pre-prepared monolayers of infected cells (IPMA and IFA). Antibody
levels can drop quite quickly in the absence of circulating virus.

==Pathology==

PRRS virus produces a multisystemic infection in pigs, but gross lesions are usually only observed in
respiratory and lymphoid tissues. Both gross and microscopic lesions are most marked in neonatal and young
weaned pigs. The gross pathology observed after uncomplicated infection of PRRS virus in finishing pigs may
be anything from severe to unremarkable.
In severe disease, lungs are mottled, tan and red, and fail to collapse; the cranioventral lobes are most affected.
Lymph nodes are moderately to severely enlarged and tan in colour and, for some strains of virus, may be
haemorrhagic. Under field conditions, most PRRS virus infected pigs are co-infected with one or more
pathogens, which complicates the diagnosis of PRRS based on pathology.

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn fetuses, but histopathology inconsistently interstitial pneumonia, myocarditis anr pulmonary arteritis. However, these changes are not specific or diagnostic for PRRS.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:30:22Z

Lizzies: /* Diagnosis */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virs then seconarily replicated in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acqure PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistance of infection occurs despite this.

==Diagnosis==

In the field, suspicion of PRRS is based on clinical signs of reproductive failure and high levels of neonatal mortality. Farm records may provide useful information for confirming reproductive failure.

The differential diagnoses for PRRS include those of respiratory and reproductive signs. Respiratory differentials include swine influenza, enzootic pneumonia, ''Haemophilus parasuis'' infection, porcine respiratory coronavirus and porcine circovirus-associated disease. Reproductive differentials include porcine parvovirus, porcine enterovirus, and Aujesky's disease.

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. Both of these tests measure IgG antibodies against PRRS virus, which can be detected from 7-10 days post-infection. Titres persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population.

Tests for the PRRS virus itself also exist. These include PCR and virus isolation on clinical samples, and immunohistochemistry on tissues. Nucleic acid sequencing of the 5' end of the virus is commercially availabe ans is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

The following specimens should be collected.
– For virus isolation and RT-PCR — whole blood (EDTA) and also serum, lung, respiratory tract, spleen
and tonsils of affected animals. Samples from mummified or aborted litters are unlikely to yield virus, but can
still be useful for RT-PCR.
– For antibody testing (serology) — serum from up to 20 exposed animals in the herd.
Specimens should be chilled and forwarded unfrozen on water ice or with frozen gel packs.
􀂃 Virus isolation
Buffy coat, serum, lung, lymph nodes, spleen and tonsils are the specimens of choice. The virus
replicates well on swine pulmonary alveolar macrophages and some strains, particularly those of
genotype 2, on Marc 145 cells. Cytopathic effects are evident in 1–4 days. Perform two 7-day
passages for maximum sensitivity.
􀂃 RT-PCR
Whole blood (EDTA), buffy coat and clarified homogenates of the above tissues are best. At this
time, there is no fully validated PCR that has international acceptability. Please consult the OIE
Manual for suggested methods.
􀂃 Serological tests
IgM can be detected within 7 days of infection and IgG can be detected within 14 days. Humoral
antibody titres reach a maximum about 5–6 weeks after infection. Antibody can be detected by ELISA
and by the indirect staining of pre-prepared monolayers of infected cells (IPMA and IFA). Antibody
levels can drop quite quickly in the absence of circulating virus.

==Pathology==

PRRS virus produces a multisystemic infection in pigs, but gross lesions are usually only observed in
respiratory and lymphoid tissues. Both gross and microscopic lesions are most marked in neonatal and young
weaned pigs. The gross pathology observed after uncomplicated infection of PRRS virus in finishing pigs may
be anything from severe to unremarkable.
In severe disease, lungs are mottled, tan and red, and fail to collapse; the cranioventral lobes are most affected.
Lymph nodes are moderately to severely enlarged and tan in colour and, for some strains of virus, may be
haemorrhagic. Under field conditions, most PRRS virus infected pigs are co-infected with one or more
pathogens, which complicates the diagnosis of PRRS based on pathology.

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn fetuses, but histopathology inconsistently interstitial pneumonia, myocarditis anr pulmonary arteritis. However, these changes are not specific or diagnostic for PRRS.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:25:46Z

Lizzies: /* Diagnosis */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virs then seconarily replicated in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acqure PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistance of infection occurs despite this.

==Diagnosis==

In the field, suspicion of PRRS is based on clinical signs of reproductive failure and high levels of neonatal mortality. Farm records may provide useful information for confirming reproductive failure.

The differential diagnoses for PRRS include those of respiratory and reproductive signs.

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. Both of these tests measure IgG antibodies against PRRS virus, which can be detected from 7-10 days post-infection. Titres persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population.

Tests for the PRRS virus itself also exist. These include PCR and virus isolation on clinical samples, and immunohistochemistry on tissues. Nucleic acid sequencing of the 5' end of the virus is commercially availabe ans is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

The following specimens should be collected.
– For virus isolation and RT-PCR — whole blood (EDTA) and also serum, lung, respiratory tract, spleen
and tonsils of affected animals. Samples from mummified or aborted litters are unlikely to yield virus, but can
still be useful for RT-PCR.
– For antibody testing (serology) — serum from up to 20 exposed animals in the herd.
Specimens should be chilled and forwarded unfrozen on water ice or with frozen gel packs.
􀂃 Virus isolation
Buffy coat, serum, lung, lymph nodes, spleen and tonsils are the specimens of choice. The virus
replicates well on swine pulmonary alveolar macrophages and some strains, particularly those of
genotype 2, on Marc 145 cells. Cytopathic effects are evident in 1–4 days. Perform two 7-day
passages for maximum sensitivity.
􀂃 RT-PCR
Whole blood (EDTA), buffy coat and clarified homogenates of the above tissues are best. At this
time, there is no fully validated PCR that has international acceptability. Please consult the OIE
Manual for suggested methods.
􀂃 Serological tests
IgM can be detected within 7 days of infection and IgG can be detected within 14 days. Humoral
antibody titres reach a maximum about 5–6 weeks after infection. Antibody can be detected by ELISA
and by the indirect staining of pre-prepared monolayers of infected cells (IPMA and IFA). Antibody
levels can drop quite quickly in the absence of circulating virus.

==Pathology==

PRRS virus produces a multisystemic infection in pigs, but gross lesions are usually only observed in
respiratory and lymphoid tissues. Both gross and microscopic lesions are most marked in neonatal and young
weaned pigs. The gross pathology observed after uncomplicated infection of PRRS virus in finishing pigs may
be anything from severe to unremarkable.
In severe disease, lungs are mottled, tan and red, and fail to collapse; the cranioventral lobes are most affected.
Lymph nodes are moderately to severely enlarged and tan in colour and, for some strains of virus, may be
haemorrhagic. Under field conditions, most PRRS virus infected pigs are co-infected with one or more
pathogens, which complicates the diagnosis of PRRS based on pathology.

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn fetuses, but histopathology inconsistently interstitial pneumonia, myocarditis anr pulmonary arteritis. However, these changes are not specific or diagnostic for PRRS.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:24:06Z

Lizzies: /* Laboratory Tests */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virs then seconarily replicated in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acqure PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistance of infection occurs despite this.

==Diagnosis==

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. Both of these tests measure IgG antibodies against PRRS virus, which can be detected from 7-10 days post-infection. Titres persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population.

Tests for the PRRS virus itself also exist. These include PCR and virus isolation on clinical samples, and immunohistochemistry on tissues. Nucleic acid sequencing of the 5' end of the virus is commercially availabe ans is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

The following specimens should be collected.
– For virus isolation and RT-PCR — whole blood (EDTA) and also serum, lung, respiratory tract, spleen
and tonsils of affected animals. Samples from mummified or aborted litters are unlikely to yield virus, but can
still be useful for RT-PCR.
– For antibody testing (serology) — serum from up to 20 exposed animals in the herd.
Specimens should be chilled and forwarded unfrozen on water ice or with frozen gel packs.
􀂃 Virus isolation
Buffy coat, serum, lung, lymph nodes, spleen and tonsils are the specimens of choice. The virus
replicates well on swine pulmonary alveolar macrophages and some strains, particularly those of
genotype 2, on Marc 145 cells. Cytopathic effects are evident in 1–4 days. Perform two 7-day
passages for maximum sensitivity.
􀂃 RT-PCR
Whole blood (EDTA), buffy coat and clarified homogenates of the above tissues are best. At this
time, there is no fully validated PCR that has international acceptability. Please consult the OIE
Manual for suggested methods.
􀂃 Serological tests
IgM can be detected within 7 days of infection and IgG can be detected within 14 days. Humoral
antibody titres reach a maximum about 5–6 weeks after infection. Antibody can be detected by ELISA
and by the indirect staining of pre-prepared monolayers of infected cells (IPMA and IFA). Antibody
levels can drop quite quickly in the absence of circulating virus.

==Pathology==

PRRS virus produces a multisystemic infection in pigs, but gross lesions are usually only observed in
respiratory and lymphoid tissues. Both gross and microscopic lesions are most marked in neonatal and young
weaned pigs. The gross pathology observed after uncomplicated infection of PRRS virus in finishing pigs may
be anything from severe to unremarkable.
In severe disease, lungs are mottled, tan and red, and fail to collapse; the cranioventral lobes are most affected.
Lymph nodes are moderately to severely enlarged and tan in colour and, for some strains of virus, may be
haemorrhagic. Under field conditions, most PRRS virus infected pigs are co-infected with one or more
pathogens, which complicates the diagnosis of PRRS based on pathology.

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn fetuses, but histopathology inconsistently interstitial pneumonia, myocarditis anr pulmonary arteritis. However, these changes are not specific or diagnostic for PRRS.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:22:58Z

Lizzies: /* Pathology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virs then seconarily replicated in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acqure PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistance of infection occurs despite this.

==Diagnosis==

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. Both of these tests measure IgG antibodies against PRRS virus, which can be detected from 7-10 days post-infection. Titres persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population.

Tests for the PRRS virus itself also exist. These include PCR and virus isolation on clinical samples, and immunohistochemistry on tissues. Nucleic acid sequencing of the 5' end of the virus is commercially availabe ans is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

==Pathology==

PRRS virus produces a multisystemic infection in pigs, but gross lesions are usually only observed in
respiratory and lymphoid tissues. Both gross and microscopic lesions are most marked in neonatal and young
weaned pigs. The gross pathology observed after uncomplicated infection of PRRS virus in finishing pigs may
be anything from severe to unremarkable.
In severe disease, lungs are mottled, tan and red, and fail to collapse; the cranioventral lobes are most affected.
Lymph nodes are moderately to severely enlarged and tan in colour and, for some strains of virus, may be
haemorrhagic. Under field conditions, most PRRS virus infected pigs are co-infected with one or more
pathogens, which complicates the diagnosis of PRRS based on pathology.

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn fetuses, but histopathology inconsistently interstitial pneumonia, myocarditis anr pulmonary arteritis. However, these changes are not specific or diagnostic for PRRS.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:22:11Z

Lizzies: /* Laboratory Tests */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virs then seconarily replicated in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acqure PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistance of infection occurs despite this.

==Diagnosis==

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. Both of these tests measure IgG antibodies against PRRS virus, which can be detected from 7-10 days post-infection. Titres persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population.

Tests for the PRRS virus itself also exist. These include PCR and virus isolation on clinical samples, and immunohistochemistry on tissues. Nucleic acid sequencing of the 5' end of the virus is commercially availabe ans is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn fetuses, but histopathology inconsistently interstitial pneumonia, myocarditis anr pulmonary arteritis. However, these changes are not specific or diagnostic for PRRS.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:16:38Z

Lizzies: /* Laboratory Tests */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virs then seconarily replicated in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acqure PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistance of infection occurs despite this.

==Diagnosis==

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. Both of these tests measure IgG antibodies against PRRS virus. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn fetuses, but histopathology inconsistently interstitial pneumonia, myocarditis anr pulmonary arteritis. However, these changes are not specific or diagnostic for PRRS.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:14:31Z

Lizzies: /* Pathology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virs then seconarily replicated in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acqure PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistance of infection occurs despite this.

==Diagnosis==

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn fetuses, but histopathology inconsistently interstitial pneumonia, myocarditis anr pulmonary arteritis. However, these changes are not specific or diagnostic for PRRS.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:09:16Z

Lizzies: /* Clinical Signs */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virs then seconarily replicated in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acqure PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistance of infection occurs despite this.

==Diagnosis==

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status of the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses.

Microscopic lesions of the fetus
and placenta include umbilical vasculitis, interstitial
pneumonia, myocarditis and pulmonary arteritis but are
inconsistent and not diagnostic for PRRS (Lager and
Ackermann, 1994; Lager and Halbur, 1996; Rossow et
al., 1996b). There may be residual effects of PRRS
virus infection in sows manifest as a reduced conception
rate (Lowe et al., 2006).

Microscopically, interstitial pneumonia
with mononuclear septal infiltration, type 2 pneumonocyte
proliferation and accumulations of necrotic
debris and macrophages in alveolar spaces is evident.
Follicular hyperplasia and necrosis may be present in
lymph nodes. Nonsuppurative meningoencephalitis and
choroiditis is commonly present, with highly variable
severity

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:04:22Z

Lizzies: /* Transmission and Epidemiology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virs then seconarily replicated in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acqure PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistance of infection occurs despite this.

==Diagnosis==

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. Severe infections may also be associated with vestibular signs, and death of up to 10% of the sow stock can occur. Reproductive failure is results in increased numbers of stillborn piglets, mummified foetuses, abortions, premature farrowings and weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with ls a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85% and increases in mortality by up to 25%. Lethargy and a loss of appetites is seen as in adult pigs, and weanling fail to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status on the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

Secondary infections commonly occur. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses.

Microscopic lesions of the fetus
and placenta include umbilical vasculitis, interstitial
pneumonia, myocarditis and pulmonary arteritis but are
inconsistent and not diagnostic for PRRS (Lager and
Ackermann, 1994; Lager and Halbur, 1996; Rossow et
al., 1996b). There may be residual effects of PRRS
virus infection in sows manifest as a reduced conception
rate (Lowe et al., 2006).

Microscopically, interstitial pneumonia
with mononuclear septal infiltration, type 2 pneumonocyte
proliferation and accumulations of necrotic
debris and macrophages in alveolar spaces is evident.
Follicular hyperplasia and necrosis may be present in
lymph nodes. Nonsuppurative meningoencephalitis and
choroiditis is commonly present, with highly variable
severity

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:02:43Z

Lizzies: /* Transmission and Epidemiology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted by infected semen. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. It has been thought that aerosol transmission may occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

Transmission of PRRS virus to swine occurs most efficiently
through direct contact. Blood, saliva, urine, milk
and semen from infected animals have been shown to
transmit PRRS virus to susceptible swine (Wills et al.,
1997). Aerosol transmission may occur but has proven
difficult to demonstrate even over relatively short distances
(meters). Transmission by semen, either
through natural service or artificial insemination is well
established (Yaeger et al., 1993).

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virs then seconarily replicated in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acqure PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistance of infection occurs despite this.

==Diagnosis==

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. Severe infections may also be associated with vestibular signs, and death of up to 10% of the sow stock can occur. Reproductive failure is results in increased numbers of stillborn piglets, mummified foetuses, abortions, premature farrowings and weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with ls a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85% and increases in mortality by up to 25%. Lethargy and a loss of appetites is seen as in adult pigs, and weanling fail to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status on the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

Secondary infections commonly occur. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses.

Microscopic lesions of the fetus
and placenta include umbilical vasculitis, interstitial
pneumonia, myocarditis and pulmonary arteritis but are
inconsistent and not diagnostic for PRRS (Lager and
Ackermann, 1994; Lager and Halbur, 1996; Rossow et
al., 1996b). There may be residual effects of PRRS
virus infection in sows manifest as a reduced conception
rate (Lowe et al., 2006).

Microscopically, interstitial pneumonia
with mononuclear septal infiltration, type 2 pneumonocyte
proliferation and accumulations of necrotic
debris and macrophages in alveolar spaces is evident.
Follicular hyperplasia and necrosis may be present in
lymph nodes. Nonsuppurative meningoencephalitis and
choroiditis is commonly present, with highly variable
severity

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:01:32Z

Lizzies: /* Pathogenesis */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted by infected semen. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. It has been thought that aerosol transmission may occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection.

Transmission of PRRS virus to swine occurs most efficiently
through direct contact. Blood, saliva, urine, milk
and semen from infected animals have been shown to
transmit PRRS virus to susceptible swine (Wills et al.,
1997). Aerosol transmission may occur but has proven
difficult to demonstrate even over relatively short distances
(meters). Transmission by semen, either
through natural service or artificial insemination is well
established (Yaeger et al., 1993).

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virs then seconarily replicated in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acqure PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistance of infection occurs despite this.

==Diagnosis==

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. Severe infections may also be associated with vestibular signs, and death of up to 10% of the sow stock can occur. Reproductive failure is results in increased numbers of stillborn piglets, mummified foetuses, abortions, premature farrowings and weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with ls a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85% and increases in mortality by up to 25%. Lethargy and a loss of appetites is seen as in adult pigs, and weanling fail to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status on the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

Secondary infections commonly occur. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses.

Microscopic lesions of the fetus
and placenta include umbilical vasculitis, interstitial
pneumonia, myocarditis and pulmonary arteritis but are
inconsistent and not diagnostic for PRRS (Lager and
Ackermann, 1994; Lager and Halbur, 1996; Rossow et
al., 1996b). There may be residual effects of PRRS
virus infection in sows manifest as a reduced conception
rate (Lowe et al., 2006).

Microscopically, interstitial pneumonia
with mononuclear septal infiltration, type 2 pneumonocyte
proliferation and accumulations of necrotic
debris and macrophages in alveolar spaces is evident.
Follicular hyperplasia and necrosis may be present in
lymph nodes. Nonsuppurative meningoencephalitis and
choroiditis is commonly present, with highly variable
severity

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T19:00:48Z

Lizzies: /* Pathogenesis */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted by infected semen. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. It has been thought that aerosol transmission may occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection.

Transmission of PRRS virus to swine occurs most efficiently
through direct contact. Blood, saliva, urine, milk
and semen from infected animals have been shown to
transmit PRRS virus to susceptible swine (Wills et al.,
1997). Aerosol transmission may occur but has proven
difficult to demonstrate even over relatively short distances
(meters). Transmission by semen, either
through natural service or artificial insemination is well
established (Yaeger et al., 1993).

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virs then seconarily replicated in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acqure PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistance of infection occurs despite this. The fact that virus replicates in pigs for such a long time contributes to the maintenance of infection within a herd.

==Diagnosis==

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. Severe infections may also be associated with vestibular signs, and death of up to 10% of the sow stock can occur. Reproductive failure is results in increased numbers of stillborn piglets, mummified foetuses, abortions, premature farrowings and weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with ls a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85% and increases in mortality by up to 25%. Lethargy and a loss of appetites is seen as in adult pigs, and weanling fail to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status on the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

Secondary infections commonly occur. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses.

Microscopic lesions of the fetus
and placenta include umbilical vasculitis, interstitial
pneumonia, myocarditis and pulmonary arteritis but are
inconsistent and not diagnostic for PRRS (Lager and
Ackermann, 1994; Lager and Halbur, 1996; Rossow et
al., 1996b). There may be residual effects of PRRS
virus infection in sows manifest as a reduced conception
rate (Lowe et al., 2006).

Microscopically, interstitial pneumonia
with mononuclear septal infiltration, type 2 pneumonocyte
proliferation and accumulations of necrotic
debris and macrophages in alveolar spaces is evident.
Follicular hyperplasia and necrosis may be present in
lymph nodes. Nonsuppurative meningoencephalitis and
choroiditis is commonly present, with highly variable
severity

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T18:49:26Z

Lizzies: /* Pathogenesis */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted by infected semen. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. It has been thought that aerosol transmission may occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection.

Transmission of PRRS virus to swine occurs most efficiently
through direct contact. Blood, saliva, urine, milk
and semen from infected animals have been shown to
transmit PRRS virus to susceptible swine (Wills et al.,
1997). Aerosol transmission may occur but has proven
difficult to demonstrate even over relatively short distances
(meters). Transmission by semen, either
through natural service or artificial insemination is well
established (Yaeger et al., 1993).

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically.
Secondary replication of PRRS virus occurs in monocyte/
macrophages in many tissues. While other cell
types, including fibroblasts, endothelial cells, seminiferous
epithelium and smooth muscle, have been reported
to be PRRS virus-positive by in situ hybridization and/or
immunohistochemistry, only cells of macrophage lineage
have been unequivocally shown to support PRRS
virus replication (Sur et al., 1997).
In most swine, viremia resolves within 4-6 weeks following
infection. However, PRRS virus can persist in
lymphoid tissues, such as tonsil, for extended periods of
time and be transmitted to susceptible swine (Zimmerman
et al., 1992). PRRS virus has been detected for up
to 225 days following inoculation, though the proportion
of positive animals appears to drop off between 80 and
100 days (Albina et al., 1994; Allende et al., 2000; Wills
et al., 2003). Persistence occurs in the face of neutralizing
and other antibodies, and cell mediated immune
responses, as indicated by gamma-interferon producing
cells. Studies indicate that a low T cell response
contributes to prolonged PRRS clearance (Xiao et al.,
2004). Persistence is of epidemiologic significance
since persistently infected animals are capable of transmitting
PRRS virus to susceptible pigs via direct contact
(Albina et al., 1994). This is likely an important mechanism
by which PRRS virus is maintained within, and
transmitted between, swine herds.

==Diagnosis==

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. Severe infections may also be associated with vestibular signs, and death of up to 10% of the sow stock can occur. Reproductive failure is results in increased numbers of stillborn piglets, mummified foetuses, abortions, premature farrowings and weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with ls a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85% and increases in mortality by up to 25%. Lethargy and a loss of appetites is seen as in adult pigs, and weanling fail to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status on the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

Secondary infections commonly occur. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses.

Microscopic lesions of the fetus
and placenta include umbilical vasculitis, interstitial
pneumonia, myocarditis and pulmonary arteritis but are
inconsistent and not diagnostic for PRRS (Lager and
Ackermann, 1994; Lager and Halbur, 1996; Rossow et
al., 1996b). There may be residual effects of PRRS
virus infection in sows manifest as a reduced conception
rate (Lowe et al., 2006).

Microscopically, interstitial pneumonia
with mononuclear septal infiltration, type 2 pneumonocyte
proliferation and accumulations of necrotic
debris and macrophages in alveolar spaces is evident.
Follicular hyperplasia and necrosis may be present in
lymph nodes. Nonsuppurative meningoencephalitis and
choroiditis is commonly present, with highly variable
severity

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T18:48:34Z

Lizzies: /* Pathogenesis */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted by infected semen. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. It has been thought that aerosol transmission may occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection.

Transmission of PRRS virus to swine occurs most efficiently
through direct contact. Blood, saliva, urine, milk
and semen from infected animals have been shown to
transmit PRRS virus to susceptible swine (Wills et al.,
1997). Aerosol transmission may occur but has proven
difficult to demonstrate even over relatively short distances
(meters). Transmission by semen, either
through natural service or artificial insemination is well
established (Yaeger et al., 1993).

==Pathogenesis==

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. Lymphatic transport
of PRRS virus and virus-infected macrophages to
regional lymph nodes is also thought to occur.
Secondary replication of PRRS virus occurs in monocyte/
macrophages in many tissues. While other cell
types, including fibroblasts, endothelial cells, seminiferous
epithelium and smooth muscle, have been reported
to be PRRS virus-positive by in situ hybridization and/or
immunohistochemistry, only cells of macrophage lineage
have been unequivocally shown to support PRRS
virus replication (Sur et al., 1997).
In most swine, viremia resolves within 4-6 weeks following
infection. However, PRRS virus can persist in
lymphoid tissues, such as tonsil, for extended periods of
time and be transmitted to susceptible swine (Zimmerman
et al., 1992). PRRS virus has been detected for up
to 225 days following inoculation, though the proportion
of positive animals appears to drop off between 80 and
100 days (Albina et al., 1994; Allende et al., 2000; Wills
et al., 2003). Persistence occurs in the face of neutralizing
and other antibodies, and cell mediated immune
responses, as indicated by gamma-interferon producing
cells. Studies indicate that a low T cell response
contributes to prolonged PRRS clearance (Xiao et al.,
2004). Persistence is of epidemiologic significance
since persistently infected animals are capable of transmitting
PRRS virus to susceptible pigs via direct contact
(Albina et al., 1994). This is likely an important mechanism
by which PRRS virus is maintained within, and
transmitted between, swine herds.

==Diagnosis==

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. Severe infections may also be associated with vestibular signs, and death of up to 10% of the sow stock can occur. Reproductive failure is results in increased numbers of stillborn piglets, mummified foetuses, abortions, premature farrowings and weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with ls a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85% and increases in mortality by up to 25%. Lethargy and a loss of appetites is seen as in adult pigs, and weanling fail to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status on the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

Secondary infections commonly occur. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses.

Microscopic lesions of the fetus
and placenta include umbilical vasculitis, interstitial
pneumonia, myocarditis and pulmonary arteritis but are
inconsistent and not diagnostic for PRRS (Lager and
Ackermann, 1994; Lager and Halbur, 1996; Rossow et
al., 1996b). There may be residual effects of PRRS
virus infection in sows manifest as a reduced conception
rate (Lowe et al., 2006).

Microscopically, interstitial pneumonia
with mononuclear septal infiltration, type 2 pneumonocyte
proliferation and accumulations of necrotic
debris and macrophages in alveolar spaces is evident.
Follicular hyperplasia and necrosis may be present in
lymph nodes. Nonsuppurative meningoencephalitis and
choroiditis is commonly present, with highly variable
severity

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T18:41:10Z

Lizzies: /* Transmission and Epidemiology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted by infected semen. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. It has been thought that aerosol transmission may occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection.

Transmission of PRRS virus to swine occurs most efficiently
through direct contact. Blood, saliva, urine, milk
and semen from infected animals have been shown to
transmit PRRS virus to susceptible swine (Wills et al.,
1997). Aerosol transmission may occur but has proven
difficult to demonstrate even over relatively short distances
(meters). Transmission by semen, either
through natural service or artificial insemination is well
established (Yaeger et al., 1993).

==Pathogenesis==

Following exposure to PRRS virus, primary replication
occurs in regional or mucosal macrophages (Rossow,
1998; Rossow et al., 1996a). Typically macrophages of
the tonsil, nasal and respiratory epithelium are sites of
primary replication after oronasal exposure. Viremia
can occur within 12 hours following exposure resulting
in systemic dissemination of the virus. Lymphatic transport
of PRRS virus and virus-infected macrophages to
regional lymph nodes is also thought to occur.
Secondary replication of PRRS virus occurs in monocyte/
macrophages in many tissues. While other cell
types, including fibroblasts, endothelial cells, seminiferous
epithelium and smooth muscle, have been reported
to be PRRS virus-positive by in situ hybridization and/or
immunohistochemistry, only cells of macrophage lineage
have been unequivocally shown to support PRRS
virus replication (Sur et al., 1997).
In most swine, viremia resolves within 4-6 weeks following
infection. However, PRRS virus can persist in
lymphoid tissues, such as tonsil, for extended periods of
time and be transmitted to susceptible swine (Zimmerman
et al., 1992). PRRS virus has been detected for up
to 225 days following inoculation, though the proportion
of positive animals appears to drop off between 80 and
100 days (Albina et al., 1994; Allende et al., 2000; Wills
et al., 2003). Persistence occurs in the face of neutralizing
and other antibodies, and cell mediated immune
responses, as indicated by gamma-interferon producing
cells. Studies indicate that a low T cell response
contributes to prolonged PRRS clearance (Xiao et al.,
2004). Persistence is of epidemiologic significance
since persistently infected animals are capable of transmitting
PRRS virus to susceptible pigs via direct contact
(Albina et al., 1994). This is likely an important mechanism
by which PRRS virus is maintained within, and
transmitted between, swine herds.

==Diagnosis==

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. Severe infections may also be associated with vestibular signs, and death of up to 10% of the sow stock can occur. Reproductive failure is results in increased numbers of stillborn piglets, mummified foetuses, abortions, premature farrowings and weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with ls a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85% and increases in mortality by up to 25%. Lethargy and a loss of appetites is seen as in adult pigs, and weanling fail to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status on the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

Secondary infections commonly occur. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses.

Microscopic lesions of the fetus
and placenta include umbilical vasculitis, interstitial
pneumonia, myocarditis and pulmonary arteritis but are
inconsistent and not diagnostic for PRRS (Lager and
Ackermann, 1994; Lager and Halbur, 1996; Rossow et
al., 1996b). There may be residual effects of PRRS
virus infection in sows manifest as a reduced conception
rate (Lowe et al., 2006).

Microscopically, interstitial pneumonia
with mononuclear septal infiltration, type 2 pneumonocyte
proliferation and accumulations of necrotic
debris and macrophages in alveolar spaces is evident.
Follicular hyperplasia and necrosis may be present in
lymph nodes. Nonsuppurative meningoencephalitis and
choroiditis is commonly present, with highly variable
severity

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T18:40:50Z

Lizzies: /* Pathogenesis */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted by infected semen. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. It has been thought that aerosol transmission may occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection.

==Pathogenesis==

Following exposure to PRRS virus, primary replication
occurs in regional or mucosal macrophages (Rossow,
1998; Rossow et al., 1996a). Typically macrophages of
the tonsil, nasal and respiratory epithelium are sites of
primary replication after oronasal exposure. Viremia
can occur within 12 hours following exposure resulting
in systemic dissemination of the virus. Lymphatic transport
of PRRS virus and virus-infected macrophages to
regional lymph nodes is also thought to occur.
Secondary replication of PRRS virus occurs in monocyte/
macrophages in many tissues. While other cell
types, including fibroblasts, endothelial cells, seminiferous
epithelium and smooth muscle, have been reported
to be PRRS virus-positive by in situ hybridization and/or
immunohistochemistry, only cells of macrophage lineage
have been unequivocally shown to support PRRS
virus replication (Sur et al., 1997).
In most swine, viremia resolves within 4-6 weeks following
infection. However, PRRS virus can persist in
lymphoid tissues, such as tonsil, for extended periods of
time and be transmitted to susceptible swine (Zimmerman
et al., 1992). PRRS virus has been detected for up
to 225 days following inoculation, though the proportion
of positive animals appears to drop off between 80 and
100 days (Albina et al., 1994; Allende et al., 2000; Wills
et al., 2003). Persistence occurs in the face of neutralizing
and other antibodies, and cell mediated immune
responses, as indicated by gamma-interferon producing
cells. Studies indicate that a low T cell response
contributes to prolonged PRRS clearance (Xiao et al.,
2004). Persistence is of epidemiologic significance
since persistently infected animals are capable of transmitting
PRRS virus to susceptible pigs via direct contact
(Albina et al., 1994). This is likely an important mechanism
by which PRRS virus is maintained within, and
transmitted between, swine herds.

==Diagnosis==

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. Severe infections may also be associated with vestibular signs, and death of up to 10% of the sow stock can occur. Reproductive failure is results in increased numbers of stillborn piglets, mummified foetuses, abortions, premature farrowings and weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with ls a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85% and increases in mortality by up to 25%. Lethargy and a loss of appetites is seen as in adult pigs, and weanling fail to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status on the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

Secondary infections commonly occur. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses.

Microscopic lesions of the fetus
and placenta include umbilical vasculitis, interstitial
pneumonia, myocarditis and pulmonary arteritis but are
inconsistent and not diagnostic for PRRS (Lager and
Ackermann, 1994; Lager and Halbur, 1996; Rossow et
al., 1996b). There may be residual effects of PRRS
virus infection in sows manifest as a reduced conception
rate (Lowe et al., 2006).

Microscopically, interstitial pneumonia
with mononuclear septal infiltration, type 2 pneumonocyte
proliferation and accumulations of necrotic
debris and macrophages in alveolar spaces is evident.
Follicular hyperplasia and necrosis may be present in
lymph nodes. Nonsuppurative meningoencephalitis and
choroiditis is commonly present, with highly variable
severity

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T18:40:18Z

Lizzies: /* Prognosis */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted by infected semen. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. It has been thought that aerosol transmission may occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection.

==Pathogenesis==

Transmission of PRRS virus to swine occurs most efficiently
through direct contact. Blood, saliva, urine, milk
and semen from infected animals have been shown to
transmit PRRS virus to susceptible swine (Wills et al.,
1997). Aerosol transmission may occur but has proven
difficult to demonstrate even over relatively short distances
(meters). Transmission by semen, either
through natural service or artificial insemination is well
established (Yaeger et al., 1993).
Following exposure to PRRS virus, primary replication
occurs in regional or mucosal macrophages (Rossow,
1998; Rossow et al., 1996a). Typically macrophages of
the tonsil, nasal and respiratory epithelium are sites of
primary replication after oronasal exposure. Viremia
can occur within 12 hours following exposure resulting
in systemic dissemination of the virus. Lymphatic transport
of PRRS virus and virus-infected macrophages to
regional lymph nodes is also thought to occur.
Secondary replication of PRRS virus occurs in monocyte/
macrophages in many tissues. While other cell
types, including fibroblasts, endothelial cells, seminiferous
epithelium and smooth muscle, have been reported
to be PRRS virus-positive by in situ hybridization and/or
immunohistochemistry, only cells of macrophage lineage
have been unequivocally shown to support PRRS
virus replication (Sur et al., 1997).
In most swine, viremia resolves within 4-6 weeks following
infection. However, PRRS virus can persist in
lymphoid tissues, such as tonsil, for extended periods of
time and be transmitted to susceptible swine (Zimmerman
et al., 1992). PRRS virus has been detected for up
to 225 days following inoculation, though the proportion
of positive animals appears to drop off between 80 and
100 days (Albina et al., 1994; Allende et al., 2000; Wills
et al., 2003). Persistence occurs in the face of neutralizing
and other antibodies, and cell mediated immune
responses, as indicated by gamma-interferon producing
cells. Studies indicate that a low T cell response
contributes to prolonged PRRS clearance (Xiao et al.,
2004). Persistence is of epidemiologic significance
since persistently infected animals are capable of transmitting
PRRS virus to susceptible pigs via direct contact
(Albina et al., 1994). This is likely an important mechanism
by which PRRS virus is maintained within, and
transmitted between, swine herds.

==Diagnosis==

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. Severe infections may also be associated with vestibular signs, and death of up to 10% of the sow stock can occur. Reproductive failure is results in increased numbers of stillborn piglets, mummified foetuses, abortions, premature farrowings and weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with ls a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85% and increases in mortality by up to 25%. Lethargy and a loss of appetites is seen as in adult pigs, and weanling fail to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status on the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

Secondary infections commonly occur. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses.

Microscopic lesions of the fetus
and placenta include umbilical vasculitis, interstitial
pneumonia, myocarditis and pulmonary arteritis but are
inconsistent and not diagnostic for PRRS (Lager and
Ackermann, 1994; Lager and Halbur, 1996; Rossow et
al., 1996b). There may be residual effects of PRRS
virus infection in sows manifest as a reduced conception
rate (Lowe et al., 2006).

Microscopically, interstitial pneumonia
with mononuclear septal infiltration, type 2 pneumonocyte
proliferation and accumulations of necrotic
debris and macrophages in alveolar spaces is evident.
Follicular hyperplasia and necrosis may be present in
lymph nodes. Nonsuppurative meningoencephalitis and
choroiditis is commonly present, with highly variable
severity

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T18:39:00Z

Lizzies: /* Pathology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted by infected semen. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. It has been thought that aerosol transmission may occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection.

==Pathogenesis==

Transmission of PRRS virus to swine occurs most efficiently
through direct contact. Blood, saliva, urine, milk
and semen from infected animals have been shown to
transmit PRRS virus to susceptible swine (Wills et al.,
1997). Aerosol transmission may occur but has proven
difficult to demonstrate even over relatively short distances
(meters). Transmission by semen, either
through natural service or artificial insemination is well
established (Yaeger et al., 1993).
Following exposure to PRRS virus, primary replication
occurs in regional or mucosal macrophages (Rossow,
1998; Rossow et al., 1996a). Typically macrophages of
the tonsil, nasal and respiratory epithelium are sites of
primary replication after oronasal exposure. Viremia
can occur within 12 hours following exposure resulting
in systemic dissemination of the virus. Lymphatic transport
of PRRS virus and virus-infected macrophages to
regional lymph nodes is also thought to occur.
Secondary replication of PRRS virus occurs in monocyte/
macrophages in many tissues. While other cell
types, including fibroblasts, endothelial cells, seminiferous
epithelium and smooth muscle, have been reported
to be PRRS virus-positive by in situ hybridization and/or
immunohistochemistry, only cells of macrophage lineage
have been unequivocally shown to support PRRS
virus replication (Sur et al., 1997).
In most swine, viremia resolves within 4-6 weeks following
infection. However, PRRS virus can persist in
lymphoid tissues, such as tonsil, for extended periods of
time and be transmitted to susceptible swine (Zimmerman
et al., 1992). PRRS virus has been detected for up
to 225 days following inoculation, though the proportion
of positive animals appears to drop off between 80 and
100 days (Albina et al., 1994; Allende et al., 2000; Wills
et al., 2003). Persistence occurs in the face of neutralizing
and other antibodies, and cell mediated immune
responses, as indicated by gamma-interferon producing
cells. Studies indicate that a low T cell response
contributes to prolonged PRRS clearance (Xiao et al.,
2004). Persistence is of epidemiologic significance
since persistently infected animals are capable of transmitting
PRRS virus to susceptible pigs via direct contact
(Albina et al., 1994). This is likely an important mechanism
by which PRRS virus is maintained within, and
transmitted between, swine herds.

==Diagnosis==

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. Severe infections may also be associated with vestibular signs, and death of up to 10% of the sow stock can occur. Reproductive failure is results in increased numbers of stillborn piglets, mummified foetuses, abortions, premature farrowings and weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with ls a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85% and increases in mortality by up to 25%. Lethargy and a loss of appetites is seen as in adult pigs, and weanling fail to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status on the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

Secondary infections commonly occur. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses.

Microscopic lesions of the fetus
and placenta include umbilical vasculitis, interstitial
pneumonia, myocarditis and pulmonary arteritis but are
inconsistent and not diagnostic for PRRS (Lager and
Ackermann, 1994; Lager and Halbur, 1996; Rossow et
al., 1996b). There may be residual effects of PRRS
virus infection in sows manifest as a reduced conception
rate (Lowe et al., 2006).

Microscopically, interstitial pneumonia
with mononuclear septal infiltration, type 2 pneumonocyte
proliferation and accumulations of necrotic
debris and macrophages in alveolar spaces is evident.
Follicular hyperplasia and necrosis may be present in
lymph nodes. Nonsuppurative meningoencephalitis and
choroiditis is commonly present, with highly variable
severity

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Prognosis==

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T18:35:17Z

Lizzies: /* Pathology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted by infected semen. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. It has been thought that aerosol transmission may occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection.

==Pathogenesis==

Transmission of PRRS virus to swine occurs most efficiently
through direct contact. Blood, saliva, urine, milk
and semen from infected animals have been shown to
transmit PRRS virus to susceptible swine (Wills et al.,
1997). Aerosol transmission may occur but has proven
difficult to demonstrate even over relatively short distances
(meters). Transmission by semen, either
through natural service or artificial insemination is well
established (Yaeger et al., 1993).
Following exposure to PRRS virus, primary replication
occurs in regional or mucosal macrophages (Rossow,
1998; Rossow et al., 1996a). Typically macrophages of
the tonsil, nasal and respiratory epithelium are sites of
primary replication after oronasal exposure. Viremia
can occur within 12 hours following exposure resulting
in systemic dissemination of the virus. Lymphatic transport
of PRRS virus and virus-infected macrophages to
regional lymph nodes is also thought to occur.
Secondary replication of PRRS virus occurs in monocyte/
macrophages in many tissues. While other cell
types, including fibroblasts, endothelial cells, seminiferous
epithelium and smooth muscle, have been reported
to be PRRS virus-positive by in situ hybridization and/or
immunohistochemistry, only cells of macrophage lineage
have been unequivocally shown to support PRRS
virus replication (Sur et al., 1997).
In most swine, viremia resolves within 4-6 weeks following
infection. However, PRRS virus can persist in
lymphoid tissues, such as tonsil, for extended periods of
time and be transmitted to susceptible swine (Zimmerman
et al., 1992). PRRS virus has been detected for up
to 225 days following inoculation, though the proportion
of positive animals appears to drop off between 80 and
100 days (Albina et al., 1994; Allende et al., 2000; Wills
et al., 2003). Persistence occurs in the face of neutralizing
and other antibodies, and cell mediated immune
responses, as indicated by gamma-interferon producing
cells. Studies indicate that a low T cell response
contributes to prolonged PRRS clearance (Xiao et al.,
2004). Persistence is of epidemiologic significance
since persistently infected animals are capable of transmitting
PRRS virus to susceptible pigs via direct contact
(Albina et al., 1994). This is likely an important mechanism
by which PRRS virus is maintained within, and
transmitted between, swine herds.

==Diagnosis==

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. Severe infections may also be associated with vestibular signs, and death of up to 10% of the sow stock can occur. Reproductive failure is results in increased numbers of stillborn piglets, mummified foetuses, abortions, premature farrowings and weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with ls a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85% and increases in mortality by up to 25%. Lethargy and a loss of appetites is seen as in adult pigs, and weanling fail to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status on the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

Secondary infections commonly occur. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses.

Microscopic lesions of the fetus
and placenta include umbilical vasculitis, interstitial
pneumonia, myocarditis and pulmonary arteritis but are
inconsistent and not diagnostic for PRRS (Lager and
Ackermann, 1994; Lager and Halbur, 1996; Rossow et
al., 1996b). There may be residual effects of PRRS
virus infection in sows manifest as a reduced conception
rate (Lowe et al., 2006).

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Prognosis==

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T18:34:31Z

Lizzies: /* Pathogenesis */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted by infected semen. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. It has been thought that aerosol transmission may occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection.

==Pathogenesis==

Transmission of PRRS virus to swine occurs most efficiently
through direct contact. Blood, saliva, urine, milk
and semen from infected animals have been shown to
transmit PRRS virus to susceptible swine (Wills et al.,
1997). Aerosol transmission may occur but has proven
difficult to demonstrate even over relatively short distances
(meters). Transmission by semen, either
through natural service or artificial insemination is well
established (Yaeger et al., 1993).
Following exposure to PRRS virus, primary replication
occurs in regional or mucosal macrophages (Rossow,
1998; Rossow et al., 1996a). Typically macrophages of
the tonsil, nasal and respiratory epithelium are sites of
primary replication after oronasal exposure. Viremia
can occur within 12 hours following exposure resulting
in systemic dissemination of the virus. Lymphatic transport
of PRRS virus and virus-infected macrophages to
regional lymph nodes is also thought to occur.
Secondary replication of PRRS virus occurs in monocyte/
macrophages in many tissues. While other cell
types, including fibroblasts, endothelial cells, seminiferous
epithelium and smooth muscle, have been reported
to be PRRS virus-positive by in situ hybridization and/or
immunohistochemistry, only cells of macrophage lineage
have been unequivocally shown to support PRRS
virus replication (Sur et al., 1997).
In most swine, viremia resolves within 4-6 weeks following
infection. However, PRRS virus can persist in
lymphoid tissues, such as tonsil, for extended periods of
time and be transmitted to susceptible swine (Zimmerman
et al., 1992). PRRS virus has been detected for up
to 225 days following inoculation, though the proportion
of positive animals appears to drop off between 80 and
100 days (Albina et al., 1994; Allende et al., 2000; Wills
et al., 2003). Persistence occurs in the face of neutralizing
and other antibodies, and cell mediated immune
responses, as indicated by gamma-interferon producing
cells. Studies indicate that a low T cell response
contributes to prolonged PRRS clearance (Xiao et al.,
2004). Persistence is of epidemiologic significance
since persistently infected animals are capable of transmitting
PRRS virus to susceptible pigs via direct contact
(Albina et al., 1994). This is likely an important mechanism
by which PRRS virus is maintained within, and
transmitted between, swine herds.

==Diagnosis==

===Clinical Signs===

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. Severe infections may also be associated with vestibular signs, and death of up to 10% of the sow stock can occur. Reproductive failure is results in increased numbers of stillborn piglets, mummified foetuses, abortions, premature farrowings and weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with ls a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85% and increases in mortality by up to 25%. Lethargy and a loss of appetites is seen as in adult pigs, and weanling fail to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status on the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

Secondary infections commonly occur. Bacteria previously reported to be associated with PRRS include ''Streptococcus suis'', ''Escherichia coli'', ''Salmonella choleraesuis'', ''Haemophilus parasuis'' and ''Mycoplasma hyopneumoniae''. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses,sup>viro.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Prognosis==

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T18:19:19Z

Lizzies: /* Clinical Signs */

Porcine Reproductive and Respiratory Syndrome

2010-08-27T18:19:02Z

Lizzies: /* Clinical Signs */

Porcine Reproductive and Respiratory Syndrome

2010-08-27T18:07:24Z

Lizzies: /* Clinical Signs */

Porcine Reproductive and Respiratory Syndrome

2010-08-27T18:01:40Z

Lizzies: /* Clinical Signs */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted by infected semen. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. It has been thought that aerosol transmission may occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection.

==Pathogenesis==
*Infects alveolar macrophages, followed by '''interstitial pneumonitis'''
*Persistent infection of '''[[Monocytes]]''' followed by '''leukopenia and thrombocytopenia'''
*Mostly affects '''piglets'''
*In adults, '''cyanotic''' appearance due to '''vascular lesions'''
*Transplacental spread leads to '''abortion, mummification, or resorption'''

==Diagnosis==

===Clinical Signs===
The clinical signs of PRRS vary with the strain of virus as well as the the immune status of the herd. Although infection may be asymptomatic, a wide variety of signs can be seen in all ages of pig. In adults, a period of acute disease is seen, which is characterised by lethargy, inappetance and pyrexia. Abortion or premature farrowing may be seen, and severe cases may result in the death of up to 10% of animals. Vestibular signs, such as loss of balance or a head tilt, occur in some cases.

Concurrent infections
with other pathogens are also common.

RRS appears to have 2 distinct clinical phases: reproductive failure and postweaning respiratory diseases. The reproductive phase of the disease includes increases in the number of stillborn piglets, mummified fetuses, premature farrowings, and weak-born pigs. Stillbirths and mummies may increase up to 25-35%, and abortions can be >10%. Anorexia and agalactia are evident in lactating sows and result in increased (30-50%) preweaning mortality. Suckling piglets develop a characteristic thumping respiratory pattern, and histopathologic examination of lung tissue reveals a severe, necrotizing, interstitial pneumonia. PRRS is capable of crossing the placenta in the third and possibly second trimester of gestation. Piglets may also be born viremic and transmit the virus for 112 days after infection. Performance after weaning is also affected. Infection with PRRS virus results in destruction of mature alveolar macrophages, which has led to the hypothesis that infection results in the suppression of the immune system; however, controlled studies indicate that the virus may actually enhance specific parameters of the immune response.
Outbreaks of the reproductive form of PRRS have been reported to last 1-4 mo, depending on the facilities and initial health status of the pigs. In contrast, the postweaning pneumonic phase can become chronic, reducing daily gain by 85% and increasing mortality to 10-25%. Numerous other pathogens are commonly isolated along with PRRS virus from affected nursery or finishing pigs. Other bacteria such as Streptococcus suis , Escherichia coli , Salmonella choleraesuis , Haemophilus parasuis , and Mycoplasma hyopneumoniae have been reported, as well as viruses such as porcine respiratory coronavirus and swine influenza virus. Finally, differences in the clinical response to PRRS virus may also be due to strain variation. Studies have demonstrated the ability of different isolates to induce varying degrees of interstitial pneumonia in CD/CD (cesarean-derived/colostrum-deprived) piglets after intranasal inoculation.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses,sup>viro.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Prognosis==

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T17:57:11Z

Lizzies: /* Clinical Signs */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted by infected semen. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. It has been thought that aerosol transmission may occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection.

==Pathogenesis==
*Infects alveolar macrophages, followed by '''interstitial pneumonitis'''
*Persistent infection of '''[[Monocytes]]''' followed by '''leukopenia and thrombocytopenia'''
*Mostly affects '''piglets'''
*In adults, '''cyanotic''' appearance due to '''vascular lesions'''
*Transplacental spread leads to '''abortion, mummification, or resorption'''

==Diagnosis==

===Clinical Signs===
The clinical signs of PRRS vary with the strain of virus, the immune status of the herd and management
factors. Infection may also be asymptomatic. Clinical disease in a herd is a consequence of acute viraemia in
individuals and transplacental transmission of virus from viraemic dams to their foetuses, which can occur at
any time, though infections in the last third of pregnancy can result in severe disease. Concurrent infections
with other pathogens are also common.

RRS appears to have 2 distinct clinical phases: reproductive failure and postweaning respiratory diseases. The reproductive phase of the disease includes increases in the number of stillborn piglets, mummified fetuses, premature farrowings, and weak-born pigs. Stillbirths and mummies may increase up to 25-35%, and abortions can be >10%. Anorexia and agalactia are evident in lactating sows and result in increased (30-50%) preweaning mortality. Suckling piglets develop a characteristic thumping respiratory pattern, and histopathologic examination of lung tissue reveals a severe, necrotizing, interstitial pneumonia. PRRS is capable of crossing the placenta in the third and possibly second trimester of gestation. Piglets may also be born viremic and transmit the virus for 112 days after infection. Performance after weaning is also affected. Infection with PRRS virus results in destruction of mature alveolar macrophages, which has led to the hypothesis that infection results in the suppression of the immune system; however, controlled studies indicate that the virus may actually enhance specific parameters of the immune response.
Outbreaks of the reproductive form of PRRS have been reported to last 1-4 mo, depending on the facilities and initial health status of the pigs. In contrast, the postweaning pneumonic phase can become chronic, reducing daily gain by 85% and increasing mortality to 10-25%. Numerous other pathogens are commonly isolated along with PRRS virus from affected nursery or finishing pigs. Other bacteria such as Streptococcus suis , Escherichia coli , Salmonella choleraesuis , Haemophilus parasuis , and Mycoplasma hyopneumoniae have been reported, as well as viruses such as porcine respiratory coronavirus and swine influenza virus. Finally, differences in the clinical response to PRRS virus may also be due to strain variation. Studies have demonstrated the ability of different isolates to induce varying degrees of interstitial pneumonia in CD/CD (cesarean-derived/colostrum-deprived) piglets after intranasal inoculation.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses,sup>viro.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Prognosis==

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T17:56:00Z

Lizzies: /* Transmission and Epidemiology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted by infected semen. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. It has been thought that aerosol transmission may occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection.

==Pathogenesis==
*Infects alveolar macrophages, followed by '''interstitial pneumonitis'''
*Persistent infection of '''[[Monocytes]]''' followed by '''leukopenia and thrombocytopenia'''
*Mostly affects '''piglets'''
*In adults, '''cyanotic''' appearance due to '''vascular lesions'''
*Transplacental spread leads to '''abortion, mummification, or resorption'''

==Diagnosis==

===Clinical Signs===

Clinical signs include non-specific illness (anorexia and dullness) in sows, with reproductive losses occuring 1-2 weels later. In piglets, PRRS is characterised by inthriftiness, respiratory illness and mortality. Signs are similar in all ages of growing stock. Effects on neonatal piglets can be severe. Respiratory distress is seen, in addition to scour, unthriftiness and high mortality. Infection of boars may lead to impaired semen quality. Blue ears, snout and vulva can be seen in 1-5% of sows. Reproductive problems include infertility (normal oestrus delated, retuns to service increased), premature farrowing, stillbriths and weakly piglets.

RRS appears to have 2 distinct clinical phases: reproductive failure and postweaning respiratory diseases. The reproductive phase of the disease includes increases in the number of stillborn piglets, mummified fetuses, premature farrowings, and weak-born pigs. Stillbirths and mummies may increase up to 25-35%, and abortions can be >10%. Anorexia and agalactia are evident in lactating sows and result in increased (30-50%) preweaning mortality. Suckling piglets develop a characteristic thumping respiratory pattern, and histopathologic examination of lung tissue reveals a severe, necrotizing, interstitial pneumonia. PRRS is capable of crossing the placenta in the third and possibly second trimester of gestation. Piglets may also be born viremic and transmit the virus for 112 days after infection. Performance after weaning is also affected. Infection with PRRS virus results in destruction of mature alveolar macrophages, which has led to the hypothesis that infection results in the suppression of the immune system; however, controlled studies indicate that the virus may actually enhance specific parameters of the immune response.
Outbreaks of the reproductive form of PRRS have been reported to last 1-4 mo, depending on the facilities and initial health status of the pigs. In contrast, the postweaning pneumonic phase can become chronic, reducing daily gain by 85% and increasing mortality to 10-25%. Numerous other pathogens are commonly isolated along with PRRS virus from affected nursery or finishing pigs. Other bacteria such as Streptococcus suis , Escherichia coli , Salmonella choleraesuis , Haemophilus parasuis , and Mycoplasma hyopneumoniae have been reported, as well as viruses such as porcine respiratory coronavirus and swine influenza virus. Finally, differences in the clinical response to PRRS virus may also be due to strain variation. Studies have demonstrated the ability of different isolates to induce varying degrees of interstitial pneumonia in CD/CD (cesarean-derived/colostrum-deprived) piglets after intranasal inoculation.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses,sup>viro.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Prognosis==

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T17:52:05Z

Lizzies: /* Transmission and Epidemiology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted by infected semen. It has been thought that aerosol transmissionmay occur, particularly under conditions of high humidity, low temperatures, and low wind speeds; but this has been difficult to reproduce. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection.
PRRS virus can also be transmitted by fomites, such as contaminated needles, boots, coveralls, transport vehicles, and shipping containers. Farm personnel are not a risk, unless hands are contaminated with blood from viremic pigs. Finally, transmission via certain species of insects (mosquitos [ Aedes vexans ] and house flies [ Musca domestica ]) has been reported. The role of migratory waterfowl has not been determined. While biologic transmission of PRRS virus has been documented in immature Mallard ducks, results have not been reproducible experimentally using adult Mallards, nor have infected pigs been able to transmit virus to adult Mallards housed under field conditions.

==Pathogenesis==
*Infects alveolar macrophages, followed by '''interstitial pneumonitis'''
*Persistent infection of '''[[Monocytes]]''' followed by '''leukopenia and thrombocytopenia'''
*Mostly affects '''piglets'''
*In adults, '''cyanotic''' appearance due to '''vascular lesions'''
*Transplacental spread leads to '''abortion, mummification, or resorption'''

==Diagnosis==

===Clinical Signs===

Clinical signs include non-specific illness (anorexia and dullness) in sows, with reproductive losses occuring 1-2 weels later. In piglets, PRRS is characterised by inthriftiness, respiratory illness and mortality. Signs are similar in all ages of growing stock. Effects on neonatal piglets can be severe. Respiratory distress is seen, in addition to scour, unthriftiness and high mortality. Infection of boars may lead to impaired semen quality. Blue ears, snout and vulva can be seen in 1-5% of sows. Reproductive problems include infertility (normal oestrus delated, retuns to service increased), premature farrowing, stillbriths and weakly piglets.

RRS appears to have 2 distinct clinical phases: reproductive failure and postweaning respiratory diseases. The reproductive phase of the disease includes increases in the number of stillborn piglets, mummified fetuses, premature farrowings, and weak-born pigs. Stillbirths and mummies may increase up to 25-35%, and abortions can be >10%. Anorexia and agalactia are evident in lactating sows and result in increased (30-50%) preweaning mortality. Suckling piglets develop a characteristic thumping respiratory pattern, and histopathologic examination of lung tissue reveals a severe, necrotizing, interstitial pneumonia. PRRS is capable of crossing the placenta in the third and possibly second trimester of gestation. Piglets may also be born viremic and transmit the virus for 112 days after infection. Performance after weaning is also affected. Infection with PRRS virus results in destruction of mature alveolar macrophages, which has led to the hypothesis that infection results in the suppression of the immune system; however, controlled studies indicate that the virus may actually enhance specific parameters of the immune response.
Outbreaks of the reproductive form of PRRS have been reported to last 1-4 mo, depending on the facilities and initial health status of the pigs. In contrast, the postweaning pneumonic phase can become chronic, reducing daily gain by 85% and increasing mortality to 10-25%. Numerous other pathogens are commonly isolated along with PRRS virus from affected nursery or finishing pigs. Other bacteria such as Streptococcus suis , Escherichia coli , Salmonella choleraesuis , Haemophilus parasuis , and Mycoplasma hyopneumoniae have been reported, as well as viruses such as porcine respiratory coronavirus and swine influenza virus. Finally, differences in the clinical response to PRRS virus may also be due to strain variation. Studies have demonstrated the ability of different isolates to induce varying degrees of interstitial pneumonia in CD/CD (cesarean-derived/colostrum-deprived) piglets after intranasal inoculation.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses,sup>viro.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Prognosis==

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T17:28:36Z

Lizzies: /* Transmission and Epidemiology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The virus is spread by contact with infected pigs, and infection also be transmitted by infected semen. Aerosol transmission of the virus has been considered to be a potential route of transmission, particularly under conditions of high humidity, low temperatures, and low wind speeds; however, this has been difficult to consistently reproduce under controlled field conditions and in the laboratory. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection.
PRRS virus can also be transmitted by fomites, such as contaminated needles, boots, coveralls, transport vehicles, and shipping containers. Farm personnel are not a risk, unless hands are contaminated with blood from viremic pigs. Finally, transmission via certain species of insects (mosquitos [ Aedes vexans ] and house flies [ Musca domestica ]) has been reported. The role of migratory waterfowl has not been determined. While biologic transmission of PRRS virus has been documented in immature Mallard ducks, results have not been reproducible experimentally using adult Mallards, nor have infected pigs been able to transmit virus to adult Mallards housed under field conditions.

==Pathogenesis==
*Infects alveolar macrophages, followed by '''interstitial pneumonitis'''
*Persistent infection of '''[[Monocytes]]''' followed by '''leukopenia and thrombocytopenia'''
*Mostly affects '''piglets'''
*In adults, '''cyanotic''' appearance due to '''vascular lesions'''
*Transplacental spread leads to '''abortion, mummification, or resorption'''

==Diagnosis==

===Clinical Signs===

Clinical signs include non-specific illness (anorexia and dullness) in sows, with reproductive losses occuring 1-2 weels later. In piglets, PRRS is characterised by inthriftiness, respiratory illness and mortality. Signs are similar in all ages of growing stock. Effects on neonatal piglets can be severe. Respiratory distress is seen, in addition to scour, unthriftiness and high mortality. Infection of boars may lead to impaired semen quality. Blue ears, snout and vulva can be seen in 1-5% of sows. Reproductive problems include infertility (normal oestrus delated, retuns to service increased), premature farrowing, stillbriths and weakly piglets.

RRS appears to have 2 distinct clinical phases: reproductive failure and postweaning respiratory diseases. The reproductive phase of the disease includes increases in the number of stillborn piglets, mummified fetuses, premature farrowings, and weak-born pigs. Stillbirths and mummies may increase up to 25-35%, and abortions can be >10%. Anorexia and agalactia are evident in lactating sows and result in increased (30-50%) preweaning mortality. Suckling piglets develop a characteristic thumping respiratory pattern, and histopathologic examination of lung tissue reveals a severe, necrotizing, interstitial pneumonia. PRRS is capable of crossing the placenta in the third and possibly second trimester of gestation. Piglets may also be born viremic and transmit the virus for 112 days after infection. Performance after weaning is also affected. Infection with PRRS virus results in destruction of mature alveolar macrophages, which has led to the hypothesis that infection results in the suppression of the immune system; however, controlled studies indicate that the virus may actually enhance specific parameters of the immune response.
Outbreaks of the reproductive form of PRRS have been reported to last 1-4 mo, depending on the facilities and initial health status of the pigs. In contrast, the postweaning pneumonic phase can become chronic, reducing daily gain by 85% and increasing mortality to 10-25%. Numerous other pathogens are commonly isolated along with PRRS virus from affected nursery or finishing pigs. Other bacteria such as Streptococcus suis , Escherichia coli , Salmonella choleraesuis , Haemophilus parasuis , and Mycoplasma hyopneumoniae have been reported, as well as viruses such as porcine respiratory coronavirus and swine influenza virus. Finally, differences in the clinical response to PRRS virus may also be due to strain variation. Studies have demonstrated the ability of different isolates to induce varying degrees of interstitial pneumonia in CD/CD (cesarean-derived/colostrum-deprived) piglets after intranasal inoculation.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses,sup>viro.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Prognosis==

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T17:24:55Z

Lizzies: /* Transmission and Epidemiology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

The primary vector for transmission of the virus is the infected pig. Contact transmission has been demonstrated experimentally, and the spread of virus from infected seedstock originating from a single source has been described. Introduction of infected seedstock can lead to the introduction and coexistence of genetically diverse isolates of PRRS virus on the same farm. Controlled studies have indicated that infected swine may be longterm carriers, with adults able to shed PRRS virus for up to 86 days after infection, while weaned pigs may harbor virus for 157 days. Experimentally infected boars can shed virus in the semen up to 93 days after infection.
Aerosol transmission of the virus has been considered to be a potential route of transmission, particularly under conditions of high humidity, low temperatures, and low wind speeds; however, this has been difficult to consistently reproduce under controlled field conditions and in the laboratory. PRRS virus can also be transmitted by fomites, such as contaminated needles, boots, coveralls, transport vehicles, and shipping containers. Farm personnel are not a risk, unless hands are contaminated with blood from viremic pigs. Finally, transmission via certain species of insects (mosquitos [ Aedes vexans ] and house flies [ Musca domestica ]) has been reported. The role of migratory waterfowl has not been determined. While biologic transmission of PRRS virus has been documented in immature Mallard ducks, results have not been reproducible experimentally using adult Mallards, nor have infected pigs been able to transmit virus to adult Mallards housed under field conditions.

==Pathogenesis==
*Infects alveolar macrophages, followed by '''interstitial pneumonitis'''
*Persistent infection of '''[[Monocytes]]''' followed by '''leukopenia and thrombocytopenia'''
*Mostly affects '''piglets'''
*In adults, '''cyanotic''' appearance due to '''vascular lesions'''
*Transplacental spread leads to '''abortion, mummification, or resorption'''

==Diagnosis==

===Clinical Signs===

Clinical signs include non-specific illness (anorexia and dullness) in sows, with reproductive losses occuring 1-2 weels later. In piglets, PRRS is characterised by inthriftiness, respiratory illness and mortality. Signs are similar in all ages of growing stock. Effects on neonatal piglets can be severe. Respiratory distress is seen, in addition to scour, unthriftiness and high mortality. Infection of boars may lead to impaired semen quality. Blue ears, snout and vulva can be seen in 1-5% of sows. Reproductive problems include infertility (normal oestrus delated, retuns to service increased), premature farrowing, stillbriths and weakly piglets.

RRS appears to have 2 distinct clinical phases: reproductive failure and postweaning respiratory diseases. The reproductive phase of the disease includes increases in the number of stillborn piglets, mummified fetuses, premature farrowings, and weak-born pigs. Stillbirths and mummies may increase up to 25-35%, and abortions can be >10%. Anorexia and agalactia are evident in lactating sows and result in increased (30-50%) preweaning mortality. Suckling piglets develop a characteristic thumping respiratory pattern, and histopathologic examination of lung tissue reveals a severe, necrotizing, interstitial pneumonia. PRRS is capable of crossing the placenta in the third and possibly second trimester of gestation. Piglets may also be born viremic and transmit the virus for 112 days after infection. Performance after weaning is also affected. Infection with PRRS virus results in destruction of mature alveolar macrophages, which has led to the hypothesis that infection results in the suppression of the immune system; however, controlled studies indicate that the virus may actually enhance specific parameters of the immune response.
Outbreaks of the reproductive form of PRRS have been reported to last 1-4 mo, depending on the facilities and initial health status of the pigs. In contrast, the postweaning pneumonic phase can become chronic, reducing daily gain by 85% and increasing mortality to 10-25%. Numerous other pathogens are commonly isolated along with PRRS virus from affected nursery or finishing pigs. Other bacteria such as Streptococcus suis , Escherichia coli , Salmonella choleraesuis , Haemophilus parasuis , and Mycoplasma hyopneumoniae have been reported, as well as viruses such as porcine respiratory coronavirus and swine influenza virus. Finally, differences in the clinical response to PRRS virus may also be due to strain variation. Studies have demonstrated the ability of different isolates to induce varying degrees of interstitial pneumonia in CD/CD (cesarean-derived/colostrum-deprived) piglets after intranasal inoculation.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses,sup>viro.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Prognosis==

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T17:03:37Z

Lizzies: /* Transmission and Epidemiology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==

Following infection of a naive herd, exposure of all members of the breeding population is inconsistent, leading to the development of naive, exposed, and persistently infected subpopulations of sows. This situation is exacerbated over time through the addition of improperly acclimated replacement gilts and leads to shedding of the virus from carrier animals to those that have not been previously exposed.

The primary vector for transmission of the virus is the infected pig. Contact transmission has been demonstrated experimentally, and the spread of virus from infected seedstock originating from a single source has been described. Introduction of infected seedstock can lead to the introduction and coexistence of genetically diverse isolates of PRRS virus on the same farm. Controlled studies have indicated that infected swine may be longterm carriers, with adults able to shed PRRS virus for up to 86 days after infection, while weaned pigs may harbor virus for 157 days. Experimentally infected boars can shed virus in the semen up to 93 days after infection.
Aerosol transmission of the virus has been considered to be a potential route of transmission, particularly under conditions of high humidity, low temperatures, and low wind speeds; however, this has been difficult to consistently reproduce under controlled field conditions and in the laboratory. PRRS virus can also be transmitted by fomites, such as contaminated needles, boots, coveralls, transport vehicles, and shipping containers. Farm personnel are not a risk, unless hands are contaminated with blood from viremic pigs. Finally, transmission via certain species of insects (mosquitos [ Aedes vexans ] and house flies [ Musca domestica ]) has been reported. The role of migratory waterfowl has not been determined. While biologic transmission of PRRS virus has been documented in immature Mallard ducks, results have not been reproducible experimentally using adult Mallards, nor have infected pigs been able to transmit virus to adult Mallards housed under field conditions.

==Pathogenesis==
*Infects alveolar macrophages, followed by '''interstitial pneumonitis'''
*Persistent infection of '''[[Monocytes]]''' followed by '''leukopenia and thrombocytopenia'''
*Mostly affects '''piglets'''
*In adults, '''cyanotic''' appearance due to '''vascular lesions'''
*Transplacental spread leads to '''abortion, mummification, or resorption'''

==Diagnosis==

===Clinical Signs===

Clinical signs include non-specific illness (anorexia and dullness) in sows, with reproductive losses occuring 1-2 weels later. In piglets, PRRS is characterised by inthriftiness, respiratory illness and mortality. Signs are similar in all ages of growing stock. Effects on neonatal piglets can be severe. Respiratory distress is seen, in addition to scour, unthriftiness and high mortality. Infection of boars may lead to impaired semen quality. Blue ears, snout and vulva can be seen in 1-5% of sows. Reproductive problems include infertility (normal oestrus delated, retuns to service increased), premature farrowing, stillbriths and weakly piglets.

RRS appears to have 2 distinct clinical phases: reproductive failure and postweaning respiratory diseases. The reproductive phase of the disease includes increases in the number of stillborn piglets, mummified fetuses, premature farrowings, and weak-born pigs. Stillbirths and mummies may increase up to 25-35%, and abortions can be >10%. Anorexia and agalactia are evident in lactating sows and result in increased (30-50%) preweaning mortality. Suckling piglets develop a characteristic thumping respiratory pattern, and histopathologic examination of lung tissue reveals a severe, necrotizing, interstitial pneumonia. PRRS is capable of crossing the placenta in the third and possibly second trimester of gestation. Piglets may also be born viremic and transmit the virus for 112 days after infection. Performance after weaning is also affected. Infection with PRRS virus results in destruction of mature alveolar macrophages, which has led to the hypothesis that infection results in the suppression of the immune system; however, controlled studies indicate that the virus may actually enhance specific parameters of the immune response.
Outbreaks of the reproductive form of PRRS have been reported to last 1-4 mo, depending on the facilities and initial health status of the pigs. In contrast, the postweaning pneumonic phase can become chronic, reducing daily gain by 85% and increasing mortality to 10-25%. Numerous other pathogens are commonly isolated along with PRRS virus from affected nursery or finishing pigs. Other bacteria such as Streptococcus suis , Escherichia coli , Salmonella choleraesuis , Haemophilus parasuis , and Mycoplasma hyopneumoniae have been reported, as well as viruses such as porcine respiratory coronavirus and swine influenza virus. Finally, differences in the clinical response to PRRS virus may also be due to strain variation. Studies have demonstrated the ability of different isolates to induce varying degrees of interstitial pneumonia in CD/CD (cesarean-derived/colostrum-deprived) piglets after intranasal inoculation.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses,sup>viro.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Prognosis==

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T16:49:30Z

Lizzies: /* Aetiology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

==Transmission and Epidemiology==
ollowing infection of a naive herd, exposure of all members of the breeding population is inconsistent, leading to the development of naive, exposed, and persistently infected subpopulations of sows. This situation is exacerbated over time through the addition of improperly acclimated replacement gilts and leads to shedding of the virus from carrier animals to those that have not been previously exposed.
The primary vector for transmission of the virus is the infected pig. Contact transmission has been demonstrated experimentally, and the spread of virus from infected seedstock originating from a single source has been described. Introduction of infected seedstock can lead to the introduction and coexistence of genetically diverse isolates of PRRS virus on the same farm. Controlled studies have indicated that infected swine may be longterm carriers, with adults able to shed PRRS virus for up to 86 days after infection, while weaned pigs may harbor virus for 157 days. Experimentally infected boars can shed virus in the semen up to 93 days after infection.
Aerosol transmission of the virus has been considered to be a potential route of transmission, particularly under conditions of high humidity, low temperatures, and low wind speeds; however, this has been difficult to consistently reproduce under controlled field conditions and in the laboratory. PRRS virus can also be transmitted by fomites, such as contaminated needles, boots, coveralls, transport vehicles, and shipping containers. Farm personnel are not a risk, unless hands are contaminated with blood from viremic pigs. Finally, transmission via certain species of insects (mosquitos [ Aedes vexans ] and house flies [ Musca domestica ]) has been reported. The role of migratory waterfowl has not been determined. While biologic transmission of PRRS virus has been documented in immature Mallard ducks, results have not been reproducible experimentally using adult Mallards, nor have infected pigs been able to transmit virus to adult Mallards housed under field conditions.

==Pathogenesis==
*Infects alveolar macrophages, followed by '''interstitial pneumonitis'''
*Persistent infection of '''[[Monocytes]]''' followed by '''leukopenia and thrombocytopenia'''
*Mostly affects '''piglets'''
*In adults, '''cyanotic''' appearance due to '''vascular lesions'''
*Transplacental spread leads to '''abortion, mummification, or resorption'''

==Diagnosis==

===Clinical Signs===

Clinical signs include non-specific illness (anorexia and dullness) in sows, with reproductive losses occuring 1-2 weels later. In piglets, PRRS is characterised by inthriftiness, respiratory illness and mortality. Signs are similar in all ages of growing stock. Effects on neonatal piglets can be severe. Respiratory distress is seen, in addition to scour, unthriftiness and high mortality. Infection of boars may lead to impaired semen quality. Blue ears, snout and vulva can be seen in 1-5% of sows. Reproductive problems include infertility (normal oestrus delated, retuns to service increased), premature farrowing, stillbriths and weakly piglets.

RRS appears to have 2 distinct clinical phases: reproductive failure and postweaning respiratory diseases. The reproductive phase of the disease includes increases in the number of stillborn piglets, mummified fetuses, premature farrowings, and weak-born pigs. Stillbirths and mummies may increase up to 25-35%, and abortions can be >10%. Anorexia and agalactia are evident in lactating sows and result in increased (30-50%) preweaning mortality. Suckling piglets develop a characteristic thumping respiratory pattern, and histopathologic examination of lung tissue reveals a severe, necrotizing, interstitial pneumonia. PRRS is capable of crossing the placenta in the third and possibly second trimester of gestation. Piglets may also be born viremic and transmit the virus for 112 days after infection. Performance after weaning is also affected. Infection with PRRS virus results in destruction of mature alveolar macrophages, which has led to the hypothesis that infection results in the suppression of the immune system; however, controlled studies indicate that the virus may actually enhance specific parameters of the immune response.
Outbreaks of the reproductive form of PRRS have been reported to last 1-4 mo, depending on the facilities and initial health status of the pigs. In contrast, the postweaning pneumonic phase can become chronic, reducing daily gain by 85% and increasing mortality to 10-25%. Numerous other pathogens are commonly isolated along with PRRS virus from affected nursery or finishing pigs. Other bacteria such as Streptococcus suis , Escherichia coli , Salmonella choleraesuis , Haemophilus parasuis , and Mycoplasma hyopneumoniae have been reported, as well as viruses such as porcine respiratory coronavirus and swine influenza virus. Finally, differences in the clinical response to PRRS virus may also be due to strain variation. Studies have demonstrated the ability of different isolates to induce varying degrees of interstitial pneumonia in CD/CD (cesarean-derived/colostrum-deprived) piglets after intranasal inoculation.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses,sup>viro.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Prognosis==

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T16:43:38Z

Lizzies: /* Aetiology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. These viruses are antigenically distinct from each other. Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the positive-sense single-stranded RNA genome is contained within an icosohedral nucleocapsid. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surfae spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasms. The genome is 13Kb in length, and is infectious itself without the capsid or envelope. The viruses are host-specific, and persistent infections are established after invasion. Inactivation is possible after treatment with ether or chloroform; however, the virus is very stable under freezing conditions, retaining its infectivity for 4 mo at -70°C. As the temperature rises, infectivity is reduced (15-20 min at 56°C).

==Transmission and Epidemiology==
ollowing infection of a naive herd, exposure of all members of the breeding population is inconsistent, leading to the development of naive, exposed, and persistently infected subpopulations of sows. This situation is exacerbated over time through the addition of improperly acclimated replacement gilts and leads to shedding of the virus from carrier animals to those that have not been previously exposed.
The primary vector for transmission of the virus is the infected pig. Contact transmission has been demonstrated experimentally, and the spread of virus from infected seedstock originating from a single source has been described. Introduction of infected seedstock can lead to the introduction and coexistence of genetically diverse isolates of PRRS virus on the same farm. Controlled studies have indicated that infected swine may be longterm carriers, with adults able to shed PRRS virus for up to 86 days after infection, while weaned pigs may harbor virus for 157 days. Experimentally infected boars can shed virus in the semen up to 93 days after infection.
Aerosol transmission of the virus has been considered to be a potential route of transmission, particularly under conditions of high humidity, low temperatures, and low wind speeds; however, this has been difficult to consistently reproduce under controlled field conditions and in the laboratory. PRRS virus can also be transmitted by fomites, such as contaminated needles, boots, coveralls, transport vehicles, and shipping containers. Farm personnel are not a risk, unless hands are contaminated with blood from viremic pigs. Finally, transmission via certain species of insects (mosquitos [ Aedes vexans ] and house flies [ Musca domestica ]) has been reported. The role of migratory waterfowl has not been determined. While biologic transmission of PRRS virus has been documented in immature Mallard ducks, results have not been reproducible experimentally using adult Mallards, nor have infected pigs been able to transmit virus to adult Mallards housed under field conditions.

==Pathogenesis==
*Infects alveolar macrophages, followed by '''interstitial pneumonitis'''
*Persistent infection of '''[[Monocytes]]''' followed by '''leukopenia and thrombocytopenia'''
*Mostly affects '''piglets'''
*In adults, '''cyanotic''' appearance due to '''vascular lesions'''
*Transplacental spread leads to '''abortion, mummification, or resorption'''

==Diagnosis==

===Clinical Signs===

Clinical signs include non-specific illness (anorexia and dullness) in sows, with reproductive losses occuring 1-2 weels later. In piglets, PRRS is characterised by inthriftiness, respiratory illness and mortality. Signs are similar in all ages of growing stock. Effects on neonatal piglets can be severe. Respiratory distress is seen, in addition to scour, unthriftiness and high mortality. Infection of boars may lead to impaired semen quality. Blue ears, snout and vulva can be seen in 1-5% of sows. Reproductive problems include infertility (normal oestrus delated, retuns to service increased), premature farrowing, stillbriths and weakly piglets.

RRS appears to have 2 distinct clinical phases: reproductive failure and postweaning respiratory diseases. The reproductive phase of the disease includes increases in the number of stillborn piglets, mummified fetuses, premature farrowings, and weak-born pigs. Stillbirths and mummies may increase up to 25-35%, and abortions can be >10%. Anorexia and agalactia are evident in lactating sows and result in increased (30-50%) preweaning mortality. Suckling piglets develop a characteristic thumping respiratory pattern, and histopathologic examination of lung tissue reveals a severe, necrotizing, interstitial pneumonia. PRRS is capable of crossing the placenta in the third and possibly second trimester of gestation. Piglets may also be born viremic and transmit the virus for 112 days after infection. Performance after weaning is also affected. Infection with PRRS virus results in destruction of mature alveolar macrophages, which has led to the hypothesis that infection results in the suppression of the immune system; however, controlled studies indicate that the virus may actually enhance specific parameters of the immune response.
Outbreaks of the reproductive form of PRRS have been reported to last 1-4 mo, depending on the facilities and initial health status of the pigs. In contrast, the postweaning pneumonic phase can become chronic, reducing daily gain by 85% and increasing mortality to 10-25%. Numerous other pathogens are commonly isolated along with PRRS virus from affected nursery or finishing pigs. Other bacteria such as Streptococcus suis , Escherichia coli , Salmonella choleraesuis , Haemophilus parasuis , and Mycoplasma hyopneumoniae have been reported, as well as viruses such as porcine respiratory coronavirus and swine influenza virus. Finally, differences in the clinical response to PRRS virus may also be due to strain variation. Studies have demonstrated the ability of different isolates to induce varying degrees of interstitial pneumonia in CD/CD (cesarean-derived/colostrum-deprived) piglets after intranasal inoculation.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses,sup>viro.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Prognosis==

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]

Porcine Reproductive and Respiratory Syndrome

2010-08-27T16:39:06Z

Lizzies: /* Aetiology */

{{unfinished}}

Also known as: PRRS, blue eared pig disease

==Description==

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

==Aetiology==

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. These viruses are antigenically distinct from each other. Arteriviruses are enveloped viruses of 45 6o 80 nm in diameterand appear spherical due to the shape of the envelope. However, the positive-sense single-stranded RNA genome is contained within The virus is enveloped and ranges in size from 45 to 80 mm. Inactivation is possible after treatment with ether or chloroform; however, the virus is very stable under freezing conditions, retaining its infectivity for 4 mo at -70°C. As the temperature rises, infectivity is reduced (15-20 min at 56°C).

This family of enveloped, positive-sense, single-stranded RNA viruses, established in 1996, was classified formerly in the Togaviridae family. It has only one genus, Arterivirus, whose virus species are antigenically distinct from each other.
Viral Characteristics

* These positive sense, single-stranded RNA viruses are medium in size (50 - 70 nm) have a spherical appearance due to the envelope, but the nucleocapsid is icosahedral in shape (see Fig. 25.1).
* They possess a lipoprotein envelope with ring-like structures on the surface, but no gross surface spikes.
* They replicate in the cytoplasm of macrophages and endothelial cells.
* The genome is 13K nucleotides in length, has a 5'-methylguanosine cap and a 3' poly A tail of approximately 50 nucleotides. The genome alone is infectious.
* Individual viruses are antigenically distinct and host specific; they establish persistent infections

o Porcine Respiratory and Reproduction Syndrome
o Lactate Dehydrogenase-elevating Virus of Mice

==Transmission and Epidemiology==
ollowing infection of a naive herd, exposure of all members of the breeding population is inconsistent, leading to the development of naive, exposed, and persistently infected subpopulations of sows. This situation is exacerbated over time through the addition of improperly acclimated replacement gilts and leads to shedding of the virus from carrier animals to those that have not been previously exposed.
The primary vector for transmission of the virus is the infected pig. Contact transmission has been demonstrated experimentally, and the spread of virus from infected seedstock originating from a single source has been described. Introduction of infected seedstock can lead to the introduction and coexistence of genetically diverse isolates of PRRS virus on the same farm. Controlled studies have indicated that infected swine may be longterm carriers, with adults able to shed PRRS virus for up to 86 days after infection, while weaned pigs may harbor virus for 157 days. Experimentally infected boars can shed virus in the semen up to 93 days after infection.
Aerosol transmission of the virus has been considered to be a potential route of transmission, particularly under conditions of high humidity, low temperatures, and low wind speeds; however, this has been difficult to consistently reproduce under controlled field conditions and in the laboratory. PRRS virus can also be transmitted by fomites, such as contaminated needles, boots, coveralls, transport vehicles, and shipping containers. Farm personnel are not a risk, unless hands are contaminated with blood from viremic pigs. Finally, transmission via certain species of insects (mosquitos [ Aedes vexans ] and house flies [ Musca domestica ]) has been reported. The role of migratory waterfowl has not been determined. While biologic transmission of PRRS virus has been documented in immature Mallard ducks, results have not been reproducible experimentally using adult Mallards, nor have infected pigs been able to transmit virus to adult Mallards housed under field conditions.

==Pathogenesis==
*Infects alveolar macrophages, followed by '''interstitial pneumonitis'''
*Persistent infection of '''[[Monocytes]]''' followed by '''leukopenia and thrombocytopenia'''
*Mostly affects '''piglets'''
*In adults, '''cyanotic''' appearance due to '''vascular lesions'''
*Transplacental spread leads to '''abortion, mummification, or resorption'''

==Diagnosis==

===Clinical Signs===

Clinical signs include non-specific illness (anorexia and dullness) in sows, with reproductive losses occuring 1-2 weels later. In piglets, PRRS is characterised by inthriftiness, respiratory illness and mortality. Signs are similar in all ages of growing stock. Effects on neonatal piglets can be severe. Respiratory distress is seen, in addition to scour, unthriftiness and high mortality. Infection of boars may lead to impaired semen quality. Blue ears, snout and vulva can be seen in 1-5% of sows. Reproductive problems include infertility (normal oestrus delated, retuns to service increased), premature farrowing, stillbriths and weakly piglets.

RRS appears to have 2 distinct clinical phases: reproductive failure and postweaning respiratory diseases. The reproductive phase of the disease includes increases in the number of stillborn piglets, mummified fetuses, premature farrowings, and weak-born pigs. Stillbirths and mummies may increase up to 25-35%, and abortions can be >10%. Anorexia and agalactia are evident in lactating sows and result in increased (30-50%) preweaning mortality. Suckling piglets develop a characteristic thumping respiratory pattern, and histopathologic examination of lung tissue reveals a severe, necrotizing, interstitial pneumonia. PRRS is capable of crossing the placenta in the third and possibly second trimester of gestation. Piglets may also be born viremic and transmit the virus for 112 days after infection. Performance after weaning is also affected. Infection with PRRS virus results in destruction of mature alveolar macrophages, which has led to the hypothesis that infection results in the suppression of the immune system; however, controlled studies indicate that the virus may actually enhance specific parameters of the immune response.
Outbreaks of the reproductive form of PRRS have been reported to last 1-4 mo, depending on the facilities and initial health status of the pigs. In contrast, the postweaning pneumonic phase can become chronic, reducing daily gain by 85% and increasing mortality to 10-25%. Numerous other pathogens are commonly isolated along with PRRS virus from affected nursery or finishing pigs. Other bacteria such as Streptococcus suis , Escherichia coli , Salmonella choleraesuis , Haemophilus parasuis , and Mycoplasma hyopneumoniae have been reported, as well as viruses such as porcine respiratory coronavirus and swine influenza virus. Finally, differences in the clinical response to PRRS virus may also be due to strain variation. Studies have demonstrated the ability of different isolates to induce varying degrees of interstitial pneumonia in CD/CD (cesarean-derived/colostrum-deprived) piglets after intranasal inoculation.

===Laboratory Tests===
The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7-10 days after infection and can persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

==Pathology==

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses,sup>viro.

==Control==
Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens have also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality.
Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses.
Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

==Prognosis==

==Links==

*[http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs The Pig Site: Porcine Reproductive and Respiratory Syndrome]

==References==

#Wise, D J and Carter, G R (2005) ''' A Concise Review of Veterinary Virology''', ''IVIS''.
#Merck & Co (2008) '''The Merck Veterinary Manual (Eight Edition)''', ''Merial''.
#Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. ''In Practice'', '''25(7)''', 410-417.
#OIE (2008) PRRS: the disease, its diagnosis, prevention and control. ''Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome''.
#Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. ''Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology''.

[[Category:Arteriviridae]]
[[Category:Pig]]
[[Category:To_Do_-_Lizzie]]
[[Category:Respiratory_Viral_Infections]]