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Goat plague, pest of sheep and goats, pneumoenteritis complex, pseudorinderpest of small ruminants, stomatitis-pneumoenteritis syndrome.

Also known as: '''''PPR — PPRV — Goat Plague — Pest of Sheep and Goats — Pneumoenteritis Complex — Pseudorinderpest of Small Ruminants — Stomatitis-Pneumoenteritis Syndrome

 

== Introduction ==

== Introduction ==

The disease was first described by workers in the Côté d’Ivoire (Gargadennec and Lalanne, 1942), and thereafter in other parts of West Africa in the 1950s and 1960s. It is now recognized to be distributed from south Asia through the Middle East, and from the horn of Africa through to West Africa. The similarity in clinical signs to that of rinderpest in cattle probably accounts for the number of reports of rinderpest in small ruminants from some countries, and delayed the recognition of the disease as a distinct entity in India until the early 1990s.

The disease was first described by workers in the Côté d’Ivoire (Gargadennec and Lalanne, 1942), and thereafter in other parts of West Africa in the 1950s and 1960s. It is now recognized to be distributed from south Asia through the Middle East, and from the horn of Africa through to West Africa. The similarity in clinical signs to that of [[rinderpest]] in cattle probably accounts for the number of reports of rinderpest in small ruminants from some countries, and delayed the recognition of the disease as a distinct entity in India until the early 1990s.

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The condition is caused by a morbillivirus of the family paramoxyviridae. The infective agent was first considered a variant of rinderpest virus adapted to small ruminants, but was later shown to be antigenically (Gibbs et al., 1979) and genetically distinct (Diallo et al., 1989). Since PPRV isolates of West African, Middle Eastern and south Asian origin comprise distinct genetic groups, it is likely that the infections have circulated largely independently for long periods in each area.

 

The condition is caused by a [[:Category:Morbilliviruses|morbillivirus]] of the family [[:Category:Paramyxoviridae|paramoxyviridae]]. The infective agent was first considered a variant of rinderpest virus adapted to small ruminants, but was later shown to be antigenically (Gibbs et al., 1979) and genetically distinct (Diallo et al., 1989). Since PPRV isolates of West African, Middle Eastern and south Asian origin comprise distinct genetic groups, it is likely that the infections have circulated largely independently for long periods in each area.

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The disease is recognized by the Office International des Epizooties (OIE) as a 'List A' pathogen on account of the high mortality and morbidity, and rapidity of spread by contagion. Recognition of PPR as a problem has increased in the 1990s, partly as a result of surveillance activities of the global rinderpest eradication programme (GREP), but also by the capacity of the infection to invade disease-free countries. The presence of infection restricts international trade in livestock and livestock products from infected countries, and is usually associated with ongoing severe losses where conditions exist that support epidemic spread among susceptible breeds, such as the incursions of infection into 'marginal' zones for persistence of infection such as humid zones of West Africa.  

The disease is recognized by the [http://www.oie.int/ Office International des Epizooties (OIE)] as a 'List A' pathogen on account of the high mortality and morbidity, and rapidity of spread by contagion. Recognition of PPR as a problem has increased in the 1990s, partly as a result of surveillance activities of the [http://www.fao.org/ag/againfo/programmes/en/grep/home.html global rinderpest eradication programme (GREP)], but also by the capacity of the infection to invade disease-free countries. The presence of infection restricts international trade in livestock and livestock products from infected countries, and is usually associated with ongoing severe losses where conditions exist that support epidemic spread among susceptible breeds, such as the incursions of infection into 'marginal' zones for persistence of infection such as humid zones of West Africa.  

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== Clinical Signs ==

== Clinical Signs ==

Signs include sudden onset of pyrexia (40- 42), marked depression, lethargy, weight loss or reducded weight gain and a reduced appetite. There will be ulcers, vesicles and erosion on the tongue and oral mucosa and the animal may be smacking its' lips, salivating excessively and grinding its teeth in pain. Gentle rubbing of the gum line will reveal a foul- smelling material and shreds of epithelial tissue. Similar changes may also be seen in the mucous membranes of the vagina and vulva. There will also be excessinve lacrimation and nasal discharge, both of which may become purulent later on in the condition, following secondary bacterial infection.  

Signs include sudden onset of pyrexia (40 - 42⁰C), marked depression, lethargy, weight loss or reduced weight gain and a reduced appetite. There will be ulcers, vesicles and erosion on the tongue and oral mucosa and the animal may be smacking its lips, salivating excessively and grinding its teeth in pain. Gentle rubbing of the gum line will reveal a foul-smelling material and shreds of epithelial tissue. Similar changes may also be seen in the mucous membranes of the vagina and vulva. There will also be excessive lacrimation and nasal discharge, both of which may become purulent later on in the condition, following secondary bacterial infection.  

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The animal will later develop foul- smelling diarrhoea, containing blood and pieces of dead gut tissue. Dyspnoea, tachypnoea and coughing may be present. Pregnant animals may abort.

The animal will later develop foul-smelling diarrhoea, containing blood and pieces of dead gut tissue. Dyspnoea, tachypnoea and coughing may be present. Pregnant animals may abort.

   

   

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== Pathology ==

== Pathology ==

The carcass is usually dehydrated, and soiled with faeces. The peri-orbital and perinasal areas are usually encrusted with muco-purulent discharges. The erosions and ulcerations in the mouth and throat are usually prominent, as is the presence of the secondary broncho-pneumonia. The underlying primary viral pneumonia may be less obvious but is manifested by areas of level red consolidation (Rowland et al., 1969). 'Zebra striping' in the colon may also be seen, and lympadenopathy.

The carcass is usually dehydrated, and soiled with faeces. The peri-orbital and perinasal areas are usually encrusted with muco-purulent discharges. The erosions and ulcerations in the mouth and throat are usually prominent, as is the presence of the secondary broncho-pneumonia. The underlying primary viral pneumonia may be less obvious but is manifested by areas of level red consolidation (Rowland et al., 1969). 'Zebra striping' in the colon may also be seen, and lymphadenopathy.

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The most important histopathological indicator of PPRV is the presence of multi-nucleated giant cells containing intra-nuclear and intra-cytoplasmic inclusions. Multi-nucleated giant cells (syncytia) are most readily detected in the lungs, but also occur in bronchial, alveolar and ileal epithelium.

The most important histopathological indicator of PPRV is the presence of multi-nucleated giant cells containing intra-nuclear and intra-cytoplasmic inclusions. Multi-nucleated giant cells (syncytia) are most readily detected in the lungs, but also occur in bronchial, alveolar and ileal epithelium.

== Diagnosis ==

== Diagnosis ==

History, signalment and clinical signs may lead to a presumptive diagnosis of this countries in countries where it is endemic.

History, signalment and clinical signs may lead to a presumptive diagnosis of this disease in countries where it is endemic.

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Other conditions which need to be eliminated as differentials are rinderpest in small ruminants, contagious caprine pleuropneumonia, bluetongue, pasteurellosis, contagious ecthyma, foot-and-mouth disease, heartwater, coccidiosis and mineral poisoning.  

 

Other conditions which need to be eliminated as differentials are ([[rinderpest]] in small ruminants), [[Contagious Caprine Pleuropneumonia|contagious caprine pleuropneumonia]], [[bluetongue]], pasteurellosis, [[Orf|contagious ecthyma]], [[Foot and Mouth Disease|foot-and-mouth disease]], [[heartwater]], [[Coccidiosis - Sheep|coccidiosis]] and mineral poisoning.  

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Rinderpest virus can cause disease in small ruminants, but where RP exists as a risk to small ruminants, disease in cattle would be expected, since many countries have ceased vaccination. Rinderpest has now been eradicated worldwide.  

Rinderpest virus can cause disease in small ruminants, but where RP exists as a risk to small ruminants, disease in cattle would be expected, since many countries have ceased vaccination. Rinderpest has now been eradicated worldwide.  

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Bluetongue infection occurs in many countries that are endemic or at-risk from PPR incursion. It can give rise to a muco-purulent discharge and high morbidity and mortality rate in susceptible sheep, but usually less so in goats. It does not usually result in a severe enteritis, although loose stools may occur, or erosions/ulcerations of epithelial surfaces. Bluetongue usually gives rise to visible signs of haemorrhage on the coronary band of the foot, in contrast to PPR.  

Bluetongue infection occurs in many countries that are endemic or at-risk from PPR incursion. It can give rise to a muco-purulent discharge and high morbidity and mortality rate in susceptible sheep, but usually less so in goats. It does not usually result in a severe enteritis, although loose stools may occur, or erosions/ulcerations of epithelial surfaces. Bluetongue usually gives rise to visible signs of haemorrhage on the coronary band of the foot, in contrast to PPR.  

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Foot-and-mouth disease affects other stock as well as sheep and goats; cattle in the region would be expected to show more severe signs than sheep or goats. On occasion though, the disease is more severe in the latter, and cattle may be absent. However, the enteritis usually present in PPR is not seen in FMD.  

Foot-and-mouth disease affects other stock as well as sheep and goats; cattle in the region would be expected to show more severe signs than sheep or goats. On occasion though, the disease is more severe in the latter, and cattle may be absent. However, the enteritis usually present in PPR is not seen in FMD.  

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The lesions of orf (contagious ecthyma) and sheep and goat pox differ in distribution to that of PPR, but animals recovering from PPR may develop proliferative growths on the lips resembling orf, and the virus may be involved in the pathogenesis of the condition.  

 

The lesions of orf (contagious ecthyma) and [[Capripox|sheep and goat pox]] differ in distribution to that of PPR, but animals recovering from PPR may develop proliferative growths on the lips resembling orf, and the virus may be involved in the pathogenesis of the condition.  

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Contagious caprine pleuropneumonia occurs in many similar countries to PPR but does not usually give a high mortality in sheep, or have an accompanying severe enteritis.  

Contagious caprine pleuropneumonia occurs in many similar countries to PPR but does not usually give a high mortality in sheep, or have an accompanying severe enteritis.  

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Heartwater can give a high mortality rate in susecptible breeds, but without a stomatitis.

 

Heartwater can give a high mortality rate in susceptible breeds, but without a stomatitis.

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Detection of virus antigens by the agar gel immunodiffusion test (AGIDT) is a relatively simple, fast and cheap process. It is extremely useful as an initial test, but it does not discriminate between PPR and rinderpest viruses and further tests are needed to do this. Histopathology combined with immunohistochemical staining (e.g. immunoperoxidase) is a useful procedure because it is performed on formalin-fixed material and can discriminate between PPR and rinderpest when performed with specific monoclonal antibodies. Virus antigens can also be detected by immunocapture ELISA.  

Detection of virus antigens by the agar gel immunodiffusion test (AGIDT) is a relatively simple, fast and cheap process. It is extremely useful as an initial test, but it does not discriminate between PPR and rinderpest viruses and further tests are needed to do this. Histopathology combined with immunohistochemical staining (e.g. immunoperoxidase) is a useful procedure because it is performed on formalin-fixed material and can discriminate between PPR and rinderpest when performed with specific monoclonal antibodies. Virus antigens can also be detected by immunocapture ELISA.  

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Antigen-capture ELISA is sensitive and specific, using monoclonal antibodies to give a result with PPR virus and enabling differentiation from rinderpest in small ruminants (Libeau et al., 1994). The availability of the ELISA as a kit has undoubtedly assisted countries in the detection of PPR epidemics. PCR may be of advantage in testing tissues where virus cannot be detected by other means, including specimens for histopathology. However, the time taken to extract RNA, and undertake the RT-PCR is usually longer than that needed for CIEP, and higher technical standards are required to avoid false-positive reactions. Despite these issues it is now commonly used alongside ELISA.

Antigen-capture [[ELISA testing|ELISA]] is sensitive and specific, using monoclonal antibodies to give a result with PPR virus and enabling differentiation from rinderpest in small ruminants (Libeau et al., 1994). The availability of the ELISA as a kit has undoubtedly assisted countries in the detection of PPR epidemics. PCR may be of advantage in testing tissues where virus cannot be detected by other means, including specimens for histopathology. However, the time taken to extract RNA, and undertake the RT-PCR is usually longer than that needed for CIEP, and higher technical standards are required to avoid false-positive reactions. Despite these issues it is now commonly used alongside ELISA.

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Antibodies are strongly induced by infection, and become detectable from the diarrheic stage onwards. The prescribed test for international trade (that which is accepted as a basis for the veterinary certification of animals as having evidence of presence or absence of antibodies) is virus neutralisation (VNT; OIE, 2000). Since there is cross-neutralisation between antibodies to PPR and RPV, a positive VNT result to PPR virus needs to be compared to the titre obtained with RPV. The OIE considers that a serum is considered to be positive for PPR when the neutralisation titre is at least two-fold higher for PPR than for rinderpest. Virus neutralisation tests involve use of live virus and cell cultures, and therefore require well-equipped laboratories and biosecurity to prevent escape of virus. VNT is therefore mainly restricted to laboratories with sufficient expertise and through-put of samples to justify the investment involved. The tests are sensitive and specific, and enable differentiation of antibodies to rinderpest virus, should these occur as a result of use of RP vaccine in small ruminants or exposure to the type 1 lineage of RPV. Haemagglutination inhibition tests for antibody have also been described with good correlation with VNT (Raj et al., 2000). After countries have been declared free of rinderpest infection, it may be sufficient to use more simple antibody detection methods that do not require differentiation of RPV infection of small ruminants.

 

Antibodies are strongly induced by infection, and become detectable from the diarrhoeic stage onwards. The prescribed test for international trade (that which is accepted as a basis for the veterinary certification of animals as having evidence of presence or absence of antibodies) is virus neutralisation (VNT; OIE, 2000). Since there is cross-neutralisation between antibodies to PPR and RPV, a positive VNT result to PPR virus needs to be compared to the titre obtained with RPV. The OIE considers that a serum is considered to be positive for PPR when the neutralisation titre is at least two-fold higher for PPR than for rinderpest. Virus neutralisation tests involve use of live virus and cell cultures, and therefore require well-equipped laboratories and biosecurity to prevent escape of virus. VNT is therefore mainly restricted to laboratories with sufficient expertise and through-put of samples to justify the investment involved. The tests are sensitive and specific, and enable differentiation of antibodies to rinderpest virus, should these occur as a result of use of RP vaccine in small ruminants or exposure to the type 1 lineage of RPV. Haemagglutination inhibition tests for antibody have also been described with good correlation with VNT (Raj et al., 2000). After countries have been declared free of rinderpest infection, it may be sufficient to use more simple antibody detection methods that do not require differentiation of RPV infection of small ruminants.

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A live, attenuated strain (PSRV 75/1) of the PPR virus has been developed for use as a vaccine and provides protection for over 3 years. Previous trials (usually with RP vaccine) usually reported reduction in mortality, particularly in weaned young stock, and positive benefit-to-cost ratios.  

A live, attenuated strain (PSRV 75/1) of the PPR virus has been developed for use as a vaccine and provides protection for over 3 years. Previous trials (usually with RP vaccine) usually reported reduction in mortality, particularly in weaned young stock, and positive benefit-to-cost ratios.  

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Risk factors for occurrence of disease are the purchase of animals from markets, and free-range husbandry of animals, when PPRV is known to be present in the region.

Risk factors for occurrence of disease are the purchase of animals from markets, and free-range husbandry of animals, when PPRV is known to be present in the region.

Movement control, at the level of total standstill of livestock movements and banning of markets may be effective if enforceable and short-lasting in duration, since the incubation period is short. However, an effective quarantine of affected and in-contact animals for one month after the recovery of the last clinically affected case has been recommended (Rossiter and Taylor, 1993). These measures may be accompanied by a slaughter policy of animals on infected and in-contact premises, in addition to the ban on livestock movements, if the aim is rapid eradication. Measures that negatively affect livelihoods will be unpopular and difficult to enforce unless accompanied by incentives, and have rarely been implemented by authorities.

Movement control, at the level of total standstill of livestock movements and banning of markets may be effective if enforceable and short-lasting in duration, since the incubation period is short. However, an effective quarantine of affected and in-contact animals for one month after the recovery of the last clinically affected case has been recommended (Rossiter and Taylor, 1993). These measures may be accompanied by a slaughter policy of animals on infected and in-contact premises, in addition to the ban on livestock movements, if the aim is rapid eradication. Measures that negatively affect livelihoods will be unpopular and difficult to enforce unless accompanied by incentives, and have rarely been implemented by authorities.

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PPR is a list A disease of the OIE, and thus member states are required to inform the OIE of the occurrence of the disease in their territory. The OIE publishes recommendations for zoo-sanitary conditions and certification of trade in animals and livestock products from countries which are not recognized as having freedom from PPR disease (OIE, 2001b). The OIE recommends sanitary prophylaxis (movement control, quarantine of infected premises, with slaughter of infected animals and in-contacts) when the disease appears in previously PPR-free countries. The use of a stamping-out policy, involving slaughter of infecteds and in-contact animals on infected premises, can lead to a reduced period of time elapsing after the last case of disease has been reported before the country is internationally recognized as free of PPR.

PPR is a list A disease of the [http://www.oie.int/ OIE], and thus member states are required to inform the OIE of the occurrence of the disease in their territory. The OIE publishes recommendations for zoo-sanitary conditions and certification of trade in animals and livestock products from countries which are not recognized as having freedom from PPR disease (OIE, 2001b). The OIE recommends sanitary prophylaxis (movement control, quarantine of infected premises, with slaughter of infected animals and in-contacts) when the disease appears in previously PPR-free countries. The use of a stamping-out policy, involving slaughter of infected and in-contact animals on infected premises, can lead to a reduced period of time elapsing after the last case of disease has been reported before the country is internationally recognized as free of PPR.

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Gibbs EPJ, Taylor WP, Lawman MJP, Bryant J, 1979. Classification of peste des petits ruminants virus as the fourth member of the genus Morbillivirus. Intervirology, 11(5):268-274.

Gibbs EPJ, Taylor WP, Lawman MJP, Bryant J, 1979. Classification of peste des petits ruminants virus as the fourth member of the genus Morbillivirus. Intervirology, 11(5):268-274.

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OIE, 2000. The Manual of Standards for Diagnostic Tests and Vaccines. Paris, France: Office International Des Epizooties.

OIE, 2000. The Manual of Standards for Diagnostic Tests and Vaccines. Paris, France: Office International Des Epizooties.

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Rossiter PB, Taylor WP, 1993. Peste des Petits Ruminants. In: Infectious Diseases of Livestock, with special reference to Southern Africa. Chapter 75.

Rossiter PB, Taylor WP, 1993. Peste des Petits Ruminants. In: Infectious Diseases of Livestock, with special reference to Southern Africa. Chapter 75.

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[[Category:To Do - CABI review]]

[[Category:CABI Expert Review]][[Category:Sheep Viruses]][[Category:Goat Viruses]][[Category:Intestinal Diseases - Sheep]][[Category:Intestinal Diseases - Goat]][[Category:Respiratory Diseases - Sheep]][[Category:Respiratory Diseases - Goat]]

[[Category:Morbilliviruses]]

[[Category:Morbilliviruses]]