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Cattle plague.

Also know as: '''''Cattle plague

 

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== Introduction ==

== Introduction ==

Rinderpest is an acute to subacute contagious viral disease of ruminants and pigs that can cause morbidity and mortality rates in excess of ninety per cent, though inapparent infections also occur. The disease is characterized by necrosis and erosions in the gastrointestinal tract that result in severe diarrhoea and dehydration. It is caused by a morbillivirus, a member of a group of enveloped viruses forming a separate genus within the family Paramyxoviridae. Viruses in this genus included rinderpest virus (RPV) infecting cattle and other large ruminants, peste des petits ruminants virus (PPRV) infecting sheep and goats, canine distemper virus (CDV) which infects carnivores, human measles virus (MV), and other members in marine mammals. Members of the genus are closely related antigenically and are distinguished from the other paramyxoviruses by their lack of neuraminidase activity.

Rinderpest was an acute to subacute contagious viral disease of ruminants and pigs that could cause morbidity and mortality rates in excess of ninety per cent, though inapparent infections did also occur. The disease wass characterized by necrosis and erosions in the gastrointestinal tract that resulted in severe diarrhoea and dehydration. It was caused by a [[:Category:Morbilliviruses|morbillivirus]], a member of a group of enveloped viruses forming a separate genus within the family [[:Category:Paramyxoviridae|Paramyxoviridae]]. Viruses in this genus included rinderpest virus (RPV) infecting cattle and other large ruminants, [[Peste des Petits Ruminants|peste des petits ruminants virus (PPRV)]] infecting sheep and goats, [[Canine Distemper Virus|canine distemper virus (CDV)]] which infects carnivores, human measles virus (MV), and other members in marine mammals. Members of the genus are closely related antigenically and are distinguished from the other paramyxoviruses by their lack of neuraminidase activity.

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In terms of economic losses in domestic animals, rinderpest is the most important member of the group. It was eradicated from the UK in 1877, but continued to be endemic in Africa and Asia until very recently. It was present in Sudan and Somalia until the 1994 Global Rinderpest Eradication Programme (GREP) succeeded in its goal in 2011.

In terms of economic losses in domestic animals, rinderpest was the most important member of the group. It was eradicated from the UK in 1877, but continued to be endemic in Africa and Asia until very recently. It was present in Sudan and Somalia until the 1994 [[http://www.fao.org/ag/againfo/programmes/en/grep/home.html Global Rinderpest Eradication Programme (GREP)] succeeded in its goal in 2011.

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Cattle and buffallo show the most severe clinical signs of Rinderpest Virus. Sheep, goats and Asiatic pigs are also susceptible and may develop clinical disease. European breeds of pig undergo subclinical infection. Infection of wild artiodactyls with strains largely maintained in cattle caused a wide spectrum of clinical disease, ranging from very severe in African buffalo (''Syncerus caffer''), giraffe (''Giraffa camelopardalis''), eland (''Taurotragus oryx'') and kudu (''Tragelaphus strepciceros, T. imberbis'') through increasingly less severe syndromes in other antelopes to mild or atypical in impala (''Aepyceros melampus'') and subclinical in hippopotami (''Hippopotamus amphibius''). There was also variation in susceptibility to clinical disease between breeds, especially cattle. Most European cattle breeds (''Bos taurus'') are more susceptible than ''Bos indicus'' breeds. African humpless cattle, such as the Ankole in East Africa, are notoriously susceptible in comparison to East African zebus.  

Cattle and buffallo show the most severe clinical signs of Rinderpest Virus. Sheep, goats and Asiatic pigs are also susceptible and may develop clinical disease. European breeds of pig undergo subclinical infection. Infection of wild artiodactyls with strains largely maintained in cattle causes a wide spectrum of clinical disease, ranging from very severe in African buffalo (Syncerus caffer), giraffe (Giraffa camelopardalis), eland (Taurotragus oryx) and kudu (Tragelaphus strepciceros, T. imberbis) through increasingly less severe syndromes in other antelopes to mild or atypical in impala (Aepyceros melampus) and subclinical in hippopotami (Hippopotamus amphibius). There is also variation in susceptibility to clinical disease between breeds, especially cattle. Most European cattle breeds (Bos taurus) are more susceptible than Bos indicus breeds. African humpless cattle, such as the Ankole in East Africa, are notoriously susceptible in comparison to East African zebus.  

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Vectors and intermediate hosts are not involved in the transmission of rinderpest.

Vectors and intermediate hosts are not involved in the transmission of rinderpest.

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Infected animals excreted infectious virus in their ocular, nasal, oral and vaginal secretions and faeces. Excretion began 1 or 2 days before the onset of fever, the first clinical sign, and continued for 9 to 10 days after the start of pyrexia. Highest titres of virus were excreted during the early stages of clinical disease when epithelial lesions, especially those in the mouth, were developing to their maximum extent. Subsequently, the titres of excreted virus waned as antibody developed. Recovered cows may have aborted an infected foetus some weeks after apparent recovery, with virus excretion in their uterine and vaginal discharges.

Infected animals excrete infectious virus in their ocular, nasal, oral and vaginal secretions and faeces. Excretion begins 1 or 2 days before the onset of fever, the first clinical sign, and continues for 9 to 10 days after the start of pyrexia. Highest titres of virus are excreted during the early stages of clinical disease when epithelial lesions, especially those in the mouth, are developing to their maximum extent. Subsequently, the titres of excreted virus wane as antibody develops. Recovered cows may abort an infected foetus some weeks after apparent recovery, with virus excretion in their uterine and vaginal discharges.

The fragility of the virus ensures that most infectivity survives for only a few hours outside the host, though some may persist under favourable conditions for up to 2 to 4 days. Carcass decomposition inactivates the virus within 1 to 3 days.

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Spread of RV is effected almost exclusively by contact between infected and susceptible animals. Transmission by infected aerosols probably only occurs under ideal conditions of close proximity and gentle air currents, i.e. amongst housed animals. There is no carrier state in rinderpest and recovered animals do not excrete infectious RV and are not involved in the maintenance and transmission of the disease. The virus is not transmitted by arthropods and the potential for transmission through abortion is limited. Consequently, RV has a short direct cycle of infection and is spread by close contact. Under experimental conditions regular contact transmission can be difficult to achieve.

The fragility of the virus ensured that most infectivity survived for only a few hours outside the host, though some may have persisted under favourable conditions for up to 2 to 4 days. Carcass decomposition inactivated the virus within 1 to 3 days.

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In the field, rinderpest is maintained by large, heterogeneous populations of animals with a sufficient supply of new susceptibles. In Africa in recent times the endemic areas have been those with large cattle populations belonging to nomadic or semi-nomadic people, which ensures good mixing of the population, especially when restricted by the availability of water during dry seasons.

Spread of RV was effected almost exclusively by contact between infected and susceptible animals. Transmission by infected aerosols probably only occured under ideal conditions of close proximity and gentle air currents, i.e. amongst housed animals. There was no carrier state in rinderpest and recovered animals did not excrete infectious RV and were not involved in the maintenance and transmission of the disease. The virus was not transmitted by [[:Category:Arthropods|arthropods]] and the potential for transmission through abortion was limited. Consequently, RV had a short direct cycle of infection and was spread by close contact. Under experimental conditions regular contact transmission was difficult to achieve.

In highly susceptible populations rinderpest behaves in epidemic fashion with the virus infecting virtually all susceptible individuals and causing severe clinical disease in most age groups. Endemic rinderpest, however, is much milder and is maintained by young animals usually less than 2 years old that have lost their maternal immunity. Intermediate patterns also exist.

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Wildlife play an important role in rinderpest. In Asia wildlife have been described with clinical disease and such infected animals can transmit infection to other susceptible species, including domestic stock. However, the sizes and densities of wildlife populations are low and they are not considered to be involved in the maintenance of the virus in Asia. In Africa, however, the greater population sizes and densities, the larger number of susceptible species, and the frequency with which the disease used to be reported in wildlife have lead to considerable study of rinderpest in these species. Until the 1960s a widely held view was that wildlife could maintain the virus independently of cattle, though some authorities considered cattle to be the main reservoir of infection. However, when cell-culture-attenuated vaccine led to the eradication of the disease from cattle in Maasailand [East Africa] in the early 1960s, clinical disease also disappeared from wildlife. The absence of antibodies in wildebeest and other species born after 1963 supported this and as a consequence opinion changed to the view that wildlife could not maintain the virus, which is still widely held today.

In the field, rinderpest was maintained by large, heterogeneous populations of animals with a sufficient supply of new susceptibles. In Africa in recent times the endemic areas have been those with large cattle populations belonging to nomadic or semi-nomadic people, which ensured good mixing of the population, especially when restricted by the availability of water during dry seasons.

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== Clinical Signs ==

== Clinical Signs ==

The animal will at first become pyrexic, dull and depressed. Signs include ulcers, vesicles and erosions on the tongue and oral mucosa, causing ptyalsim, smacking of the lips and bruxism due to pain. There may also be diarrhoea +/- blood and mucous. Diarrhoea and breath will usually have a foul odour. Generally the animal will be weak, lethargic and have a reluctance to eat. There may be signs of weight loss or reduced weight gain and if in milk, the yield will be severely reduced. There may be occular signs such as excess lacrimation, blepharospasm and reddened conjunctiva. The animal may also be in respiratory distress with dyspnoea, tachypnoea, coughing and nasal dishcarge all possible clinical signs.

The animal would at first become pyrexic, dull and depressed. Signs included ulcers, vesicles and erosions on the tongue and oral mucosa, causing ptyalism, smacking of the lips and bruxism due to pain. There may also have been diarrhoea +/- blood and mucous. Diarrhoea and breath would usually have a foul odour. Generally the animal would be weak, lethargic and have a reluctance to eat. There may have been signs of weight loss or reduced weight gain and if in milk, the yield would be severely reduced. There may have been ocular signs such as excess lacrimation, blepharospasm and reddened conjunctiva. The animal may have also been in respiratory distress with dyspnoea, tachypnoea, coughing and nasal discharge all possible clinical signs.

 

== Diagnosis ==

== Diagnosis ==

History, clinical signs and signalment/ region etc are characteristic of the disease. A presumptive diagnosis of rinderpest can be made on the basis of the clinical signs and gross pathology. However, in countries where the disease is not prevalent, and especially in regions dependent on livestock exports, it is essential to obtain laboratory confirmation of the diagnosis as soon as possible. Countries where rinderpest is either endemic or a high risk should treat any syndrome resembling rinderpest as such until proven otherwise. This will allow immediate steps to be taken to control the disease and restrict losses.

History, clinical signs and signalment/ region etc were characteristic of the disease. A presumptive diagnosis of rinderpest could be made on the basis of the clinical signs and gross pathology. However, in countries where the disease was not prevalent, and especially in regions dependent on livestock exports, it was essential to obtain laboratory confirmation of the diagnosis as soon as possible. Countries where rinderpest was either endemic or a high risk should treat any syndrome resembling rinderpest as such until proven otherwise. This would allow immediate steps to be taken to control the disease and restrict losses.

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The collection of adequate quantities of appropriate specimens greatly increases the chances of an accurate laboratory diagnosis. A sample of animals in the acute stage of the disease should be sampled. Animals that are dead, moribund or have had diarrhoea and mucopurulent discharges for more than 3 days are less reliable sources of virus or antigen as the levels of these decline with the onset of antibody development. From each selected animal, whole blood should be collected for serum antibody assay, and in anti-coagulant for virus isolation from leukocytes, a biopsy from a superficial lymph node, debris from oral lesions, and ocular and nasal swabs for virus isolation and antigen or nucleic acid detection. If possible, two or more animals should be killed for necropsy examination and collection of up to three universal bottles of spleen and mesenteric lymph nodes. All specimens should be collected and bottled aseptically, kept cool on ice (but not frozen) and transported as rapidly as possible to a diagnostic laboratory. Glycerol should not be used as a preservative because it inactivates RV. The use of anti-proteases increases the survival of RV antigens in tissue suspensions and reduces the degradation of RNA.

The collection of adequate quantities of appropriate specimens greatly increases the chances of an accurate laboratory diagnosis. A sample of animals in the acute stage of the disease should be sampled. Animals that are dead, moribund or have had diarrhoea and mucopurulent discharges for more than 3 days are less reliable sources of virus or antigen as the levels of these decline with the onset of antibody development. From each selected animal, whole blood should be collected for serum antibody assay, and in anti-coagulant for virus isolation from leukocytes, a biopsy from a superficial lymph node, debris from oral lesions, and ocular and nasal swabs for virus isolation and antigen or nucleic acid detection. If possible, two or more animals should be killed for necropsy examination and collection of up to three universal bottles of spleen and mesenteric lymph nodes. All specimens should be collected and bottled aseptically, kept cool on ice (but not frozen) and transported as rapidly as possible to a diagnostic laboratory. Glycerol should not be used as a preservative because it inactivates RV. The use of anti-proteases increases the survival of RV antigens in tissue suspensions and reduces the degradation of RNA.

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