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| − | Animal Health and Production Compendium
| + | == Synonyms == |
| | + | Goat plague, pest of sheep and goats, pneumoenteritis complex, pseudorinderpest of small ruminants, stomatitis-pneumoenteritis syndrome. |
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| − | Selected sections for: peste des petits ruminants
| + | == Introduction == |
| − | Identity Pathogen/s Overview Distribution Distribution Table Hosts/Species Affected Host Animals Systems Affected List of Symptoms/Signs Epidemiology Zoonoses and Food Safety Pathology Diagnosis Disease Course Disease Treatment Table Disease Treatment Vaccines Prevention and Control References Links to Websites Images
| + | 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 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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| − | Datasheet Type(s): Animal Disease
| + | 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. |
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| − | Identity
| + | The development of tests for the confirmation of the agent and the differentiation from rinderpest was only achieved in the late 1980s, and recent recognition of the infection in many African and Asian countries can be attributed to availability of methods for specific detection of virus and antibodies. However, given the rapidity of spread of epidemics and the lack of a carrier state, it is likely that infection is not maintained in some areas because of inadequate supply of susceptible animals and some incursions of disease appear self-limiting. Presence of infection in a country in one year does not imply endemic infection. However, the risk of trans-boundary spread of this disease is high because sheep and goats are easily transported and trade across borders is difficult to control. |
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| − | Preferred Scientific Name
| + | Disease occurs in goats and sheep, and has been recognized in captive wild ungulates from families of Gazellinae (Dorcas gazelle), Caprinae (Nubian ibex and Laristan sheep) and Hippotraginae (gemsbok). Experimentally, severe disease also occurs in white-tailed deer. Cattle undergo mainly subclinical reactions, and pigs develop a viraemia. |
| − | peste des petits ruminants
| + | Seasonality in breeding, in marketing and in crop production all appear related to disease occurrence. In arid and semi-arid zones, surplus animals are sold during the dry season, which may lead to spread of infection into other areas, especially if sale occurs via markets. In humid zones, sale of surplus animals may occur at the start of the rains, with tethering of animals to avoid crop damage. Both sale of animals and close housing/tethering can increase risk of transmission if virus is introduced. The wet season can also predispose to secondary bacterial infections, exacerbating the viral pneumonia. |
| − | International Common Names
| + | <br> |
| − | English acronym
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| − | PSR
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| − | French acronym
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| − | PPR
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| − | English
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| − | goat plague, pest of sheep and goats, pest of small ruminants, peste des petits ruminants - exotic, pneumoenteritis complex, pseudorinderpest of small ruminants, stomatitis-pneumoenteritis syndrome
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| − | Local Common Names
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| − | Nigeria
| + | PPRV has a direct life cycle, maintained by infected animal to susceptible animal transmission, without involvement of carrier animals or vectors. The underlying requirement is a regular supply of susceptible hosts plus sufficient animal movement to allow mixing of the population (Rossiter and Taylor, 1993). Risk factors include unconfined husbandry, whether in urban or rural settings. The population size required to maintain infection is not known, but small populations probably cannot maintain infection for long and, therefore, given the rapid population turnover of small ruminants, disease associated with re-introduction can be severe. Severe epidemics probably reflect introduction of virus into areas with mainly susceptible populations and breeds, rather than endemic presence of infection throughout the year (Rossiter and Taylor, 1993). There is one serotype of virus, and immunity is long-lasting, probably life-long. Because colostral antibody protects young animals, in endemic areas most disease occurs in animals after waning of colostral immunity, from 4 months to 2 years of age, with protection of animals which have had previous exposure. Mortality rate in areas considered endemic may be in the region of 4-5% whereas rates from 20% to 90% in outbreaks have frequently been reported under epidemic conditions (Rossiter and Taylor, 1993). Climate appears to play a role in increasing the severity of disease, via secondary infections exacerbating the infection of the lung, but also affects the migration of pastoralist flocks in response to rainfall and drought and the resultant exposure to infection. |
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| | + | == Clinical Signs == |
| | + | Signs include pyrexia, 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. The animal will have diarrhoea which may have mucous or blood in. |
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| | + | There may also be a foul odour to the breath and nasal discharge, dyspnoea, tachypnoea and coughing may be present. The animal may also be lacrimating excessively. |
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| − | Overview
| + | <br> |
| − | 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, but not south of a line from Cameroon to the Sudan. 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 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). Although it had been previously proposed that PPR virus (PPRV) emerged from rinderpest virus (RPV) more recently than RPV diverged from measles virus and canine distemper virus, comparison of gene sequences suggest PPRV is no more related to RPV than to non-ruminant morbilliviruses (Das et al., 2000). 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. Under such conditions there is a high social impact of disease, since small ruminants often represent a readily convertible currency in smallholder agriculture. Control by vaccination is merited in many endemic countries, and the benefit-to-cost ratio is usually high. The disease is also important as a complication in the eradication of rinderpest, since PPRV can infect cattle and resultant antibodies must be distinguished. The use of rinderpest vaccine to protect against PPR is no longer recommended, to avoid the possibility of RP antibody detection in cattle or small ruminants.
| + | == Diagnosis == |
| | + | A manual on the diagnosis of PPR has been produced (FAO, 1998). Suspicion of PPR would be raised by signs of stomatitis – or pneumonitis, with enteritis in several animals. A high mortality and morbidity rate would be expected in outbreaks occurring in non-endemic areas, or where outbreaks have not occurred for some time and animals are not vaccinated. |
| | + | <br> |
| | + | 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. 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. 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. 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. 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. 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. Heartwater can give a high mortality rate in susecptible breeds, but without a stomatitis. |
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| − | This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's Handistatus database on disease occurrence. Please see the AHPC library for further information on this disease from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.
| + | PPRV is present at a high concentration in secretions and tissue samples in the early stages of the disease, but rapidly becomes difficult to detect after development of antibody responses. Collection of specimens from animals which have a serous ocular-nasal discharge and fever is preferable compared to later-stage signs of necrotic stomatitis-enteritis. In live animals, swabs should be made of the conjunctival discharges from the nasal and buccal mucosae. Whole blood should be collected in anticoagulant for virus isolation, polymerase chain reaction (PCR) and haematology. From the necropsy examination of two to three animals, lymph nodes, especially the mesenteric and bronchial nodes, lungs, spleen and intestinal mucosae should also be collected aseptically, chilled on ice and transported under refrigeration. Fragments of organs collected for histopathology are placed in 10% formalin. At the end of the outbreak, blood can be collected for serological diagnosis. Post-mortem examination of carcasses can be valuable, particularly in wildlife and in situations where samples cannot be kept in suitable conditions during transport to the laboratory, with a view to collection of specimens for detection of multi-nucleated giant cells by histopathology. Infection can be confirmed by identification of the agent with specific tests. Detection of a rise in titre of antibody could also be used, with paired samples collected 14-21 days apart. |
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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. |
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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. |
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| − | Distribution
| + | == Pathology == |
| − | The development of tests for the confirmation of the agent and the differentiation from rinderpest was only achieved in the late 1980s, and recent recognition of the infection in many African and Asian countries can be attributed to availability of methods for specific detection of virus and antibodies. However, given the rapidity of spread of epidemics and the lack of a carrier state, it is likely that infection is not maintained in some areas because of inadequate supply of susceptible animals and some incursions of disease appear self-limiting. Presence of infection in a country in one year does not imply endemic infection. However, the risk of trans-boundary spread of this disease is high because sheep and goats are easily transported and trade across borders is difficult to control. Recent extension of infection into Turkey highlights the risk to previously free areas.
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| − | In addition to the countries listed in the table, the disease may also occur in the following countries (OIE, 2001a): Kuwait, Lebanon, Burkina Faso, Central African Republic, Chad, Egypt, Gambia, Mauritania, Somalia, Sudan. Disease is suspected in Bahrain and Uganda (OIE, 2001a).
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| − | Distribution Table
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| − | Hosts/Species Affected
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| − | Disease occurs in goats and sheep, and has been recognized in captive wild ungulates from families of Gazellinae (Dorcas gazelle), Caprinae (Nubian ibex and Laristan sheep) and Hippotraginae (gemsbok). Experimentally, severe disease also occurs in white-tailed deer. Cattle undergo mainly subclinical reactions, and pigs develop a viraemia. A PPR-like virus was recently detected in a disease in camels (Roger et al., 2001). West African Dwarf goats are more susceptible than European breeds (Scott, 1990), and sheep and goats of the Sahelian zones are more resistant than dwarf types from humid zones to the south (Bourdin, 1983). Seasonality in breeding, in marketing and in crop production all appear related to disease occurrence. In arid and semi-arid zones, surplus animals are sold during the dry season, which may lead to spread of infection into other areas, especially if sale occurs via markets. In humid zones, sale of surplus animals may occur at the start of the rains, with tethering of animals to avoid crop damage. Both sale of animals and close housing/tethering can increase risk of transmission if virus is introduced. The wet season can also predispose to secondary bacterial infections, exacerbating the viral pneumonia.
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| − | Host Animals
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| − | Animal name Context
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| − | Bos indicus (zebu) Domesticated host
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| − | Bubalus bubalis (buffalo)
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| − | Capra hircus (goats) Domesticated host
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| − | Ovis aries (sheep) Domesticated host
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| − | Systems Affected
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| − | Digestive - Large Ruminants
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| − | Digestive - Small Ruminants
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| − | Respiratory - Large Ruminants
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| − | Respiratory - Small Ruminants
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| − | Skin - Large Ruminants
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| − | Skin - Small Ruminants
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| − | List of Symptoms/Signs
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| − | Sign Life Stages Type
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| − | Digestive Signs
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| − | Tongue ulcers, vesicles, erosions, sores, blisters, cuts, tears Sign [C]
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| − | Mucous, mucoid stools, faeces Sign [C]
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| − | Bloody stools, faeces, haematochezia Sign [C]
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| − | Anorexia, loss or decreased appetite, not nursing, off feed Sign [C]
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| − | Congestion oral mucous membranes, erythema, redness oral mucosa Sign [C]
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| − | Excessive salivation, frothing at the mouth, ptyalism S1 ( All Stages ) Sign [C]
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| − | Diarrhoea S1 ( All Stages ) Diagnosis [C]
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| − | Oral mucosal ulcers, vesicles, plaques, pustules, erosions, tears S1 ( All Stages ) Diagnosis [C]
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| − | General Signs
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| − | Fever, pyrexia, hyperthermia S1 ( All Stages ) Sign [C]
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| − | Dehydration S1 ( All Stages ) Sign
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| − | Tenesmus, straining, dyschezia S1 ( All Stages ) Sign
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| − | Weight loss Sign [C]
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| − | Generalized weakness, paresis, paralysis Sign [C]
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| − | Inability to stand, downer, prostration Sign [C]
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| − | Sweating excessively, hyperhidrosis Sign [C]
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| − | Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift Sign [C]
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| − | Nervous Signs
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| − | Dullness, depression, lethargy, depressed, lethargic, listless Sign [C]
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| − | Ophthalmology Signs
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| − | Purulent discharge from eye Sign [C]
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| − | Chemosis, conjunctival, scleral edema, swelling Sign [C]
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| − | Conjunctival, scleral, redness Sign [C]
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| − | Corneal edema, opacity Sign [C]
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| − | Lacrimation, tearing, serous ocular discharge, watery eyes S1 ( All Stages ) Diagnosis [C]
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| − | Pain/Discomfort Signs
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| − | Mouth, oral mucosal or tongue pain S1 ( All Stages ) Sign
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| − | Reproductive Signs
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| − | Abortion or weak newborns, stillbirth S1 ( All Stages ) Sign [C]
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| − | Papule, pustule, vesicle, ulcer penis or prepuce Sign [C]
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| − | Vaginal or cervical ulcers, vesicles, erosions, tears, papules, pustules Sign [C]
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| − | Agalactia, decreased, absent milk production Sign [C]
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| − | Respiratory Signs
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| − | Dyspnea, difficult, open mouth breathing, grunt, gasping Sign [C]
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| − | Abnormal breathing sounds of the upper airway, airflow obstruction, stertor, snoring Sign [C]
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| − | Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs Sign [C]
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| − | Epistaxis, nosebleed, nasal haemorrhage, bleeding Sign [C]
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| − | Coughing, coughs S1 ( All Stages ) Sign [C]
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| − | Dull areas on percussion of chest, thorax S1 ( All Stages ) Sign
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| − | Purulent nasal discharge S1 ( All Stages ) Diagnosis [C]
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| − | Mucoid nasal discharge, serous, watery S1 ( All Stages ) Diagnosis [C]
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| − | Abnormal breath odor, foul odor mouth S1 ( All Stages ) Sign
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| − | Increased respiratory rate, polypnea, tachypnea, hyperpnea S1 ( All Stages ) Sign [C]
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| − | Sneezing, sneeze S1 ( All Stages ) Sign
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| − | Skin/Integumentary Signs
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| − | Skin crusts, scabs Sign [C]
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| − | Epidemiology
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| − | PPRV has a direct life cycle, maintained by infected animal to susceptible animal transmission, without involvement of carrier animals or vectors. The underlying requirement is a regular supply of susceptible hosts plus sufficient animal movement to allow mixing of the population (Rossiter and Taylor, 1993). Risk factors include unconfined husbandry, whether in urban or rural settings. The population size required to maintain infection is not known, but small populations probably cannot maintain infection for long and, therefore, given the rapid population turnover of small ruminants, disease associated with re-introduction can be severe. Severe epidemics probably reflect introduction of virus into areas with mainly susceptible populations and breeds, rather than endemic presence of infection throughout the year (Rossiter and Taylor, 1993). Re-introduction of infection at intervals appear frequently related to livestock movement into areas, for example introduction for slaughter at festivals (Bonniwell, 1980). There is one serotype of virus, and immunity is long-lasting, probably life-long. Because colostral antibody protects young animals, in endemic areas most disease occurs in animals after waning of colostral immunity, from 4 months to 2 years of age, with protection of animals which have had previous exposure. Serological studies indicate that many, if not most, infections are subclinical or insufficiently severe to attract attention, and this may be related to breed resistance. Mortality rate in areas considered endemic may be in the region of 4-5% whereas rates from 20% to 90% in outbreaks have frequently been reported under epidemic conditions (Rossiter and Taylor, 1993). Climate appears to play a role in increasing the severity of disease, via secondary infections exacerbating the infection of the lung, but also affects the migration of pastoralist flocks in response to rainfall and drought and the resultant exposure to infection.
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| − | The virus will infect a range of ruminant hosts, but appears to cause disease in only goats, sheep, certain antelope species and occasionally water buffalo (Govindarajan et al, 1997). The virus will infect cattle and pigs, but subclinically; potentially these species might be involved in transmission between small-ruminant populations, although evidence that this is important in the field is lacking. Infection of cattle with PPRV protects against rinderpest virus, and the exposure rates of cattle in West Africa to PPRV may have contributed to a failure to induce antibodies to RPV after vaccination (Anderson and McKay, 1994), and also to the rapidity of eradication efforts against RPV in this region. Antibodies to most virulent RPV strains can be distinguished from those to PPRV in cattle by use of monoclonal antibody based tests, although some low-virulence RPV strains appear to share antigenic determinants with PPRV. PPR virus isolates differ in their pathogenicity for each host, with some strains resulting in more disease in sheep than goats. However, the outcome of infection is also markedly affected by animal breed, with some breeds from Sahelian countries showing marked resistance in contrast to those of West African humid zones (Bourdin, 1983).
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| − | Zoonoses and Food Safety
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| − | PPR virus has not been shown to present any risk to human health. However, the carcasses of animals suffering from PPR are unlikely to provide good-quality meat and should be buried or destroyed by heat.
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| − | 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 lympadenopathy. |
| − | | + | <br> |
| | 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. |
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| − | Diagnosis
| + | == Treatment and Control == |
| − | Clinical Diagnosis
| + | Chloramphenicol, penicillin, streptomycin can each be used and should be given intramuscularly for 5 days. Fluid therapy is also useful as a supportive treatment aswell as electrolyte replacement. |
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| − | A manual on the diagnosis of PPR has been produced (FAO, 1998). Suspicion of PPR would be raised by signs of stomatitis – or pneumonitis, with enteritis in several animals. A high mortality and morbidity rate would be expected in outbreaks occurring in non-endemic areas, or where outbreaks have not occurred for some time and animals are not vaccinated. The occurrence of both stomatitis, with erosions/ulcerations of epithelial surfaces in the oral cavity, together with diarrhoea, occurs in few other single diseases of sheep and goats. In an outbreak situation, early signs of infection, such as oculo-nasal discharges and fever, would be expected for in-contact animals, if some of the group have reached the late stage of the disease or have died. In most countries PPR is a notifiable disease and the authorities require to be informed if the infection is suspected. Given the infectivity of individual animals, immediate actions or advice to community leaders to contain movement of in-contact animals are important to reduce local spread while investigations are proceeding.
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| − | Differential Diagnosis
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| − | Other conditions to be considered are: rinderpest in small ruminants, contagious caprine pleuropneumonia, bluetongue, pasteurellosis, contagious ecthyma, foot-and-mouth disease, heartwater, coccidiosis, 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.
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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.
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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.
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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. 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. Heartwater can give a high mortality rate in susecptible breeds, but without a stomatitis.
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| − | Laboratory Diagnosis
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| − | Detection of the virus
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| − | PPRV is present at a high concentration in secretions and tissue samples in the early stages of the disease, but rapidly becomes difficult to detect after development of antibody responses. Collection of specimens from animals which have a serous ocular-nasal discharge and fever is preferable compared to later-stage signs of necrotic stomatitis-enteritis. The Manual of Standards of the Office International des Epizooties (OIE, 2000) gives a description of the recommended samples to be collected. In live animals, swabs should be made of the conjunctival discharges from the nasal and buccal mucosae. Whole blood should be collected in anticoagulant for virus isolation, polymerase chain reaction (PCR) and haematology. From the necropsy examination of two to three animals, lymph nodes, especially the mesenteric and bronchial nodes, lungs, spleen and intestinal mucosae should also be collected aseptically, chilled on ice and transported under refrigeration. Fragments of organs collected for histopathology are placed in 10% formalin. At the end of the outbreak, blood can be collected for serological diagnosis. The priority is therefore to collect suitable specimens from early cases, after discussion with the national veterinary laboratory and Government officers of the country concerned as to their capability and preferred system for laboratory confirmation. Post-mortem examination of carcasses can be valuable, particularly in wildlife and in situations where samples cannot be kept in suitable conditions during transport to the laboratory, with a view to collection of specimens for detection of multi-nucleated giant cells by histopathology. Infection can be confirmed by identification of the agent with specific tests. Detection of a rise in titre of antibody could also be used, with paired samples collected 14-21 days apart.
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| − | | |
| − | Several methods for detection of virus are recognized by the Office International des Epizooties (OIE, 2000). Of these, agar gel immuno-diffusion (AGID) and counter-immuno-electrophoresis (CIEP) are relatively simple and suitable for small-scale field centres and simple laboratories. The latter gives a faster result than the former, enabling detection in less than 2 hours. Where polyclonal antisera are used, a positive result will not be distinguished from rinderpest virus and subsequent tests to confirm the identity are required. 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. Molecular tests using gene probes have been superseded by PCR-based tests (Forsyth and Barrett, 1995). 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. Other tests have been described, including simple staining methods for detecting syncitia in conjunctival cells collected onto glass slides which are suitable for simple field use (Sumption et al., 1998), and monoclonal-based staining of such cells, or infected cells in histopathological sections (Saliki et al., 1994).
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| − | | |
| − | The OIE Manual (OIE, 2000) recommends efforts are made to isolate the virus from outbreaks of disease, and this is particularly relevant, although more difficult, in countries where it is suspected for the first time. The FAO (Food and Agriculture Organization of the United Nations) Reference Laboratory for PPR is given on the OIE website, and is currently at CIRAD-EMVT, Montpellier, France; they can advise on the use of this technique for virus identification in field samples.
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| − | | |
| − | | |
| − | Serological tests
| |
| − | | |
| − | | |
| − | 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 development of competition ELISA (C-ELISA) tests using monoclonal antibodies to either H (Anderson and McKay, 1994) or N (Libeau et al., 1995) antigens has extended the access to serological tests, and proved valuable in investigation of PPR epidemiology in the field. 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. Kits are available from international organizations (IAEA, Vienna) and from the World Reference Laboratory for PPR in France, and the Institute for Animal Health in Pirbright, UK. 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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| − | | |
| − | | |
| − | Disease Course
| |
| − | The pathogenesis is little studied but is assumed to be essentially similar to rinderpest virus, with infection occurring via aerosols, or ingestion by nuzzling or licking, with entry through the oropharynx and subsequent multiplication in the draining lymph nodes, and thereafter in lymph nodes through the body. Virus is then released which enters the circulation and is transported to the epithelium, where it multiplies in susceptible cells, resulting in the development of lesions and disease signs associated with damage to these sites (Rossiter and Taylor, 1993).
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| − | | |
| − | The course of infection is swift, with an incubation period of 2 to 6 days, with death usually occurring within 14 days of infection, 5 to 7 days after onset of pyrexia. The course of infection is development of fever, followed by ocular and nasal discharges and later erosions of the epithelial surfaces of the mouth and/or gums and onset of diarrhoea. Death occurs by dehydration, complicated by pneumonia.
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| − | | |
| − | The first signs are of fever, with a serous nasal discharge, followed within hours by depression. Pale areas of necrosis become visible on the gums, which develop into erosions develop in the mucous membranes lining the upper alimentary, upper respiratory and uro-genital tracts 1 to 2 days after onset of fever. Salivation becomes profuse, and the nasal discharge becomes muco-purulent and may block the nostrils, and muco-purulent ocular secretions may mat the eyelids together. Ulceration of the lesions in the alimentary tract contributes to a debilitating diarrhoea, and rapid loss of condition. Pneumonia commonly occurs, with frequent secondary infections with Pasteurella, and other latent infections including Mycoplasma capri, adenoviruses, orf virus and dermatophilosis. The condition is rapidly debilitating and death may rapidly occur after development of the diarrhoea/pneumonia. Affected animals have an exceptionally miserable appearance, and recovery is slow, often accompanied by growths on the lips, attributed to recrudescence of orf virus and/or exacerbation of Dermatophilus congolense infection (Scott, 1990).
| |
| − | | |
| − | | |
| − | Disease Treatment Table
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| − | | |
| − | Drug Dosage, administration and withdrawal times Life stages Adverse affects Drug resistance Type
| |
| − | norfloxacin For treatment of secondary bacterial pneumonia - intramuscular at 2.5 mg/kg body weight together with oral and intravenous administration of electrolytes. Always seek veterinary advice before administering treatment. All Stages No Drug
| |
| − | PSRV75/1 (attenuated strain of PPR virus) According to manufacturer's instructions. Always seek veterinary advice before administering treatment. All Stages No Vaccine
| |
| − | | |
| − | | |
| − | Disease Treatment
| |
| − | | |
| − | Chloramphenicol 10 ml/kg body weight, penicillin 10,000 IU/kg, streptomycin 10 mg/kg, each given intramuscularly for 5 days), intestinal sedatives (Entero Sediv, 20 ml/kg for 4 days orally) and fluid therapy (Pedialyte, 30 ml/kg, for 4 days subcutaneously) were used to treat pneumonia, diarrhoea and restore body fluid ionic balance (Wosu, 1989).
| |
| − | | |
| − | | |
| − | Vaccines
| |
| − | | |
| − | Vaccine Dosage, Administration and Withdrawal Times Life Stages Adverse Affects
| |
| − | PSRV75/1 (attenuated strain of PPR virus) According to manufacturer's instructions. Always seek veterinary advice before administering treatment. -Sheep & Goats: All Stages
| |
| − | | |
| − | | |
| − | Prevention and Control
| |
| − | Immunization and Vaccines
| |
| − | | |
| − | | |
| − | 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. This vaccine has superseded the use of an attenuated rinderpest vaccine, whose use is no longer recommended to avoid any potential problem with the serological identification of residual foci of rinderpest circulation. Previous trials (usually with RP vaccine) usually reported reduction in mortality, particularly in weaned young stock, and positive benefit-to-cost ratios. A reduction in mortality of 24% was reported in Nigeria compared to controls, for a combined vaccination and dipping programme (Reynolds and Francis, 1988). In Cameroon, a benefit to cost ratio of between 2.26 and 4.23 was reported for goats and sheep through use of PPR vaccination and strategic anthelminthic treatment (Awa et al., 2000). In Niger, Stem (1993) estimated an internal rate of return of 900% for a PPRV vaccination programme over 5 years.
| |
| − | | |
| − | | |
| − | Husbandry methods and good practice
| |
| − | | |
| − | | |
| − | 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. In Oman, animals under controlled grazing (e.g. fenced or paddocked) were at lower risk than free-ranging urban livestock (Taylor et al., 1990).
| |
| − | | |
| − | | |
| − | Local Control
| |
| − | | |
| | | | |
| | + | 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. |
| | + | <br> |
| | + | 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. |
| − | | + | <br> |
| − | | |
| − | National and International Control Policy
| |
| − | | |
| | | | |
| | 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 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. |
| | | | |
| − | The Animal Health Code of the OIE (OIE, 2001b) considers:
| + | <br> |
| − | the period for quarantine purposes, ('incubation period') for the peste des petits ruminants (PPR) to be 21 days.
| |
| − | A country may be considered free from PPR when it has been shown that PPR has not been present for at least the past 3 years.
| |
| − | Or, this period shall be 6 months after the slaughter of the last affected animal for countries in which a stamping-out policy is practised with or without vaccination against PPR.
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| − | | |
| − | The Code also recognizes the presence of zones of infection, which shall be considered as infected with PPR until:
| |
| − | at least 21 days have elapsed after the confirmation of the last case and the completion of a stamping-out policy and disinfection procedures, or
| |
| − | until 6 months have elapsed after the clinical recovery or death of the last affected animal if a stamping-out policy was not practised.
| |
| − | | |
| − | The risk of entry of PPR into PPR-free countries is dealt with mainly by a strict prohibition of the import of live animals, recognizing that the majority of importations of virus have been via entry of live animals. The Animal Health Code of the OIE recognizes that Veterinary Administrations of PPR-free countries may prohibit importation or transit through their territory, from countries considered infected with PPR:
| |
| − | | |
| − | of domestic and wild ruminants,
| |
| − | semen of ruminants,
| |
| − | embryos/ova of ruminants,
| |
| − | fresh meat of domestic and wild ruminants,
| |
| − | meat products of domestic and wild ruminants that have not been processed to ensure the destruction of the PPR virus,
| |
| − | products of animal origin (from ruminants) intended for use in animal feeding or for agricultural or industrial use which have not been processed to ensure the destruction of the PPR virus,
| |
| − | products of animal origin (from ruminants) intended for pharmaceutical or surgical use which have not been processed to ensure the destruction of the PPR virus,
| |
| − | pathological material and biological products (from ruminants) which have not been processed to ensure the destruction of the PPR virus.
| |
| − | For each of the above, the Animal Health Code recommends the use of sanitary measures, including (where required) laboratory test results, backed by international veterinary certificates to ensure that within the boundary of error asociated with test or quarantine procedures, the animals and animal products are free of disease and/or infection at the time of importation. For example, for importation of small ruminants from countries not free of PPR, Veterinary Administrations should require the presentation of an international veterinary certificate attesting that the animals:
| |
| − | | |
| − | showed no clinical sign of PPR on the day of shipment;
| |
| − | were kept since birth, or for the past 21 days, in an establishment where no case of PPR was officially reported during that period, and that the establishment was not situated in a PPR-infected zone; and/or
| |
| − | were kept in a quarantine station for the 21 days prior to shipment;
| |
| − | have not been vaccinated against PPR; or were vaccinated against PPR: not less than 15 days and not more than 4 months prior to shipment in the case of animals for breeding or rearing; or not less than 15 days and not more than 12 months prior to shipment in the case of animals for slaughter.
| |
| − | Importing countries may in addition impose additional conditions on the importation, that is, do not allow importation despite these conditions being fulfilled; they might be challenged in international courts, with the OIE acting as independent assessors of the risk involved in the importation.
| |
| − | | |
| − | There is at present no international programme for PPR control; the situation differs in each country according to the level of state subsidy, if any, for disease control programmes and the degree of emphasis on the private sector to undertake vaccination under a demand and supply system. Positive ratios for benefit-to-cost of national programmes have been reported (Stem, 1993) and increase in small-ruminant numbers in Oman was attributed to control of PPR by vaccination (Rossiter and Taylor, 1993). Additional controls on PPRV may be required if the infection adapts to fill the void left by lack of immunity to RP after eradication of rinderpest, since PPRV can infect cattle and in almost all PPR-endemic countries, RP has been present for at least the twentieth century. Morbilliviruses are highly adaptable, and the potential of PPRV to adapt to transmission via cattle requires monitoring, and continued vigilance for RP-like infections after RP eradication.
| |
| − | | |
| − | | |
| − | References
| |
| | | | |
| − | Anderson J, McKay JA, 1994. The detection of antibodies against peste des petits ruminants virus in cattle, sheep and goats and the possible implications to rinderpest control programmes. Epidemiology and Infection, 112(1):225-231; 7 ref.
| + | == References == |
| − | Awa DN, Njoya A, Ngo Tama AC, 2000. Economics of prophylaxis against peste des petits ruminants and gastrointestinal helminthosis in small ruminants in north Cameroon. Tropical Animal Health and Production, 32(6):391-403; 17 ref.
| |
| − | Ayaz MM, Muhammad G, Rehman MS, 1997. Pneumo-enteritis syndrome among goats in Dera Ghazi Khan. Pakistan Veterinary Journal, 17(2):97-99; 9 ref.
| |
| − | Bonniwell MA, 1980. The use of tissue culture rinderpest vaccine (TCRV) to protect sheep and goats against "peste des petits ruminants" in the Ashanti region of Ghana. Bulletin de L'Office International des Epizooties, 92(11/12):1233-1238.
| |
| − | Bourdin P, 1983. History, epidemiology and economic significance of PPR in west Africa and Nigeria in particular. In: Hill DH, ed. Peste des petitis ruminants (PPR) in sheep and goats. Proceedings of the International Workshop, Ibadan, Nigeria, 1980. Addis Ababa, Ethiopia: International Livestock Centre for Africa.
| |
| − | Das SC, Baron MD, Barrett T, 2000. Recovery and characterization of a chimeric rinderpest virus with the glycoproteins of peste-des-petits-ruminants virus: homologous F and H proteins are required for virus viability. Journal of Virology, 74(19):9039-9047; 50 ref.
| |
| | Diallo A, Barrett T, Barbron M, Subbarao SM, Taylor WP, 1989. Differentiation of rinderpest and peste des petits ruminants viruses using specific cDNA clones. Journal of Virological Methods, 23(2):127-136; 24 ref. | | Diallo A, Barrett T, Barbron M, Subbarao SM, Taylor WP, 1989. Differentiation of rinderpest and peste des petits ruminants viruses using specific cDNA clones. Journal of Virological Methods, 23(2):127-136; 24 ref. |
| | + | <br> |
| | FAO, 1998. Recognising peste des petits ruminants. A field manual. Rome, Italy: Food and Agriculture Organisation (FAO). | | FAO, 1998. Recognising peste des petits ruminants. A field manual. Rome, Italy: Food and Agriculture Organisation (FAO). |
| − | Forsyth MA, Barrett T, 1995. Evaluation of polymerase chain reaction for the detection and characterisation of rinderpest and peste des petits ruminants viruses for epidemiological studies. Virus Research, 39(2/3):151-163; 22 ref.
| + | <br> |
| | Gargadennec L, Lalanne A, 1942. La peste-des-petits-ruminants. Bulletin du Service Zootechnique Epizootique du Afrique Occidentale Francaise, 5:16-21. | | Gargadennec L, Lalanne A, 1942. La peste-des-petits-ruminants. Bulletin du Service Zootechnique Epizootique du Afrique Occidentale Francaise, 5:16-21. |
| | + | <br> |
| | 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. |
| − | Govindarajan R, Koteeswaran A, Venugopalan AT, Shyam G, Shao^tail~una S, Shaila MS, Ramachandran S, 1997. Isolation of pestes des petits ruminants virus from an outbreak in Indian buffalo (Bubalus bubalis). Veterinary Record, 141(22):573-574; 10 ref.
| + | <br> |
| − | Hamdy FM, Dardiri AH, Nduaka O, Breese SS, Ihemelandu EC, 1976. Etiology of the stomatitis pneumonenteritis complex in Nigerian dwarf goats. Canadian Journal of Comparative Medicine, 40:276-284.
| |
| − | ICTV, 1995. Virus taxonomy: classification and nomenclature of viruses. In: Murphy FA, Fauquet CM, Bishop DHL, Ghabrial SA, Jarvis AW, Martelli GP, Mayo MA, Summers MD, eds. Sixth report of the International Committee on Taxonomy of Viruses. Wien, Austria: Springer-Verlag.
| |
| − | Kulkarni DD, Bhikane AU, Shaila MS, Varalakshmi P, Apte MP, Narladkar BW, 1996. Peste des petits ruminants in goats in India. Veterinary Record, 138(8):187-188; 6 ref.
| |
| − | Lefevre PC, 1982. Peste des petitis ruminants et infection bovipestique des ovins et caprins. Maisons-Alfort, France: Institut d'Elevage et de Medicine Veterinaire des Pays Tropicaux.
| |
| − | Libeau G, Diallo A, Calvez D, Lefèvre PC, 1992. A competitive ELISA using anti-N monoclonal antibodies for specific detection of rinderpest antibodies in cattle and small ruminants. Veterinary Microbiology, 31(2-3):147-160; 13 ref.
| |
| − | Libeau G, Diallo A, Colas F, Guerre L, 1994. Rapid differential diagnosis of rinderpest and peste des petits ruminants using an immunocapture ELISA. Veterinary Record, 134(12):300-304; 24 ref.
| |
| − | Libeau G, Préhaud C, Lancelot R, Colas F, Guerre L, Bishop DHL, Diallo A, 1995. Development of a competitive ELISA for detecting antibodies to the peste des petits ruminants virus using a recombinant nucleoprotein. Research in Veterinary Science, 58(1):50-55; 29 ref.
| |
| − | OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties.
| |
| − | OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties.
| |
| − | OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.
| |
| | 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. |
| − | OIE, 2001. The International Animal Health Code. Paris, France: Office International Des Epizooties.
| + | <br> |
| − | OIE, 2001. World Animal Health in 2000. Parts 1 and 2. Paris, France: Office International Des Epizooties.
| |
| − | OIE, 2003. Peste des petits ruminants in Israel, follow-up report number 1. Disease Information, 16, No. 37.
| |
| − | OIE, 2004. Peste des petits ruminants in Côte d’Ivoire in July 2004. Disease Information, 17(40).
| |
| − | OIE, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.
| |
| − | OIE, 2009. World Animal Health Information Database - Version: 1.4. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int
| |
| − | Raj GD, Nachimuthu K, Nainar AM, 2000. A simplified objective method for quantification of peste des petits ruminants virus or neutralizing antibody. Journal of Virological Methods, 89(1/2):89-95.
| |
| − | Reynolds L, Francis PA, 1988. The effect of PPR control and dipping on village goat populations in southwest Nigeria. ILCA Bulletin, No. 32:22-27; 11 ref.
| |
| − | Roger F, Guebre Yesus M, Libeau G, Diallo A, Yigezu LM, Yilma T, 2001. Detection of antibodies of rinderpest and peste des petits ruminants viruses (Paramyxoviridae, Morbillivirus) during a new epizootic disease in Ethiopian camels (Camelus dromedarius). Revue de Médecine Vétérinaire, 152(3):265-268; 25 ref.
| |
| | 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. |
| | + | <br> |
| | Rowland AC, Scott GR, Hill HD, 1969. The pathology of an erosive stomatitis and enteritis in West African Dwarf goats. Journal of Pathology, 98:83-87. | | Rowland AC, Scott GR, Hill HD, 1969. The pathology of an erosive stomatitis and enteritis in West African Dwarf goats. Journal of Pathology, 98:83-87. |
| − | Saliki JT, Brown CC, House JA, Dubovi EJ, 1994. Differential immunohistochemical staining of peste des petits ruminants and rinderpest antigens in formalin-fixed, paraffin-embedded tissues using monoclonal and polyclonal antibodies. Journal of Veterinary Diagnostic Investigation, 6(1):96-98; 16 ref.
| |
| − | Scott GR, 1990. Peste-des-petits-ruminants (goat plague) virus. Virus infections of ruminants., 355-361; 15 ref.
| |
| − | Seth S, Shaila MS, 2001. The hemagglutinin-neuraminidase protein of peste des petits ruminants virus is biologically active when transiently expressed in mammalian cells. Virus Research, 75(2):169-177.
| |
| − | Shaila MS, Shamaki D, Forsyth MA, Diallo A, Goatley L, Kitching RP, Barrett T, 1996. Geographic distribution and epidemiology of peste des petits ruminants viruses. Virus Research, 43(2):149-153; 25 ref.
| |
| − | Stem C, 1993. An economic analysis of the prevention of peste des petits ruminants in Nigerian goats. Preventive Veterinary Medicine, 16(2):141-150; 22 ref.
| |
| − | Sumption KJ, Aradom G, Libeau G, Wilsmore AJ, 1998. Detection of peste des petits ruminants virus antigen in conjunctival smears of goats by indirect immunofluorescence. Veterinary Record, 142(16):421-424; 25 ref.
| |
| − | Taylor WP, Busaidy SA, Barrett T, 1990. The epidemiology of peste des petits ruminants in the Sultanate of Oman. Veterinary Microbiology, 22(4):341-352; 10 ref.
| |
| − | Wosu LO, 1989. Management of clinical cases of peste des petits ruminants (PPR) disease in goats. Beiträge zur Tropischen Landwirtschaft und Veterinärmedizin, 27(3):357-361; 17 ref.
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| − |
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| − |
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| − | Links to Websites
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| − |
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| − | Website URL Comment
| |
| − | World Organisation for Animal Health (OIE) http://www.oie.int Website of the World Organisation for Animal Health (formerly Office International des Epizooties).
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| − |
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| − | Images
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| − |
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| − | Picture Title Caption Copyright
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| − | Symptoms Natural case of PPR in a goat, Ghana. Late-stage infection, ulceration of the hard palate, erosive stomatitis. Max Bonniwell
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| − | Symptoms Natural case of PPR in a goat, Ghana. Mucopurulent nasal and ocular discharge. Max Bonniwell
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| − | Pathology Natural case of PPR in a goat, Ghana. Evidence of 'zebra striping' in intestine on necropsy examination. Max Bonniwell
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| − | Histopathology PPR in a goat, Nigeria. Multi-nucleate giant cell in the lung (original magnification x400). A.C. Rowland
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| − | External symptoms Dried exudate on the muzzle and around the eye resulting from rhinitis and conjunctivitis. USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal _ Plant Health Inspection Service
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| − | Pathology Necrosis of the epithelium (whitish areas) on the tongue and pharynx. USDA, 2002. Foreign Animal Diseases Training Set. USDA - Animal _ Plant Health Inspection Service
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| − | Date of report: 04/04/2011
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| − | © CAB International 2010
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| − | [[Category:To Do - CABI]] | + | [[Category:To Do - CABI review]] |
| | [[Category:Morbilliviruses]] | | [[Category:Morbilliviruses]] |