Peste Des Petits Ruminants (PPR)

Nature of the disease

    • PPR is an acute highly contagious viral disease of goats, less commonly sheep and closely related wild bovidae, and is clinically mimics cattle plague, characterized by fever, errosive stomatitis, enteritis, pneumonia, and death.
    • PPR is regarded as the most economically important viral disease of small ruminants particularly goats in areas where these animals are intensively reared. In the regions where PPR occurs in an epizootic form it may have dramatic consequences for animal owners due to high mortality rates. In endemic areas where subacute reactions is usually occurs, it opens the door to many other infections and its impact on animal production is certainly considerable.
    • OIE classification: list (A).
    • Latent infections may be activated and complicate the clinical picture.

History and Occurrence

    • PPR was first described in 1942 in Cote d'Ivoire , and it was soon recognized in Benin, Sengal, and Nigeria. PPR is wide spread in the northly countries of sub-saharan Africa and has been identified in the Sudan, Ethiopia, Egypt, Arab peninsula, and Middle East. Recently PPR has been reported in India and Jordan. PPR is endemic in the Sahel area west of Africa and central Africa.
      • In Egypt the first epidemic was recorded in January 1987 in goats at Kafr Hakim, Embeba, Giza governorate and in lambs in 1989 at Fayoum Governorate.


    • PPR virus is a Morbillivirus of the Family Paramyxoviridae, RNA genome and has a particular affinity for lymphoid and epithelial tissues of the GI tract, in which it produces characteristic lesions. PPR viruse strains are antigenically homogeneous.
    • PPR and RP viruses are distinct pathogens with close antigenic relationship and cross-protection. Also, it has some antigenic relationship to viruses of canine distemper in dogs, measles in humans, and equine influenza recently described in Australia .
    • PPR virus can be isolated in primary sheep and goat kidney and vero cells producing cytopathic effect "CPE" similar to that RP virus characterized by syncytium formation, intracytoplasmic and intranuclear inclusion bodies.
    • As with RP virus, PPR virus is very fragile it does not survive outside the host for many hours; also the virus is inactivated by putrefaction, and inactivated in sunlight within 2 hours.
      • PPR virus is inactivated by strong acid or alkaline conditions within 10 minutes, and chemical agents as 5 % chloroform, 2 % phenol, and 2 % formalin.


    • The natural hosts are goats, sheep, and closely related wild bovidae as Laristan sheep, Dorcas gazelles, and Nubian ibex.
    • Goats are clearly more susceptible than sheep and the disease often occurs in goats without affecting sheep in close proximity.The highest incidences are found in young stock less than two years old.
    • Cattle and pigs when infected experimently develop serum-neutrlizing antibodies without symptoms "dead-end hosts".
      • Nomadic goats and sheep in the Sahel area west of Africa have a high innate resistance and undergo subclinical infections whereas settled flocks south of the Sahel and indigenous goats and sheep in the Middle East posses a low innate resistance.


    • The virus is present in all body excretions and secretions such as tears, nasal discharge, sputum, and diarrheic feces.
    • As in RP, PPR virus spreads by direct contact or close indirect contact and infection is mainly by inhalation of infective aerosols but could also occur through the conjunctiva and oral mucosa.
    • As with RP, the transimission cycle of PPR virus is maintained through a regular supply of susceptible hosts plus sufficient animal movment to allow mixing of the population.
      • As in RP, it is generally accepted that there is no carrier state in PPR.

Key signs

PPR has acute and subacute forms.

The acute form

    • The acute form occurs frequently in goats with a clinical course mimics that of cattle plague but crusty scabs and pneumonia development is more prominent in PPR.
    • After an IP 2-6 days the first clinical sign is short fever 40-41°C accompanied by dullness, serous oculonasal discharge that rapidly becomes profuse and purulent. The nasal discharge may block the nares and encrust the muzzle, causing the animal to snort and sneeze, whereas the ocular discharge may mat the eye lids together.
    • Congestion and necrosis affects the gums, the lower lip, and may extend over the entire oral mucosa. The tongue becomes coated with fetid diphtheric plaques, the lips swollen, and the animal unable to eat.
    • Profuse diarrhea begins 2-4 days after the onset of fever and feces may be mucoid and blood tinged.
    • Pulmonary involvement usually occurs during the later stage of the disease and the death usually occurs within a week of the onset of illness. The mortality rate in goats is generally high and ranges from 77-90%, but goats of the endemic Sahel area have a lower rate.
    • In the absence of complications recovery may occur within 8-10 days from illness.

Subacute form

    • Subacute reactions are more common in sheep but they also occur in goats and are manifested by low-grade signs and lesions.
    • Most affected animals recover wthin 2 weeks and a few dye. Sheep fatality rate is less than 10 %.
    • Bacterial bronchopneumonia and labial orf lesions are the commonest complications, but other latent enteric pathogens and blood parasites may be exacerbated.


Surviving goats and sheep develop a strong lifelong immunity associated with the presence of humoral neutralizing antibodies.


    • The carcass is dehydrated and solid with fluid fetid feces.
    • Eyelids, nares, and lips are usually encrusted with discharges.
    • Necrotic erosions are found throughout the oral cavity, pharynx, and less frequently esophagus.
    • As in RP, Congestion of capillaries along the crests of the longitudinal folds in the large intestine and rectal mucosa "Zebra Striping."
    • The abomasum and small intestine are congested rather than eroded.
    • Mesenteric lymph nodes are congested and edematous.
    • Purulent bronchopneumonia is a prominent finding that masks the underlying viral Broncho-
    • Pneumonia manifested as areas of red consolidation.


A presumptive diagnosis of the acute forms of PPR can be made from the epidemiology, clinical signs, and lesions but subacute form may require laboratory diagnosis.

Samples and specimens

    • For virus isolation or viral antigen detection, from live animals during early stages of fever until the beginning of the erosions, ocular or nasal swabs, scrapings of early oral lesions, blood with heparin or EDTA "buffy coat". From deceased animals portions of the spleen, lymph nodes, and lungs collected within 2 hours of death. The specimens should be chilled on ice, but not frozen, and examined as soon as possible.
    • For serology collect serum from acutely ill and recovered animals.
    • For histopathology slices of lymph node, spleen, tonsils, and mucosal lesions are collected in 10 % formalin saline for.
    • The virus is isolated by inoculation of buffy coat, swab material, or 10% tissue suspention onto lamb or kid kidney, CPEs develops after 4 days which are indistinguishable from that of RP virus. CPEs specificity is confirmed serologically by comparative titration against antisera to homologous and heterologous antisera, the homologous titre usually being much higher than the heterologous. The isolates can be examined with cELISA based on monoclonal antibodies and specific cDNA probes.
    • Specific viral antigens in 30% tissue suspentions or in undiluted swap material of suspected cases is detected by hyperimmune sera to RP or PPR viruses by AGID and counter immunoelectrophoresis "CIEP". Antigen can also be detected by immunohistochemical staining of tissues "immunoperoxidase staining" and dot-ELISA.
    • In survivors, a four-fold or greater increase in neutralizing antibodies in paired serum samples confirms the presumptive diagnosis. Seroconvertion in paired serum samples is mainly used only for disease serviullance.
    • Confirmation by the experimental transimission of the disease requires strict isolation facilities and can done by i.v inoculation of 5 ml blood from suspected animal at the height of the disease into susceptible goat, sheep, and cattle. PPR usually causes severe disease in goats, miler disease in sheep and subclinical infection in cattle.

Differential diagnosis

PPR should be differentiated clinically from RP, bluetongue, contagious caprine pleuropneumonia "CCPP", contagious ecthyma, foot and mouth disease, sheep and goat pox, Nairobi sheep disease, heartwater, bacterial and parasitic diarrhea, and viral and parasitic pneumonia.


There is no specific treatment and the disease is notifiable. In valuable individuals, good nursing, fluid replacment to compensate electrolyte losses from diarrhea, and antibiotics to suppress bacterial infections that complicate viral pneumonia should be considered.

Prevention and control measures

    • Eradication is the usual goal in countries which PPR appears for the first time.
    • PPR management in endemic areas:
    • Control is enhanced by segregation of new stock from unknown sources or that bought at live stock markets, or that retruned unsold unless the entire herd has been vaccinated.
    • The tissue culture attenuated RP vaccine is effectively used to protect sheep and goats for at least one year. In endemic areas kids and lambs should be vaccinated at 3-4 months of age. Furthermore, a homologous PPR tissue culture vaccine have been developed giving long-live immunity in small ruminants.


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