Peste des Petits Ruminants (PPR, Sheep and Goat Plague) and Rinderpest (Cattle Plague)
Bradford P. Smith
Definition and Etiology
Peste des petits ruminants (PPR) and rinderpest are acute, highly contagious, and usually fatal viral diseases of ruminants. PPR is still active and threatens goats and sheep, but OIE and the Food and Agriculture Organization have the goal of eradication by 2030.1,2 Rinderpest was officially declared by the OIE to be globally eradicated in 2011, mainly through vaccination.
It is the second disease after smallpox to be eliminated.3 Cattle and water buffaloes were most frequently affected by rinderpest, but the disease also occurred in yaks, gaur, sheep, goats, pigs, and other cloven-hoofed animals, in which it is usually less severe. It was rarer in camelids. Many wild animals in Africa are susceptible, including buffalo, lesser kudu, eland, giraffe, warthog, and wildebeest.The viruses causing PPR and rinderpest are closely related RNA viruses in the Paramyxoviridae family, genus Morbillivirus. The viruses can remain viable for at least 1 year in frozen tissue but are killed by direct sunlight in 2 hours. Other morbilliviruses pathogenic for animals include canine distemper and the Hendra virus, which caused disease in horses and humans in Australia in 1994.
PPR is a highly virulent virus of goats, sheep and occasionally camels. There is only one serotype. It occurs in Africa, the Near East, Middle East, and Asia; outbreaks have occurred in approximately 76 countries. In 2016 it reached the edge of Europe in Georgia.1 There do not appear to be any carriers or reservoirs besides domestic goats and sheep.1 PPR has important negative economic effects in agricultural societies. An effective single-dose vaccine that confers lifelong immunity is available. There are also accurate diagnostic assays. Thus it is hoped that massive vaccination programs in domestic animals can eradicate PPR by 2030.
PPR morbidity rates can reach 100%, and the mortality rate can be between 50% and 100% in goats and sheep. Cattle and pigs develop inapparent infections. The disease also occurs in wild species, including several gazelles, gemsbok, ibex, and wild sheep. In 2015, a massive outbreak occurred among Mongolian wild Saiga antelope, triggering a die-off due to PPR. The reader is referred to the OIE website1 for current information.
Clinical Signs and Differential Diagnosis
Clinical signs of PPR in goats and sheep are similar to those of rinderpest in cattle. For both PPR and rinderpest, the incubation period is usually 3 to 10 days, which is followed by sudden onset of fever, depression, and anorexia. The nose is dry, and mucous membranes are congested. Within days oral erosions appear where necrotic foci have sloughed. Purulent occular and nasal discharge occurs. Diarrhea is severe and may be bloody. Interstitial pneumonia occurs, and secondary bacterial bronchopneumonia is common. Dehydration and starvation often lead to death.
In small ruminants with signs of PPR, bluetongue and Nairobi sheep disease must be ruled out.
In endemic areas, rinderpest is suspected in cattle when the signs described earlier occur in groups of animals. In nonendemic areas diseases that appear similar clinically are BVD- related mucosal diseases, MCF, arsenic poisoning, severe coccidiosis, and severe fulminating infectious bovine rhinotracheitis, as well as FMD and vesicular stomatitis.
Laboratory Diagnosis
A rapid strip test for PPR can be used in the field.4 Laboratory confirmation of PPR or rinderpest virus can be accomplished by virus isolation; PCR; ELISA; detection of viral antigen by fluorescent antibody testing, virus neutralization, or agar gel immunodiffusion; counterimmunoelectropheresis; detection of rising antibody titer by ELISA or virus neutralization5; and histopathologic evaluation, including immunohistopathologic study. Virus isolation is most successful in the first days of infection (often before the onset of diarrhea).
Blood should be taken in heparin. The lymph nodes and spleen are reliable sources of virus, as are tears and ocular discharges. Lymph node biopsy after day 3 of infection is the most reliable means of diagnosis in a living goat. Tissues should be shipped frozen on ice to the laboratory for virus isolation or detection of antigen. Detection of a rising antibody titer can help diagnose the disease retrospectively. Leukopenia may be noted in the acute early stages.Pathophysiology
The virus usually enters through the respiratory mucosa. Lymphoid tissue and epithelial cells of the GI and respiratory systems are the primary targets of rinderpest virus. Lymphocytes are destroyed in the germinal centers of the lymph nodes, Peyer's patches, tonsils, splenic corpuscles, and cecal lymphoid tissue. Immunosuppression occurs as lymphoid tissue is destroyed. The virus also attacks the alimentary tract mucosa; Peyer patches are the most severely affected. As alimentary mucosa is lost, diarrhea and emaciation become severe, and secondary bronchopneumonia usually develops as the respiratory epithelium is destroyed.
Epidemiology
PPR and rinderpest are highly contagious and spread mainly through airborne droplets, direct contact, feces, and contaminated fomites such as human beings. All secretions and feces of infected animals are contagious throughout the course of the disease. Wild ruminants with active disease may be a source of infection for livestock. Because the mortality rate is high, treatment is unrewarding and the prognosis is poor, although individual animals can be helped by good nursing, fluid therapy, and antimicrobials to control bronchopneumonia. Innate or specific resistance may protect individuals or herds from clinical signs after infection. Recovered animals do not appear to act as carriers for more than a few months.
Necropsy Findings
Lesions are found mainly in the alimentary tract, lymphoid tissues and lungs. Subendocardial hemorrhages may also be seen in animals that die of acute illness.
Oral erosions, edema, and congestion of the abomasum are typical, and ulcers and hemorrhagic to necrotic Peyer's patches occasionally are present. The cecal and colonic mucosae are hemorrhagic, ulcerated, or necrotic. The lymph nodes are enlarged and have necrotic germinal centers. Severe interstitial pneumonia frequently occurs,5 and secondary bronchopneumonia is common.Prevention and Control
Because there is only one known strain of PPR and one of rinderpest virus, protection after infection or vaccination usually is lifelong. Vaccination of susceptible animals at 6 months of age and older in endemic areas with a live attenuated virus is an effective means of control.1,6 The vaccine does not produce adverse reactions, has a long shelf life if refrigerated, and produces solid immunity. Its major disadvantages are that the lyophilized virus has to be kept cold, and once a vial has been reconstituted, it must be used quickly before the virus dies. Research is yielding more stable vaccine without a cold chain for up to 30 days. 7
Control of epidemics in areas where the disease is not endemic involves quarantine and slaughter of infected and exposed animals, as well as other contact ruminants and swine. Disinfection of premises while they are under government quarantine is essential for controlling the disease. The virus is susceptible to most disinfectants and survives in the environment for only 2 to 3 days. A comprehensive review was published in 2014.8