Overview of Peste des Petits Ruminants

The causal virus, a member of the Morbillivirus genus in the family Paramyxoviridae, preferentially replicates in lymphoid tissues and epithelial tissue of the GI and respiratory tracts, where it produces characteristic lesions.

PPR has been reported in virtually all parts of the African continent, except for the southern tip; the Middle East; and the entire Indian subcontinent. In the last 15 yr, PPR has rapidly expanded within Africa and to large parts of Central Asia, South Asia, and East Asia (including China).

Because PPR virus and the now-eradicated rinderpest virus (see Rinderpest) are cross-protective, it is possible that the recent rapid expansion of the PPR virus within endemic zones and into new regions may be because of disappearance of the cross-protection previously afforded by natural rinderpest infection of small ruminants and/or the hitherto use of rinderpest vaccine to prevent small ruminant infection with PPR virus in certain endemic areas. Based on this theory, PPR virus has the potential to cause severe epidemics, or even pandemics, in more small ruminant populations in an increasingly expanding area of the developing world.

At a local level, such epidemics may eliminate the entire goat or sheep population of an affected village. Between epidemics, PPR can assume an endemic profile. Mortality and morbidity rates vary within an infected country, presumably due to two factors: the varying immune status of the affected populations and varying levels of viral virulence.

Transmission is by close contact, and confinement seems to favor outbreaks. Secretions and excretions of sick animals are the sources of infection. Transmission can occur during the incubation period. It is generally accepted that there is no carrier state. The common husbandry system whereby goats roam freely in urban areas contributes to spread and maintenance of the virus. There are also numerous instances of livestock dealers being associated with the spread of infection, especially during religious festivals when the high demand for animals increases the trade in infected stock.

Several species of gazelle, oryx, and white-tailed deer are fully susceptible; these and other wild small ruminants may play a role in the epidemiology of the disease, but few epidemiologic data are available for PPR in wild small ruminants. Cattle, buffalo, and pigs can become naturally or experimentally infected with PPR virus, but these species are dead-end hosts, because they do not exhibit any clinical disease and do not transmit the virus to other in-contact animals of any species.

The acute form of PPR is accompanied by a sudden rise in body temperature to 40°–41.3°C (104°–106°F). Affected animals appear ill and restless and have a dull coat, dry muzzle, congested mucous membranes, and depressed appetite. Early, the nasal discharge is serous; later, it becomes mucopurulent and gives a putrid odor to the breath. The incubation period is usually 4–5 days. Small areas of necrosis may be observed on the mucous membrane on the floor of the nasal cavity. The conjunctivae are frequently congested, and the medial canthus may exhibit a small degree of crusting. Some affected animals develop a profuse catarrhal conjunctivitis with matting of the eyelids. Necrotic stomatitis affects the lower lip and gum and the gumline of the incisor teeth; in more severe cases, it may involve the dental pad, palate, cheeks and their papillae, and the tongue. Diarrhea may be profuse and accompanied by dehydration and emaciation; hypothermia and death follow, usually after 5–10 days. Bronchopneumonia, characterized by coughing, may develop at late stages of the disease. Pregnant animals may abort. Morbidity and mortality rates are higher in young animals than in adults.

A presumptive diagnosis is based on clinical, pathologic, and epidemiologic findings and may be confirmed by viral isolation and identification. Historically, simple techniques such as agar-gel immunodiffusion have been used in developing countries for confirmation and reporting purposes. However, PPR virus cross-reacts with rinderpest virus in these tests. Virus isolation is a definitive test but is labor intensive, cumbersome, and takes a long time to complete. Currently, antigen capture ELISA and reverse transcription-PCR are the preferred laboratory tests for confirmation of the virus. For antibody detection (such as might be needed for epidemiologic surveillance, confirmation of vaccine efficacy, or confirmation of absence of the disease in a population), competitive ELISA and virus neutralization are the OIE-recommended tests. The specimens required are lymph nodes, tonsils, spleen, and whole lung for antigen or nucleic acid detection, and serum (from unclotted blood) for antibody detection, The virus neutralization test may also be used to confirm an infection if paired serum samples from a surviving animal yield rising titers of ≥4-fold. PPR must be differentiated from other GI infections (eg, GI parasites), respiratory infections (eg, contagious caprine pleuropneumonia), and such other diseases as contagious ecthyma, heartwater, coccidiosis, and mineral poisoning.

Local and federal authorities should be notified when PPR is suspected. PPR is also an OIE-reportable disease worldwide. Eradication is recommended when the disease appears in previously PPR-free countries. There is no specific treatment, but treatment for bacterial and parasitic complications decreases mortality in affected flocks or herds. An attenuated PPR vaccine prepared in Vero cell culture is available and affords protection from natural disease for >1 yr. Encouraged by the successful global eradication of rinderpest, international organizations such as OIE, Food and Agriculture Organization of the United Nations (FAO), and International Atomic Energy Agency (IAEA) are making plans (2015) for global eradication of PPR. The available homologous PPR vaccine would play an important role in that effort.