Peste des petits ruminants is an internationally notifiable disease of small domestic and wild ruminants. It is caused by a Morbillivirus closely related to but distinct from rinderpest virus. The main organ systems affected are the respiratory and digestive systems. Treatment is restricted to supportive care; a vaccine is available for prevention.
Peste des petits ruminants (PPR) is an acute or subacute viral disease of goats and sheep characterized by fever, necrotic stomatitis, gastroenteritis, pneumonia, and sometimes death. It was reported first in Côte d’Ivoire (the Ivory Coast) in 1942, and subsequently in other parts of West Africa. Goats and sheep appear to be equally susceptible to the virus; however, goats exhibit more severe clinical signs. The virus also affects several wild small ruminant species. Cattle, buffalo, and pigs are only subclinically infected. Humans are not at risk.
Etiology and Epidemiology of Peste des Petits Ruminants
The causative virus of PPR, a member of the Morbillivirus genus in the family Paramyxoviridae, preferentially replicates in lymphoid tissues and in epithelial tissue of the GI and respiratory tracts, where it produces characteristic lesions.
PPR has been reported in all parts of the African continent except the southern tip; in the Middle East; and in the entire Indian subcontinent. Since the year 2000, PPR has rapidly expanded within Africa and to large parts of Asia and more recently, Europe.
PPR virus and rinderpest virus are cross-protective. Because rinderpest virus has been eradicated, however, the rapid expansion of the PPR virus within endemic zones and into new regions may be due to the disappearance of the cross-protection previously afforded by natural rinderpest infection of small ruminants. In addition, in certain endemic areas rinderpest vaccine has been used to prevent PPR virus infection in small ruminants. These factors suggest that PPR virus has the potential to cause severe epidemics, or even pandemics, in more populations of small ruminants in an increasingly expanding area of the world.
At a local level, PPR 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 because of two factors: the varying immune status of the affected populations and varying extents of viral virulence.
Transmission of Peste des Petits Ruminants
PPR is transmitted by close contact, and confinement favors 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 transmission and maintenance of the virus. In addition, production animal handlers have been associated with the transmission of infection in numerous instances, especially during religious festivals when the high demand for animals increases the trade in infected animals.
Several species of gazelle, oryx, and white-tailed deer are fully susceptible to PPR infection. These and other wild small ruminants may play a role in the epidemiology of the disease; however, 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 exhibit no clinical signs and do not transmit the virus to other in-contact animals of any species.
Clinical Findings of Peste des Petits Ruminants
The acute form of PPR is accompanied by a sudden rise in body temperature to 40°C–41.3°C (104°F–106°F). The incubation period is usually 4–5 days. Morbidity and mortality are variable but can be as high as 80%–100% in some outbreaks.
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. 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 show a small amount of crusting. Some affected animals develop a profuse catarrhal conjunctivitis with matting of the eyelids.
Necrotic stomatitis affects the lower lip and gum, as well as the gumline of the incisor teeth. In more severe cases, necrotic stomatitis may involve the dental pad, palate, cheeks and their papillae, and 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.
Lesions
Emaciation, conjunctivitis, and stomatitis are common clinical signs of PPR; necrotic lesions are observed inside the lower lip and on the adjacent gum, on the cheeks near the commissures, and on the ventral surface of the tongue.
In severe cases, the lesions may extend to the hard palate and pharynx. The erosions are shallow, with a red, raw base and later become pinkish white; they are bounded by healthy epithelium that provides a sharply demarcated margin.
The rumen, reticulum, and omasum are rarely involved. The abomasum exhibits regularly outlined erosions that have red, raw floors and ooze blood.
Courtesy of Plum Island, USDA.
Severe PPR lesions are less common in the small intestines than in the mouth, abomasum, or large intestines. Streaks of hemorrhages, and less frequently erosions, may be present in the first portion of the duodenum and terminal ileum. Peyer’s patches are severely affected; entire patches of lymphoid tissue may be sloughed.
The large intestine is usually more severely affected, with lesions developing around the ileocecal valve and at the cecocolic junction and rectum. The latter exhibits streaks of congestion along the folds of the mucosa, resulting in the characteristic zebra-striped appearance.
Petechiae may appear in the turbinates, larynx, and trachea. Patches of bronchopneumonia may be present.
Diagnosis of Peste des Petits Ruminants
Antigen detection by ELISA or PCR
A presumptive diagnosis of PPR 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 regions of limited resources for confirmation and reporting. However, PPR virus cross-reacts with rinderpest virus in these tests.
Virus isolation is definitive for PPR diagnosis; however, it is labor intensive, cumbersome, and time-consuming. Currently, antigen capture ELISA and reverse-transcription PCR assay 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 tests recommended by the World Organisation for Animal Health (WOAH). The specimens required are lymph nodes, tonsils, spleen, and whole lung for antigen or nucleic acid detection, and serum for antibody detection.
The virus neutralization test may also be used to confirm PPR infection if paired serum samples from a surviving animal yield rising titers ≥ 4-fold. PPR must be differentiated from other GI infections (eg, GI parasite infestations), respiratory infections (eg, contagious caprine pleuropneumonia), and such other diseases as contagious ecthyma, heartwater, coccidiosis, and mineral toxicoses.
Control of Peste des Petits Ruminants
Supportive care
Local and federal authorities should be notified when PPR is suspected. PPR is also a WOAH-reportable disease worldwide. Eradication is recommended when the disease appears in previously PPR-free countries.
There is no specific treatment for PPR; however, treatment for bacterial and parasitic complications decreases mortality rates in affected flocks or herds. A live, attenuated PPR vaccine prepared in Vero cell culture affords protection from natural disease for > 1 year. Encouraged by the successful global eradication of rinderpest, international organizations such as WOAH and the Food and Agriculture Organization of the United Nations (FAO) are actively pursuing global eradication of PPR by 2030. The available homologous PPR vaccine is playing an important role in that effort.
Key Points
Peste des petits ruminants (PPR) is a severe viral disease of domestic and wild small ruminants.
PPR affects primarily the respiratory and digestive systems, inducing high rates of morbidity and mortality.
PPR is widespread in Asia, Africa, and the Near and Middle East, and was detected in Europe in 2016.
Presumptive diagnosis is based on clinical signs; PCR and ELISA are used for definitive diagnosis.
There is no specific treatment for PPR; a vaccine is available for disease prevention.
For More Information
World Organisation for Animal Health: Peste des Petits Ruminants
Benfield CTO, Legnardi M, Mayen F, et al. Peste Des Petits Ruminants in the Middle East: Epidemiological Situation and Status of Control and Eradication Activities after the First Phase of the PPR Global Eradication Program (2017-2021). Animals (Basel). 2023;13(7):1196. doi: 10.3390/ani13071196. PMID: 37048452; PMCID: PMC10093352.
