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Overview of Peste des Petits Ruminants


Peste des petits ruminants (PPR) is an acute or subacute viral disease of goats and sheep characterized by fever, necrotic stomatitis, gastroenteritis, and pneumonia. It was first reported in the Ivory Coast in 1942 and subsequently in Senegal, Ghana, Togo, Benin, and Nigeria. Sheep and goats are probably equally susceptible to the virus, but sheep may be somewhat more resistant to its clinical effects. While serosurveillance of affected flocks often shows higher prevalence levels in sheep, this may reflect the fact that a higher proportion of the affected goats have died. Cattle are only subclinically infected. Humans are not at risk.

The causal virus, a morbillivirus of the family Paramyxoviridae, has a particular affinity for lymphoid tissues and epithelial tissue of the GI and respiratory tracts, where it produces characteristic lesions.

PPR is present in west, central, north, and east Africa; the Middle East; and the Indian subcontinent as far east as Bangladesh. On both landmasses the virus is still extending its range. It recently spread through Afghanistan into Central Asia (Uzbekistan, Tajikistan, and Turkmenistan) and in a separate incursion has now spread to Tibetan China. In Africa a poorly understood barrier that prevented the virus from moving south from Sudan and Ethiopia has now been breached and both Kenya and Uganda are currently infected. In the north of the continent, the disease is now present in Morocco.

With the global eradication of rinderpest an accomplished fact, and the realization that rinderpest was never a common disease of small ruminants, the true nature of PPR as a virus with the potential to cause severe epidemics, or even pandemics, in small ruminants is now being increasingly realized.

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; it is suspected that the varying levels of viral virulence account for the differing scenarios that can arise within an infected country.

Transmission is by close contact, and confinement seems to favor outbreaks. Secretions and excretions of sick animals are the sources of infection. It is generally accepted that there is no carrier state; however, cases of PPR may spread the infection during the incubation period. According to the husbandry system, it appears that urban, free-roaming goats can contribute to maintenance of the virus. There are also numerous instances of livestock dealers being associated with the spread of infection, and the requirements of animals for religious festivals often increases the trade in infected stock.

Several species of gazelle, oryx, and white-tailed deer are fully susceptible; these and other wild ruminants may play a role in the epidemiology of the disease, but little or no data are available for infection in wild small ruminants. Pigs are dead-end hosts and do not transmit the disease to susceptible pigs or goats, and it is unlikely that they play a role in PPR epidemiology. Although cattle and domestic buffalo are susceptible to infection, there is no evidence that they exhibit clinical signs following natural or experimental infection or that they transmit the disease to susceptible 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 is 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.


Emaciation, conjunctivitis, and stomatitis are seen; necrotic lesions are observed inside the lower lip and on the adjacent gum, 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 normal 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.

Severe 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 broncho-pneumonia may be present.

A presumptive diagnosis is based on clinical, pathologic, and epidemiologic findings and may be confirmed by viral isolation and identification. At the local field level, both the agar-gel immuno-diffusion test and the PPR penside test provide adequate confirmation for reporting purposes. However, due to the difficulty and time required for virus isolation, techniques such as immune capture ELISA and reverse transcriptase-PCR are the preferred reference laboratory techniques. The specimens required are unclotted blood, lymph nodes, tonsils, spleen, and whole lung. Detection of virus-neutralizing antibodies with a rising titer in surviving animals is diagnostic. PPR must be differentiated from other acute GI infections (eg, rinder-pest), 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. 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 vaccine has been prepared in Vero cell culture; it affords protection from natural disease for >1 yr. Rinderpest cell culture vaccine also has been used to successfully immunize against PPR but, due to the global eradication of rinderpest, the use of this vaccine would mask evidence of any re-emergence of that virus, or could be misconstrued as evidence of such re-emergence. Homologous PPR vaccines are now widely used to control the disease.

Last full review/revision March 2012 by William Taylor, ; Thomas Barrett, MSc, PhD, Deceased

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