PPR, kata, or goat plague is caused by peste des petits ruminants virus (PPRV), a morbillivirus (family Paramyxoviridae) closely related to the morbilliviruses of rinderpest, measles (in humans), carnivores, and marine mammals.
The disease occurs mostly in goats and sheep and has spread extensively across national and continental boundaries. Outbreaks in sheep and goats invariably occur when new stock is introduced into a farm. Factors that contributed to the spread of that outbreak included communal grazing and the cheap prices of sick animals bought by livestock keepers for slaughtering in other villages.
Methods of Transmission
PPRV is transmitted mainly by aerosols when animals live in close contact. Large amounts of the virus are present in exhaled air and in all body excretions and secretions including feces, saliva, ocular and nasal discharges, and urine that can contaminate fomites. Diarrheic feces are especially infectious. Infection is mainly by inhalation but could also occur through the conjunctiva and oral mucosa.
Kids over four months and under one year of age are most susceptible to the disease, corresponding to decreasing maternal antibody from immune dams.
PPR is regarded as the most important disease of goats and sheep in all countries in which the disease occurs.
The disease can be peracute, acute, or subacute. The peracute and acute forms are seen mainly in goats and are similar to rinderpest in cattle except that severe respiratory distress is a common feature of caprine PPR. Signs generally appear 3 to 6 days after being in contact with an infected animal.
High fever (above 40°C) is accompanied by dullness, sneezing, and serous discharge from the eyes and nostrils. A day or two later, discrete necrotic lesions develop in the mouth and extend over the entire oral mucosa, forming diphtheritic plaques.
There is profound halitosis and the animal is unable to eat because of a sore mouth and swollen lips. Nasal and ocular discharges become mucopurulent and the exudate dries up, matting the eyelids and partially occluding the external nares.
Diarrhea develops 3 to 4 days after the onset of fever. It is profuse and feces may be mucoid and blood tinged. Dyspnea and coughing occur later, and the respiratory signs are aggravated when there is secondary bacterial pneumonia.
Death usually occurs within 1 week of the onset of illness and earlier in peracute cases.
Subacute forms are more common in sheep but they also occur in goats. The signs and lesions are less marked and a few animals may die within 2 weeks, but most recover.
The carcass is severely dehydrated; the hindquarters are soiled with fluid feces; and crusts of exudate are present around eyes, nose, and lips. Discrete or extensive areas of erosion, necrosis, and ulceration are present in the oral mucosa, pharynx and upper esophagus.
Hemorrhagic ulceration is marked in the ileocecal region, colon, and rectum in which they may produce typical “zebra stripes.”
Regional lymph nodes are enlarged and wet and the spleen may be enlarged.
Severe lesions are often present throughout the respiratory tract. A mucopurulent exudate extends from the nasal opening to the larynx, whereas the trachea and bronchi may be hyperemic and contain froth caused by pulmonary congestion and edema.
For diagnostic purposes, specimens should be collected from several live animals and should include swabs of conjunctival, nasal, and buccal mucosae, as well as whole blood in anticoagulant for virus isolation and other tests.
At necropsy, the following specimens should be collected for histopathology and virology, including PCR detection:
- Small and large intestines
- Oral mucosa
- Mesenteric lymph nodes
Treatment of goats showing clinical signs of PPR is of little value and is generally not recommended. However, valuable sick animals in the early stages of the disease could be isolated and given supportive treatment i.e. fluid therapy for dehydration and antibiotics to prevent secondary bacterial infections.
Lesions around the eyes, nostrils, and mouth should be cleaned and good nursing provided.
The disease can be prevented by vaccination and by not introducing new stock from unknown sources, especially animals bought at livestock markets. In addition, animals returned unsold from markets should be segregated unless the entire herd or flock has been vaccinated.
Kids and lambs born to immunized or exposed dams should be vaccinated at 3 to 4 months of age by which time maternal antibodies start to wane.