Peste des Petits Ruminants

Also known as: PPR — PPRV — Goat Plague — Pest of Sheep and Goats — Pneumoenteritis Complex — Pseudorinderpest of Small Ruminants — Stomatitis-Pneumoenteritis Syndrome

Introduction

The condition is caused by a morbillivirus of the family paramoxyviridae. The infective agent was first considered a variant of rinderpest virus adapted to small ruminants, but was later shown to be antigenically and genetically distinct.

Recognition of PPR as a problem has increased in the 1990s, partly as a result of surveillance activities of the global rinderpest eradication programme (GREP), but also by the capacity of the infection to invade disease-free countries. The presence of infection restricts international trade in livestock and livestock products from infected countries, and is usually associated with ongoing severe economic losses.

The disease is recognized by the Office International des Epizooties (OIE) as a List A pathogen on account of the high mortality and morbidity, and rapidity of spread by contagion.

Signalment

Disease occurs in goats and sheep, and has been recognized in captive wild ungulates.

Cattle undergo mainly subclinical reactions, and pigs develop a viraemia.

Because colostral antibody protects young animals, in endemic areas most disease occurs in animals after waning of colostral immunity, from 4 months to 2 years of age. Mortality rates in endemic areas may be in the region of 4-5% whereas rates from 20% to 90% in epidemic outbreaks have frequently been reported.

Seasonality in breeding, in marketing and in crop production all appear related to disease occurrence. In arid and semi-arid zones, infection may spread when animals are sold in the dry season. In humid zones, tethering and sale of surplus animals may occur at the start of the rains, thus aiding transmission. The wet season can also predispose to secondary bacterial infections, exacerbating the viral pneumonia.

Distribution

From South Asia through the Middle East, and from the horn of Africa through to West Africa.

PPRV has a direct life cycle, maintained by infected animal to susceptible animal transmission, without involvement of carrier animals or vectors. The only requirement is a regular supply of susceptible hosts plus sufficient animal movement to allow mixing of the population.

Clinical Signs

Signs include sudden onset of pyrexia (40 - 42⁰C), marked depression, lethargy, weight loss or reduced weight gain and a reduced appetite. There will be ulcers, vesicles and erosion on the tongue and oral mucosa and the animal may be smacking its lips, salivating excessively and grinding its teeth in pain. Gentle rubbing of the gum line will reveal a foul-smelling material and shreds of epithelial tissue. Similar changes may also be seen in the mucous membranes of the vagina and vulva.

There will also be excessive lacrimation and serous nasal discharge, both of which may become purulent later on in the condition, following secondary bacterial infection.

The animal will later develop foul-smelling diarrhoea, containing blood and pieces of dead gut tissue. Dyspnoea, tachypnoea and coughing may be present. Pregnant animals may abort.

Pathology

The carcass is usually dehydrated, and soiled with faeces. The peri-orbital and perinasal areas are usually encrusted with muco-purulent discharges. The erosions and ulcerations in the mouth and throat are usually prominent, as is the presence of the secondary broncho-pneumonia. The underlying primary viral pneumonia may be less obvious but is manifested by areas of red consolidation.

Zebra striping in the colon may also be seen, and lymphadenopathy.

The most important histopathological indicator of PPRV is the presence of multi-nucleated giant cells containing intra-nuclear and intra-cytoplasmic inclusions. Multi-nucleated giant cells (syncytia) are most readily detected in the lungs, but also occur in bronchial, alveolar and ileal epithelium.

Diagnosis

History, signalment and clinical signs may lead to a presumptive diagnosis of this disease in countries where it is endemic.

Other conditions which need to be eliminated as differentials are (rinderpest in small ruminants), contagious caprine pleuropneumonia, bluetongue, pasteurellosis, contagious ecthyma, foot-and-mouth disease, heartwater, coccidiosis and mineral poisoning.

Rinderpest virus can cause disease in small ruminants, but where RP exists as a risk to small ruminants, disease in cattle would be expected. Rinderpest has now been eradicated worldwide.

PPRV is present at a high concentration in secretions and tissue samples in the early stages of the disease, but rapidly becomes difficult to detect after development of antibody responses. Collection from animals which have a serous ocular-nasal discharge and fever is preferable. Gum debris, conjunctival swabs, clotted blood and whole blood and tissues from post mortem are all valuable.

From the necropsy examination of two to three animals, lymph nodes, especially the mesenteric and bronchial nodes, lungs, spleen and intestinal mucosae should also be collected aseptically, chilled on ice and transported under refrigeration. Fragments of organs collected for histopathology are placed in 10% formalin.

Detection of virus antigens by the agar gel immunodiffusion test (AGIDT) is a relatively simple, fast and cheap process. It is extremely useful as an initial test, but it does not discriminate between PPR and rinderpest viruses and further tests are needed to do this.

Histopathology combined with immunohistochemical staining (e.g. immunoperoxidase) is a useful procedure because it is performed on formalin-fixed material and can discriminate between PPR and rinderpest when performed with specific monoclonal antibodies. Virus antigens can also be detected by immunocapture ELISA.

Antigen-capture ELISA is sensitive and specific, using monoclonal antibodies to give a result with PPR virus and enabling differentiation from rinderpest but taking longer than counter-immuno-electrophoresis (CIEP).

Antibodies are strongly induced by infection, and become detectable from the diarrhoeic stage onwards.

The prescribed test for international trade (that which is accepted as a basis for the veterinary certification of animals as having evidence of presence or absence of antibodies) is Virus Neutralisation. There is however cross-neutralisation between antibodies to PPR and RPV. The OIE considers that a serum is said to be positive for PPR when the neutralisation titre is at least two-fold higher for PPR than for rinderpest.

Treatment

Chloramphenicol, penicillin, streptomycin can each be used and should be given intramuscularly for 5 days. Fluid therapy is also useful as a supportive treatment along with electrolyte replacement.

Control

A live, attenuated strain (PSRV 75/1) of the PPR virus has been developed for use as a vaccine and provides protection for over 3 years. Previous trials (usually with RP vaccine) usually reported reduction in mortality, particularly in weaned young stock, and positive benefit-to-cost ratios.

Movement control, at the level of total standstill of livestock movements and banning of markets may be effective if enforceable and short-lasting in duration, since the incubation period is short. However, an effective quarantine of affected and in-contact animals for one month after the recovery of the last clinically affected case has been recommended. These measures may be accompanied by a slaughter policy of animals on infected and in-contact premises, in addition to the ban on livestock movements, if the aim is rapid eradication.

PPR is a list A disease of the OIE, and thus member states are required to inform the OIE of the occurrence of the disease in their territory. The OIE publishes recommendations for zoo-sanitary conditions and certification of trade in animals and livestock products from countries which are not recognized as having freedom from PPR disease.

The OIE also recommends sanitary prophylaxis when the disease appears in previously PPR-free countries. The use of a stamping-out policy, involving slaughter of infected and in-contact animals on infected premises, can lead to a reduced period of time elapsing after the last case of disease has been reported before the country is internationally recognized as free of PPR.

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References

FAO (1998) Recognising peste des petits ruminants. A field manual. Rome, Italy: Food and Agriculture Organisation (FAO).

Gargadennec, L., Lalanne, A (1942) La peste-des-petits-ruminants. Bulletin du Service Zootechnique Epizootique du Afrique Occidentale Francaise, 5:16-21.

Libeau, G., Diallo, A., Colas, F., Guerre, L (1994) Rapid differential diagnosis of rinderpest and peste des petits ruminants using an immunocapture ELISA. Vet Record, 134(12):300-304; 24.

OIE (2001) World Animal Health in 2000. Parts 1 and 2. Paris, France: Office International Des Epizooties.

Raj, G. D., Nachimuthu, K., Nainar, A. M (2000) A simplified objective method for quantification of peste des petits ruminants virus or neutralizing antibody. J Virological Methods, 89(1/2):89-95.