Rinderpest: Introduction - The Merck Veterinary Manual

Rinderpest: Introduction
(Cattle plague)

Rinderpest is a disease of cloven-hoofed animals characterized by fever, necrotic stomatitis, gastroenteritis, lymphoid necrosis, and high mortality. In epidemic form, it is the most lethal plague known in cattle. All species of the order artiodactyla are variably susceptible to rinderpest. Susceptibility is high in African buffalo, giraffes, wild Suidae, Tragelaphinae, and breeds of cattle such as Ankole, Channel Islands, and Japanese Black; moderate in wildebeest and East African zebus; and mild in gazelles and small domestic ruminants. Rinderpest is subclinical in European pigs and hippopotami. It is endemic in many countries of Asia and Africa. Historically, rinderpest virus has been widely distributed throughout Europe and Africa but has never established itself in North America, Central America, the Caribbean Islands, South America, Australia, or New Zealand. Rinderpest is included in OIE List A.

Etiology and Pathogenesis:

The infectious agent is a morbillivirus, closely related to the viruses causing peste des petits ruminants ( Peste Des Petits Ruminants: Introduction), canine distemper ( Canine Distemper: Introduction), and measles. Strains of rinderpest virus may vary markedly in host range and virulence. Sera from recovered or vaccinated cattle cross-react with all strains in neutralization tests, but minor antigenic differences have been demonstrated. The virus is fragile and becomes rapidly inactivated by heat and light, but remains viable for long periods in chilled or frozen tissues.

Rinderpest virus is present in small amounts of nasal secretions 1-2 days before fever; levels are high in secretions and excretions during the first week of clinical disease and decrease rapidly as animals develop specific antibodies and begin to recover. Transmission requires direct or close indirect contact; infection is via the nasopharynx. There is no carrier state; the virus maintains itself by continual transmission among susceptible animals. In endemic areas, young cattle become infected after maternal immunity disappears and before vaccine immunity begins, with possible auxiliary cycles in sheep, goats, and wild ungulates. In epidemic areas, the virus infects most susceptible animals and tends to limit itself unless the population is large enough to support endemicity.

Following primary growth in lymph nodes associated with the nasopharynx, the virus proliferates throughout the lymphoid tissue and spreads via the blood to the mucosa of the GI and upper respiratory tracts. Tissue damage is caused by viral cytopathology. Viral antigens induce a potent immune response that controls the infection and allows recovery if tissue damage is not too severe.

Clinical Findings:

An incubation period of 3-15 days is followed by fever, anorexia, and depression; oculonasal discharge develops 1-2 days later. Within 2-3 days, pinpoint necrotic lesions, which rapidly enlarge to form cheesy plaques, appear on the gums, buccal mucosa, and tongue. The hard and soft palates are often affected. The oculonasal discharge becomes mucopurulent, and the muzzle appears dry and cracked. Diarrhea, the final clinical sign, may be watery and contain blood, mucus, and mucous membranes. Animals show severe abdominal pain, thirst, and dyspnea and may die from dehydration. Convalescence is prolonged and may be complicated by concurrent infections due to immunosuppression. In endemic areas, morbidity is low and clinical signs are often mild; in epidemic areas, morbidity is often 100% and mortality is up to 90%.

Lesions:

Rinderpest, necrosis and fibronecrotic exudate

Gross pathologic changes are evident throughout the GI and upper respiratory tracts, either as areas of necrosis and erosion, or congestion and hemorrhage, the latter creating classic “zebra-striping” in the rectum. Lymph nodes may be enlarged and edematous, with white necrotic foci in the Peyer’s patches. Histologic examination reveals lymphoid and epithelial necrosis with viral-induced syncytia and intracytoplasmic inclusions.

Diagnosis:

Clinical and pathologic findings may be sufficient for diagnosis in endemic areas and after initial laboratory confirmation of an outbreak. In areas where rinderpest is uncommon or absent, laboratory tests must be used to differentiate it from bovine viral diarrhea in particular, as well as East Coast fever, foot-and-mouth disease, infectious bovine rhinotracheitis, and malignant catarrhal fever. Viral isolation and detection of specific viral antigens in affected tissues are standard tests, and demonstration of rising antibody titers is useful. Simple, rapid tests for antigen detection (immunodiffusion, counterimmunoelectrophoresis, and competitive ELISA) are valuable in the field.

Specimens for the laboratory must be collected from several animals during the early stages of clinical disease, preferably before the onset of diarrhea. Whole blood, lymphoid tissue, spleen, and gut lesions should be collected aseptically and transported swiftly at 4°C or on ice.

Control:

Treatment usually is not attempted, but nursing care with supportive fluid and antibiotic therapy (for secondary bacterial infections) may aid recovery of valuable animals. Active immunity is usually lifelong; maternal immunity lasts 6-11 mo. Control in endemic areas is by immunization of all cattle and domestic buffalo >1 yr old with attenuated cell culture vaccine. In these areas, outbreaks are controlled by quarantine and “ring vaccination” and sometimes by slaughtering. In epidemic areas, the disease is best eliminated by imposing quarantine and slaughtering affected and exposed animals. Control of animal movement is paramount because most outbreaks are due to introduction of infected cattle. Countries that are free of the disease and that border endemic areas must be extremely vigilant or vaccinate as a precaution.

In the last 15 yr, the prevalence of rinderpest has been declining. The Food and Agriculture Organization (FAO) of the United Nations, with the leading veterinary officials of rinderpest-affected countries and international experts on rinderpest, has developed a strategy for the worldwide eradication of rinderpest. The OIE has promoted this goal by encouraging disease reporting, sharing information, and developing international animal sanitary standards. Article 2.1.4.4 of the OIE International Animal Health Code requires that, for a country to declare itself or a zone free of rinderpest, it should fulfill certain conditions, including disease absence for at least 2 yr in the presence of disease surveillance and monitoring, a reporting system, a preventive program, and cessation of vaccination. Many countries have now achieved that status; others have made progress in rinderpest eradication and have declared provisional free zones.