Historically, rinderpest virus was widely distributed throughout Europe, Asia, and Africa but it never established itself in North America, Central America, the Caribbean Islands, South America, Australia, or New Zealand. Until late 20th century rinderpest was endemic in a number of countries in Africa and Asia Minor, but it now appears to have been eradicated globally. The Food and Agriculture Organization (FAO) of the United Nations, with the leading veterinary officials of rinderpest-affected countries and international experts on rinderpest, developed a strategy for worldwide eradication which eventually evolved into the Global Rinderpest Eradication Programme (GREP). It is the view of GREP that no confirmed cases of rinderpest have been reported since 2001.
The OIE have also promoted this goal by promulgating a list of member states free from infection with rinderpest either on historical grounds (never part of an infected continent; no cases and no rinderpest vaccination for 25 years) or, in the case of countries with a history of recent endemicity, the acceptance of national evidence based on disease searching, disease reporting, and serosurveillance in unvaccinated animals. Most formerly endemic countries have now achieved this status. The aim of FAO is to formally declare that the world is free of rinderpest in the year 2010. It is in this context that a description of the disease and the methods used in its control are provided here.
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 although in practical terms the virus has always been maintained by transmission between domestic cattle, domestic buffalo, and yaks. Among cattle, Bos taurus breeds show more severe clinical involvement than Bos indicus breeds. In South Asia, where peste des petits ruminants and rinderpest existed side by side, the frequent failure to make a differential diagnosis often led to peste des petits ruminants-infected sheep or goats being incorrectly diagnosed with rinderpest. In some cases, however, small ruminants were infected with rinderpest, possibly subclinically, and were of some epidemiologic importance as virus transmitters. Rinderpest also affects some breeds of pigs and a large variety of wildlife species within the order Artiodactyla through contact with infected bovines.
Etiology and Pathogenesis
The infectious agent is a morbillivirus, closely related to the viruses causing peste des petits ruminants (see Peste des Petits Ruminants), canine distemper (see Canine Distemper), and measles. Strains of rinderpest virus have been shown to vary markedly in virulence for cattle. In addition to the vaccine strain, 3 distinct phylogenetic lineages can be differentiated (1 Asian and 2 African), but sera from recovered or vaccinated cattle cross-react with all strains in neutralization tests. 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 and ocular 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 or lung. There is no carrier state; the virus maintains itself by continual transmission among susceptible animals. In endemic areas, young cattle became infected after maternal immunity disappeared and before vaccinal immunity began, with possible auxiliary cycles in wild ungulates. In epidemic areas, the virus infected most susceptible animals and tended to limit itself unless the population was 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.
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. Morbidity is often 100% and mortality is up to 90% in epidemic areas, but in endemic areas morbidity is low and clinical signs are often mild.
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 and intranuclear inclusions are often seen.
Clinical and pathologic findings were sufficient for diagnosis in endemic areas and after initial laboratory confirmation of an outbreak. In areas where rinderpest was uncommon or absent, laboratory tests had to 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 using an immunodiffusion test was the standard, but simpler, more rapid and more discriminating tests, such as immune capture ELISA and reverse transcriptase-PCR, were favored toward the end of the eradication campaign. The reverse transcriptase-PCR technique allowed phylogenetic characterization of the virus and helped trace the origin of the viruses in new outbreaks. A simple lateral flow device penside test for field use also proved useful in the latter stages of the eradication campaign.
Before the official declaration of eradication, all cases of erosive stomatitis in susceptible animals should be tested for rinderpest. Laboratory specimens should 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.
Treatment was not usually attempted, but nursing care with supportive fluid and antibiotic therapy aided recovery of valuable animals. Active immunity was regarded as lifelong while maternal immunity lasted 6–11 mo. Control in endemic areas was by immunization of all cattle and domestic buffalo >1 yr old with an attenuated cell culture vaccine. In these areas, outbreaks were controlled by quarantine and “ring vaccination” and sometimes by slaughtering. In epidemics the disease was best eliminated by imposing quarantine and slaughtering affected and exposed animals. Control of animal movement was paramount in controlling rinderpest; many outbreaks were due to the introduction of infected cattle to hitherto uninfected herds.
Last full review/revision March 2012 by William Taylor, ; Thomas Barrett, MSc, PhD, Deceased