Overview of Rinderpest

Rinderpest virus is a Morbillivirus, closely related to the viruses causing peste des petits ruminants, canine distemper (see Canine Distemper), and measles. Strains of varying virulence for cattle occurred and could be differentiated genetically. However, a single serotype of the virus existed, and a vaccine prepared from any strain could protect against all strains.

Rinderpest virus is shed in nasal and ocular secretions and can be transmitted during the incubation period (1–2 days before onset of fever). Transmission required direct or close indirect contact between susceptible animals and sick animals shedding the virus. The role of fomites in transmission was negligible, because the virus is fragile, being inactivated within 12 hr of exposure to atmospheric heat and light. There was no carrier state, and recovered animals acquired lifelong immunity. In endemic areas, young cattle became infected after maternal immunity disappeared and before vaccinal immunity began, with possible auxiliary cycles in wild ungulates.

After an incubation period of 3–15 days, fever, anorexia, depression, and oculonasal discharges developed, followed by necrotic lesions on the gums, buccal mucosa, and tongue. The hard and soft palates were often affected. The oculonasal discharge became mucopurulent, and the muzzle appeared dry and cracked. Diarrhea, the final clinical sign, could be watery and bloody. Convalescence was prolonged and could be complicated by concurrent infections due to immunosuppression. Morbidity was often 100% and mortality was up to 90% in epidemic areas, but in endemic areas morbidity was low and clinical signs were often mild.

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 transcription-PCR (RT-PCR), were favored toward the end of the eradication campaign. The RT-PCR technique allowed phylogenetic characterization of the virus and helped trace the origin of strains in new outbreaks. A simple lateral flow penside test for field use also proved useful in the final stages of the eradication campaign. In the 10-yr period between occurrence of the last outbreak and the official declaration of eradication, active rinderpest surveillance in recent endemic areas included the testing of all susceptible cloven-hoofed animals presenting with erosive stomatitis.

Active immunity was lifelong, whereas 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 by slaughtering affected and exposed animals. Control of animal movements was paramount to control rinderpest; many outbreaks were due to the introduction of infected cattle to hitherto uninfected herds. The lessons learned from this huge success will be instrumental in the fight against peste des petits ruminants.