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Nature of the Disease

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Nature of the Disease Manual on the preparation of rinderpest contingency plans 5 Chapter 2 Nature of the disease DEFINITION EPIDEMIOLOGICAL FEATURES Rinderpest, or cattle plague, is an acute, highly Susceptible species contagious viral disease of wild and domesti- Large domestic ruminants. Although all clo- cated ruminants and pigs. It is characterized by ven-hoofed animals are probably susceptible to sudden onset of fever, oculonasal discharges, infection, severe disease occurs most commonly necrotic stomatitis, gastroenteritis and death. in cattle, domesticated water buffaloes and yaks. In a fully susceptible population, as is the Breeds of cattle differ in their clinical response to case in non-endemic areas, morbidity and rinderpest virus. Some breeds have developed a mortality can approach 100 percent. With high innate resistance through selection by long some strains of the virus, however, the dis- association with the disease. ease may be mild with low mortality from Sheep and goats are generally less suscep- infection. tible but may develop clinical disease. Asiatic pigs are susceptible and may suffer WORLD DISTRIBUTION clinical disease. European breeds are less sus- Formerly widespread throughout Europe, Asia ceptible. The latter tend to undergo subclinical and Africa, rinderpest has now been limited to infection and play little or no part in the fairly well-defined locations in South Asia, the maintenance of the disease. Near East and eastern Africa. This has been Camels are apparently not infected and ap- achieved through various national and regional pear to have no role in rinderpest transmission rinderpest eradication programmes. Global and maintenance. rinderpest eradication, which is being targeted for 2010, is being coordinated by FAO. Wildlife. Some species, such as African buffalo, eland, giraffe, lesser kudu and warthog and Asian AETIOLOGY antelopes, bovids and swine, are highly suscep- Rinderpest virus belongs to the morbillivirus tible. Others, such as antelopes, hippopotamus genus of the paramyxovirus family. Other mem- and Indian blackbuck are less susceptible. There bers of the genus include the measles virus of is no evidence to suggest that wildlife popula- humans, the peste des petits ruminants virus of tions can maintain the disease indefinitely with- domesticated and some small wild ruminants, out concurrent disease in cattle. the canine distemper virus of dogs and wild Rinderpest does not infect humans. carnivores and the morbilliviruses of aquatic mammals. Transmission There is only one serotype of rinderpest Almost invariably, rinderpest spreads between virus, but the different strains vary in their herds and to new areas by the movement of pathogenicity. infected animals. Infected cattle start shedding 6 Nature of the disease virus one or two days before the appearance of serve as a source of infection for pigs, which clinical signs. They continue to shed virus for may then transmit the disease to cattle. about nine to ten days after the onset of fever, and Rinderpest is not transmitted by insect vec- generally harbour the virus for no more than tors. three weeks. Infected cattle may spread virus through markets and transport it long distances Virus stability before clinical evidence of the disease is ob- At 4°C, rinderpest virus is most stable at pH values served. of 7.2 to 7.9 and is rapidly inactivated at pH less Rinderpest virus is found in expired air, than 5.6 or greater than 9.6. The virus is inacti- nasal and ocular discharges, saliva, faeces, vated rapidly at environmental temperatures by milk, semen, vaginal discharge and urine. In- solar radiation and desiccation. Pasture is infec- fection is transmitted primarily by inhalation tive for six hours if unshaded or 18 to 48 hours if of expired air contaminated by infected drop- shaded. Contaminated bare enclosures are infec- lets or by contact with secretions and excre- tive to cattle for no more than 48 hours and contami- tions from infected animals. Transmission oc- nated buildings for a maximum of 96 hours. curs mainly over short distances, but occasion- The virus is highly susceptible to many lipid- ally may occur over distances of up to 100 m or solvent disinfectants because it is enveloped. It more at night, when the effects of high tem- is also susceptible to both acid and alkaline perature and sunlight are minimal, especially conditions. It is inactivated rapidly by autoly- in conditions of very high humidity. sis and putrefaction and hence does not survive Transmission through the oral route by in- for more than 24 hours in the carcass of an gestion of contaminated feed and water is animal that has died from the disease. possible. Infected meat stored at 4°C can The virus is present in milk one or two days remain infective for at least seven days. Feed- before appearance of clinical signs. Heat treat- ing of infected meat and feed contaminated ment or pasteurization of milk is sufficient to with infective secretions and excretions may inactivate the virus. DOMESTICATED WATER BUFFALOES The national rinderpest contingency plan should include provisions for this species, as the disease is commonly seen in buffaloes Manual on the preparation of rinderpest contingency plans 7 CLINICAL SIGNS from between three and five days to two Cattle weeks, before returning to normal. This is Rinderpest is capable, in certain situations, of accompanied by restlessness, depression, causing devastating losses in cattle herds, but inappetence and a significant fall in milk tends to have less impact in endemic areas and on yield. Respirations are shallow and rapid. partially immune populations. The disease may One or two days later, serous oculonasal dis- be peracute, acute or mild, depending on a num- charges and severe congestion of the mucous ber of factors inherent in the virus strain, the host membranes of the eyes and nose are typically and the system of management of the animals. seen. Two to five days after the onset of fever, Peracute rinderpest. In peracute rinderpest, there tiny, pinpoint greyish areas of necrosis appear is a sudden onset of fever, inappetence, depres- on the gum and lips. The lesions increase in sion, congestion of the visible mucous mem- number, enlarge and coalesce to form a thick, branes and death within two to three days, before yellow pseudo-membrane covering the oral oral erosions develop. mucosa including the lateral and ventral as- pects of the tongue. The necrotic debris easily Acute rinderpest. The OIE International animal desquamates, leaving shallow erosions with health code puts the incubation period of red layers of basal cells. Similar erosions can rinderpest as 21 days for purposes of zoosanitary also be seen on the mucous membranes of the measures. The route of infection, the dose and nose, the vulva and the vagina. Salivation is the virulence of the strain of virus may modify stimulated, the saliva being initially mucoid the incubation period. In general, the period and then mucopurulent. A distinctive foul between the first index case and the appearance odour exudes from the mouth. of secondary cases is about two weeks. Diarrhoea starts one to three days after the Typically, the disease is heralded by a sud- appearance of oral lesions. The faeces are den onset of pyrexia, which may last anything initially thin and dark in colour, and may later A COMMON WATERING-POINT Rinderpest transmission and spread are enhanced by congregation of different herds of animals, as occurs at common watering- points 8 Nature of the disease become watery and contain mucus, shreds of are more likely to be PPR. However, acute epithelium and specks of clotted blood. Occa- rinderpest can occasionally be seen in small sionally the liquid faeces may be red in colour. ruminants. Clinical manifestations are similar to Affected animals arch their backs and strain, those seen in cattle, and consist of fever (rectal sometimes exposing congested and eroded temperatures of 41 to 42°C), focal to coalescent rectal mucosae. necrotic stomatitis, oculonasal discharges, Respirations are laboured and painful and conjunctivitis, pneumonia and diarrhoea. there may be an audible grunt on expiration. In fatal cases the diarrhoea continues to worsen, Pigs causing rapid dehydration and visible wast- Asiatic breeds of pigs may suffer peracute or ing. Sternal recumbency follows and death acute rinderpest. Peracute disease is character- supervenes 6 to 12 days after the onset of ized by sudden onset of fever and death without fever. If animals survive, the erosions heal, further premonitory signs. Acute disease in these diarrhoea stops and a prolonged convales- breeds of pigs is manifested by sudden onset of cence follows, with recovery to full health fever, inappetence, depression, shivering, vom- taking many weeks. Pregnant cows commonly iting and epistaxis. Shallow erosions, diarrhoea, abort in the convalescent period. progressive but rapid dehydration and emacia- Skin lesions, which appear as a maculo- tion precede death. papular rash on the less hairy parts of the body such as the groin and axillae, have been de- scribed. Mild rinderpest. The evolution and clinical signs of mild rinderpest are similar to those of the classic syndrome but are less marked. One or more of the cardinal features may be absent or only present transiently, particularly oral ero- sions, which may be meagre. Most affected cattle recover, and convalescence is short. A frequent sequel of mild infections is activation of latent pathogens, notably protozoa, occurring four to six days after
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