Cattle and buffalo diseases
Rinderpest: Rinderpest is the most destructive of the virus diseases of cloven-footed animals, viz. cattle, buffaloes, sheep, goats, pigs and wild ruminants. Before the advent of vaccination programme, in India alone, an annual loss of millions of rupees through deaths and indirect losses due to rinderpest has been accounted. The incidence of the disease came down from 1960 outbreaks to 12 outbreaks per 1 million bovine population during 1970 to 2000. The National Project on Rinderpest Eradication (NPRE) was instituted by the Government of India in 1991 by implementing mass immunization programmes with the assistance of European Economic Community (EEC). The NPRE has accomplished significant results and there has been no report of occurrence of rinderpest in the country since. The role of sheep and goats, in the perpetuation of the virus and transmission of the disease has given increasing evidence to the presence of Peste des petits ruminants (PPR) virus in outbreaks which were suspected of rinderpest in many parts of the country. During the 75th General Session the International Committee adopted the proposed update in the "OIE rinderpest pathway" of the Terrestrial Code. In view of the progress in global rinderpest eradication, the provisions of Chapter 2.2.12. of the Terrestrial Code 2007 were restricted the sole recognition of rinderpest free status representing a country-wide infection free status. Therefore, new applications of Members for zones free from rinderpest or rinderpest disease free status are no longer applicable. India is recognized as free from rinderpest, according to the provisions of Chapter 2.2.12. of the Terrestrial Code. (Adopted by the International Committee of the OIE on 27 May 2008).
Epidemiology: The disease occurred in endemic form in South Asia, especially in India, Nepal, Afghanistan, Democratic Yemen, and Gulf States. The virus causing the rinderpest is classified in the family Paramyxoviridae, subfamily Paramyxovirinae under the genus Morbillivirus. The rinderpest virus shares a common antigen with human measles and canine distemper viruses. It has an affinity for lymphoid and epithelial cells. It lives in the white blood cells of affected animals in later stages of its growth and existence. It can be propagated in cattle or buffaloes in which the virus maintains its full virulence. It can also be propagated in goats, rabbits, embryonated eggs and cell cultures. However, continued cultivation of a virulent virus in these hosts results in a lowering of the virulence or attenuation.
Exotic cattle or those with an admixture of foreign blood and water buffaloes are more susceptible than the indigenous zebu cattle of the plains of India. The mortality rate varies from 8 to 100 %. In the cattle from the plains, originating in northern India, the mortality varies from 20 to 50%. Domestic pigs can develop clinical signs and are regarded as an important virus reservoir in Asia. Among wild animals, wild beast, deer, antelope and hippopotamuses are susceptible.
In the infected animal, the virus is found notably in saliva, discharge from eyes and nostrils, in urine and faeces. Virus is present in the blood during the febrile stage and later concentrated in different organs, especially in the spleen, lymph-nodes and liver. The best specimens for virus isolation are tissues from mucosal lesions or lymph nodes; cocultivation of washed buffy coat cells from suspect animals with bovine kidney cells. Outside the animal body, the virus is rapidly destroyed by direct sunlight and disinfectants. Frozen conditions preserve the virus. Susceptible animals get exposed to infection through contaminated feed and water.
Outbreaks had often been followed after wars and civil disturbance where movement of troops and refugees with live animals disseminates the virus. Rinderpest also reappeared in Turkey in 1990s, possibly as a consequence of Gulf War.
Symptoms: Rinderpest is an acute febrile disease with morbidity in susceptible population approaching 100% and mortality 90-100%. The incubation period of the disease is 3 to 7 days. After 4 to 6 days, the animal develops a temperature of 40o to 41.1oC which reaches the peak in 24 to 48 hrs (prodromal phase). The peak lasts for 2 to 7 days. The animal becomes dull, with congested conjunctiva, lachrymation and dryness of the muzzle (mucosal phase). There is arching of the back with the rigors, loss of appetite and constipation. These symptoms are followed by the passing of soft faeces. This soon develops into diarrhoea with foetid smell. The faeces is often stained with blood. After 7 to 9 days, the characteristic lesions of rinderpest appear on the buccal mucous membrane, the inside of the lips and on the gums. These lesions are at first of the size of pin points but later coalesce into ulcers and are often covered with bran like deposits. Similar lesions develop through the gastrointestinal tract. Mucus and epithelial shreads are often passed in the faeces. The presence of raw ulcers in the mouth render the animal incapable of feeding and the severe diarrhoea causes the animal rapidly to loose condition. The animal dies in 7 to 10 days from the onset of the symptoms. Skin lesions have also, in some instances, been observed in affected animals. Recovered animals continue to remain emaciated for a considerable length of time.
Postmortem examination generally shows evidence of emaciation and diarrhoea.
Skinning of the animal discloses a parched appearance of the entire body. The lesions are found in the internal organs and, in particular, in the intestines and the abomasum. The mucous membrane is extremely congested. The folds of the abomasum are thickened, flabby and dark chocolate in color. Some necrotic ulcers covered with bran- like deposits are also seen. The posterior part of the large intestine reveals intense congestion, the so-called zebra marking. Other organs also show a certain degree of congestion which, however, is not typical of rinderpest infection alone.
Diagnosis: The early symptoms of rinderpest present a certain degree of similarity to those of malignant catarrhal fever, but oral ulcers and diarrhoea at a later stage of the disease occur only in rinderpest. However, malignant catarrhal fever is a protracted disease and does not result in immediate death.
In coccidiosis, fever is not a symptom. The oocysts which can be readily seen under the microscope are passed in the faeces and mouth lesions do not occur in this disease. Coccidiosis generally occurs as a complication of rinderpest, especially in young ones. Calves before 6 mouths of age are very susceptible to coccidiosis.
The foot lesions, highly characteristic of foot-and-mouth disease, do not occur in rinderpest. The ulcers in the mouth are of a different character. Further, rinderpest is invariably associated with diarrhoea.
The result of postmortem examination should remove any doubt as to the identity of the disease. A provisional diagnosis can be further obtained by inoculation tests in the laboratory animal with pieces of spleen, collected soon after the death of an affected animal. The material may be dispatched in a leak-proof sterile bottle without any preservative and the bottle is immersed in crushed ice. The confirmation of a provisional diagnosis can be obtained by demonstrating virus specific antigen by counter immuno electrophoresis (CIE) or agar gel immuno-diffusion (AGID) test using reference antisera or by virus isolation in cell culture. The virus infects a wide range of cells, but isolation for the laboratory diagnosis is carried out routinely in primary bovine kidney cell cultures. A marmoset lymphoblastoid cell lines (B95a) and Theilaria parva transformed bovine lymphocytes cell lines are also used. The best specimens for virus isolation are tissues from mucosal lesions or lymph-nodes. Co-cultivation of washed buffy coat cells from suspected animals with bovine kidney cells may be used to avoid the effects of presence of early antibodies. Cyto-pathology is evident in 3-12 days. Neutralization and enzyme immunoassays are used to confirm the identity of the isolates and for serological diagnosis. For the differential diagnosis with PPR, monoclonal antibody based ELISA and multiplex PCR using H gene has been developed.
Treatment: Symptomatic treatment with penicillin, streptomycin, sulphadimidine and intestinal antiseptics help in the recovery of less severe cases of rinderpest, as these control secondary complications caused by bacteria. It is beneficial to keep the animal on light diet like rice gruel with kaolin which acts as an intestinal astringent and reduces the intestinal effusions and controls diarrhoea.
Prevention and control: If one of the infected animals, viz. cattle, buffaloes and goats survives, it carries the infection. Others animals, especially those in close contact, will contract the infection and introduce the disease in their respective localities. It is, however, in cattle fairs that the disease usually spreads from affected to healthy cattle. The affected animals have to be detected well in time for segregation, although this is by no means easy, especially when the animals concerned are in incubation stage.
It is not until 3 to 7 days after the animal has contracted the infection that the owner notices symptoms of illness in the animal. In the mean time, the infection spreads to a number of other susceptible animals in a herd. A cattle owner usually observes the infection when about 25 to 50% of animals are infected and when one animal after another starts showing the typical symptoms. At this stage, isolate the affected and incontact animals from those that are apparently healthy and remove them to distant place with separate arrangements for feeding and watering, by separate attendants.
Prevention means limited measures applied for a small community or herd. Control implies to mass treatment for the region or for the country periodically, as a routine vigilance measure to keep the disease out. Eradication means the complete elimination of the infectious agent from the host population and its environment.
Rinderpest vaccines: Rinderpest vaccines are the live modified vaccines, viz. goat-adapted tissue vaccine (250th passage), lapinized vaccine (700-800 passage in rabbit), lapinized-avianized vaccine (rabbit passaged virus is again passaged in chicken embryo), avianized vaccine and tissue cultures based vaccines. Mass immunization of about 75% of susceptible cattle in the plains and buffaloes with the goat tissue vaccine (GTV) carried out under the All- India scheme for the Eradication of Rinderpest during the first three Plan periods brought down the incidence of outbreaks and deaths to a very low figure. European breeds of cattle, crossbred cattle, hill cattle at very high altitudes, Mithuns in Assam and NEFA, Yaks in Indo-Tibetian border areas and sheep and goats reacted severely to the inoculation with GTV. With the use of tissue culture based live virus vaccine, however, these reactions have not been observed.
Cell-culture rinderpest vaccine: Cell-culture rinderpest virus vaccine, Kabete 'O' strain of RP virus, after repeated passages in calf-kidney cell culture or propagated on VERO cell line (92-96 passages), got attenuated. Vaccination of all calves should be undertaken when they are 6 to 8 months old and again within 12 months. The protection induced is expected to last for at least 5 to 7 years. However, it is advisable to carry out revaccination every 5 years. The vaccine can be used in the face of an outbreak with advantage in those animals not showing fever or any other clinical symptom of the disease. Since the disease has been eradicated from India, vaccination is no more done.