Rinderpest is a highly contagious and fatal disease of cattle caused by a Morbillivirus. It was historically one of the most devastating diseases for cattle populations in Africa and Asia, with mortality rates up to 90%. Clinical signs include fever, oral lesions, diarrhea, and death within 6-12 days. The virus primarily affects lymphoid tissues and the gastrointestinal tract. An international eradication effort successfully eliminated rinderpest by 2011. Diagnosis can be made through various serological and molecular tests.
Rinderpest is a highly contagious and fatal disease of cattle caused by a Morbillivirus. It was historically one of the most devastating diseases for cattle populations in Africa and Asia, with mortality rates up to 90%. Clinical signs include fever, oral lesions, diarrhea, and death within 6-12 days. The virus primarily affects lymphoid tissues and the gastrointestinal tract. An international eradication effort successfully eliminated rinderpest by 2011. Diagnosis can be made through various serological and molecular tests.
Rinderpest is a highly contagious and fatal disease of cattle caused by a Morbillivirus. It was historically one of the most devastating diseases for cattle populations in Africa and Asia, with mortality rates up to 90%. Clinical signs include fever, oral lesions, diarrhea, and death within 6-12 days. The virus primarily affects lymphoid tissues and the gastrointestinal tract. An international eradication effort successfully eliminated rinderpest by 2011. Diagnosis can be made through various serological and molecular tests.
Rinderpest is a highly contagious and fatal disease of cattle caused by a Morbillivirus. It was historically one of the most devastating diseases for cattle populations in Africa and Asia, with mortality rates up to 90%. Clinical signs include fever, oral lesions, diarrhea, and death within 6-12 days. The virus primarily affects lymphoid tissues and the gastrointestinal tract. An international eradication effort successfully eliminated rinderpest by 2011. Diagnosis can be made through various serological and molecular tests.
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Rinderpest
• Also known as cattle plague
• An acute, highly contagious disease of cattle caused by Morbilli virus • Foremost cause of death in cattle in most of African and asian countries • Establishment of first Veterinary college in 1762 in Lyon , France • Mortality varies from 25-90% depending on the strain and resistance of the animals • Rinderpest eradication campaign successfully completed in Nepal • Clinically the disease is characterised by high fever, necrotic stomatitis, diarrhoea and high mortality • Buffaloes, sheep, pigs, goats and camels are also susceptible • In wild life rinderpest has been reported in deer, antelope, wild buffaloes, wild boars, bushbuck, and giraffe • The rinderpest virus is antigenically closely related to the virus of canine distemper, peste des petits ruminants(PPR) of sheep and goats and measles of human • Incubation period varies from 6-9 days Spread
• The rinderpest virus is quite fragile
• Therefore close contact between infected and healthy animals is necessary for spread of disease • The virus does not survive for long outside the host • The virus is excreted by infected animals in urine, faeces, nasal discharges, saliva, tears and sweat • Transmission occurs through contaminated feed or by inhalation of aerosal (infected droplets) • Ingestion of contaminated food and water by the discharges of clinical cases or animals in the incubation stage may also be important mode of infection especially in pigs Pathogenesis • The virus is inhaled in infected droplets • It penetrates through the epithelium of upper respiratory tract and multiplies in the tonsils and regional lymph nodes • It enters blood in mononuclear cells which disseminate the virus to other lymphoid organs, the lungs, and epithelial cells of mucous membranes • The virus has high degree of affinity for lymphoid tissue and alimentary mucosa • There is a pronounced destruction of lymphocytes in tissues with pyknosis and fragmentation of nucleus and germinal centers devoid of lymphocytes • This is the cause of marked leukopenia • The focal necrotic stomatitis and enteritis are the direct result of the viral infection and replication • Death is usually from severe dehydration Signs • Rise in temperature(104-105⁰F) accompanied by restlessness, dryness of the muzzle and constipation • Photophobia(intolerance to light), excessive thirst, shining coat, retarded rumination, anorexia, and excessive salivation • Fever usually reaches peak on the 3rd or 5th day but drops abruptly with the onset of diarrhoea • Lesions in oral mucosa appear by 2nd or 3rd day of fever but become clearly visible after onset of diarrhoea • Abdominal pain, arched back, increased respiration, severe dehydration and emaciation followed by prostration , subnormal temperature and death(6-12 days) Lesions • The virus has a particular affinity for epithelial tissues of the gastrointestinal tract • In lymphoid tissue the virus causes necrosis of lymphocytes • Striking in microscopic sections of lymph nodes, spleen and payers patches • Multinucleated giant cells containing eosinophillic cytoplasmic inclusion bodies are present • Grossly changes are most marked in the Peyer’s patches – haemorrhages, slaughing leaving deep craters(ulcers) in intestinal wall • In cattle- the virus carried to oral mucosa by blood stream and causes necrosis of epithelial cells stratum malpighii • These cells have pyknotic and fragmented nuclei with eosinophillic cytoplasm • The necrotic areas increase in size and multinucleated giant cells form in the stratum spinosusm • Eosinophillic cytoplasmic inclusion bodies form in the mucosal epithelial cells and giant cells • Vesicles are not formed in this disease • With time the foci of necrosis coalesce to form large areas of erosions • The erosions are shallow with a red raw floor and a sharply demarcated margin • The lesion in oral mucosa have selective distribution: inside the lower lip, the adjacent gum, the cheeks near commissures and the ventral surface of the free portion of the tongue • In severe cases lesions extend to the hard palate and pharynx, in fulminant cases to all surface of the tongue • The abomasum is the most common sites of the lesions of rinderpest • They are most severe in pyloric region where necrotic foci of microscopic size in the epithelium with congestion and haemorrhages in underlying lamina propria • Grossly irregular superficial bright red to dark brown streaks extending into fundus and becomes more numerous and diffuse in pylorus • In small intestine payer’s patches are affected, necrotic and slough out leaving deep crater in the intestinal wall • The large intestine is more seriously damaged than the small intestine with prominent lesion in ileocaecal valve, caeco-colic junction and the rectum • The crest of folds of mucous membrane throughout the caecum is bright red due to petechiae • Streaks of congestion along the folds of mucosa of rectum produce a characteristic “ zebra – striped” (zebra marking) • As the disease progresses the mucosa becomes eroded, diffuse congestion and bleeding from the raw surfaces occur in large areas • Lesions in caecocolic junction include congestion, erosion and increased thickness of the wall due to oedema of the submucosa and muscularis • The changes in colon and rectum vary from a few longitudinal streaks of congestion along the crest of the folds of the mucosa to erosions of mucosal epithelium • The streaks and congestion and haemorrhages are more common in the rectum than colon • In respiratory system, petechiae occur on the mucosa of upper respiratory tract in the larynx and trachea • In trachea streaks of haemorrhages in the mucosa are almost always found • Common in anterior third of trachea • The lungs involve only secondarily. • In long standing cases lesions include both interstitial and alveolar emphysema and small areas of consolidation • In the urinary bladder the epithelium may be desquamated and underlying stroma infiltrated with erythrocytes • Acute congestion and edema of conjunctiva followed by purulent conjunctivitis Diagnosis • AGID • CFT • Virus isolation on tissue cultures • Virus neutralisation • Counter immuno electrophoresis • Immunofluorescence • Immmunoperoxidase test • ELISA • PCR