Peste des petits ruminants
It is also known as goat plague or kata resulting in high fever, diarrhoea and respiratory distress. In India, the disease was reported in the village of Arasur, Tamil Nadu State in 1989, and subsequently the disease was recorded from other parts of the country and is now endemic in goat and sheep.
Etiology: PPR virus is a morbillivirus of the family paramyxoviridae, closely related to rinderpest and canine distemper viruses. The disease is seen both in sheep and goat and occurs in more severe form in goat than sheep. Kids of 4-12 months of age are more susceptible. The morbidity rates are 75-90% while mortality rates are 70-80%. Close contact between infected and susceptible animals is essential for spread of the disease.
Pathogenesis: The virus is excreted in all the excretions and secretions of infected animals. After gaining entry, virus penetrates the retropharyngeal mucous membrane and causes viraemia. Due to this, gastrointestinal, respiratory and lymphoid systems are damaged resulting in diarrhoea and respiratory distress.
Clinical signs: The disease usually occurs in acute form and symptoms appear after 4-7 days. Initially there is high rise of body temperature followed by anorexia, depression, watery ocular and nasal discharge which becomes mucopurulent later on. This discharge becomes catarrhal later on and crusts are formed which occlude the nasal passage. Necrotic areas also develop in some cases on nasal mucosae. On the lips, gums, cheeks, and corners of mouth, mucosal erosions develop and tongue becomes thick with necrotic areas. Conjunctivae of animals are congested and there is profuse catarrhal discharge. After 3-4 days of development of fever, animals show diarrhoea which is profuse and mucoid followed by dysentery. In the later stages, animals show coughing and dyspnoea. Due to secondary bacterial contamination, bronchopneumonia occurs. Animals usually die within one week of onset of diarrhoea.
On postmortem examination of dead animals, erosions and ulcerations of mucosae of digestive tract and buccal cavity are seen. There is haemorrhagic inflammation of abomasum, caecum and colon. Pneumonia, pleuritis and hydrothorax have been reported. The lymphnodes and spleen are enlarged.
Diagnosis: It is diagnosed by clinical signs and postmortem lesions of dead animals. Blood analysis reveals haemoconcentration, polycythemia, leukopenia, lymphopenia, eosinopenia and monocytosis. Plasma volume and serum sodium and potassium are progressively declined. Agar gel precipitation, counter immunoelectrophoresis, haemagglutination and ELISA tests may be used for the confirmation of disease.
Treatment: Broad-spectrum antibiotics like gentamycin, erythromycin, neomycin or streptopenicillin may be used to check secondary bacterial infection. Antihistaminics, antipyretic and expectorants are also helpful. In dehydrated animals, dextrose or normal saline should be given intravenously. Infected animals recover quickly if hyperimmune serum is given intravenously @ 5 ml in infected goats.
Control: Live attenuated homologous vaccine against peste des petits ruminants of sheep and goats is produced on a large in India using seed virus developed at the Indian Veterinary Research Institute, Muktheswar, India. Vero cells between 130-150 passages with six percent foetal calf serum is used for the production of vaccine. The freezedried vaccine is monitored to have a titre of minimum of 105/100 doses. The tissue culture rinderpest vaccine (TCRP) earlier used for the control of PPR had the side effects of abortion in goats and sheep, that has been substituted by homologous PPR vaccine. Proper maintenance of animals hygienically, avoidance of stress, regular deworming and proper nutrition can reduce the susceptibility of the animals to the disease.