It is an acute disease predominantly in goat and goat kids having the age range of 3-8 weeks characterised by lameness, fever and recumbency.
Distribution
The disease is widely prevalent in various states of the country. Epizootiology studies of the disease has been reported from West Bengal.
Aetiology
The disease is caused by Mycoplasma spp. Mycoplasma mycoides capri, M. mycoides large colony and M. argini have been considered as aetiology of the disease from various countries. PPLO broth is required for culture. The culture shows ‘nipple shaped’ appearance after 24 hours of incubation at 37 C. In India, polyarthritis in goats has been incriminated to be caused by M. mycoides sub spp, mycoides.
Susceptible Hosts
Goat and goat kids are mostly affected. The disease has been noted in sheep. Polyarthritis has been reported in pigs caused by M. hyorhinis. Polyarthritis in calf has been found to be associated with M. bovis, where pneumonic signs are also present. Black Bengal goats suffer most.
Mode of Transmission
Transmission of infection may be due to direct contact with infected animal. Intercurrent infection through inhalation is possible. The infection may spread from milk of goat suffering from mycoplasmal mastitis. Sheep may also suffer from similar manner. Ear mite psoroptes cuniculi have been identified as possible spreader of infection. Goat fleas of the order Siphonaptera may act as vectors for spontaneous caprine polyarthritis associated with septicaemia. The kid may acquire the infection from green grass as the organisms are wide spread in nature.
Clinical Findings
The disease is mostly prevalent in young goats of 1 to 8 weeks of age but highest in 3-8 weeks of age. Black Bengal goats mostly suffer in India. There is high rise of temperature, stiffness of gait and lameness. There is reduced appetite and gradual loss of body weight. The affected one is unable to move due to swollen joints causing pain. All the diarthrodial joints are involved. Some goats may remain in lateral recumbency. Prolonged recumbency may lead to the formation of decubital ulcer. There is thickening and oedema of synovial membranes. Other signs like pneumonia, lymphadenitis, pericarditis, peritonitis, enteropathies, nephritis and conjunctivitis may be observed with polyarthritis.
Diagnosis
This is based on the following
(a) Clinical findings: Characterised by appearance of joint lesions in number of kids in a flock with signs of systemic involvement with a mortality rate of 35%.
(b) Isolation of organisms: Synovial fluid is to be aspired aseptically from affected joints. About 0.1 ml of the material is to be transferred to PPLO broth containing 20% horse serum and to be incubated at 37 C at reduced oxygen tension. Blind passages are to be followed three times and finally the growths are to be tested in PPLO agar plates by incubating them at 37 C for 4 days. Isolates are to be characterised based on cultural, morphological, biochemical and growth inhibition tests and thus confirmation of isolates can be made. In India, culture can be sent to PL 480 Research Centre for animal mycoplasmas, Mathura Veterinary College, Mathura for confirmation of mycoplasmal isolates. Typical poached egg shaped colonies will appear. Isolates may take royal blue colour when stained with Diene’s stain.
(c) Serology: Mycoplasma can be detected by employing the tests like complement fixation test, latex agglutination test, indirect haemagglutination test, enzyme linked immunosorbent assay and indirect immunofluorescent test.
(d) Biochemical changes: There may be reduction of haemoglobin, PCV and toral erythrocyte values indicating signs of anaemia. Anaemia may result due to huge destruction of RBC or effect of endotoxin liberated by mycoplasma. There is leucocytosis.
Biochemical changes include reduction of calcium and phosphorous levels. But, increase in the levels of blood sugar, SGOT and SGPT.
Changes in synovial effusions.
Arthritis should also be differentiated from other infections causing such changes. Arthritis and synovitis, in different species of domestic animals may be caused by different organisms.
Synovial fluid study may help in differentiating septic changes from degenerative joint diseases of large ruminants.
Treatment
Drugs like oxytetracycline, doxycycline, Tylosin, tiamulin, lincomycin, enrofloxacin can be used against this malady. Tylosin tartrate @ 10 mg/kg body weight by intramuscular route for 10 days along with dexamethasone sod phos. @ 0.25 mg/kg body weight orally for 7 days may give complete recovery with no reisolation of the organisms.
Tiamulin solution @ 1.5 ml per 12.5 body weight through intramuscular injection along with prednisolone injection @ 2.5 to 5 nig per kid for 6 days could bring disappearance of swelling of joints, restoration of normal gait, improvement of appetite and disappearance of fever..
Control
- On detection, the affected animals should be segregated and treated.
- Entry of the suspected goat should not be permitted in goatery unless cultural examination proves negative.
- Test and slaughter will be the ideal way of eradication from a goat farm.
- Culture of the milk should be done before purchase of goat to be introduced in a new farm. Kid may be fed wih cow’s milk while performing the milk culture of the doe since the kids acquire the infection through mother’s milk.
- Treated animals following recovery may remain as carrier. Therefore, it is suggested to sell the animal for meat purposes.
- Mite and flea have been incriminated as possible transmitting vectors. These vectors are to be controlled through insecticide spray.
- Long term oral alincomycin or tiamulin may be used as preventive measure in endemic zones.
- Formalized vaccine as used against cattle may be tried to control the disease.
