Avian Encephalomyelitis is an infectious viral disease of young chicken and is characterized by nervous signs of incoordination, ataxia, tremors of head, neck and even whole body and paresis. The disease also affects birds, but most flocks show no clinical signs of the disease other than a drop in egg production, which is transitory and usually passes unnoticed.
Distribution
Jones (1932), first reported the disease in 2 weeks old Rhode Island Red chicks from a commercial flock. From that the disease was reported in all the corners of the world.
Avian Encephalomyelitis is an emerging disease in India. Rao (1968) mentioned the occurrence of the disease in India and suspected the presence of infection on clinical manifestation. Mohanty (1971) investigated the disease in the laboratory and studied the pathogenicity and pathology. Singh (1972) reported the occurrence of the disease in Punjab. The disease is now prevalent in all the states of India.
Aetiology
The disease is caused by Picornavirus, a RNA virus measuring 20-30 micrometre in diameter. The virus is relatively resistant to physical and chemical agents as well as heat and cold. All the strains are antigenically more or less uniform. Virus has got the affinity for enteric and nervous tissues.
Susceptible Hosts
Natural infection occurs in poultry, turkeys, Japanese quail and pheasants. Ducklings, young pigeons and guinea fowl are also susceptible to the virus. Baby chicks of 1-2 weeks of age are mostly susceptible. Adult birds are also affected. Mice, guinea pigs, rabbit and monkeys are refractory to the virus. Human being is not affected.
Transmission
The disease is observed in all the seasons. There may be low seasonal incidence during winter months, which increases during spring.
- The infection is disseminated through the egg or through infected chicks to the healthy ones during hatching. The present stock that has experienced a recent infection shows a transient drop in egg production, the virus being eliminated in the egg and passed to the chicks during this phase of infection, which is followed by development of antibodies and recovery in egg production.
- Virus is excreted in droppings for long period. Very young chicks may shed the virus for more than 2 weeks. So, through infected litters the infection may also spread, as the disease is essentially an enteric infection.
- Contaminated fomites may transmit the virus.
- Virus spread is less in caged birds than those on the floor.
Pathogenesis
Chicks infected vertically has an incubation period of 1-7 days and chicks infected horizontally show the incubation period of about 11 days. Morbidity of the natural disease has been observed only in young chicks. The average mortality rate is around 10% and in some instances may exceed 50%. The mortality is due to inability of the chicks to reach to food and water. Viral antigen localises primarily in the alimentary tract in the birds exposed to oral infection. There is rapid viraemia and the virus is deposited in pancreas. Purkinje cell and molecular layer of the cerebellum are the favourable sites for viral multiplication.
Clinical Findings
Young chicks are primarily affected with high morbidity and mortality. Severity of the disease reduces on attainment of age of more than 5 weeks. The average set of signs will be visible at 17 to 21 days following hatch. Affected young chicks will show nervous signs. The nervous signs are characterized by dullness, depression, ataxia, incoordination, sitting on haunches, inability to walk and paralysis. Birds may show signs of tremor of head and opacity of lens. 36.9% of histologically positive cases show ataxia, 18.3% show tremor, 35% show both and 9.2% show no clinical signs. Tremors can be aggravated by handling the birds. Birds die due to trembling and inability to take food. In adult birds, signs are intestinal in nature and diarrhoea may be evident in them. There is 10-20% drop in egg production. The appetite is retained. Birds usually remain drowsy but, if any sound is made they will get up and walk and finally go to tremor.
Lesions
The only gross lesion observed in dead chicks is whitish areas in the muscles of gizzard and proventriculus caused by masses of infiltrating lymphocytes.
Histological examination of pon, medulla and spinal cord show eccentricity and chromatolysis of nucleus. Striking perivascular infiltration occurs in these areas. Non-purulent encephalomyelitis and hanglionitis are observed. Gliosis occurs in molecular layer of cerebellum. Two nuclei of mild brain or fundus and ovoidalis show the microgliosis and considered as pathognomic. Central chromatolysis of neurons of brain stem is also pathognomic. Huge lymphocytic proliferation is observed in proventriculus, pancreas, gizzard an heart muscles.
Diagnosis
- Age of the bird and typical clinical signs.
- Histopathological changes.
- Isolation of the virus on experimental production of the disease in newly hatched chicks by inoculating infected material in the embryonated eggs via intra-yolk sac route or alternatively by intracerebral inoculation in the young chicks.
- Virus neutralization test: Van Roekel embryo adopted strain is recommended to determine the neutralising capacity of the serum. Six-day old embryos are inoculated via yolk sacs with virus dilutions mixed with serum are examined for characteristic lesion on 10-12 days post inoculation.
- Fluorescent antibody technique to demonstrate the virus in tissues.
- Agar-gel precipitation test.
- Embryo susceptibility test.
- ELISA.
The disease should be differentiated from the following affections/disease:
- Ranikhet disease
- Vitamin E deficiency
- Muscular dystrophy
- Marek’s disease
- Exudative diathesis
- Arsenal involvement
Treatment
There is no effective treatment for the infected birds.
Control
- In case of an outbreak, affected birds are to be segregated immediately and it is advisable to destroy the affected birds.
- Sanitation and hygienic measures are to be adopted.
- Strict, hygienic measures are to be adopted in the hatchery.
- Birds should be purchased from the disease free stock.
- Vaccination is practised in foreign countries with live embryo-propagated viral strain 1143 via drinking water or by spraying. Vaccination is to be done at 10-16 weeks of age, prior to egg laying. In India, no commercial vaccine is available.
