Avian Encephalomyelitis
(Epidemic tremor)
Avian encephalomyelitis is a worldwide viral disease of
Japanese quail, turkeys, chickens, and pheasants,
characterized by ataxia and tremor of the head, neck, and
limbs. Ducklings, pigeons, and guinea fowl are susceptible to
experimental infection. The causative picornavirus can be
grown in chicken embryos from nonimmune hens. It is
transmitted for ~ 1wk through a portion of eggs laid by
infected hens, and then spreads laterally in the hatcher or
brooder to susceptible hatchmates .
Clinical Findings :
Signs commonly appear at 11-7days of age, although they
may be present at hatching or delayed for several weeks. The
main signs are unsteadiness, sitting on hocks, paresis, and
even complete inability to move. Muscular tremors are best
seen after exercising the bird; holding the bird on its back in
the cupped hand helps in detection. Typically, about %5of the
flock is affected, although morbidity and mortality may be
much higher. The disease in adult birds is inapparent except
for a transient drop in egg production. The disease in turkeys
is often milder than in chickens .
Lesions: No gross lesions of the nervous system are seen.
Lymphocytic accumulations in the gizzard muscle may be
visible as grayish areas. Lens opacities may develop weeks
after infection. Microscopic lesions in the CNS consist of
neuronal axon-type degeneration (“ghost” cells) in the brain,
particularly in the brain stem and in the anterior horn cells of
the spinal cord. Gliosis and lymphocytic perivascular cuffing
can also be seen. Visceral microscopic lesions consist of
lymphoid follicles in the muscular tissue of the gizzard,
proventriculus, and myocardium, while numerous lymphoid
follicles can be found in the pancreas .
Diagnosis :
Avian encephalomyelitis must be differentiated from avian
encephalomalacia (vitamin E deficiency), rickets, vitamin B 1
or B 2deficiency, Newcastle disease, eastern encephalitis,
Marek’s disease, and encephalitis caused by bacteria, fungi
(eg, aspergillosis), or mycoplasmas. Diagnosis is based on
history, signs, and histologic study of brain, spinal cord,
proventriculus, gizzard, and pancreas. Virus isolation in eggs
free of avian encephalomyelitis antibody is sometimes
necessary for confirmation. Serologic testing of paired
samples is helpful, using virus neutralization or ELISA tests.
Microscopic lesions are sparse and may not be found in
infected adults .
Prevention and Treatment :
Immunization of breeder pullets 15-11wk old with a
commercial live vaccine is advised to prevent vertical
transmission of the virus to progeny and to provide them with
maternal immunity against the disease. Vaccination of tableegg flocks is also advisable to prevent a temporary drop in
egg production. Affected chicks and poults are ordinarily
destroyed because few recover. A combination vaccine for
fowlpox and avian encephalomyelitis for wing-web
administration is widely used. The disease does not affect
humans or other mammals .