Avian Encephalomyelitis

Etiology

Avian Encephalomyelitis (AE) is a viral disease that affects immature chickens, turkeys, pheasants, and coturnix quail, characterized by ataxia and rapid tremors of the head, neck, and limbs. The disease is caused by the avian encephalomyelitis virus, a small envelope-free RNA virus, included in the Picornaviridae family.

Host Range

AE has a limited host range, naturally infecting chickens, turkeys, coturnix quail, and pheasants. Other avian species, as well as non-avian species, appear to be refractory to the infection. The virus presents no public health concern to humans.

Epidemiology

The AE virus is shed into the feces of infected birds. Shedding occurs for a period of several days to weeks, depending on the age of the infected bird. Ingestion of contaminated feces, direct bird-to-bird contact, and exposure to contaminated personnel and fomites are the usual sources of horizontal transmission. The virus is resistant to environmental conditions and remains infectious in the environment for long periods of time. Vertical transmission also plays an important role in the spread of the virus. Embryos and chicks, from eggs laid 5-12 days following virus exposure of the hen, become infected.

Nearly all chicken flocks worldwide become infected with AE. However, clinical signs are mostly seen in young birds, between 1 to 3 weeks of age. Unvaccinated adults that become infected after they begin laying eggs, typically do not show signs of clinical disease but do transmit the infection to their offspring.

Clinical Signs

The clinical signs of AE depend on the age of the bird at the time of virus exposure. In chicks, signs may be present at the time of hatch but usually occur between 1-2 weeks of age. Early signs include depression and a dull expression to the eyes. This is followed by progressive neurologic signs. Neurologic signs may begin with hock-sitting and progress to ataxia, paralysis, prostration, and fine muscle tremors of the head and neck. The tremors may be exacerbated when the bird is frightened or exercised. Birds exposed to the virus after 2-3 weeks of age, typically show resistance to the infection and may not develop clinical signs. Mature birds that are exposed may experience a slight drop in egg production but do not exhibit neurologic signs.

Morbidity in chicks may go as high as 60%, while the average mortality is 25%. A few birds may recover completely, but survivors often fail to grow and produce eggs normally. Survivors may develop a bluish opacity of the lens and blindness. AE often produces milder disease in turkeys compared to chickens.

Post-mortem Lesions

AE is typically not associated with any gross lesions on post-mortem examination. The neurologic signs associated with AE are caused by CNS involvement; however these lesions are not visible on gross examination. The only subtle post-mortem findings that may be observed in some birds are white infiltrations in the muscle wall of the ventriculus (gizzard). These lesions are cause by large amounts of lymphocytic infiltrates. Birds that survive the acute infection may have bluish lens opacities.

Differential Diagnosis

Avian encephalomyelitis must be differentiated from other diseases that cause signs of CNS in young birds, such as Newcastle disease, equine encephalomyelitis, Marek's disease, mycotic encephalitis, brain abscesses, nutritional disturbances (rickets, encephalomalacia, riboflavin deficiency), and toxicities (salt, some pesticides etc.). AE can be distinguished on the basis of age (less than 5 weeks) of onset of clinical signs, general absence of gross lesions, and characteristic histopathology (i.e. gliosis, neuronal and Purkinje cell degeneration, perivascular cuffing, and hyperplastic lymphoid follicles) in certain visceral organs. A confirmatory diagnosis is made by histopathologic, virologic or serologic testing.

Diagnosis

Viral diagnosis is possible by inoculating susceptible chicks or embryos at 5-7 days and observing the hatched chicks for clinical signs and pathognomonic lesions associated with AE. Tissue samples collected from the brain (cerebellum), gizzard, pancreas, spleen and heart lesions can be submitted for histopathology. One of the lesions of pathognomonic significance is central chromatolysis (axonal reaction) of the neurons in the nuclei of the brain stem, particularly those of the medulla oblongata and also a dense lymphocytic foci in the muscular wall of proventriculus Serologic assays using ELISA, immunodiffusion test, standard VN test, indirect FA test, and passive hemagglutination can be used. Rising titers in sequential blood samples are highly suggestive of active infection.

Prevention and Control

Although live and inactivated vaccines are available, inactivated vaccines are not commonly used. Live vaccines can be given in the drinking water, by coarse spray, or by wing web stab. However, live vaccines should not be used within four weeks of the onset of egg production. The most common control approach used in the poultry industry is to vaccinate layers and breeder flocks during the growing period with live vaccines. In the case of breeders, this approach prevents susceptible flocks from becoming infected and transmitting the virus to the progeny by the egg-borne route. Vaccination induces good levels of maternal antibodies that will protect the progeny during the critical first two or three weeks of life. Early vaccination in layers (pullets) prevents drops in egg production, associated AE infection.

Selected References

1. Calnek, B.W. 2008. Avian Encephalomyelitis. In Diseases of Poultry, 12th ed. Y.M. Saif. et al. (ed.). Blackwell Publishing, Ames, Iowa.
2. Calnek, B.W. 1998. Control of avian encephalomyelitis: A historical account. Avian Dis 42:632-647.
3. Calnek, B.W., P.J. Taylor, and M. Sevoian. 1961. Studies on avian encephalomyelitis V. Development and Application of an Oral Vaccine. Avian Dis 5:297-312.
4. Charlton, B. R. (ed). 2006. Avian Disease Manual, 6th ed. American Association of Avian Pathologists (AAAP), 953 College Station Road, Athens, Georgia 30602-4875.
5. Glisson, J.R. and O.J. Fletcher. 1987. Clinical encephalitis following avian encephalomyelitis vaccination in broiler pullets. Avian Dis 31:383-385.
6. van der Heide, L. 2008. Avian Encepalomyelitis. In A Laboratory Manual for the Isolation and Identification of Avian Pathogens, 5th edition. L. Dufour-Zavala Louise et al. (ed.) OmniPress, Inc., Madison, Wisconsin.
7. World Organization for Animal Health (OIE) website. 2008. www.oie.int

Thank you to the following individuals for reviewing these materials:

Jaime Ruiz
Pedro Villegas
Jose Bruzual