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Avian Encephalomyelitis

(Epidemic Tremor)


Rüdiger Hauck

, DVM, PhD, DECPVS, Department of Pathobiology, College of Veterinary Medicine, Auburn University

Reviewed/Revised Sep 2023
Topic Resources

Avian encephalomyelitis is a viral infection affecting the CNS of several species of birds. Signs include tremors, ataxia, and weakness that progresses to paralysis. Diagnosis is based on history, clinical signs, histopathologic findings, virus isolation, and detection of virus genome by RT-PCR assay. Live vaccines are available to prevent transmission and decrease egg losses.

Avian encephalomyelitis (epidemic tremor) is a viral disease of the CNS of poultry. Avian encephalomyelitis is of economic importance.

Etiology of Avian Encephalomyelitis

The etiological agent of avian encephalomyelitis is avian encephalomyelitis virus (AEV), a nonenveloped RNA virus (family Picornaviridae, genus Tremovirus, species tremovirus A).

Natural field strains of the virus are enterotropic and multiply in the intestine. Infected birds shed the virus in their feces for a few days to a few weeks, which serves to transmit the infection to hatchmates.

Epidemiology of Avian Encephalomyelitis

Avian encephalomyelitis has a worldwide distribution.

Natural infection with AEV causes encephalomyelitis in chicks, turkey poults, Japanese quail, pheasants, and pigeons. Turkeys are less susceptible to natural infection and generally develop milder clinical signs of disease than chickens. Ducklings and guinea fowl are susceptible to experimental infection.

AEV does not cause disease in humans or other mammals.

Infection occurs via vertical and horizontal transmission. If a breeder flock becomes infected during egg production, the virus is vertically transmitted to the offspring, and a major outbreak occurs. The disease often appears in a series of flocks hatched from the infected breeder flock.

Morbidity and mortality rates vary and depend on the level of egg transmission and extent of immunity in the flock. In severe outbreaks, morbidity and mortality rates may exceed 50%.

There is no convincing evidence that the virus persists in infected birds.

Clinical Findings for Avian Encephalomyelitis

  • Ataxia

  • Tremors

  • Weakness that progresses to paralysis and recumbency

Avian encephalomyelitis, clinical signs

Avian encephalomyelitis is characterized by neurologic signs. The outcome after infection with AEV depends on the infection route, age and immune status of the bird, and whether the virus is wild-type or embryo adapted ().

Vertically infected chicks commonly show clinical nervous system signs of avian encephalomyelitis during the first week after hatching, although signs may be present in a few birds at hatching. Clinical signs appear later in hatchmates that are horizontally infected by the fecal-oral route. Vertical infection followed by horizontal infection causes a characteristic biphasic mortality pattern.

The main clinical signs of avian encephalomyelitis are ataxia and leg weakness that varies from sitting on hocks to paresis that progresses to paralysis and recumbency.

Fine tremors of the head and neck are evident in some birds and are characteristic of the disease. They are responsible for the common name epidemic tremor.

Tremors vary in frequency and severity and are best observed after birds are disturbed or excited. This can be done by placing the bird on its back and letting it right itself. Cupping the bird in one's hands often results in a buzzing feeling because of rapid, fine tremors. Severely affected birds lie on their side and exhibit intermittent fine tremors of the head, neck, and legs.

Horizontally infected chicks usually show clinical signs at 2–4 weeks old; thus, clinical signs of avian encephalomyelitis progress through the flock for the first few weeks, and the episode is usually over by the time the flock is ~4 weeks old.

By 4 weeks old, chickens are resistant to disease but not to infection. An exception occurs occasionally in immunocompromised older chickens.

In laying chickens, there is a sudden 5%–10% decrease in egg production, which usually lasts for < 2 weeks, followed by a return to normal production. There is no deterioration in eggshell quality.

Hatchability may decrease as much as 5% during the decrease in egg production due to late embryonic death. Infected eggs are laid during the period of viremia, which usually lasts 1–2 weeks.

The virus can inadvertently become embryo-adapted during serial passages in chicken embryos. This has happened during vaccine production; however, no recent cases have been documented. Single nucleotide polymorphisms in the VP2 and VP3 genes have been implicated in embryo adaptation.

Chick-embryo-adapted strains are highly neurotropic and can cause clinical signs of disease after parenteral administration. Affected birds exhibit typical neurologic signs like those observed in younger chicks.



No gross lesions are seen in the brains of birds with avian encephalomyelitis. Gray to white foci may be visible on cut surfaces of the muscle of the gizzard. Weeks after infection, opacity of eye lenses (cataracts) may occur in a small percentage of chickens that survive the infection.

Microscopic lesions in the CNS are found in the brain (cerebral peduncle, cerebellum, brainstem) and spinal cord and consist of degeneration and necrosis of neurons, perivascular lymphocytic cuffing, and gliosis with formation of glial nodules.

  • In the cerebellum, there are areas of necrosis or loss of Purkinje cells and replacement by glial nodules that extend into the molecular layer of the gray matter.

  • Neuronal lesions of central chromatolysis, shrinkage and increased basophilia, satellitosis, and neuronophagia are best found in neuron clusters (nuclei) in the brainstem, arbor vitae of the cerebellum, and lateral horn (gray matter) of the spinal cord.

  • Central chromatolysis of neurons is characterized by rounding of the cell contour and displacement of Nissl granules to the periphery.

  • Dorsal root ganglia have multifocal nodular collections of lymphocytes.

A common microscopic lesion outside the CNS is diffuse or nodular lymphocytic infiltrates in the gizzard muscle, muscular layer of the esophagus and proventriculus, myocardium, and pancreas.

Except for cataracts, microscopic lesions generally are not found in infected adults unless they are showing clinical nervous signs, in which case they will have CNS lesions similar to those in young birds.

Diagnosis of Avian Encephalomyelitis

  • Characteristic clinical signs

  • Histopathologic lesions

  • Viral isolation

  • RT-PCR assay


Diagnosis of avian encephalomyelitis is based on history, clinical signs, and characteristic histopathologic lesions in the brain and spinal cord.

The diagnosis is best confirmed by isolation and identification of the virus. Tissues collected for virus isolation must include the brain and duodenum with the pancreas.

Demonstration of AEV antigen in the brain, spinal cord, and other tissues by immunofluorescent and immunohistochemical staining is a reliable method of diagnosis. The same tissues can be used for detection of the virus by RT-PCR assay. However, because of variance between isolates, not all published primer pairs will amplify all isolates.

ELISAs to detect antibodies against AEV are commercially available and can be used to monitor success of vaccination.

The major differential diagnosis for neurologic signs in very young chicks is bacterial or mycotic encephalitis, as well as neurotropic virulent Newcastle disease Newcastle Disease in Poultry Newcastle disease is a severe, systemic, and fatal viral disease of poultry due to virulent strains of avian paramyxovirus type 1. Clinical signs in unvaccinated birds include sudden death,... read more Newcastle Disease in Poultry . Rickets and nutritional encephalomalacia are additional differential diagnoses that should be considered, although the clinical signs of these diseases differ from those in avian encephalomyelitis.

Treatment and Prevention of Avian Encephalomyelitis

  • Vaccination

No treatment is available for avian encephalomyelitis. Control therefore relies on removal of affected birds and vaccination.

Vaccination of broiler breeder pullets with a commercial chick-embryo-propagated live vaccine prevents vertical transmission of the AEV and provides progeny with maternal immunity. Vaccine is administered to broiler breeders 8 weeks or older but at least 4 weeks before start of lay.

Vaccination of table-egg flocks is also advisable to prevent decreases in egg production. Avian encephalomyelitis vaccine is usually combined with fowlpox vaccine and administered to chickens by wing-web stab. Also available is a live fowlpox-vectored infectious laryngotracheitis and avian encephalomyelitis combination vaccine.

Chicks and turkey poults with neurologic signs are ordinarily euthanized because they rarely recover.

Because AEV is nonenveloped, it is resistant to environmental conditions and may remain infectious for long periods.

Key Points

  • Avian encephalomyelitis is a viral disease of the CNS of young birds, characterized by neurologic signs.

  • Diagnosis of avian encephalomyelitis is based on history, clinical signs, and characteristic histopathologic lesions. Useful diagnostic tests include virus isolation, RT-PCR assay, and ELISA.

  • No treatment is available; control relies on vaccination.

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