Avian encephalomyelitis (AE), also known as epidemic tremor, is a contagious viral disease that affects the nervous system of birds. It is caused by a picornavirus and occurs worldwide, primarily in young chickens between 1–3 weeks of age, as well as pheasants, quail, and turkeys. Infected birds typically develop ataxia (incoordination and stumbling), which can progress to paralysis along with characteristic rapid tremors of the head and neck. The disease is most commonly seen in chicks sourced from unvaccinated breeding flocks, making it largely preventable.
Clinical Signs
Early signs in affected chicks may include a dull or less alert appearance, particularly in the eyes, followed by progressively worsening ataxia. As the disease advances, chicks are more frequently observed sitting on their hocks. When stimulated, they often struggle to control their movements, appearing unsteady and prone to falling onto their sides. In severe cases, paralysis may develop.
Transmission
The virus is most commonly transmitted vertically from infected breeding hens to their chicks through the egg. Infected chicks can then spread the virus horizontally through their feces for up to two weeks after hatching. By approximately 6 weeks of age, birds typically develop sufficient immune protection, reducing susceptibility to infection.
Incubation Period
Chicks infected through vertical transmission may show clinical signs as early as one day up to three weeks after hatching. When infection occurs through direct contact with infected birds, signs usually take at least 11 days to appear.
Treatment
There is no specific treatment for avian encephalomyelitis, and care is primarily supportive. Affected chicks should be housed separately in a safe recovery area to prevent injury or trampling and provided with easy access to food and water.
Chicks that recover may have ongoing coordination issues. Survivors often will develop cataracts at around 18-20 weeks of age, which present as a bluish lens opacity and impaired vision.
Recovered birds may continue to exhibit coordination issues. Many survivors develop cataracts between 18–20 weeks of age, which appear as a bluish opacity of the lens and can impair vision.
Adult chickens are typically asymptomatic, though some may experience a temporary drop in egg production and hatchability.
Ataxia (incoordination, stumbling)
Rapid head and neck tremors
- History
- Clinical signs
- Virus isolation
- Serology
- Case 1: Avian encephalomyelitis in a Chicks Avian encephalomyelitis (AE) caused the death of approximately 20 of 300 12-day-old chicks that developed neurologic signs (ataxia, down on hocks and unable to walk) and died. Three chicks were submitted for necropsy and AE was diagnosed as the cause of death based on histopathology. None of the chicks had antibodies to AE virus indicating the chicks did not have maternal antibodies that would have protected them. Since the virus incubation period is 11-12 days minimum, and chicks began to die prior to 11 days, they were most likely infected via vertical transmission from the breeders. All chicks should come from breeder flocks that are vaccinated for AE. Chicks exposed to AE virus that are older than three weeks of age are typically resistant to developing clinical disease. Ref
- Case 2: Avian encephalomyelitis in a White Leghorn pullets Avian Encephalomyelitis (AE) was diagnosed in a flock of 11,500, 10 to 12-week-old White Leghorn pullets. About 8% of the flock exhibited neurological signs and ~2% either died or were killed a few weeks after vaccination for AE. Necropsy of 12 chickens did not reveal any gross lesions but histopathology revealed characteristic lesions of avian encephalomyelitis in the brain and spinal cord, and mild neuritis. AE virus was confirmed by PCR on the brain and peripheral nerves. It is suspected that AE vaccine used in this flock was probably egg-adapted and might have caused AE in these chickens. Ref
- Case 3: Avian encephalomyelitis in a Multiple California chickens Avian Encephalomyelitis virus infection was diagnosed as the cause of trembling, ataxia, circling, lateral recumbency, head tremors, wing walking, unsteady gait and/or inability to stand in multiple flocks in the past two months. Affected birds ranged from 10 days to 10 weeks old. Diagnosis was based on typical histologic changes of meningoencephalitis and neuron changes most severely affecting the brainstem and cerebellum. Ref
- Case 4: Avian encephalomyelitis in a Commercial laying hens An outbreak occurred in a commercial flock in Northeastern Brazil in 2018 which affected several flocks of hens of various age groups. The breeder hens had received the vaccine against AE. The chicks and pullets developed clinical signs of muscle tremors and motor incoordination, resulting in difficulty accessing water and food, which lead to starvation and death. In the adult laying flock, 60% of the hens developed bilateral opacities of the cornea and lens, tremors of the head and neck, lateral deviation of the head (wry neck) and motor incoordination (ataxia). In these laying hens, ataxia ranged from mild incoordination to lateral decubitus. No significant changes were observed during the necropsy of adult birds. Microscopic findings in the central nervous system consisted of hyperemia from the blood vessels of the leptomeningeal and cerebral cortex. The neurons of the cerebral cortex, midbrain, and cerebellum had an eosinophilic, shrunken aspect and intensely basophilic, thin, sometimes pyknotic or karyolytic nuclei. Ref
- Case 5: Avian encephalomyelitis in a Pigeons The pathological and immunohistochemical findings of avian encephalomyelitis (AE) were described in various tissues of naturally infected pigeons of a flock from a outbreak in Turkey. Clinically, paresis, paralysis, circling movement and torticollis of the head associated with nervous signs were marked symptoms among the diseased pigeons. At necropsy, small or large white–greyish foci were detected in the pancreas, and erosive-ulcerative foci along with petechial hemorrhages in ingluves. Histopathologically, lesions in central nervous system, particularly in the cerebullum molecular layer, consisted of non-suppurative encephalomyelitis. Lesions in the pancreas revealed non-suppurative pancreatitis along with acinar degeneration and necrosis and/or lymphoid aggregations. Immunohistochemical staining of formalin-fixed, paraffin-embedded tissues was performed using a direct-fluorescein antibody technique with chicken anti-AE virus serum flourescein isothiocyanate conjugate. Viral antigen was strongly stained in cytoplasm of epithelial cells of the exocrin glands, and neurons of the cerebral hemispheres and midbrain. In addition, viral antigen was also marked in the kidneys and tissues of the digestive system. Ref
- Case 6: Avian encephalomyelitis in a Pheasants An outbreak of neurological disease occurred in pheasant chicks on a game farm in 2007. The disease was first seen in the 10th hatching of chicks on the farm. Affected chicks showed trembling and incoordination from the time of hatching, and subsequently blindness and cataract formation was seen in some of the affected chicks at 3 weeks of age. The peak mortality and culling figure was 21.0% in the worst affected hatch, compared with a maximum of 11.7% in the first nine hatches. No further cases were evident by 7.5 weeks of age. Histopathological examination showed a moderate acute encephalomyelitis in some, but not all, of the chicks with neurological signs. The clinical presentation and histopathological findings were typical of vertically transmitted avian encephalomyelitis as seen in chickens, although avian encephalomyelitis virus could not be detected in inoculated embryonated chicken eggs. However, serological testing by enzyme-linked immunosorbent assay for antibodies to the virus was positive in four of five affected 3-week-old birds and in 23 out of 29 adult breeding birds, and reverse transcriptase-polymerase chain reaction testing of RNA extracted from brain and pancreas tissue of affected chicks yielded nucleotide sequences aligned 82% and 83% with three avian encephalomyelitis sequences in a sequence database. The evidence suggested that the neurological disease was attributable to infection with a strain of avian encephalomyelitis virus that appeared to have entered the flock at the start of the breeding season, and was possibly introduced by carrier pheasants brought on to the farm early in the season. Ref
Supportive care: Isolate the bird from the flock and place in a safe, comfortable, warm location (your own chicken "intensive care unit") with easy access to water and food. Limit stress.:
Live vaccination is recommended for breeder pullets at 10–15 weeks of age. This prevents vertical transmission of the virus through eggs and provides maternal immunity to their offspring.
Chickens who survive the disease have a higher chance of developing cataracts later in life.
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