Avian encephalomyelitis (AE), also referred to as epidemic tremor, is an infectious neurological disease caused by a picornavirus. The disease occurs worldwide in young (usually between 1-3 weeks old) chickens, pheasants, quail, and turkeys. Infected birds develop ataxia (incoordination, stumbling), which often progresses to paralysis and rapid trembling of the head and neck. It occurs most commonly in chicks purchased from backyard breeders who didn't vaccinate their breeding flocks.
Chicks with avian encephalomyelitis may initially develop a slightly dull expression of the eyes, followed by a progressive ataxia. Chicks will eventually be seen more frequently sitting on their hocks. When disturbed, they may appear like they have little to no control over their speed and gait, and often will fall on their sides.
Chicks may also become paralyzed, and observed lying spread out on the ground in a severely weakened state. Without intervention with supportive care to ensure the chick stays hydrated and eating, they will often die from starvation or from getting trampled to death by other flock members.
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.
If adult chickens are infected, they usually won't develop any clinical signs, other than an occasional decrease in egg production and hatchability.
Avian encephalomyelitis virus is usually transmitted vertically to chicks by infected adult breeding hens. Their offspring will then transmit the virus horizontally into the environment for up to two weeks, through their feces. After 6-weeks of age, chicks are usually protected via increased immunocompetence and protective humoral response.
Avian Encephalomyelitis Incubation Period
Chicks infected by vertical egg transmission start to develop clinical signs anywhere from one day to three weeks after they hatch. When infected by direct contact with diseased birds, signs of infection may take at least 11 days to start to present.
Ataxia (incoordination, stumbling)
Rapid trembling of the head and neck
- Clinical signs
- Virus isolation
- 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. Call your veterinarian.
Live vaccination: Given to breeder pullets at 10-15 weeks old to prevent vertical transmission of the virus to their eggs, to provide their offspring with maternal immunity against the disease.
Chickens which survive the disease have a higher chance of developing cataracts later in life.
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