Avian encephalomyelitis

Avian encephalomyelitis is a viral infection affecting the CNS of several species of birds.
Signs include tremors, ataxia, and weakness that progresses to paralysis. In severe
outbreaks, morbidity and mortality may exceed 50%. Diagnosis is based on history,
clinical signs, histopathology, and isolation of the virus. A live vaccine is available to
prevent transmission and reduce egg losses.
Avian encephalomyelitis (AE) is a viral disease of the CNS of young chickens, turkeys,
Japanese quail, pheasants, and pigeons. Turkeys are less susceptible to natural infection and
generally develop a milder clinical disease than chickens. Ducklings and guinea fowl are
susceptible to experimental infection.

AE is characterized by neurologic signs that result from infection of the CNS with an RNA
virus. The virus species is Tremovirus A in the genus Tremovirus of the family Picornaviridae.
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.
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 spread the infection
to hatchmates. There is no convincing evidence that the virus persists in infected birds. AE
virus is resistant to environmental conditions and may remain infectious for long periods.

Clinical Findings for Avian Encephalomyelitis

• Ataxia

• Tremors

• Weakness that progresses to paralysis and recumbency

Avian encephalomyelitis, clinical signs

Vertically infected chicks commonly show clinical 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 tremors. Tremors vary in frequency and severity
and are best seen after birds are disturbed or excited. This can easily 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 lay 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 of age; thus, clinical
disease progresses through the flock for the first few weeks, and the episode is usually over by
the time the flock is ~4 weeks old. Morbidity and mortality rates vary and depend on the level
of egg transmission and degree of immunity in the flock. In severe outbreaks, both morbidity
and mortality may exceed 50%.

After 4 weeks of age, chickens are resistant to disease but not to infection. An exception occurs
occasionally in older chickens after vaccination with chick-embryo–propagated vaccines in
which the vaccine virus inadvertently becomes embryo-adapted during production of the
vaccine. Chick-embryo-adapted strains are highly neurotropic and can cause clinical disease
after parenteral administration. Affected birds exhibit typical neurologic signs like those seen
in younger chicks.

In laying chickens, there is a sudden 5%–10% drop in egg production, which usually lasts for <
2 weeks, followed by a return to normal production. There is no deterioration in egg shell
quality. Hatchability may drop as much as 5% during the decline in egg production due to late
embryonic mortality. Infected eggs are laid during the period of viremia, which usually lasts 1–
2 weeks.
Lesions
Avian encephalomyelitis, brain lesions, histopathology
No gross lesions are seen in the brain of birds infected 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, brain stem) 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 brain stem, 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 nervous signs, in which case they will have CNS lesions similar to
those in young birds.

Diagnosis of Avian Encephalomyelitis

• Characteristic clinical signs and histopathology

• Viral isolation

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 AE virus antigen in the brain, spinal
cord, and other tissues by immunofluorescent and immunohistochemical staining is a reliable
method of diagnosis. The major differential diagnosis for neurologic signs in very young
chicks is bacterial or mycotic encephalitis. Rickets and nutritional encephalomalacia are next
in the list of differential diagnoses, although the clinical manifestations of these diseases differ
from those in AE. In adults, serologic testing of acute and convalescent sera to demonstrate an
increase in antibody titers helps establish a diagnosis.

Prevention of Avian Encephalomyelitis

• Vaccination at least 4 weeks before start of laying

Immunization of broiler breeder pullets with a commercial chick-embryo-propagated live

vaccine prevents vertical transmission of the AE virus 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. AE vaccine is usually combined with fowlpox vaccine and given to chickens by
wing-web stab. Also available is a live fowlpox-vectored infectious laryngotracheitis and AE
combination vaccine. Chicks and turkey poults with neurologic signs are ordinarily euthanized
because they rarely recover.

AE virus does not cause disease in people or other mammals.

Avian Encephalomyelitis Other Names: New England Disease, Epidemic Tremor 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. Clinical Signs 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. Transmission 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. Clinical Signs Seizure like activity Wry neck Spinning Ataxia
(incoordination, stumbling) Rapid trembling of the head and neck Paralysis Blindness in
offspring Diagnosis Reported Cases Treatment 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.: Support Prevention 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.

Avian Encephalomyelitis (AE) in chickens

Avian encephalomyelitis (AE) or epidemic tremor is an infectious viral disease affecting

chickens, turkeys, pheasants and quail.
Avian encephalomyelitis virus (AEV) is an enterotropic virus, infectious by the oral route. The
virus replicates in the intestine and is excreted in the feces.

Infected litter spreads the virus either via direct bird to bird contact or via fomites (contaminated
equipment, vehicles, people, …).

Besides this horizontal transmission, AEV can also be vertical transmitted. When susceptible
parent stock flocks get infected after sexual maturity, they will infect part of their progeny during
the period of viremia (about 2 weeks).

In young birds, primary infection takes place in the alimentary tract, followed by a viremia and
subsequent infection of the central nervous system (CNS). In older birds, infected orally, no viral
antigen is found in the CNS, explaining why infected adults show no neurological signs.

AEV is a Picorna virus, quite resistant to environmental conditions.

Clinical Signs

Ataxia and tremors of the head and neck in 1-2 weeks old chicks are typical. No significant
macroscopic lesions are seen in affected birds, but some survivors can develop cataracts at later
age.

There seems to be a marked age resistance starting around 3 weeks of age.

Mature birds can show a temporary drop in egg production but do not develop neurologic signs.
In breeder flocks, hatchability also drops due to late embryonic mortality.
Diagnosis

Clinical history, histology of the brain and antigen detection are conclusive. The brain is the best
source for PCR or virus isolation.

Serology can be done with Elisa.

Control & Vaccination

Maternal derived antibodies (MDA’s) fully protect chicks against disease. Parent stock must be
vaccinated at least 4 weeks before the onset of lay.

It is also advised to vaccinate commercial layers to prevent a drop in egg production.