Avian encephalomyelitis (AE) is a disease of the central nervous system that affects young chickens, turkeys, quail, pheasants and pigeons. The virus is transmitted vertically from infected hens to chicks through eggs and spreads within flocks through direct contact or indirect fecal contamination. Clinical signs appear 7-10 days after infection and include tremors, ataxia and paralysis. There is no treatment for acute cases, but vaccination 4 weeks before laying can prevent vertical transmission and provide protection.

1. AVIAN ENCEPHALOMYELITIS (AE)
Dr. Anand Mohan
Assistant Professor

2. INTRODUCTION
 AE is a disease of CNS in young chickens, turkeys,
Japanese quail, pheasants, and pigeons.
 First reported of AE in 1932, the virus grows in the yolk
sac and brain of the chicken embryo in eggs from
nonimmune hens.
 AE virus is resistant to environmental conditions and
may remain infectious for long periods
 Most prevalent in chickens 1 to 6 weeks of age.

3. CONT.
 Susceptible chickens are of more than 5 weeks old,
will develop antibodies to AE, but do not show clinical
signs at the time of infection.
 AE occurs world wide and occurs in all seasons of the
year, but most cases are reported from January to
June.

4. ETIOLOGY
 The virus species is Tremovirus A in the
genus Tremovirus of the family Picornaviridae.
 Natural field strains of the virus are enterotropic and
multiply in the intestine.

5. TRANSMISSION
 Vertical transmission: Infected hen to chick is the most
common mode of spread via egg
 Direct contact of susceptible hatchlings with infected
birds accounts for spread within the flock.
 Indirect spread via fecal contamination of feed and
water also occurs.
 The virus can survive at least 4 weeks in droppings.

6. CLINICAL SIGNS
 Clinical signs appear at 7 to 10 days of age.
 Chickens of all ages are susceptible, but clinical signs of
encephalitis only develop in younger than 4 weeks.
 Tremors of the head and neck are presumptive of the
disease in the flock hence the name "Epidemic
tremor".
 Muscular tremors are best seen by exercising the bird.

7. Ataxia, Tremors, Weakness that progresses to
paralysis and recumbency in chicks

8. CONT.
 Affected birds are inactive; some may refuse to walk or
walk on their hocks.
 Ataxia progresses to paralysis and death results from
inability to feed or drink, or through being trampled.
 Some birds recover, and others may survive with
persistent clinical signs.
 In susceptible adult birds, infection is usually sub-clinical,
although there may be a transient drop in egg production

9. CONT.
 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.
 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.
 The disease is similar in turkeys and chickens.

10. DIAGNOSIS & DD
 Diagnosis is confirmed by FAT, virus isolation and
AGPT.
 AE must be differentiated from other encephalitic
diseases such as ND, EEE, MD etc.

11. TREATMENTS
 There is no treatment for acute outbreaks.
 Affected birds should be removed, killed and
incinerated.
 Provide good nursing during outbreaks will reduce the
mortality.
 Control is through prevention
 Selecting hatching eggs from immune breeder flocks.

12. VACCINATION
 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.
 AE vaccine is usually combined with fowl pox vaccine
and given to chickens by wing-web stab.
 Also available is a live fowl pox-vectored ILT & AE
combination vaccine.