Brief introduction of poultry disease - avian encephalomyelitis

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.