1. Avian Encephalomyelitis (AE)

2. Plan of Talk
 Introduction
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention and control

3. Plan of Talk
 Introduction
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention and control

4. Introduction
 Avian encephalomyelitis (AE) is a viral disease of young
chickens, turkeys, Japanese quail, pheasants and pigeons.
 AE is characterized by neurologic signs that result from
infection of the CNS with an RNA virus in the family
Picornaviridae.

5. Cont. …
Turkeys
 They are less susceptible to natural
infection
 They generally develop a milder clinical
disease than chickens.

6. Cont. …
 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.

7. Cont. …
 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 hatch
mates.
 AE virus is resistant to environmental conditions and may
remain infectious for long periods.

8. Plan of Talk
 Introduction
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention and control

9. Etiology
 AEV
 Serologic uniformity, strains differ in virulence.

10. Strain Classification and Pathogenicity
Pathotype One
 Represented by natural field strains,
is enterotropic.
 These strains infect chickens readily
via the oral route, multiply in the
intestine, and are shed in the feces.

11. Cont. …
Pathotype Two
 Embryo-adapted strains constitute
the other pathotype.
 They do not infect via the oral route
except with very high doses, and
they do not spread horizontally.
X
X

12. Cont. …
 Adaptation may occur after
multiple passages in antibody-free
chicken embryos.

13. Plan of Talk
 Introduction
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention and control

14. Transmission
Egg transmission is the major route of transmission.
Infected breeders will transmit the A.E. virus for several
weeks and cause a decrease in egg hatchability.
Infected chicks that hatch will show clinical signs of the
disease and spread the infection in the incubator to other
new hatched susceptible chicks.
Young chicks can also be infected on the farm.

15. Transmission
 The horizontal transmission by direct contact may be more
common, but vertical transmission is clinically more
important.
 The incubation period varies from 5 to 14 days depending on
the route of infection.

16. Plan of Talk
 Introduction
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention and control

17. Clinical Signs
Vertically infected chicks
 Clinical signs appear during the first week after hatching,
although signs may be present in a few birds at hatching.
 Vertical infection followed by horizontal infection causes a
characteristic biphasic mortality pattern.

18. Cont. …
Horizontally infected chicks
 Clinical signs appear at 2–4 week of age, incubation period of
5-14 days.
 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.
 After 4 weeks of age, chickens are resistant to disease but not
infection.
 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%.

19. The main clinical signs are ataxia and leg weakness that varies
from sitting on hocks to paresis that progresses to paralysis and
decumbency.

20.  Fine tremors of the head and neck.
Cupping the bird in one's hands often results in a buzzing
feeling because of rapid and fine tremors.

21. Severely affected birds lay on their side and exhibit intermittent
fine tremors of the head, neck and legs.

26. Clinical Signs
 In laying chickens, there is a sudden, 5%–10% drop in egg
production, which usually lasts for less than 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 wk.

27. Plan of Talk
 Introduction
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention and control

28. Post Mortem Lesions
 No gross lesions are seen in the brain of infected birds.
 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.

29. Plan of Talk
 Introduction
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention and control

30. Diagnosis
Diagnosis is based on:
1. History
2. Clinical signs
3. Characteristic histopathologic lesions in the brain and spinal
cord.

31. Cont. …
The following methods may help in making a diagnosis for Avian
Encephalomyelitis.
1. Virus Neutralization test.
2. Agar Gel test.
3. Elisa test.
4. Embryo Susceptibility test.
The above tests are only indicative of antibody present but not
necessarily disease.

32. Cont. …
The diagnosis is best confirmed by isolation and identification of
the virus.
1. Tissues collected for virus isolation must include the brain
and duodenum with the pancreas.
2. Demonstration of AE virus antigen in the brain, spinal cord,
and other tissues by immunofluorescent and
immunohistochemical staining is a reliable method of
diagnosis.

33. Plan of Talk
 Introduction
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention and control

34. Treatment
 Sick birds should be isolated and potentially destroyed as few
of them recover.
 Good supportive care may be helpful in some cases.
 Sanitize the premises.

35. Plan of Talk
 Introduction
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention and control

36. Prevention and Control
 Immunization of breeder pullets 10-15 weeks old with a
commercial live vaccine is advised to prevent vertical
transmission of the virus to progeny and to provide them with
maternal immunity against the disease.
 Vaccination of layers is advisable to prevent a temporary drop
in egg production.