Infectious bursal disease (IBD), commonly known as Gumboro disease, is a highly contagious viral infection affecting chickens. It was first identified in Delaware in 1962. The disease destroys lymphocytes in the bursa of Fabricius, causing immunosuppression. Clinical signs include depression, diarrhea, and increased susceptibility to other diseases. The virus is transmitted orally and spreads rapidly between flocks. Prevention relies on vaccination programs and biosecurity to control spread between birds.

1. oCOMMONLY KNOWN AS GUMBOROCOMMONLY KNOWN AS GUMBORO
oPREPARED & PRESENTED BY:PREPARED & PRESENTED BY:
oRED GROUPRED GROUP
o2K14-AV-08, 09, 11, 12, 16, 172K14-AV-08, 09, 11, 12, 16, 17
Infectious Bursal DiseaseInfectious Bursal Disease
(IBD)(IBD)

2. Introduction
Infectious bursal disease (IBD, Gumboro) is an
acute, highly contagious viral infection in chickens
manifested by inflammation and subsequent
atrophy of the bursa of Fabricius, and various
degrees of nephritis and immunosuppression.
The disease was first discovered in Gumboro,
Delaware (USA) in 1962.

3. Etiology
IBDV is a double stranded RNA virus .
Belongs to the genus Avibirnavirus of family
Birnaviridae .
There are two distinct serotypes of the virus, but only
serotype 1 viruses cause disease in poultry

4. Mode of transmission
Via Ingestion ( horizontally through contaminated
feed and water )
Mechanical transmission via people , animals ,vehicles
and equipments when transferred from diseased flock
to healthy one.
May be via the conjunctiva or respiratory tract, with
an incubation period of 2-3 days.
There is no vertical transmission
The infected birds shed virus for 14 days in their
faeces. Feed, water, and poultry house litter become
contaminated.

5. Pathogenesis
The most likely route of infection is oral ingestion of
contaminated faeces or other contaminated organic
material.
Virus was present within 4-5 hours in the macrophages and
lymphatic cells of the duodenum, jejunum and caecum.
Duodenum, jejunum and caecum are the first sites of viral
replication.
IBDV reaching the main bloodstream is circulated to other
organs including the bursa of Fabricius.

6. Pathogenesis
Immature B-lymphocytes in the follicles of the bursa are
the target cells for viral replication.
By 13 hours post-infection most follicles in the bursa are
virus positive.
By 16 hours post infection a second massive viraemia
occurs.
There is infection and secondary viral replication in other
lymphatic organs.
Clinical disease and death occurs within 64-72 hrs post-
infection

7. Clinical findings
 Infectious bursal disease follows one of two courses,
depending on the age at which chickens infected,
breed and virulence of field virus
 1-clinical form
 2-subclinical form

8. Clinical form
Clinical IBD occurs usually between 3-8 weeks of age
depending on maternal antibody levels.
A ected birds are depressed, pale, huddlingff
producing watery white diarrhea, soiled vent
feathers, vent picking, and inflammation of the
cloaca.

9. Continue…
Disease may appear suddenly and morbidity
typically reaches 100%
Mortality varies. Usually new cases of IBD have a
mortality rate of about 5 to10% but can be as high as
60% depending on the pathogenicity of the strain
involved.
 Highly pathogenic strains are called “very virulent”
IBD (vvIBD) resulting in high mortality.

10. Subclinical form
Subclinical IBD occurs with infections before 3
weeks of age.
Early IBD infection result in permanent
immunosuppression without mortality.
Immunosuppression is economically important due
to increased susceptibility to secondary infections
especially in the respiratory tract.
In broilers this form of the disease results in bad
performance with lower weight gains and higher feed
conversion ratios.

11. Post Mortem Lesions
Oedematous bursa (may be slightly enlarged, normal
size or reduced in size depending on the stage), may
have haemorrhages, rapidly proceeds to atrophy.
Five days after infection, the BF diminishes in size
rapidly.
Haemorrhages in skeletal muscle (especially on
thighs and pectoral) and junction of the
proventriculus and gizzard because the IBD virus
interferes with the normal blood clotting
mechanism.

12. Continue…
Swollen kidneys with urates. Such lesions probably
result form severe dehydration, not direct viral
damage.
Dehydration.
Chickens that have recovered from IBDV infections
have small, atrophied, cloacal bursas due to the
destruction and lack of regeneration of the bursal
follicles.

13. Severe hemorrhagic inflammation of bursa

16. Hemorrhage on thigh pectoral muscles

17. Affected kidneys with uretes

18. Histopathological changes
Destruction of
lymphocytes in the
bursa of fabrics of
infected animals

19. Diagnosis
1-flock history
2-symptoms
3-postmortem examination
4-histopathology
5- virus isolation and identification
6- Serology and fluorescent antibody techniques
7- PCR was designed for the detection of IBDV
genome
8- Serological tests such as agar gel precipitation and
ELISA, for detecting antibodies

20. Prevention and control
good management and suitable vaccination
programme at 1–21 days of age.
An effective IBD prevention and control program
must involve an effective breeder vaccination
program, an effective biosecurity program, and an
effective broiler vaccination program
All infected litter and carcases of infected birds must
be suitably disposed of away from the site or any
other poultry operation.