INFECTIOUS BURSAL DISEASE (IBD)
Infectious bursal disease is an acute, highly contagious, lymphocytolytic, immunosuppressive disease of predominantly young chickens (3-6 weeks), characterized by necrosis and depletion of lymphoid tissues, particularly the bursa of Fabricius.
Infectious bursal disease is also known as avian infectious
bursitis and Gumboro disease as the first outbreaks occurred in the area of
Gumboro, Delaware, USA
OIE listed diseases
The economic importance of this disease is manifested in two ways.
Up to 60% mortality in chickens 3 weeks of age and older
Severe, prolonged immunosuppression
ETIOLOGY:
Infectious bursal disease virus : DS bisegmented RNA
Genus: Avibirnavirus
Family: Birnaviridae
IBDV can be divided into two main serotypes by virus neutralization
tests
Serotypes 1 and 2 of IBDV; only type 1 is pathogenic
Serotypes 1 and 2 affect ducks and turkeys but do not cause disease in
these
Species Serotype 2 does not protect against Serotype 1 infection Very
virulent IBD (vvIBD) is a highly pathogenic strain present in Europe, Asia, S.
America and Africa
HOST
Clinical disease occurs solely in chickens
Only chickens younger
than 10 weeks are usually clinically affected. Older chickens usually show no
clinical signs
White leghorns are especially susceptible
Birds 1-14 days of age are less sensitive because of maternal antibodies
Although turkeys, ducks, guinea fowl, pheasants and ostriches may be
infected but no clinical signs found.
TRANSMISSION
Faecal–oral route
Direct contact with contaminated feed, water, droppings and litter
PATHOGENESIS
IBDV serotype have a tropism for
precursor B lymphocytes (actively dividing,
⇓
surface-immunoglobulin-M-bearing B
cells) of the bursa
⇓
In chicken, bursa is at its maximum
development between 3 to 6 weeks of age and have highest numbers of precursor B
lymphocytes, hence 3 to 6 weeks of age is most susceptible for infection
⇓
After oral infection virus enter in to
body
⇓
infect gut-associated lymphoid tissues
⇓
virus replication → reach to liver →
primary viremia
⇓
virus reaches the bursavia the blood
stream
⇓
infect precursor B lymphocytes → virus
replication
⇓
most follicles of bursa affected
⇓
lysis of precursor B lymphocytes release
of large amounts of virus into the circulation
second and pronounced viraemia
⇓
Infection of other organs like spleen,
Harderian gland, caecal tonsils and thymus
⇓
Releases of interferon (IFN)1, tumour
necrosis factor (TNF) α, interleukin (IL) 6 or IL8 by activated T-lymphocytes
⇓
cytokine storm induces a shock in the
bird, which becomes prostrated and reluctant to move and death
⇓
Birds that survive initial infection are immune suppressed due to decreased humoral immunity as well as impaired cell-mediated immunity and phagocytosis
⇓
secondary bacterial, viral or other infection
⇓
During viral replication in bursa antigen-antibody-complement complexes are formed and deposited in bursa induce chemotactic factors
cause oedema, necrosis, haemorrhage, and
large numbers of polymorph nuclear leukocytes infiltration
⇓
This Arthus reaction (Type III hypersensitivity) reaction responsible for marked hemorrhagic oedematous bursa
⇓
Increased clotting times in
IBDV-infected chickens responsible for hemorrhages in different organs
CLINICAL SIGNS
Incubation period: 2-3 days
Earliest signs of infection – Birds pick at their own vents
Anorexia,
Depression,
Ruffled feathers,
Soiled vent feathers,
whitish or watery diarrhea,
dehydration,
trembling,
severe prostration and
finally, death
Macroscopic Pathology
Day 3-5, the bursa may enlarge about twice normal size; after day 5,
bursa atrophies and may contain necrotic foci and hemorrhages
Haemorrhage of the thigh and pectoral muscles and occasionally on the
mucosa of the proventriculus and increased mucous in the intestine
The spleen and liver may be enlarged with small gray foci on the surface
In some birds, there are accumulation of urates in the kidney results in
enlarged/swollen kidney. This lesions is attributed to enlarged bursa occlude the
ureter and/or dehydration
Microscopic Pathology
Bursa:
Acute (when bursa is enlarged and oedematous)
Degeneration and necrosis of lymphocytes
Infiltration of heterophils
Hyperplasia of reticuloendothelial cells
Oedema and hemorrhages
o Chronic ( when bursa is grossly shrunken)
Cystic cavitation in the medullary region
Necrosis and phagocytosis of heterophils with interfollicular
fibroplasia
Hyperplasia of the bursal epithelium with formation of glandular structures
Spleen, cecal tonsil and thymus:
Acute:
Hyperplasia of reticuloendothelial cells
Chronic:
multifocal lymphoid necrosis
Kidney: Acute nephrosis characterized by large tubular casts composed
of homogenous material infiltrated by heterophils
DIAGNOSIS
Based on clinical
signs
Gross and microscopic
lesions
Sample collected for
laboratory diagnosis: cloacal bursa and spleen
Serological test includes
Agar gel immunodiffusion assay (AGID)
Antigen-capture enzyme-linked immunosorbent assay (AC-ELISA)
Virus neutralisation (VN)
Immunofluorescence (IF)
RT-PCR
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