Infectious Bursal Disease - causes, pathophysiology,

clinical signs, diagnosis, treatment

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Infectious bursal disease is also known as Gamboro disease because it was first recognized in
Gamboro, Delaware in 1962.

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It is caused by the infectious bursal disease virus, the sole member of the genus Avi berna virus.

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It belongs in the family Berna viridae by meaning to RNA referring to ribonucleic acid and viridae
meaning virus family.

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Oh and Avi here refers to avians.

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The infectious bursal disease virus is a non envelope virus that has two linear segments of double
stranded RNA.

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There are two serotypes.

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Serotype one causes disease in chickens only whereas serotype 2 can infect chickens and turkeys but
do not cause clinical disease.

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Serotype one has three antigenic subgroups, classic variant and very virulent with the following
mortality rates.

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Pathophysiology The infectious bursal disease virus has a tropism for certain B lymphocytes in the
Bursa of Fabricius.

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The Bursa of Fabricius is an organ unique to birds.

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It is a SAC like structure located dorsal to the cloaca.

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Hence it is also called the cloacal Bursa.
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Histologically it looks like this folds of pseudostratified columnar epithelium project into the lumen.

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Within these folds are lymphoid follicles with a dark cortex and light medulla.

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This is where we can find maturing B cells.

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It is a primary lymphoid organ that serves as the site of maturation of B cells in birds.

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The B in B cells refers to Bursa after all, as opposed to the T&T cells for the thymus.

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B cells play important roles in humoral immunity, that is, immunity involving antibodies.

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The infectious bursal disease virus likes to infect very specific kinds of B cells.

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These are B lymphoblasts that do not bear any immunoglobulins yet and B lymphocytes bearing
immunoglobulin M Interestingly, the virus does not replicate in stem cells and peripheral B cells.

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This trope is in for B lymphocytes at a very specific stage of differentiation results in age dependent
clinical disease.

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Chicks infected before three weeks of age may simply develop a subclinical infection because they
only have a few immature B cells and still possess maternal antibodies to protect them.

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Even though this is a subclinical infection, production losses can still result.

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The chicks may become poor responders to vaccination and have increased susceptibility to infections
that are normally harmless.

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The subclinical infection simply means that the chicks do not manifest the clinical signs of IPD during
the course of the disease.

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The Bursa of Fabricius may simply atrophy without significant inflammation.
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At three to six weeks of age, however, is when IPD V infection is most severe.

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This is when there are many immature B cells in the cloical Bursa.

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The Bursa has reached its maximum size and maternal antibodies have waned after a two to four day
incubation period.

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Chickens may show signs of prostration, incoordination, anorexia, watery diarrhea leading to soiled
vent feathers, vent picking, and inflammation of the cloaca.

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The Bursa of Fabricius can become up to five times bigger from the inflammation appearing
edematous, hyperemic and yellowish B lymphocyte.

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Destruction leads to the collapse of the normal follicular structure of the Bursa and multiple foci of
necrosis throughout the Bursa.

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This has been called a viral bursectomy because, just like in surgically bursectomized birds, there is a
significant decrease in the chicken's ability to produce antibodies.

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This also results in poor response to vaccination, recurrent opportunistic infections, and more severe
illness when infected with common diseases.

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Very virulent strains may also affect the thymus, spleen and bone marrow.

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Chickens infected after six weeks of age already have a physiologically atrophied bursal fabricius.

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This primary lymphoid organ atrophies would age just like the thymus, and most of their B cells have
already matured, so they don't really develop clinical signs of the disease.

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Diagnosis necropsy is usually done in the field, but diagnosis is confirmed by electron microscopy of
bursal specimens, virus isolation in embryonating eggs or cell cultures or RTPCR control.

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There is no treatment for infectious bursal disease.
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Being a non envelope virus it is extremely stable in the environment.

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It can be inactivated with phenolic base compounds, iodine complexes, formalin and chloramine
compounds, but take note that these must be used at the correct concentration with sufficient contact
time.

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Vaccination is the best method to prevention.

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Many vaccines against IBD are available, such as live vaccines, vectored vaccines, and immune
complex vaccines, some of which can be administered in Alva or while the chick is still in the egg.

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To recap, infectious bursal disease or Gomboro disease is caused by the infectious bursal disease
virus, a non envelope double stranded RNA Avi Burna virus of the family Burnaviridae.

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It has a tropism for B lymphocytes at a specific stage of maturation in the Bursa of Fabricius.

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Clinical disease is age dependent.

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Necropsy is commonly done in the field, but diagnosis can be confirmed through electron
microscopy, virus isolation, and RTPCR.

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The infectious bursal disease virus is very stable in the environment and is best prevented through
vaccination.