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INFECTIOUS BURSAL DISEASE (GUMBORO) IN COMMERCIAL BROILERS

Gary D. Butcher and Richard D. Miles

Infectious bursal disease (IBD) is an acute and highly contagious viral
infection of immature chickens. IBD is characterized by destruction of
lymphocytes in the bursa of Fabricius (BF) and to a lesser extent in other
lymphoid organs. The disease is a major problem in concentrated poultry
production areas throughout the world. However, it is often not recognized due
to a subclinical form. Affected chickens have reduced antibody response to
vaccinations, strong post vaccinal reactions, and increased susceptibility to
concurrent or secondary infections.


CHARACTERISTICS OF THE IBD VIRUS

IBD is caused by a birnavirus. The virus is resistant to many disinfectants and
environmental factors, and remains infectious for at least four months in the
poultry house environment. Because of the resistant nature of the IBD virus,
once a poultry house becomes contaminated, the disease tends to recur in
subsequent flocks.


PATHOGENESIS OF IBD

To better understand how the IBD virus adversely affects the chicken's immune
system, relevant factors of this system's early development will be described.
During embryonic development, and through approximately 10 weeks of age, immune
system cells (lymphocytes) travel to the BF to become programmed to become
antibody-producing cells. If the IBD virus damages the BF in young chickens, the
BF will not be capable of programming sufficient numbers of lymphocytes. Thus,
the chickens will experience reduced immune system capabilities
(immunosuppression).

The earlier the damage to the BF occurs, the few lymphocytes with
antibody-producing capability will be programmed. Therefore, any IBD virus
control program should attempt to protect the BF as long as possible. In
practical terms, if the BF can be protected against disease until at least 3
weeks of age, an adequate number of lymphocytes should be programmed, and the
immunosuppressive effects of an IBD outbreak should be inininal.


TRANSMISSION OF IBD VIRUS

Chickens infected with the IBD virus shed the virus in their feces. Feed, water,
and poultry house litter become contaminated. Other chickens in the house become
infected by ingesting the virus. The lesser mealworm (Alphitobus diaperinus) has
been shown to carry the virus. Because of the resistant nature of the IBD virus,
it is easily transmitted mechanically among the farms by people, equipment and
vehicles.


SUBCLINICAL AND CLINICAL IBD

Infectious bursal disease follows one of two courses, depending on the age at
which chickens are infected. The subclinical form of the disease occurs in
chickens less than 3 weeks of age. Chickens present no clinical signs of
disease, but experience permanent and severe inirnunosuppression. The reason
young chickens exhibit no clinical signs of disease is not known. However,
immunosuppression occurs due to damage to the BF. The majority of field
infections are subclinical, and this form is the more economically important
form of the disease.

Broiler integrations commonly have farms described as problem farms. Broilers
grown on these farms typically have poor body weights and feed conversions, high
mortality, excessive reactions to respiratory vaccines, and high rates of
condemnation at processing. In many cases, investigations have shown that these
farms are heavily contaminated with the IBD virus. The poor performance of the
broilers is due to factors relating to immunosuppression caused by subclinical
IBD.

The clinical form of IBD usually occurs in chickens from 3 to 6 weeks of age.
The clinical disease has a sudden onset, and the mortality rate in the flock
increases rapidly. Clinical signs of disease include dehydration, trembling,
ruffled feathers, vent pecking, and depression. Affected chickens experience a
transient immunosuppression. On necropsy, the principle lesions are found in the
BF.


GROSS LESIONS

Initially, the BF is swollen (inflamed); appears edematous and hyperemic; and
has a gelatinous yellowish transudate covering the serosal surface. Hemorrhage
and areas of necrosis may be present in more severe cases. Five days after
infection, the BF diminishes in size rapidly (atrophies).

Necrosis and depletion of lymphocytes also occur in the secondary lymphoid
organs, including the spleen, glands of Harder, and cecal tonsils. These organs
are typically affected less severely than the BF and may recover following
infection.

Hemorrhage may be present in the thigh and pectoral muscles, because the IBD
virus interferes with the normal blood clotting mechanism. The kidneys may
appear swollen in birds that die or that are in the advanced stages of the
disease. Such lesions probably result form severe dehydration, not direct viral
damage.


MICROSCOPIC LESIONS

Microscopically, lymphocyte necrosis is present in the BF within 36 hours after
infection. By 48 hours, few lymphocytes are present. Edema, hyperemia, and
inflammatory cell infiltration are evident, which account for the enlarged BF
during the initial days following IBD virus infection. By 8 to 12 days after
infections, the BF is shrunken to less than one-fourth of its original size. The
lymphoid follicles are cystic and depleted of lymphocytes. The epithelium lining
the BF is irregular and infolded. Fibroplasia is present in the interfollicular
connective tissue.

In severe cases of IBD, all the follicles are affected simultaneously. In less
severe cases, only scattered follicles are affected, and the lesions spread to
other follicles. Typically, the follicles in the tips of bursal folds are
affected first. Factors that determine the severity of an infection include
virulence of the IBD virus, concentration of IBD virus exposure, level of
immunity against IBD virus, and management factors.


DIAGNOSIS OF IBD

Diagnosis of IBD involves consideration of the flocks' history, and of the
clinical signs and lesions. Obviously, chickens less than 3 weeks of age present
no clinical signs of disease, while chickens greater than 3 weeks of age present
clinical signs as described. The severity of the clinical signs will depend upon
the factors described. Confirmation of a diagnosis of clinical IBD can be made
at necropsy by examining the BF during the early stages of disease for
characteristic gross lesions.

During later stages of disease it is difficult to confirm a diagnosis of IBD by
examining only shrunken, atrophied BF, as other diseases (for example, Marek's
disease, mycotoxicosis) produce similar changes. In birds less than 3 weeks of
age or in young chickens with maternal antibodies, IBD virus infections are
usually subclinical. Thus, typical clinical signs are not present, and diagnosis
should be supported by histopathologic study of suspect BF, serologic studies,
or by virus isolation.


PREVENTION AND CONTROL OF IBD

An effective IBD prevention and control program must involve an effective
breeder vaccination program, an effective biosecurity program, and an effective
broiler vaccination program. Immunization of breeders is an important part of
the IBD control program. Antibodies produced by the hen are passed through the
egg to the broiler chick. These maternal antibodies, if present in adequate
levels, protect the chicks against subclinical IBD. An example of a
comprehensive breeder vaccination program where subclinical IBD is a problem
might have a vaccine schedule such as this: at 12 to 15 days of age—IBD live; at
30 to 33 days of age—IBD live; at 85 days of age—IBD live or inactivated; and at
120 days of age—IBD inactivated.

Revaccinate at 38 to 42 weeks of age with an inactivated IBD vaccine if breeder
titers are low or of poor uniformity. Routinely monitor breeder IBD antibody
titers to ensure vaccines are administered properly and that the chickens
respond appropriately.

Effective control of IBD in commercial broilers requires that field virus
exposure be reduced by proper clean-up and disinfection between flocks, and that
traffic (people, equipment and vehicles) onto the farm be controlled. The
development and enforcement of a comprehensive biosecurity program is the most
important factor in limiting losses due to IBD.

Phenolic and formaldehyde compounds have been shown to be effective for
disinfection of contaminated premises. Efforts at biosecurity (cleaning,
disinfecting, traffic control) must be continually practices, as improvement is
gradual and often only seen after 3 or 4 flocks.

A third factor to consider in the IBD prevention and control program is
vaccination of the broilers to prevent clinical IBD. Three categories of
vaccines, based on their pathogenicity, have been described: 1) mild, 2)
intermediate, and 3) virulent. The intermediate type IBD vaccines are most
commonly used. These vaccines can stimulate the broiler to produce antibodies
earlier than the mild-type vaccines, without significant damage to the BF as may
occur with the virulent type vaccines.

The timing of broiler vaccination depends on the level of maternal antibody
present in the chicks. High levels of maternal antibody at the time of
vaccination will neutralize the vaccine virus. Thus, only a limited active
immune response results, and chickens will be susceptible to disease as maternal
titers decrease. If low levels of maternal IBD titers are present in the chicks,
vaccination may not be effective on farms contaminated with virulent field
virus.

Approximately 10 to 12 days are required after vaccination for chickens to
develop minimal protective titers. During this "lag time," chickens are
susceptible to IBD. In addition, virulent IBD viruses are able to break through
higher maternal titers than milder vaccine viruses. Thus, if IBD field virus
contamination on a broiler farm is high, nor broiler vaccination can stimulate
protection in the flock before damage occurs.

If the maternal antibody titer is not uniform in the broiler flock, multiple
costly vaccinations will be required. For example, some producers may vaccinate
broilers at one day of age and again at fourteen days of age. This multiple IBD
vaccination would be recommended when maternal titers are poorly uniform, which
results from poor vaccine administration in breeders or when mixing broilers
from different breeder flocks. In a recent study, even a group of breeders that
had fairly uniform IBD titers had chicks with titers that were variable, with
many chicks have little or no maternal antibody protection.

Although the 1 day of age vaccination would be of little direct benefit to
broilers with high maternal titer levels, multiple vaccinations would provide
some protection to chicks with lower levels of maternal antibody and would help
reduce replication of IBD field virus and subsequent shed in the poultry house
environment.

The important factors to consider in the control of IBD are the prevention of
broiler losses through an effective IBD breeder vaccination program (maternal
titers) and decreasing exposure through a comprehensive biosecurity program.
Relying on broiler vaccination has met with only limited success when not
coordinated with effective breeder vaccination and biosecurity programs.


VARIANT STRAINS OF IBD

Control of IBD has been further complicated by the recognition of variant
strains of the IBD virus. Variant viruses induce damage in the BF in chickens,
even when high and uniform antibody titers are present. Variant strains do not
cause obvious clinical disease, but induce severe immunosuppression. The BF of
affected chickens undergo rapid atrophy (lymphocyte depletion) without the
inflammatory changes observed early in the infection with the classical IBD
viruses. These variants are not from a different serotype, but are antigenically
different enough to cause problems.

Often IBD is a serious problem in an integration, and losses occur despite
persistent efforts at reducing field virus exposure through a biosecurity
program, maintenance of adequate and uniform maternal titers, and an effective
broiler vaccination program. In this case, consideration should be given to
vaccinating breeders with inactivated vaccines containing standard and variant
strains of the IBD virus.

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PUBLICATION #VM84

Release Date:February 20, 2019

Reviewed At:June 10, 2022

RELATED EXPERTS

MILES, RICHARD D.

University of Florida

BUTCHER, GARY D.

Specialist/SSA/RSA

University of Florida

RELATED UNITS

VETERINARY MEDICINE-LARGE ANIMAL CLINICAL SCIENCES

RELATED TOPICS

POULTRY DISEASES

 * Critical Issue: 1. Agricultural and Horticultural Enterprises





ABOUT THIS PUBLICATION

This document is VM84, one of a series of the Veterinary Medicine-Large Animal
Clinical Sciences Department, UF/IFAS Extension. Original publication date
November 1995. Visit the EDIS website at https://edis.ifas.ufl.edu for the
currently supported version of this publication.


ABOUT THE AUTHORS

Gary D. Butcher, DVM, Ph.D., professor and Avian Veterinarian, Department of
Large Animal Clinical Sciences; and Richard D. Miles, Ph.D., professor and
Poultry Nutritionist, College of Veterinary Medicine; UF/IFAS Extension,
Gainesville, FL 32611.


CONTACTS

 * Gary Butcher


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