Infectious Bursal Disease of
Chickens
(Gumboro Disease)
Table of Contents
- Cause
- Clinical Signs
- Disease
- Diagnosis
- Treatment and Control
This syndrome was first recognized near Gumboro, Delaware
in 1962. It was first recognized in this province in 1970. It appears
to be almost universal in broiler-growing areas.
Cause
Gumboro Disease is caused by a small, hardy virus, which shares many
characteristics of the reovirus group. The organism is resistant to a
great range of temperature and pH, but is killed by most disinfectants
(formalin, cresol, iodine, etc.). The virus is rapidly spread by direct
contact between birds and can survive for extended periods of time on
inanimate objects, contaminated feed, etc. It does not appear to spread
through the air.
Clinical Signs
Whitish, watery or mucoid diarrhea may be evident in the flock, with
very sticky litter and soiling of vent feathers. Many birds may be reluctant
to move with a tendency to sit. There is listlessness, dehydration and
some deaths, with poor feed conversions. Secondary disease conditions,
such as E. Coli infection, Marek’s disease, gangrenous dermatitis
and inclusion body hepatitis may increase in incidence, and condemnation
rates may be elevated. The mortality pattern may range from the normal
acceptable levels to a total of 15%, but the usual rate is low. Four days
after the onset of clinical signs, the mortality peaks and returns to
normal within a week. The number of affected birds in a flock (morbidity)
is variable and can approach 100%. Sick birds do not die if management
is good and stresses kept to a minimum. Apparently subclinical disease
can occur and destroy the birds immune system without causing obvious
illness in a flock until secondary diseases develop.
Disease
The bursa of Fabricius, which is the organ responsible for disease protection
in young birds, is the main target for the virus. Normally, the bursa
of Fabricius regresses by early maturity. Hence, infectious bursal disease
is most important in birds up to 4 months of age, and most critical between
2 and 4 weeks of age. The virus destroys many of the cells in the bursa
of Fabricius and the resultant inflammation causes the organ to enlarge
in size. Fever may develop and may cause depression and dehydration. Kidney
damage (nephrosis) may result from the dehydration. Hemorrhagic lesions
throughout the body on the breast and leg muscles are seen on occasion.
The post-mortem findings include pale, swollen kidneys, abnormally large
or small bursa, hemorrhagic muscle lesions and possibly damage to the
spleen, thymus or cecal tonsils.
Diagnosis
Diagnosis is made on the flock history and postmortem examination, and
confirmed by virus isolation and identification. Serology and fluorescent
antibody techniques are now available and help identify the disease agent.
Histopathology of the bursa can also lead to a diagnosis.
Treatment and Control
No known chemotherapeutic or antibiotic agent is effective in the treatment
or control of infectious bursal disease. Drug therapy is often inadvisable
in the presence of severe kidney damage. Electrolyte and/or multiple vitamin
administration may be helpful in flocks where the disease is of relatively
long standing and appetites poor. Good ventilation, warm temperatures
and fresh water will help to reduce mortality. If secondary diseases become
a problem, antibiotic therapy may be required, but this should be kept
to a minimum.
After marketing a diseased flock, the farm should be completely
depopulated of all species of birds. All litter and unused feed must be
discarded and the building and equipment thoroughly cleaned and disinfected.
Fumigation with formaldehyde is recommended if possible. (This is a hazardous
procedure and must not be administered by inexperienced personnel.) The
building should be left vacant for 3 weeks. Vaccines are available in
some countries, although they have not been introduced into Canada. Control
of rodents, insects and wild birds is also important in the control of
infectious disease.
