Infectious Bursal Disease
Table of Contents
- Clinical Signs
- 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.
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.
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, Mareks 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.
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 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
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.