Infectious Bursal Disease of Chickens
(Gumboro Disease)

Table of Contents

1. Cause
2. Clinical Signs
3. Disease
4. Diagnosis
5. 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.

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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.


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