Infectious bursal disease IBD, Gumboro is an acute, highly contagious viral infection in chickens manifested by inflammation and subsequent atrophy of the bursa of Fabricius, various degrees of nephroso-nephritis and immunosuppression. Clinically the disease is seen only in chickens older than 3 weeks. The feathers around the vent are usually stained with faeces containing plenty of urates. The period of most apparent clinical symptoms and high death rate is at the age of 3 - 6 weeks. IBD could however be observed as long as chickens have a functioning bursa up to the age of 16 weeks. In chickens younger than 3 weeks, IBD could be subclinical, but injured bursa leads to immunosuppression.

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In the clinical acute form vvIBDV , the disease causes significant economic losses due to mortality, reduced performance and immunosupression that lead to increased susceptibility to other diseases.

The IBD virus is extremely resistant to environmental conditions and chemicals. Therefore the control of the disease must take into consideration strict biosecurity combined with an effective vaccination program. The following articles review the available knowledge about the disease, the virus, the clinical signs and the role of different elements of the immune system.

At the conclusion of these articles, a prevention program is offered, which includes elements of biosecurity and a comprehensive list of vaccination programs for breeders, broilers and commercial layers that in my experience have worked effectively in Asian countries.

What is Gumboro disease? What causes infectious bursal disease more commonly known as Gumboro Disease? Gumboro disease is caused by the infectious bursal disease virus IBDV.

This is a small, hardy Avibirnavirus belonging to the family Birnaviridae. There are two serotypes. Serotype 1 is a pathogenic type isolated from chickens. Serotype 2 is apathogenic does not cause any clinical disease and was originally isolated from turkeys. Both serotypes can be differentiated by cross-neutralisation assays.

The organism is resistant to a great range of temperatures, disinfectants and pH. It is therefore very stable during environmental exposure and can survive for up to four months. Certain disinfectants like formaldehyde, glutaraldehyde, chlorine and iodophore based products are however able to destroy it. How does the virus cause disease in chickens? The BF is the organ responsible for disease protection in young birds, as it is where B lymphocytes cells of the humoral immune system are programmed to produce specific antibodies in response to disease and also to vaccine agents in birds.

If the IBD virus damages the BF in young chickens, it will destroy the immature B lymphocytes, causing lymphoid depletion of the bursa. The BF will then not be capable of programming sufficient numbers of lymphocytes and the chicken becomes immunosuppressed not capable of protecting itself against any disease agent.

The severity of the disease is directly related to the number of susceptible B cells present in the Bursa at the time of infection. The time when chickens are most susceptible is therefore between 3 and 6 weeks, when the Bursa of Fabricius is at its maximum rate of development and the follicles are filled with immature B lymphocytes. Virus replication also occurs in other lymphoid organs like the spleen and cecal tonsils but to a lesser extent.

Which birds are at risk of Gumboro disease? The population at risk includes broiler flocks and young pullets destined for breeder and commercial egg laying flocks. Light weight laying breeds are more susceptible then heavy broiler breeds. Males are more susceptible then females. How is the virus transmitted? Chickens infected with the IBD virus shed the virus in their faeces.

Virus shedding starts 48 hours after infection and lasts for 14 days. Feed, water, and poultry house litter become contaminated. Other chickens in the house become infected by ingesting the virus. It is also transmitted mechanically among the farms by people, equipment and vehicles, but also by wild birds, flies and other insects. IBDV does not appear to spread through the air.

How common is it? Since the first description of the disease in the USA by Cosgrove in the sixties, serological surveys have shown a high prevalence of IBD antibody in breeder flocks, which has been acquired either following vaccination or sub-clinical infection. This immunity is passively transmitted to the offspring via the egg yolk, protecting them at a young age for about the first two weeks against the clinical disease.

Before , in most parts of the world IBD was essentially a sub-clinical disease. This form of IBD was satisfactory controlled by vaccination of the breeders. Since the virus has gone through an evolutionary process. Two major epidemiological events causing vaccination failures have been described in different parts of the world.

Thus clinical acute IBD became predominant with additional losses due to specific mortality. In Europe and Asia, the new strains still belong to classical serotype 1 but are characterised by a marked increase in pathogenicity.

First described in Belgium at the end of the eighties, the hyper-virulent or very virulent forms of the disease vvIBD were then described in Japan in the early nineties and have rapidly spread all over the Asiatic and European continents and to major parts of the world. Latin America has been the latest victim of this epidemic. As a probable consequence of strict import controls, Australia and the USA are, so far, still unhurt.

What is the incubation period of IBD? The incubation period time between infection and the appearance of clinical disease of IBDV in chickens is about 2 to 4 days. How does the disease manifest in chickens? Infectious bursal disease follows one of two courses, depending on the type of virus to infect the chicken, the age of the infected chicken, breed of chicken and the presence or not of maternally derived antibodies passive immunity.

When the disease occurs in chickens less than 3 weeks of age, deficient of maternally derived antibodies, the chickens have no clinical signs of disease but experience permanent and severe immunosupression. The affected birds cannot respond properly to any infection, and are not capable of developing effective immunity following vaccination. The reason why young chickens exhibit no clinical signs of disease is related to relatively low levels of circulatory B lymphocytes which might be destroyed by IBDV during the first two weeks.

However, immunosupression occurs due to damage of the BF. This form is almost absent in commercial production due to the routine vaccination of breeders. When the subclinical form of the disease occurs in chickens older than 3 weeks of age, chickens do not display clinical signs of disease but experience reduction in overall performance, with high feed conversion ratios and slow growth rates.

This is the more economically important form of the disease. It is caused by the hyper virulent strains of infectious bursal disease virus. The clinical disease has a sudden onset. The first symptom in infected chickens is an acute onset of depression. Birds are listless and may be reluctant to move with a tendency to sit.

Clinical signs of disease include fever, dehydration, trembling and ruffled feathers. Whitish, watery or mucoid diarrhoea may be evident in the flock, with very sticky litter and soiling of vent feathers, often followed by vent pecking. Affected flocks show this depression for days. There is also poor feed conversion and deaths. The mortality rate has a typical bell shape curve, rising rapidly for the first two days.

Four days after the onset of clinical signs, the mortality peaks and returns to normal within a week. Affected chickens experience a transient immunosupression. Secondary disease conditions, such as E. Sick birds do not die if management is good and stresses kept to a minimum.

What effect do the variant strains of IBD have? Variant viruses induce damage in the BF in chickens, causing vaccine failure, even when high and uniform antibody titres are present. Variant strains do not cause obvious clinical disease, but induce severe immunosupression. The BF of affected chickens undergoes rapid atrophy lymphocyte depletion.

These variants are not from a different serotype, but are antigenically different enough to cause problems. Recent research from the University of Arkansas has demonstrated a new form of the disease caused by variant strain of IBD virus, characterised by an enlarged and flabby proventriculus, distension of the intestine airsaculitis, dermatitis, reduced body weight gain and immunosupression. What is seen at post mortem? In the clinical acute form of the disease the Bursa of Fabricius is the first internal organ to show lesions.

This occurs within 24 hours of infection. During the initial stages of the disease the BF is swollen due to inflammation. By day three it has increased in size and weight, appears oedematous and hyperemic and has a gelatinous yellowish transudate covering the serosal surface.

By day four the BF has doubled in weight. The transudate disappears as the bursa returns to its normal size and becomes grey in colour, undergoing atrophy. At day 8, the bursa is usually one-third of its original weight. The infected bursa always shows necrotic foci and petechial haemorrhages on the mucosal surface. Necrosis and depletion of lymphocytes also occurs in the secondary lymphoid organs, including the spleen, Harderian glands, and cecal tonsils although these organs are typically affected less severely than the BF.

The spleen therefore appears slightly enlarged with small grey foci dispersed uniformly on the surface. Haemorrhage 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 and pale with an accumulation of crystalline urate in the tubules 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. A filtered homogenate of the bursa of Fabricius from infected birds, collected 2 to 10 days post infection, is inoculated into an embryonated egg. The homogenate is preferably inoculated into the chorion allantoic membrane CAM or into the yolk sac. Embryo death occurs 3 to 7 days post inoculation. Typically an oedematous congested embryo is seen with gelatinous appearance of the skin and haemorrhages in the toes or the encephalon.

The liver appears pale, bile stained and with wide necrotic foci. What kind of virus is IBD? VP2 and VP3 are structural proteins which form the viral capsid. But as the hyper-variable region of VP2 is subject to mutations, it often leads to changes in virus antigenicity and pathogenicity. What are the criteria used to describe an isolate of IBDV?


Infectious bursal disease (or Gumboro)

In the clinical acute form vvIBDV , the disease causes significant economic losses due to mortality, reduced performance and immunosupression that lead to increased susceptibility to other diseases. The IBD virus is extremely resistant to environmental conditions and chemicals. Therefore the control of the disease must take into consideration strict biosecurity combined with an effective vaccination program. The following articles review the available knowledge about the disease, the virus, the clinical signs and the role of different elements of the immune system.


Infectious Bursal Disease in Poultry

Good Practice At one time the disease was considered as primarily affecting commercial broiler flocks. A virulent strain appeared in Europe in and since then it has become an important disease of layer and breeding flocks. Widespread vaccination is now conducted, and the immunocompetence status of breeder flocks and hatcheries is determined by the degree of exposure to the virus. Flocks maintained under strict biosecurity are particularly susceptible to field exposure as they would not previously have been exposed to the disease.


Infectious bursal disease

There are two distinct serotypes of the virus, but only serotype 1 viruses cause disease in poultry. Viruses belonging to one of these antigenic subtypes are commonly known as variants, which were reported to break through high levels of maternal antibodies in commercial flocks, causing up to 60 to percent mortality rates in chickens. With the advent of highly sensitive molecular techniques, such as reverse transcription polymerase chain reaction RT-PCR and restriction fragment length polymorphism RFLP , it became possible to detect the vvIBDV, to differentiate IBDV strains, and to use such information in studying the molecular epidemiology of the virus. IBDV genome consists of two segments, A and B, which are enclosed within a nonenveloped icosahedral capsid. The larger segment A 3. Among them, VP2 protein contains important neutralizing antigenic sites and elicits protective immune response and most of the amino acid AA changes between antigenically different IBDVs are clustered in the hypervariable region of VP2. Thus, this hypervariable region of VP2 is the obvious target for the molecular techniques applied for IBDV detection and strain variation studies.

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