infectious bursal disease

Preferred Scientific Name

• infectious bursal disease

International Common Names

• English: Gumboro disease; infectious avian nephrosis; infectious bursitis

English acronym

• IBD

Infectious bursal disease (IBD) is an acute, highly contagious disease of young chickens, caused by infectious bursal disease virus (IBDV) (van den Berg, 2000; Eterradossi and Saif, 2008; Mahgoub, 2012; Muller et al., 2012). First recognized in Gumboro, Delaware (USA) in 1962, the disease was initially referred to as avian nephrosis, and later became known as Gumboro disease or infectious bursitis. The virus responsible is a bisegmented, double-stranded RNA virus, belonging to the Avibirnavirus genus in the family Birnaviridae. IBDV shows selective tropism for lymphoid tissue and in particular the Bursa of Fabricius in the young bird. Economic losses are high and are manifested in two ways. First, in the case of classical IBD, as a result of high mortality in chickens of 3 -6 weeks and second as a result of a severe and prolonged immunosuppression that may pave the way for gangrenous dermatitis, E. coli infections and vaccination failures.

The virus occurs worldwide, and despite intensive vaccination regimes, outbreaks of disease occur frequently, and various variants of IBDV occur, each with a different virulence. At the end of the 1980s, very virulent variants of IBDV (vvIBDV) emerged. They were first recognized in Europe, and subsequently in Asia, the Middle East and South America. These viruses may cause acute disease in susceptible flocks over the entire growing period of broilers, with the virus also present in non-bursal and haematopoetic organs, such as the thymus, spleen and bone marrow. Classical vaccines failed in many cases to provide sufficient protection against vvIBD. These vvIBDVs pose a severe challenge to design of new vaccines and vaccination strategies. Because highly potent vaccines are required to protect broilers during the whole growing period, vaccine research currently focuses on new technologies. The aim is to develop new, tailor-made live or inactivated (subunit) vaccines that protect against both classical and vvIBDV strains. They should have the potency of ‘hot’ live vaccines, without the accompanying dangers of causing immunosuppression. In particular the interference of maternal derived antibodies must be overcome. The development of marker vaccines that provide the ability to distinguish between vaccinal and infectious antibodies, would allow monitoring of the epidemiological field situation.

The distribution section contains data from OIE's WAHID database on disease occurrence. Please see the AHPC library for further information on this disease from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.

The chickens that succumb to IBDV infections are dehydrated, with darkened discoloration of the pectoral muscles (Lukert and Saif, 1991). Many petechial haemorrhages may be present in the thigh and pectoral muscular tissue (Becht, 1994). There is increased mucus in the intestine and renal changes may be present in advanced stages of the disease.

In IBDV affected chickens, depending on the stage of the disease, the Bursa of Fabricius will usually be enlarged, oedematous, and may contain haemorrhages. A few days after infection, the Bursa has a gelatinous yellowish transudate covering the serosal surface. The colour of the Bursa turns from white to cream. On approximately the third day of infection, the size of the Bursa enlarges because of oedema and hyperaemia. After the fourth or fifth day the size recedes, and continues to atrophy. From the eighth day onwards, it is approximately one-third of its original weight (Lukert and Saif, 1991). The spleen may become enlarged and may contain grey foci on the surface.

Histologically, degeneration and necrosis of lymphocytes in the medullary areas of the bursal follicles may be observed. The depletion of the lymphoid cells in the bursa is caused by massive apoptosis. Importantly, some strains of IBDV do not cause severe inflammation of the bursa, but only cause depletion of lymphocytes (Jungmann et al., 2001). The cellular traffic in the inflamed bursa is complex, as demonstrated by depletion of B-cells, but also concomitant with influx of inflammatory cells, such as neutrophils, phagocytes, and T-cells (Tanimura and Sharma, 1997). T-cells that migrate into the Bursa of Fabricius are predominantly CD3+ and TCR2+ cells, and appear at the site where viral antigens are present. The CD3+ cells continue to persist in the bursa after most of the IgM+ cells and IBDV antigen-positive cells have disappeared. The role these T cells may play in the pathogenesis of IBDV infection remains to be established (Tanimura and Sharma, 1997).

In the spleen, hyperplasia of reticuloendothelial cells around the adenoid sheath arteries may be observed. Germinal follicles may show necrosis as well as the peri-arterial lymphoid sheaths. In the thymus and caecal tonsils, damage of the lymphoid tissue may be present but is less severe. If present, after classical IBD, kidney lesions are non-specific, and are a result of the severe dehydration suffered (Lukert and Saif, 1991). For vvIBDV strains, apart from the inflammation and atrophy (after 7-10 days) of the Bursa of Fabricius, the kidneys may be swollen, and ecchymotic changes in the muscles and the mucosa of the proventriculus can be observed in the majority of affected birds (van den Berg, 2000).

At necropsy, the enlarged bursa shows necrosis of the lymphoid follicles and is totally depleted of B-cells. Haemorrhages may be present in the Bursa of Fabricius and the muscular tissue (Becht , 1994).

The depletion of B-cells in the bursa is caused by necrosis and apoptosis, induced by IBDV replication in productively infected cells, as well as in antigen-negative cells in their vicinity (Jungmann et al., 2001). IBDV affects thrombocytes, and the frequently found disseminated haemorrhages are probably related to the impairment of the clotting mechanism as a result of the depletion of thrombocytes (van den Berg, 2000).

The incubation period of infectious bursal disease virus (IBDV) is very short. After an incubation period of 2-4 days, young chickens show symptoms of apathy and distress, and death may follow 1-3 days later. Mortality will peak and recede usually in a period of 5-7 days (Lukert and Saif, 1991; Becht, 1994). Morbidity approaches 100% and mortality may be up to 20%-30%, but may also be 0% (Lukert and Saif, 1991, McFerran, 1993). Characteristically, chickens may pick at their own vents in the early stage of the disease (Lukert and Saif, 1991).

Initial outbreaks on farms are the most acute and recurrent outbreaks in succeeding flocks are less severe.

For vvIBDV infections, the virus primarily replicates in the lymphocytes and macrophages of the gut-associated tissues after oral infection or inhalation. The virus then travels to the Bursa via the blood stream, where replication will occur. After 13h post-inoculation, most follicles are positive for virus and by 16h post-inoculation a second viraemia occurs leading to disease and death (van den Berg, 2000).

Outbreaks of vvIBDVs are characterized by the sudden onset of depression in susceptible flocks. The incubation period is similar to conventional serotype I infections, but animals are prostrate and reluctant to move, with ruffled feathers and frequently watery or white diarrhoea (van den Berg, 2000).

When birds are somewhat older, IBDV infection will not lead to a direct lethal infection, but the resulting severe general immunosuppression will pave the way for many opportunistic infections by various agents. This may lead to high mortality rates. The destruction of the Bursa block’s peripheral supply of mature B-cells, results in a complete lack of immunocompetent cells (Becht, 1994).

The exact mechanism for IBDV infection leading to death in young chicks remains unclear. Bursectomy does not lead to acute death in young chickens and other mechanisms must play a role that cause damage to other vital body organs and ultimately lead to the death of the birds (Becht, 1994).

Secondary infections

Chickens infected with infectious bursal disease virus (IBDV) commonly develop secondary infection of the respiratory tract with Escherichia coli, resulting in significant economic losses. Also vaccination failures may occur. IBDV alone markedly reduces opsonizing ability of antibodies, and this effect is significantly exacerbated by IBV infection (Naqi et al., 2001). Lack of adequate IgA- and IgG-associated antibody production in IBDV-infected chickens has been demonstrated, and this may account for their increased susceptibility to secondary IBV infection (Thompson et al., 1997).

Infectious bursal disease virus (IBDV) is highly contagious. Transmission of IBDV predominantly takes place via the faecal-oral route, because the virus is shed in the faeces for up to 2 weeks post infection in high amounts. The high resistance of the virus contributes to this mode of transmission. Airborne spread is not important and there is no evidence for egg-transmission or virus carriers. Wild birds or rodents might transport the virus and act as mechanical vectors (McFerran, 1993). It has been demonstrated that the lesser mealworm (Alphitobius diaperinus) taken 8 weeks after an outbreak can act as a vector for IBDV when fed as a ground-suspension (Lukert and Saif, 1991).

Birds are most susceptible between 3-6 weeks of age. Susceptible chickens that are younger than 3 weeks become infected but do not show clinical signs. However, they do develop severe immunosuppression, as was first recognized by Allen et al. (1972) and Faragher et al. (1974). The reason for the age-related resistance is not fully understood.

Molecular epidemiology

Comparisons of the immunogenic dominant IBDV VP2 protein sequences of the IBDVs offer the best evolutionary clue for vvIBDVs. The VP2 protein contains the antigenic region responsible for induction of neutralizing antibodies and for serotype specificity. The VP2 protein has a high mutation rate. Asiatic vvIBDVs probably originated from the European vvIBDVs, and phylogenetic analysis of vvIBDVs isolated in Africa, demonstrates that these IBD viruses also belong to the common very virulent lineage. However, there are significant differences between the African, and European and Asian vvIBDV strains, suggesting independent evolution (Van den Berg, 2000).

The economic impact of IBD in fowl is serious. Clinical IBDV leads to direct losses due to high mortality, but indirect losses are probably more important due to the severe immunosuppression observed (McFerran, 1993). In addition, condemnation of carcasses due to skeletal muscle, thigh and pectoral muscle haemorrhages can be an important cause of economic losses (McFerran, 1993). The occurrence of vvIBDVs has increased the economic importance of the disease. Until 1987, the strains of the virus were of low virulence, causing less than 2% mortality, and vaccination was able to satisfactorily control the disease. However, the occurrence of vvIBDV has led to vaccination failures, and increased mortality and morbidity (van den Berg, 2000). In 80% of the OIE member countries, acute clinical disease due to IBDV has been reported (van den Berg, 2000).

IBDV does not infect humans and is therefore not a zoonosis. The disease has no public health significance (Lukert and Saif, 1991; McFerran 1993; Eterradossi and Saif, 2008).

There is no treatment available in the case of clinical IBDV. The usually rapid recovery of a flock after an IBD outbreak frequently suggests response to a given treatment, but no therapeutic or supportive treatment is known. Antiviral drugs are not yet available.