Selected content from the Animal Health and Production Compendium (© CAB International 2013). Distributed under license by African Union – Interafrican Bureau for Animal Resources.
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Identity Pathogen/s Overview Distribution Distribution Map for Africa Distribution Table for Africa Hosts/Species Affected Host Animals Systems Affected Epidemiology Impact: Economic Zoonoses and Food Safety Pathology Diagnosis Disease Course Disease Treatment Table Disease Treatment Vaccines Prevention and Control References Links to Websites OIE Reference Experts and Laboratories Images
Preferred Scientific Name
infectious bursal disease
International Common Names
Gumboro disease, infectious avian nephrosis, infectious bursitis
infectious bursal disease virus
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.
Classical IBD viruses occur worldwide, with the probable exception for New Zealand (Lukert and Saif, 1991; Becht , 1994; McFerran, 1993). In the USA, antibodies against IBDV serotype 2 are widespread in chicken and turkey flocks, indicating the common prevalence of the infection. Since the recognition of very virulent IBD viruses (vvIBDVs), in the late 1980s in Europe, acute forms of the disease have been described in Japan during the early 1990s. Currently, vvIBDVs have been isolated in Asia, Central Europe, Russia, the Middle East, and South America (Yamaguchi et al., 1997; Di Fabrio et al., 1999; Liu et al., 2001; Meir et al., 2001). To date, Australia, New Zealand, Canada and the USA are unaffected with vvIBDVs (Proffitt et al., 1999). It is estimated that vvIBDVs are present in 95% of the Office International des Epizooties member countries (van den Berg, 2000).
For current information on disease incidence, see OIE's WAHID Interface.
= Present, no further details = Widespread = Localised
= Confined and subject to quarantine = Occasional or few reports
= Evidence of pathogen = Last reported... = Presence unconfirmed
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further information for individual references may be available in the Animal Health and Production Compendium. A table for worldwide distribution can also be found in the Animal Health and Production Compendium.
|Country||Distribution||Last Reported||Origin||First Reported||Invasive||References||Notes|
|Africa||Present||van den Berg, 2000|
|Algeria||Disease not reported||OIE, 2012|
|Angola||Disease not reported||OIE, 2012|
|Benin||No information available||OIE, 2012|
|Burkina Faso||Present||OIE, 2012|
|Burundi||No information available||OIE, 2012|
|Cameroon||Reported present or known to be present||OIE, 2012|
|Cape Verde||Reported present or known to be present||OIE, 2012|
|Central African Republic||Reported present or known to be present||OIE, 2012|
|Chad||No information available||OIE, 2012|
|Congo||No information available||OIE, 2012|
|Congo Democratic Republic||No information available||OIE, 2012|
|Côte d'Ivoire||Reported present or known to be present||OIE, 2012|
|Djibouti||Disease not reported||OIE, 2012|
|Egypt||Disease not reported||OIE, 2012|
|Gabon||Disease not reported||OIE, 2012|
|Gambia||No information available||OIE, 2012|
|Guinea||No information available||OIE, 2012|
|Guinea-Bissau||No information available||OIE, 2012|
|Lesotho||Disease not reported||OIE, 2012|
|Libya||Reported present or known to be present||OIE, 2012|
|Mali||No information available||OIE, 2012|
|Mauritius||Disease not reported||OIE, 2012|
|Morocco||No information available||OIE, 2012|
|Mozambique||Disease not reported||OIE, 2012|
|Namibia||Disease not reported||OIE, 2012|
|Réunion||No information available||OIE, 2012|
|Sao Tome and Principe||Serological evidence and/or isolation of the agent||OIE, 2012|
|Senegal||Disease not reported||OIE, 2012|
|Seychelles||Reported present or known to be present||OIE, 2012|
|Somalia||No information available||OIE, 2012|
|South Africa||Disease not reported||OIE, 2012|
|Sudan||Restricted distribution||OIE, 2012|
|Swaziland||Disease not reported||OIE, 2012|
|Togo||No information available||OIE, 2012|
|Tunisia||Disease not reported||OIE, 2012|
Chickens, turkeys, ducks and guinea fowl may be infected with IBDV, but clinical disease only occurs in chickens. Mortality is higher in lighter breeds than heavier breeds (van den Berg, 2000). Serotype 1 viruses mainly infect fowl, and turkeys to a lesser extent, although the widespread use of serotype 1 vaccines makes it difficult to determine the true prevalence.
IBDV Type 2 viruses are widely distributed in turkeys (McFerran, 1993). In several other species, IBDV or IBDV-specific antibodies have been detected, such as in coturnix quail, pigeons, pheasants, village weavers (Ploceus cuncullatus), pied cordon bleus (Uraeginthus bengalus), magpie geese (Anseranus semipalmata), shearwaters (Puffineus carneips, P. pacificus), soothy terns (Sterna fuscata), common noddy (Anous stolidus), silver gulls (Larus novaehollandiae), and black ducks (Anas superciliosa) (Wilcox et al., 1983; McFerran, 1993).
|Anser (geese)||Domesticated host|
|Gallus gallus domesticus (chickens)||Domesticated host|
|Muscovy duck||Domesticated host|
|Pekin duck||Domesticated host|
Multisystem - Poultry
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.
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).
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).
In fully susceptible flocks, acute clinical disease may easily be recognized. The disease manifests itself with a rapid onset, high morbidity, spiking mortality and rapid recovery (Lukert and Saif, 1991; Eterradossi and Saif, 2008). At necropsy, the bursa will show changes depending on the stage of the disease. In early stages the bursa is enlarged, whilst in later stages the bursa is reduced in size due to atrophy.
Subclinical infections occur in very young chickens, or chickens carrying maternal antibodies, or are due to variant IBD viruses.
Differential diagnosis for sudden onset and ruffled feathers should include coccidiosis, especially when there is some blood in the droppings. However, an enlarged oedematous bursa and haemorrhages in the muscle tissue would suggest IBD. Some strains of infectious bursitis virus, in particular vvIBDVs can cause nephrosis, and should be considered when changes in the kidneys are observed. Changes in the bursa will readily point towards IBD (Lukert and Saif, 1991; van den Berg, 2000).
Laboratory diagnosis is necessary to confirm the presumptive diagnosis. For detection of the antigen, the cloacal bursa or the spleen are the tissues of choice. (Lukert and Saif, 1991). IBDV-specific antigen can most economically be demonstrated using an agar gel precipitation test. Alternatively, impression smears of frozen sections of the bursa may be tested by immunofluorescence.
Reverse transcription PCR (RT-PCR), followed by restriction enzyme digestion or restriction fragment length polymorphism (RFLP) analysis of the amplified fragment is common for the detection of IBDV and for the differentiation of pathotypes (Ghorashi et al., 2011; Hernandez et al., 2011; Tomas et al., 2012). Nucleotide sequencing is commonly used to confirm RFLP analysis and for epidemiological studies, including the study of the evolution of the virus in different geographic locations (Cortey et al., 2012). FTA cards have been used successfully for the collection of nucleic acid of IBDV and for the safe transport of the samples, including internationally, to diagnostic laboratories (Moscoso et al., 2006).
Virus isolation can be performed in embryonated eggs of CEC. Tissues should be macerated in an antibiotic-containing medium and centrifuged to remove larger tissue particles. The supernatant fluid is then used to inoculate embryonating eggs or cell cultures.
For serological diagnosis, VNT or IBDV-specific ELISAs should be performed (Becht, 1994). The ELISA is the most commonly used serological test to evaluate presence of IBDV antibodies in poultry flocks. The ELISA has the advantage over the VNT that results can be quicker obtained. For evaluation of the flock immunity, a minimum of 30 samples is required (Lukert and Saif, 1991). The antibody profile may be performed with breeders or with day-old progeny, in the progeny sera the titres are usually about 60-80% lower than in those of the breeders (Lukert and Saif, 1991). The VNT has the advantage that it can differentiate between serotype 1 and 2 IBDV strains, in contrast to the ELISAs. Given the antigenic variation between the IBDV strains, the reference strain used in the VNT is of utmost importance.
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).
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).
|Drug||Dosage, administration and withdrawal times||Life stages||Adverse affects||Drug resistance||Type|
|inactivated virus vaccine||Intramuscular injection||Mature female||Sometimes a tissue reaction is observed.||No||Vaccine|
|live virus vaccine||Intramuscular injection, by spray or by drinking water||Mature female/Young poultry||Sometimes immunosuppression||No||Vaccine|
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.
|Vaccine||Dosage, Administration and Withdrawal Times||Life Stages||Adverse Affects|
|inactivated virus vaccine||Intramuscular injection||-Poultry: Mature female||Sometimes a tissue reaction is observed.|
|live virus vaccine||Intramuscular injection, by spray or by drinking water||Sometimes immunosuppression|
Disease prevention aims at prevention of infection. The stability of the virus largely contributes to the likelihood that transmission will occur for prolonged periods of time and from an infected premises towards uninfected farms. Therefore, routine sanitary precautions must rigorously be followed for IBDV. Although disinfection may be difficult, thorough disinfection with appropriate disinfectants will reduce the virus load and therefore will reduce the risk of transmission. Eradication of mechanical vectors such as mosquitoes, mealworms, and smaller rodents must also be pursued (Lukert and Saif, 1991). On farms where IBDV outbreaks have occurred, the virus may be considered endemic. Young birds will be exposed to the virus at a very early age, when cleaning between broods is not thorough (Lukert and Saif, 1991).
An early method of control involved intentional exposure of young chickens to IBDV (Lukert and Saif, 1991; Lasher and Davis, 1997). This technique lowered IBD mortality but often resulted in immunosuppression and further dissemination of the field virus. Live attenuated vaccines were developed, based on mild field isolates passaged in specific-pathogen-free eggs. They are still widely used today in breeders as a primer and in the control of very virulent IBD in many countries. Until the 1980s, mortality caused by IBD was effectively controlled by vaccination. However, the effects of immunosuppression and the tremendous economic impact of the disease were just starting to be appreciated. Recognition of Delaware variants in the USA in the mid-1980s and the emergence of very virulent forms of the condition in Europe and Asia in 1989 illustrated the continuing importance of IBD (Lasher and Davis, 1997; Lütticken, 1997; van den Berg, 2000; Eterradossi and Saif, 2008).
It is essential to prevent infection at an early age, so that the immunosuppressive effect of IBDV can be circumvented. This can be achieved by immunization of the breeders. When oil-adjuvanted vaccines are used to boost the immune response, the maternal immunity may be extended to 4-5 weeks. Normally maternal immunity lasts 1-3 weeks, protecting the chicks from early immunosuppressive infections (Lukert and Saif, 1991). When young chickens are to be vaccinated with attenuated vaccines, an important problem is the timing of vaccination, due to the suppressive effects of maternal antibodies to vaccination. Monitoring of the antibody level in a breeder flock or its progeny can aid in determining the right time to vaccinate (Lukert and Saif, 1991; Eterradossi and Saif, 2008).
Vaccines may be administered by intramuscular injection, by spray or by drinking water. When maternally derived antibodies are not present, vaccination is possible at 1 day of age. If maternally derived antibodies are suspected, serological monitoring is required to determine the right time of vaccination (OIE, 2000).
Attenuated vaccines are referred to as mild, intermediate, or 'intermediate plus' (hot) vaccines. Mild vaccines do not cause bursal damage in chicks but may be poorly efficacious in the presence of certain levels of maternal antibody or infection by vvIBDV. Vaccines of greater intrinsic pathogenicity (intermediate, or 'intermediate plus' (hot) may break through high levels of maternal immunity but may also cause damage to the bursa, with subsequent immunosuppression. In addition they may also not protect against infection with vvIBDV (Rautenschlein et al., 2005) or antigenic variants.
Mild vaccines are frequently used to prime broiler breeders prior to vaccination with an inactivated, frequently oil-adjuvanted vaccine. Intermediate and 'hot' vaccines are mostly used to overcome the maternally derived antibodies in young broilers (OIE, 2000).
Given the difficulties of achieving effective vaccination with live IBDV vaccines in the face of differing levels of maternal immunity, challenge strains of different pathogenicity, and the danger of inducing immunosuppression with 'hotter' vaccines, several different approaches to the development of IBDV vaccines have been explored. These include: genetic modification of IBDV to attenuate pathogenicity very precisely; subunit vaccines, based on the protection-inducing VP2 structural protein; DNA vaccines; immune complex vaccines (Icx); and live viral vector vaccines. All these have been reviewed by Muller et al. (2012). One of these approaches (Icx) is already in use commercially, whilst another (live vector vaccines) are close to commercial application.
An Icx vaccine comprises live pathogenic IBDV mixed with anti-IBDV antibodies derived from hyperimmunised chickens. It can be administered sub-cutaneously at day-old in the presence of various levels of maternal antibody, resulting in active immunity without causing any vaccine-induced immunosuppression (Haddad et al., 1997; Ivan et al., 2005). Icx vaccines are also used to vaccinate in ovo at day 18 of incubation using automated technology to achieve very precise vaccination.
Live virus vector vaccines comprise a gene from one pathogen e.g. VP2 of IBDV, within the genome of another, live virus – the vector. Vectors investigated with VP2 include Newcastle disease virus, fowlpox virus, Marek's disease virus, herpesvirus of turkeys (HVT) and avian adenovirus. Of these the HVT-vectored VP2 vaccines have been introduced commercially in some countries. HVT vaccines are widely used, having been used successfully for decades to control Marek's disease. HVT vaccines have an advantage of not being interfered by maternally-derived antibody. HVT-VP2 vaccines, depending on the manufacturer, can be applied in ovo or subcutaneously in day-old chicks (Bublot et al., 2007; le Gros et al., 2009; Perozo et al., 2009).
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(http://www.oie.int, accessed 5 June 2013)
Dr Nicolas Eterradossi
Agence Nationale de Sécurité Sanitaire de l'Alimentation, de l'Environnement et du Travail (Anses)
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Ohio State University
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Date of report: 03/06/2013
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