Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide


infectious bursal disease



infectious bursal disease


  • Last modified
  • 03 February 2022
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • infectious bursal disease
  • Overview
  • Infectious bursal disease virus (IBDV), a double stranded RNA virus belonging to the genus Avibirnavirus and family Birnaviridae, is the causative agent of infectious bursal disease (IBD) (...

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Infectious bursal disease; Broiler infected with infectious bursitis. July 2016.
TitleInfected broiler
CaptionInfectious bursal disease; Broiler infected with infectious bursitis. July 2016.
Copyright©Lucien Mahin (Lucyin)/via Wikimedia Commons - CC BY-SA 3.0
Infectious bursal disease; Broiler infected with infectious bursitis. July 2016.
Infected broilerInfectious bursal disease; Broiler infected with infectious bursitis. July 2016.©Lucien Mahin (Lucyin)/via Wikimedia Commons - CC BY-SA 3.0
Infectious bursal disease; bursal enlargment and yellow-greyish coloured in 35-day-old broiler with bursal disease (though duly vaccinated in 7 and 15 days, the second time with a "hot" vaccine. September 2012.
TitlePathological signs
CaptionInfectious bursal disease; bursal enlargment and yellow-greyish coloured in 35-day-old broiler with bursal disease (though duly vaccinated in 7 and 15 days, the second time with a "hot" vaccine. September 2012.
Copyright©Lucien Mahin (Lucyin)/via Wikimedia Commons - CC BY-SA 3.0
Infectious bursal disease; bursal enlargment and yellow-greyish coloured in 35-day-old broiler with bursal disease (though duly vaccinated in 7 and 15 days, the second time with a "hot" vaccine. September 2012.
Pathological signsInfectious bursal disease; bursal enlargment and yellow-greyish coloured in 35-day-old broiler with bursal disease (though duly vaccinated in 7 and 15 days, the second time with a "hot" vaccine. September 2012.©Lucien Mahin (Lucyin)/via Wikimedia Commons - CC BY-SA 3.0
IBD infection of 28 days old broiler with muscle haemorrhage.
CaptionIBD infection of 28 days old broiler with muscle haemorrhage.
CopyrightSri Poernomo
IBD infection of 28 days old broiler with muscle haemorrhage.
PathologyIBD infection of 28 days old broiler with muscle haemorrhage.Sri Poernomo
Infectious bursal disease; haemorrhages in proventriculus and gizzard. November 2007.
TitlePathological signs
CaptionInfectious bursal disease; haemorrhages in proventriculus and gizzard. November 2007.
Copyright©Lucien Mahin (Lucyin)/via Wikimedia Commons - CC BY-SA 3.0
Infectious bursal disease; haemorrhages in proventriculus and gizzard. November 2007.
Pathological signsInfectious bursal disease; haemorrhages in proventriculus and gizzard. November 2007.©Lucien Mahin (Lucyin)/via Wikimedia Commons - CC BY-SA 3.0
Infectious bursal disease; Urate precipitation on pericardis of broilers with infectious bursitis. July 2016.
TitlePathological signs
CaptionInfectious bursal disease; Urate precipitation on pericardis of broilers with infectious bursitis. July 2016.
Copyright©Lucien Mahin (Lucyin)/via Wikimedia Commons - CC BY-SA 3.0
Infectious bursal disease; Urate precipitation on pericardis of broilers with infectious bursitis. July 2016.
Pathological signsInfectious bursal disease; Urate precipitation on pericardis of broilers with infectious bursitis. July 2016.©Lucien Mahin (Lucyin)/via Wikimedia Commons - CC BY-SA 3.0


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Preferred Scientific Name

  • infectious bursal disease

International Common Names

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

English acronym

  • IBD


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Infectious bursal disease virus (IBDV), a double stranded RNA virus belonging to the genus Avibirnavirus and family Birnaviridae, is the causative agent of infectious bursal disease (IBD) (Luque et al., 2009). IBDV shows selective tropism for lymphoid tissues especially bursa of Fabricius and causes an acute and highly contagious viral disease which is manifested with inflammation and subsequently atrophy of the bursa of Fabricius, immunosuppression and various degrees of nephroso-nephritis in chickens between 3 weeks and 3 months of age (Berg, 2000; Eterradossi and Saif, 2008; Mahgoub, 2012; Müller 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. Economic losses are high and are manifested in two ways. First, in the case of classical IBD, because of high mortality in chickens of 3-6 weeks and prolonged immunosuppression leading to secondary infections and vaccination failures (Ingrao et al., 2013).

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, initially in Europe, and subsequently in Asia, the Middle East and South America. vvIBDV may cause acute disease in susceptible flocks over the entire growing period of broilers, in which the virus invades non-bursal and haematopoietic organs, such as the thymus, spleen and bone marrow. In many cases, the classical vaccines failed to provide sufficient protection against vvIBD (Fan et al., 2020). Thus novel vaccine technologies are being applied to design more effective vaccine and vaccination strategies against vvIBDV. 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 (Alkie and Rautenschlein, 2016).

The distribution section contains data from OIE's WAHIS database on disease occurrence. For more information from OIE, see the website:

Host Animals

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Animal nameContextLife stageSystem
Anser (geese)Domesticated hostPoultry|Young poultry
Gallus gallus domesticus (chickens)Domesticated hostPoultry|Young poultry
Muscovy duckDomesticated hostPoultry|Young poultry
NumidaDomesticated hostPoultry|Young poultry
Pekin duckDomesticated hostPoultry|Young poultry

Hosts/Species Affected

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Chickens, turkeys, ducks, pigeons and guinea fowl may be infected with IBDV, but clinical disease only occurs in chickens. Mortality is higher in lighter breeds than heavier breeds (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 cucullatus), pied cordon bleus (Uraeginthus bengalus), magpie geese (Anseranas semipalmata), shearwaters (Puffinus carneipes [Ardenna carneipes], P. pacificus [A. pacifica]), soothy terns (Sterna fuscata), common noddy (Anous stolidus), silver gulls (Larus novaehollandiae) and black ducks (Anas superciliosa) (Wilcox et al., 1983; McFerran, 1993).

Systems Affected

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multisystemic diseases of poultry


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Classical IBD viruses occur worldwide, with the probable exception for New Zealand (Lukert and Saif, 1991; McFerran, 1993; Becht, 1994). 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; Fabio 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 World Organisation for Animal Health (OIE) member countries (Berg, 2000).

For current information on disease incidence, see OIE's WAHIS database.

Distribution Table

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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 details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Last updated: 10 Dec 2021
Continent/Country/Region Distribution Last Reported Origin First Reported Invasive Reference Notes


Burkina FasoAbsentJul-Dec-2019
Cabo VerdeAbsentJul-Dec-2019
Central African RepublicAbsentJul-Dec-2019
Congo, Democratic Republic of theAbsentJul-Dec-2019
Côte d'IvoirePresent, LocalizedJul-Dec-2019
GabonAbsent, No presence record(s)
KenyaPresent, LocalizedJul-Dec-2019
Saint HelenaAbsent, No presence record(s)Jan-Jun-2019
São Tomé and PríncipePresentJul-Dec-2019
Sierra LeoneAbsentJan-Jun-2018
South AfricaPresentJul-Dec-2019


BhutanPresent, LocalizedJan-Jun-2020
ChinaPresent, LocalizedJul-Dec-2018
GeorgiaAbsent, No presence record(s)Jul-Dec-2019
Hong KongAbsentJul-Dec-2019
IndiaPresent, LocalizedJan-Jun-2019
IsraelPresent, LocalizedJul-Dec-2020
-Peninsular MalaysiaPresent, Serological evidence and/or isolation of the agent
MaldivesAbsent, No presence record(s)Jan-Jun-2019
MongoliaAbsent, No presence record(s)Jan-Jun-2019
PhilippinesPresent, LocalizedJul-Dec-2019
Saudi ArabiaAbsentJan-Jun-2020
South KoreaPresentJul-Dec-2019
Sri LankaPresentJul-Dec-2018
TajikistanAbsent, No presence record(s)
United Arab EmiratesAbsentJul-Dec-2020


Bosnia and HerzegovinaAbsentJul-Dec-2019
CroatiaAbsent, No presence record(s)
Faroe IslandsAbsent, No presence record(s)Jul-Dec-2018
FinlandAbsent, No presence record(s)
JerseyAbsent, No presence record(s)
LuxembourgAbsent, No presence record(s)
North MacedoniaPresentJul-Dec-2019
-Russia (Europe)Present, WidespreadOriginal citation: van den Berg (2000)
San MarinoAbsent, No presence record(s)Jan-Jun-2019
Serbia and MontenegroPresent
SpainPresent, LocalizedJul-Dec-2020
United KingdomPresentJul-Dec-2019
-Northern IrelandPresent

North America

AnguillaPresent, Widespread
BahamasAbsent, No presence record(s)Jul-Dec-2018
BermudaAbsent, No presence record(s)
British Virgin IslandsAbsent, No presence record(s)
Cayman IslandsAbsentJan-Jun-2019
Costa RicaPresentJul-Dec-2019
DominicaAbsent, No presence record(s)
Dominican RepublicPresentJan-Jun-2019
GreenlandAbsent, No presence record(s)Jul-Dec-2018
MexicoPresent, LocalizedJul-Dec-2019
Saint Kitts and NevisAbsent, No presence record(s)
Saint LuciaAbsentJul-Dec-2018
Saint Vincent and the GrenadinesAbsentJan-Jun-2019
Trinidad and TobagoAbsentJan-Jun-2018
United StatesPresentJul-Dec-2019


Federated States of MicronesiaAbsent, No presence record(s)Jan-Jun-2019
French PolynesiaPresentJan-Jun-2019
Marshall IslandsAbsent, No presence record(s)Jan-Jun-2019
New CaledoniaPresentJul-Dec-2019
New ZealandPresentJul-Dec-2020

South America

Falkland IslandsAbsent, No presence record(s)Jul-Dec-2019
French GuianaAbsentJul-Dec-2019
GuyanaPresent, LocalizedJul-Dec-2018


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Following oral infection, IBDV infects and replicates in immune cells including intestinal macrophages within gut-associated lymphoid organs within 4 h post infection, followed by primary viremia. The virus reaches the bursa of Fabricius at 11 hpi and then secondary viremia which results in spread of the virus to various tissues. Virus replication in the bursa, caecal tonsils and cecum can be detected several weeks post-infection. IBDV causes programmed cell death (apoptosis) in lymphoid cells and depletion of B lymphocytes which has a major role in IBDV pathogenesis and immunosuppression (Ingrao et al., 2013).

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). A high level of programmed cell death is observed in chicken peripheral blood lymphocytes or lymphoid organs infected with IBDV.

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 (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).


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In summary, the diagnosis can be achieved by observation of (1) clinical signs (2) gross pathological lesions in the cloacal bursa (3) microscopic analysis of the bursa for B cell depletion in the follicles (4) laboratory diagnosis using RT-PCR for detection of VP2 viral gene in bursa tissues (5) Sequence alignments and phylogenetic analysis of the VP2 region to characterize the isolated viruses into genogroups.

Clinical and gross pathological evaluation: 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; Berg, 2000).

Laboratory 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; Hernández et al., 2011; Tomás 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, however, this is not necessary for routine diagnosis. Bursal 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, the presence of IBDV antibodies could be determined using IBDV-specific commercially available ELISAs (Becht, 1994). The presence of IBDV antibodies in chicks is not always an indication of infection because most young chicks have maternal antibodies. ELISA is mainly used to evaluate the flock immunity (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). Another serological method is virus neutralization test (VNT) which can differentiate between serotype 1 and 2 of IBDV strains. Given the antigenic variation between the IBDV strains, the reference strain used in the VNT is of utmost importance (Jackwood et al., 2004).

List of Symptoms/Signs

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SignLife StagesType
Digestive Signs / Diarrhoea Poultry|Young poultry Sign
General Signs / Dehydration Poultry|Young poultry Sign
General Signs / Discomfort, restlessness in birds Poultry|Young poultry Sign
General Signs / Inability to stand, downer, prostration Poultry|Young poultry Sign
General Signs / Sudden death, found dead Poultry|Young poultry Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Poultry|Young poultry Sign
Skin / Integumentary Signs / Ruffled, ruffling of the feathers Poultry|Young poultry Sign

Disease Course

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The incubation period of IBDV is generally 2-3 days, by which time the infected chickens show clinical signs including distress, depression, ruffled feathers, anorexia, diarrhoea, trembling, dehydration and death. Morbidity may approach 100%, while mortality is usually low, but some very virulent strains are capable of causing 90%. The most severe clinical manifestations are seen in chicks of 3 to 6 weeks of age, when the bursa of Fabricius approaches its maximal stage of development. Maternal antibodies provide a level of protection in chickens up to 14 days of age, while infected chickens more than 6 weeks old rarely show clinical signs of IBD (Mahgoub, 2012).

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

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

IBDV targets B lymphocytes and induces programmed cell death in the infected cells, leading to atrophy of lymphoid tissues and immunosuppression. Impairment of immune system cells increases susceptibility to secondary bacterial and viral infections. It has been shown that the lack of adequate IgA- and IgG-associated antibody production in IBDV-infected chickens may be involved in the increased susceptibility to secondary infection (Thompson et al., 1997).

Specifically, the infected chickens commonly develop secondary respiratory tract with Escherichia coli, resulting in significant economic losses. In addition, an increased severity of bacterial infection in gastrointestinal tract of IBDV infected chicken with immunosuppression are reported. For example, an exacerbated Salmonella multi-organ colonization, pathogenicity, faecal shedding and persistence are reported in chickens exposed to infections at early ages (Barrow et al., 2012; Pan and Yu, 2014). IBDV-induced immunosuppression can also exacerbate Campylobacter jejuni colonization and shedding in chickens (Subler et al., 2006).

IBDV alone markedly reduces opsonizing ability of antibodies, and this effect is significantly exacerbated by IBV infection (Naqi et al., 2001).


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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 Allan 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 (Berg, 2000).

Impact: Economic

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Early subclinical infections have the greatest economic impact in the poultry industry as they cause severe, long-lasting immunosuppression due to destruction of immature lymphocytes in the bursa of Fabricius, thymus and spleen. The humoral immunity is most severely affected; and thus, the infected chickens do not respond well to vaccination and are predisposed to infections with even non-pathogenic avian bacteria or viruses. In addition, clinical infections can reduce growth and causes mortality resulting in severe economic impact. Being resistant to most of the disinfectants and environmental factors, the poultry house remains contaminated with IBDV that persists on the premises and tends to reappear in subsequent flocks (Dey et al., 2019). 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 (Berg, 2000). In 80% of the OIE member countries, acute clinical disease due to IBDV has been reported (Berg, 2000).

Zoonoses and Food Safety

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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).

Disease Treatment

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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.

Prevention and Control

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Management procedures

Disease prevention aims at prevention of infection by strict hygiene measures and vaccination. 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).


The control of IBD is largely dependent upon the use of effective vaccines and vaccination strategies resulting in protection against the disease. Humoral immunity has a major role in protection against IBD. Indeed, there is a close correlation between neutralizing antibody titres and protection against the disease. To induce high levels of maternal antibodies in the progeny, parent stocks are usually vaccinated between 4 and 10 weeks of age with live vaccine and again at approximately 16 weeks with inactivated oil-adjuvanted vaccine. Maternal antibody provides protection in young chicks, and this depends on antibody titre. Therefore, determination of antibody titre in chicks is important for planning an effective vaccination strategies as maternal antibodies can interfere with vaccination.

Another consideration in vaccine development against IBV is point mutations and recombination events, which have led to the antigenic drift and antigenic variation in IBDV strains. Thus, selecting an effective vaccine has become critical to controlling IBDV strains which have undergone antigenic divergence. Because of antigenic drift in different geographical sites, development of a universal IBDV vaccine which can be used worldwide is impractical (Hon et al., 2008; Jackwood and Sommer-Wagner, 2011; Jackwood, 2012).

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; 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). However, maternal antibody can interfere with the replication of live attenuated vaccines. If the vaccines are administered too early, the vaccine virus will not replicate effectively, while if it is administered too late, the birds will become vulnerable to virulent IBDV (Mahgoub, 2012). Therefore, 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).

The reverse genetics (RG) system opens a new avenue for the development of IBDV live attenuated vaccines which are highly immunogenic while the resulting live attenuated vaccine have low chance of revert phenotype. Several recombinant attenuated IBDV have been rescued and characterized for live attenuated vaccine purpose. Rational attenuation strategies using RG may lead to a new generation of safer, more widely applicable live attenuated vaccines for IBDV (Yang et al., 2020).

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 production of IBDV recombinant protein subunits in heterologous expression systems such as plants, yeast, bacteria and insect cells. Other vaccines include DNA vaccines; immune complex vaccines (Icx), viral like particles and live viral vector vaccines. All these have been reviewed by Müller et al. (2012).

An Icx vaccine comprises live pathogenic IBDV mixed with anti-IBDV antibodies derived from hyperimmunized chickens. It can be administered subcutaneously 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; Iván 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. Unlike live IBDV vaccines, HVT vaccines do not cause immunosuppression and these vaccines are not interfered by maternally-derived antibody. HVT-VP2 vaccines, depending on the manufacturer, can be applied in ovo or subcutaneously in day-old chicks. A single injection of HVT based vaccine, which is not influenced by MDA, induces protection in 1-day. However, the main limitation to its wide use is the need of cold storage in liquid nitrogen, which increases the cost of vaccinations (Bublot et al., 2007; Gros et al., 2009; Perozo et al., 2009; Jackwood, 2017; Rage et al., 2020).


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African Union-Interafrican Bureau for Animal Resources, 2011. Pan African animal health yearbook 2011, Nairobi, Kenya: African Union Inter-African Bureau for Animal Resources (AU-IBAR) 2011: xiii + 90 pp.

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Distribution References

CABI, Undated. Compendium record. Wallingford, UK: CABI

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OIE Manual of Diagnostic Tests and Vaccines for Terrestrial Animals Manual of Diagnostic Tests and Vaccines for Terrestrial Animals (Terrestrial Manual) aims to facilitate international trade in animals and animal products and to contribute to the improvement of animal health services world-wide. The principal target readership is laboratories carrying out veterinary diagnostic tests and surveillance, plus vaccine manufacturers and regulatory authorities in Member Countries. The objective is to provide internationally agreed diagnostic laboratory methods and requirements for the production and control of vaccines and other biological products.

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