Maternally Derived Antibodies: An Overview of Their Role in Infectious Bursal Disease of Chickens

Orakpoghenor O, Markus TP, Abdu PA, Woziri OA and Andamin AD

Published on: 2023-01-28


The high susceptibility of neonates to diseases in early life due to their undeveloped immune system has necessitated the need for protection provided by the dam in the form of maternally derived antibodies (MDA). Maternally derived antibodies are produced by natural infection or active immunization of the dams and they consist mainly of immunoglobulin G (IgG) in mammals and IgY in birds. In avian species, MDA are transferred from the dam to the chicks via the egg yolk thus forming the basis for protection against avian diseases. Attempts made to curb the economic losses resulting from infectious bursal disease (IBD) in poultry involved immunization of breeders using IBDV vaccine to generate MDA transferred to the chicks. The extent to which the chicks are protected from IBD depends on their MDA titres determined by the immunization program of the breeders. Infectious bursal disease MDA titre above 396 (as determined by ELISA) is generally considered protective for the disease. The IBD MDA decays in a linear pattern and rate of decay is dependent on the type of bird. Despite the benefit of MDA against IBD in chicks, complete protection is not guaranteed evident by IBD outbreaks in chicks with adequate MDA levels. Maternally derived antibodies against IBD could pose risk to the chicks by possible neutralization during early infection or vaccination. Hence, this review focused on the dynamics, transfer and significance of MDA, their relationships in IBD as it related to interference with vaccination and the breakthrough MDA titres for IBD virus strains and vaccines.


Maternally derived antibodies; Immunoglobulin; Infectious bursal disease; Immunization; Neutralization; Breakthrough


Due to the rudimentary immune defence in vertebrate neonates, protection against infection by maternally derived antibodies (MDAs) transfer is highly significant [1,2]. Maternally derived antibodies are antibodies usually produced in the dam and can confer acquired immunity in neonates when transferred [3]. These antibodies are produced in the dam’s humoral immune system following induction by natural infection or active immunization [4]. Studies have shown that immunoglobulin G (IgG) isotype constitutes majority of MDA and sometimes IgA contained in breast milk of mammals [1,5]. In avian species, IgY, which is a functional homolog of mammalian IgG, occurs in high concentrations although IgA and IgM have been detected at low amounts in the yolk sac [6,7].

Infectious bursal disease (IBD), also called Gumboro, is a highly infectious and economically important disease of poultry [8]. The disease is caused by a bisegmented, nonenveloped RNA virus belonging to the family Birnaviridae, genus Avibirnavirus [9]. The virus has tropism for actively dividing precursor B lymphocytes, primarily in the BF, but other immune organs are also affected [10,11]. Infectious bursal disease virus affects young birds, with chickens 3- to 6-week-old reported to be more susceptible [12]. The disease has been documented to be controlled by immunization of breeders which then transfer MDA to the chicks [13].

Dynamics of Maternally Derived Antibodies

Maternal antibodies enhance the neonatal responses against pathogens prior to maturation of their immune system and commencement of endogenous antibody production [14,15]. The age at which neonatal endogenous antibody production begins and MDA disappears have been reported to vary with species [16].  This could take several weeks in poultry and rodents, and several months in humans as documented by several researchers [2,17-19]. However, increased levels of MDA within 10-14 days post-hatch in some birds have been documented [19]. Disappearance of most MDA in birds occurs within 5-14 days [18], and due to lactation prolonged to 5-10 weeks in rodents [16,20] and approximately 9 months in humans [2]. Hence, the protection provided by MDA is short-lived since these antibodies are continuously catabolized [21].

Transfer of Maternally Derived Antibodies

In mammals, MDAs have been reported to be transferred to neonates via the placenta pre-natal and in the intestine from colostrum within the first 24 hours post-natal [2,3,22]. Maternal antibody transfer via the egg yolk to the offspring has been demonstrated in birds, reptiles and ?shes [1,16,23,24]. The types and amounts of MDA in neonates reflect the level of antibodies present in the dams and are directly related to the prevailing pathogens in that environment [25-27]. So, neonates can only get MDA against pathogens that the dam has previously been exposed to during her lifetime [1,28].

In chickens, transfer of MDA occurs during oogenesis and the mechanism involves movement of antibodies into the yolk across the follicular epithelium in the hen [29,30]. This transfer of MDA is achieved by attachment of IgY in maternal circulation to IgY receptors (IgY-Fc) present in the ovarian follicles [29,31]. This is followed by migration of the absorbed IgY from the egg yolk to the embryonic circulation via attachment to characterized receptors (FcRY, a phospoholipase A2 receptor homolog) on the yolk sac membrane [15,32] (Figure 1). Previous studies have shown that the movement of IgY into embryonic circulation from the egg yolk across the yolk sac occurs at a slow rate from embryonic day 7, and begins to increase by day 14 up to day 19-21 [33,34]. However, the levels of IgY transferred to the egg yolk and to the hatchlings have been reported to be directly proportional to serum IgY concentrations of the hen [35,36]. Although low concentration of IgM is also absorbed from the yolk sac, there is limited information on IgA transfer into hatchlings’ circulation from the egg yolk [30]. Maternal antibodies are catabolized by the developing chick, and the rate of loss is thought to be tied to developmental rate, with fast-developing species catabolizing maternal antibodies more rapidly than slowly developing species [16].

Figure 1: Flow chart showing the transfer of maternal antibody (IgY) from hen to the chick.

Significance of Maternally Derived Antibodies

Development of the immune system involves the immature stage in early life, followed by a period of maturation and final maturation [2]. In the immature stage, there is relatively high level of MDA which tend to decline as the immune system continues to mature [16,17]. Maturation of the immune system is achieved by priming effect on development and activation of B- and T-cells [2]. The period of maturation of the immune system has been reported to vary with species of animal ranging from 2-6 months in chickens, 6-7 weeks mallards ducks and macaws, greater than 2 weeks rodents and 1-2 years humans [16,37]. The benefits of MDA in neonates thus include improvement of immunity, decreasing challenge to acute phase responses, and increase in growth rate [38-40]. However, in domestic poultry, the benefits of MDA is directed towards providing immunity with insignificant nutritional role and this results in remarkably low levels of MDA in avian eggs [18,40,41].

There is some evidence regarding the positive effect of MDA on development of immune system through immunological imprinting [18]. Although the exact mechanism is still unclear, however, it has been reported that the B-cell repertoire may somehow model itself after antibodies in circulation [2]. Also, it has been suggested that the immunization of offsprings with the same antigen to which dams have been exposed does not lead to a strong innate immune response due to the presence of maternally-derived antigen-specific antibodies that had been passively transferred to the progenies [15]. In addition, MDAs persist for a longer period of time in chicks when initial maternal antibody levels are high [15]. The capacity for short-term passive protection is thus determined by the amount of antibody transferred from the mother to her offspring and the length of time the antibodies persist in the offspring. In addition to short-term passive protection against infection, MDAs can help prime the offspring’s immune system for future antigen exposure [18,42]. Immunological priming results in a more robust specific response [43] and/or a stronger nonspecific response [16]. Similarly, there is accumulating evidence that lack of MDAs has long-lasting negative impacts on the offsprings [44].

Despite the benefits of MDA in neonates, they have been reported to impact negative effects such as interference with vaccination, compromising immune development and triggering of autoimmune disorders [42,45,46]. The compromise of development of the immune system involves destructive priming effect, blocking and inactivation of B- and T-cells [25]. Following final maturation of the immune system, MDA have no positive effects on endogenous immunity as they continuously undergo catabolism [43,44,47]. The immunosuppressive effect of MDA on post-vaccine antibody-mediated immune response has been attributed to neutralization of vaccine virus by MDA. Maternal antibodies can also block or suppress antibody production in the offspring [19]. The degree of endogenous antibody suppression is thought to be dependent on the amount of maternal antibody transferred to the offspring as well as on the amount of antigen the offspring is exposed to [19].

Maternally Derived Antibodies and Infectious Bursal Disease

Globally, IBD has been reported to cause severe economic losses in the poultry industry resulting from high morbidity and mortality, decreased production and immunosuppression [48-50]. The control of IBD in farms has been focused on strict hygienic practices and adequate immunization of breeder flock and chicks [8,51].

The immunization of breeders has been achieved by the use of live attenuated or inactivated IBDV vaccines after which the induced antibodies (MDA) are transferred via the egg yolk to the chicks. These transferred IBDV MDA now form the basis for protection of newly hatched chicks from morbidity and mortality due to IBD in their early life [52-54]. The IBDV vaccines that have been developed include live (mild, intermediate and intermediate plus/hot), killed, non-replicative (DNA and subunit), replication-competent (viral vectors) and immune complex vaccines [55-57].

Decay of Infectious Bursal Disease Maternally Derived Antibodies

The decay time of IBD maternal antibodies is helpful in determining the appropriate time to vaccinate chicks so as to minimize chicks’ susceptibility to the disease [58,59]. The time of vaccination has been reported to vary depending on the level of MDA, route of vaccination and virulence of the vaccine virus [60-62]. The MDA level against IBD is in turn dependent on the immunization protocol and type of vaccine used in breeder flock [35,63,64]. Infectious bursal disease MDA level is said to be protective in chicks when the titre is greater than 396 using indirect enzyme linked immunosorbent assay (IELISA) [65].

The decay pattern of MDA is dependent on the type of chickens (related to metabolism and growth rates) and antibody status of breeders from which the progeny were derived [66]. Evidences of half-life estimates from several studies have shown that IBD MDA decay pattern appear to be linear. Using virus neutralisation (VN) test, half-life of 3 to 3.5 days for broilers, 4.5 days for breeders and about 5.5 days for layers, have been documented [55]. From studies of MDA half-life estimates using ELISA, 3-8 days was reported for white leghorn [67] and 5 days for broiler chickens [66,68]. In unvaccinated chicks, persistence of MDA for up to 21 days with complete decay by 28 and 35 days has been documented [69]. Maternal antibody protective level has been reported to last 1-3 weeks, but this could be extended to 4-5 weeks following immunization of breeders using oil-adjuvant vaccines [70,71].

Increased level of IBDV MDA post-hatching has been achieved through priming of breeders with live attenuated virus vaccine at 8-12 weeks of age and boosting with inactivated oil-emulsion vaccine at 20-21 weeks [54,67,71]. Infection bursal disease vaccine virus has been reported to show no effect on the decay rates of IBDV MDA evidenced by lack of difference in rate of MDA depletion in unvaccinated and IBDV-vaccinated chicks [52,72]. However, booster vaccination using inactivated oil-emulsion IBD vaccine has been reported to enhance higher immune response in hens, and consequently prolonged MDA persistence in their progeny [73].

Maternally Derived Antibodies In Infectious Bursal Disease Virus Infection

Due to the importance of MDA, their varying roles in providing protection against IBDV infection have been reported by several researchers. Since the BF is the primary target of the virus, the protection of the BF against lesions of IBD by MDA becomes necessary [74]. High initial MDA levels were reported to protect chicks against IBDV infection. At low initial level, MDA was unable to prevent bursal lesions though mortalities were decreased or prevented thus may not prevent immunosuppression [75]. In chickens with medium level of MDA, evidence of IBDV infection has been detected from 2 weeks of age, but from 5 weeks of age in chickens with high MDA level (> 4000) [35]. Chance of infection within 15-20 days in broilers has been suggested resulting from significant decline in MDA below protective level hence, the need for vaccination [66].

Interference of Maternally Derived Antibodies with Infectious Bursal Disease Vaccines

The susceptibility of chickens to IBDV is highest during their first few weeks of life hence early induction of active immunity to the virus after hatching is necessary [55]. Several studies have demonstrated whether or not the presence of MDA interferes with responses of chickens to vaccination against IBD. Alam et al. [66] and Wood et al. [75] showed that high and low initial levels of MDA produce no immune response at 1 and 14 days of age but observed better immunization by day 28 irrespective of initial MDA levels following revaccination. Outbreaks of IBD have been reported in flocks with MDA following vaccination before 10 days of age [76]. Maternal antibody interference with IBDV vaccination for up to 21 days has been demonstrated in chicks [77]. In a study involving observation of bursal lesions, vaccination could not provide protection against challenge in chicks having MDA [78,79]. Also, maternal antibodies have been shown to inhibit milder IBDV vaccine [80,81]. This suggests that following vaccination of chicks with adequate MDA (> 396), the vaccine virus replication is significantly ceased or delayed leading to decreased onset of active immunity [59,82,83].

A proposed mechanism of MDA interference in IBDV vaccination involves partial or complete neutralization of IBD vaccine virus by MDA [53,66,84]. Despite the significant roles of MDA, there seems to be interference with vaccination. Generally, live IBD vaccines tend to be neutralized by MDA while the others evade neutralization by MDA. Although studies have associated high MDA level with neutralization of IBDV vaccines when administered to day-old chicks, there has been speculation of complex formation between vaccine virus and MDA [83].

Mild IBD vaccine virus tends to be neutralized by high level of MDA during the early life [80,85] and so their use for initial vaccination of chicks is often discouraged [86]. The intermediate and intermediate plus vaccine virus though capable of being neutralized by MDA, stimulate the development of active immunity in chickens thus providing protection against challenge by field IBDV [80,83]. Despite the stimulatory role of intermediate IBDV live vaccines, they have been reported to be less effective in inducing IBDV antibody following oral or ocular administration to day-old chicks having high MDA levels [84]. The efficacy of DNA vaccines has been suggested to be affected by presence of MDA hence, MDA interference need to be overcome by high dose of the vaccine to ensure adequate immune response in chickens [87]. There is less interference of IBD MDA with recombinant viral vectors and so such vaccines could evade possible neutralization by the MDA [86].

Breakthrough MDA Titre for Infectious Bursal Disease Virus And Vaccines

Breakthrough titre is the amount of MDA that can be overwhelmed by a virus or vaccine to stimulate infection or active immunity respectively [88,89]. The breakthrough VN titre documented for classical (Faragher 52/70) and very virulent (D6948) IBDV strains were 6log2 and 8log2 [90]. The breakthrough VN titre established for IBDV live vaccines are ≤ 4log2 (ELISA (IDEXX standard) titre 100) for mild, ≤ 6log2 (ELISA (IDEXX standard) titre 125) for intermediate and ≤ 8log2 (ELISA (IDEXX standard) titre 500) for intermediate plus/hot vaccines [55]. Efficacy study using V877-based IBD vaccine (intermediate plus) in broilers having varying levels of MDA has shown breakthrough titres greater than 1100 as determined by ELISA [89]. IBD vaccines with high breakthrough MDA titres have often been considered to present lower safety profile due to their ability to induce bursal lesions and consequent immunosuppression [85,89].


Maternally derived antibodies are important in providing protection to neonates against certain diseases in early life. In chickens, the decay of IBD MDA varies between types of chicken and provides protection against IBD. The MDA also interferes with vaccination so knowledge of their decay rates and prior levels are essential for the development of an effective vaccination strategy.

Disclosure Statement

The authors declare no potential conflict of interest.


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