Genetic basis of disease resistance to coccidiosis and necrotic enteritis in chickens

The chicken has served as a valuable model organism for studying various biological systems, including the development and delineation of the various arms of the immune system. Central to more recent discoveries have been the characterization of the major histocompatibility complex (MHC) and the sequencing of the chicken genome. Even prior to those events, disease resistance in poultry had been linked to bird genetics, particularly in the context of the MHC and other alloantigen systems. Disease outbreaks pose significant challenges across the global poultry industry. Enteric challenges such as avian coccidiosis and its 'sidekick' necrotic enteritis (NE) are two critical diseases affecting chickens and threatening sustainable poultry production. As early as the 1950's, scientists documented the role of genetic components in resistance and susceptibility to coccidiosis in chickens. Later studies with various chicken lines reported that specific MHC-B haplotypes were associated with either resistance or susceptibility to coccidiosis. In response to a mixed Eimeria spp. infection, we found that the MHC B21 haplotype was associated with improved feed conversion and increased severity of coccidiosis lesions. Further, those studies assessed the association between haplotypes of the alloantigen systems A, D, E, and I with resistance or susceptibility to mixed Eimeria infection. The E-H02/H02 genotype exhibited the lowest lesion scores in the duodenum compared to other genotypes of the E alloantigen system. Similarly, the I-H01 and I-H03 haplotypes showed positive and negative associations, respectively, with jejunal and cecal gross lesions showing improved resistance to this mixed Eimeria infection model. Other studies investigating similar associations influencing birds' responses to NE highlighted the importance of host genetics in resistance to this impactful enteric disease. Yet, much of the research focused on phenotypic outcomes among different genetic lines without in-depth characterization of the specific genotypic variations. Therefore, upcoming research could utilize the genetic markers linked to responses to coccidiosis to investigate their involvement in NE and any potential resistance in the context of host genetics.