Abstract

BackgroundCoccidiosis is a major contributor to losses in poultry production. With emerging constraints on the use of in-feed prophylactic anticoccidial drugs and the relatively high costs of effective vaccines, there are commercial incentives to breed chickens with greater resistance to this important production disease. To identify phenotypic biomarkers that are associated with the production impacts of coccidiosis, and to assess their covariance and heritability, 942 Cobb500 commercial broilers were subjected to a defined challenge with Eimeria tenella (Houghton). Three traits were measured: weight gain (WG) during the period of infection, caecal lesion score (CLS) post mortem, and the level of a serum biomarker of intestinal inflammation, i.e. circulating interleukin 10 (IL-10), measured at the height of the infection.ResultsPhenotypic analysis of the challenged chicken cohort revealed a significant positive correlation between CLS and IL-10, with significant negative correlations of both these traits with WG. Eigenanalysis of phenotypic covariances between measured traits revealed three distinct eigenvectors. Trait weightings of the first eigenvector, (EV1, eigenvalue = 59%), were biologically interpreted as representing a response of birds that were susceptible to infection, with low WG, high CLS and high IL-10. Similarly, the second eigenvector represented infection resilience/resistance (EV2, 22%; high WG, low CLS and high IL-10), and the third eigenvector tolerance (EV3, 19%; high WG, high CLS and low IL-10), respectively. Genome-wide association studies (GWAS) identified two SNPs that were associated with WG at the suggestive level.ConclusionsEigenanalysis separated the phenotypic impact of a defined challenge with E. tenella on WG, caecal inflammation/pathology, and production of IL-10 into three major eigenvectors, indicating that the susceptibility-resistance axis is not a single continuous quantitative trait. The SNPs identified by the GWAS for body weight were located in close proximity to two genes that are involved in innate immunity (FAM96B and RRAD).

Highlights

  • Coccidiosis is a major contributor to losses in poultry production

  • Eigenanalysis separated the phenotypic impact of a defined challenge with E. tenella on weight gain (WG), caecal inflammation/pathology, and production of interleukin 10 (IL-10) into three major eigenvectors, indicating that the susceptibilityresistance axis is not a single continuous quantitative trait

  • The SNPs identified by the genome-wide association study (GWAS) for body weight were located in close proximity to two genes that are involved in innate immunity (FAM96B and RRAD)

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Summary

Introduction

Coccidiosis is a major contributor to losses in poultry production. With emerging constraints on the use of in-feed prophylactic anticoccidial drugs and the relatively high costs of effective vaccines, there are commercial incentives to breed chickens with greater resistance to this important production disease. Seven species of Eimeria (Apicomplexa, Coccidia) are responsible for the debilitating and sometimes fatal disease coccidiosis that is estimated to cost the international poultry industry around US$3 billion per year, mainly due to reduced productivity and the cost of Boulton et al Genet Sel Evol (2018) 50:63 of traits that may contribute towards selective breeding of chickens to control the consequences of coccidiosis is of great importance to industry. Some native chicken breeds, such as the Egyptian Fayoumi, appear to tolerate the pathological impacts of Eimeria infection [12, 13], while distinct inbred lines of White Leghorn chickens support variable levels of parasite replication by different Eimeria species [14]. Definitions of the immune categories used in this study are presented in Fig. 1 [4, 7, 11, 17, 18]

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