Abstract

Eimeria species cause the intestinal disease coccidiosis, most notably in poultry. While the direct impact of coccidiosis on animal health and welfare is clear, its influence on the enteric microbiota and by-stander effects on chicken health and production remains largely unknown, with the possible exception of Clostridium perfringens (necrotic enteritis). This study evaluated the composition and structure of the caecal microbiome in the presence or absence of a defined Eimeria tenella challenge infection in Cobb500 broiler chickens using 16S rRNA amplicon sequencing. The severity of clinical coccidiosis in individual chickens was quantified by caecal lesion scoring and microbial changes associated with different lesion scores identified. Following E. tenella infection the diversity of taxa within the caecal microbiome remained largely stable. However, infection induced significant changes in the abundance of some microbial taxa. The greatest changes were detected in birds displaying severe caecal pathology; taxa belonging to the order Enterobacteriaceae were increased, while taxa from Bacillales and Lactobacillales were decreased with the changes correlated with lesion severity. Significantly different profiles were also detected in infected birds which remained asymptomatic (lesion score 0), with taxa belonging to the genera Bacteroides decreased and Lactobacillus increased. Many differential taxa from the order Clostridiales were identified, with some increasing and others decreasing in abundance in Eimeria-infected animals. The results support the view that caecal microbiome dysbiosis associated with Eimeria infection contributes to disease pathology, and could be a target for intervention to mitigate the impact of coccidiosis on poultry productivity and welfare. This work highlights that E. tenella infection has a significant impact on the abundance of some caecal bacteria with notable differences detected between lesion score categories emphasising the importance of accounting for differences in caecal lesions when investigating the relationship between E. tenella and the poultry intestinal microbiome.

Highlights

  • Over the last 20 years global poultry production has tripled with approximately 90 million tonnes of chicken meat and 1.1 trillion eggs produced every year [1]

  • Research investigating the effect that Eimeria has on the caecal microbiome of poultry is sparse, and to our knowledge this study is the first to analyse the microbiome according to severity of caecal lesions, following exposure to a defined high dose of a single Eimeria species

  • Similar results were obtained when each individual symptomatic group was compared to LS 0 samples, with increasing numbers of differential operational taxonomic units (OTUs) as lesion score severity increased. These results indicate that OTUs belonging to these two genera may play a pivotal role in susceptibility or resistance to E. tenella infection

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Summary

Introduction

Over the last 20 years global poultry production has tripled with approximately 90 million tonnes of chicken meat and 1.1 trillion eggs produced every year (http://www.fao.org/ faostat/) [1]. Further global expansion is predicted, most notably in Africa and Asia [2], emphasising the importance to food security of effective control against poultry pathogens including the protozoan Eimeria species. Members of the phylum Apicomplexa, these parasites can cause the intestinal disease coccidiosis in many animals including poultry. Seven species infect the domestic chicken (Gallus gallus domesticus) causing malabsorptive (Eimeria acervulina, E. maxima, E. mitis, E. praecox) or haemorrhagic (E. brunetti, E. necatrix, E. tenella) enteritis, with species-specific sites of development and foci of pathology within the intestinal tract [3]. E. acervulina, E. maxima and E. tenella are most frequently found in intensively reared chickens and the latter is highly pathogenic [4,5,6]. The presence of Eimeria species can exacerbate the outcome of co-infection with bacterial pathogens such as C. perfringens (contributing to necrotic enteritis) or Salmonella enterica serovars Enteritidis or Typhimurium [14,15,16]

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