Abstract

Coccidiosis, caused by Eimeria spp. presents a self-limiting intestinal infection of poultry. Intestinal replication of the parasite causes severe morphological alterations to the host gastrointestinal tract, marked, among others, by the disruption of the intestinal barrier. We have previously reported a significant reduction in merozoite replication and oocyst shedding in E. tenella in vitro and in vivo. The objective of this study was to investigate the pathogenesis of E. maxima infection in broiler chickens under heat stress (HS) and mRNA expression of host cytokines that might affect the curtailed development of the parasite. We herein demonstrate that there is a significant detrimental effect of HS on the pathogenesis of E. maxima infection in broilers. There was a restricted replication of the parasite in HS chickens evidenced by significantly reduced oocyst shedding and disruption of the intestinal blood barrier. Gene expression of parasite genes demonstrated curtailed sexual reproduction of E. maxima in HS chickens. There was downregulation of Eimeria spp. genes related to gamete fusion, oocyst shedding, mitosis and spermiogenesis. Host gene expression indicates alterations in the cytokine expression that could be related to reduced parasite development in vivo.

Highlights

  • Coccidiosis, caused by Eimeria spp. presents a self-limiting intestinal infection of poultry

  • Between 7 and 14 dpi (14–21 days of age), TNi chickens showed an overall tendency to recover from infection faster, as demonstrated by higher Body weight (BW), feed intake (FI) and Relative growth (RG) as compared to HSi chickens

  • We demonstrate that heat stress (HS) by itself exerts severe detrimental effects for poultry production, independent of coccidiosis infection, such as lower development and weight gain

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Summary

Introduction

Coccidiosis, caused by Eimeria spp. presents a self-limiting intestinal infection of poultry. The objective of this study was to investigate the pathogenesis of E. maxima infection in broiler chickens under heat stress (HS) and mRNA expression of host cytokines that might affect the curtailed development of the parasite. The objective of this study was to investigate the effect of HS on the pathogenesis of E. maxima infection in broilers, as well as differential expression of host cytokines that might affect the curtailed development of the parasite. Together, these data indicate that HS of the host significantly reduces the sexual stages of E. maxima in vivo. We provide information on the relevance of HS control in the host response of birds for animal welfare and health, and for their response to pathogens

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