Host response to Eimeria infections

Abstract

The protozoan parasite Eimeria is responsible for the disease coccidiosis and has a worldwide distribution. Intestinal Eimeria infections are the dominating class of diseases in poultry causing great economical damage and considerably affecting animal welfare. In the Netherlands in chickens raised for meat (broilers) the three most diagnosed coccidiosis infections are E.acervulina, E.maxima and E. tenella. After recovery of primary infections, chickens generate protective immune responses and can even develop a full protective immunity to homologous re-infections. The work presented in this thesis is part of a joint research program. The goal of this program was to link insight into the within-animal dynamics with insight into the between-animal transmission of Eimeria parasites of poultry. We want to investigate how these two processes interact to determine the infection dynamics within flocks and between subsequent flocks, thus being able to develop intervention methods. In this thesis we investigated a selection of factors that may influence the development of the host-pathogen interactions and therefore modulate the response of the host to the Eimeria infection; the factors that we investigated were: number of parasites in a single primary infection, different Eimeria species, genetic background of the broilers, age of the host and the effect of a preceding infection. In our experiments, we analysed the immune response of the host. As immune parameters we used T-cell population analysis in the intestine, and cytokine mRNA expression levels in the intestine. A species-specific real-time PCR was used to quantify total amount of Eimeria DNA in the intestine. Summarizing all the experiments described in this thesis, all tested variables: amount of parasites, Eimeria species, genetic background of the broilers, age of the host and the effect of a preceding infection, had an influence on the host immune reaction. Though all factors investigated influenced the host response to Eimeria infections, some general principles could be identified. An Eimeria infection induces a typical biphasic response consisting of an early and a late response. The bi-phasic responses to the Eimeria infections have a Th1 reaction profile. Though host responses to a primary infection became more Th1 biased as hosts increased in age, the primary response did not correlate with protection to a re-infection. Increased capacity to mount a Th1 type of reaction to a primary infection with E.maxima did not result in a decreased amount of excretion of parasites or in an increased protection to re-infection. Finally, a low responsiveness to re-infection was found in animals that received a homologous E.maxima or E.acervulina challenge. No T-cell subsets were identified specifically playing a role in protection to re-infection. The reaction to a primary infection is diverse and robust, but the reaction to a secondary response is more subdued. A small subset of a measured cell types might be responsible for protection to re-infection. New cell type markers might reveal the cells responsible. Next to this a pathway analysis of the data generated with a micro-array might provide new information to our work.