Characterization of immune response to Eimeria tenella antigens in a natural immunity model with hosts which differ serologically at the B locus of the major histocompatibility complex

Abstract

A model to simulate natural immunity to Eimeria tenella was developed in three chicken lines which differ at the B locus of the major histocompatibility complex. Homozygous, 1-day-old chicks of the B 19 B 19 , B 24 B 24 , or B 30 B 30 genotype were trickle immunized by being orally fed a small infectious dose of E. tenella oocysts for 5 consecutive days. These naturally exposed birds were then challenged at different times between 5 and 24 days after the final dose, and the level of protection was assessed 6 days after challenge, using body weight gain and intestinal lesion scores. The duration of immunity in naturally exposed birds differed among the major histocompatibility complex lines. Trickle immunization of the B 19 B 19 haplotype afforded the longest and strongest level of protection compared to the other two haplotypes tested. In addition, in vitro splenic and peripheral blood lymphocyte proliferative responses in trickle-immunized birds were measured against sporozoite, merozoite, and tissue culture-derived E. tenella parasite antigens isolated from the recently described SB-CEV-1/F7 established cell line. The lymphocytes obtained from B 19 B 19 birds trickle immunized responded in vitro to the E. tenella-infected SB-CEV-1/F7 tissue culture-derived parasite antigen. Furthermore, antigen-specific immune responses appeared earlier in immune, challenged B 19 B 19 birds than in their naive, challenged counterparts. The development of a model simulating natural immunization will serve as a foundation to further characterize both humoral and cell-mediated responses to E. tenella tissue culture-derived parasite antigens and to better understand host protective immune responses to avian coccidiosis.

Poultry Coccidiosis: Design and Interpretation of Vaccine Studies

“…Infection with each species induces a robust protective immune response against homologous challenge (7). However, the numbers of parasites and rounds of infection required to induce immunity that is sufficient to protect against disease varies depending on the infecting Eimeria species, dosing schedule and chicken breed (7)(8)(9)(10). There is little or no immune protection against challenge infection with a heterologous species, and in some cases even infection with a different strain of the same species can escape immune protection (11,12).…”

Eimeria falciformisBayerHaberkorn1970 and novel wild derived isolates from house mice: differences in parasite lifecycle, pathogenicity and host immune reactions

“…Infection causes damage in the intestinal mucosa resulting in malabsorption of nutrients and weight loss (Haberkorn, 1970;Chapman et al, 2013). As this has an economic impact in livestock, coccidiosis is an important focus in veterinary research (Brake et al, 1997;Laurent et al, 2001;Gadde et al, 2009;Swaggerty et al, 2011). Eimeria species capable of natural infection of the house mouse (Mus musculus) have been proposed as a model for e.g.…”

Chicken line-dependent mortality after experimental infection with three type IIxIII recombinant Toxoplasma gondii clones

“…Similar observations, suggesting differences in susceptibility between chickens with differences in their genetic background, were also observed for other diseases. Genetic variability for resistance to chicken coccidiosis caused by Eimeria tenella has been demonstrated (Bumstead and Millard, 1987;Clare et al, 1985) and was found to be associated with genes coding for MHC molecules (Brake et al, 1997;Caron et al, 1997;Clare et al, 1985;Lillehoj et al, 1989). Based on more recent QTL analyses also other immunity related candidate genes were in the discussion, potentially contributing to the resistance against coccidiosis (Pinard-van der Laan et al, 2009).…”