Submitted to: Infection and Immunity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: March 5, 1996
Publication Date: N/A
Interpretive Summary: Avian Coccidiosis causes greater than $450 million annual loss to poultry industry. No vaccine is available and poultry industry uses medication as a means of major control. Ability to develop coccidial vaccine will have a major effect on poultry industry. In this paper, ARS scientists describe mechanisms that chickens use to defend against coccidiosis. Comprehensive understanding of how the host immune system kills parasites will lead to the development of an effective control strategy against coccidiosis.
This study evaluated the effects of selective depletion of T lymphocytes on Eimeria infections in chickens. Cell depletions were initiated in day- or week-old Hyline SC strain chickens using intra-peritoneal injections of monoclonal antibodies to CD4, CD8, or TCR alpha/beta. Control chickens received injections of irrelevant monoclonal antibody or PBS. Following the establishment of cell depletion, chickens were infected orally with E. acervulina or E. tenella, 1x10 4 oocysts for primary infections and 2x10 5 oocysts for secondary infections. Chickens treated with anti-CD4 monoclonal antibody produced significantly more oocysts than controls following primary E. tenella but not E. acervulina infections. Development of resistance to challenge infection was unaffected. These results suggest that CD4+ lymphocytes are important in controlling primary infection with E. tenella. Chickens treated with anti-CD8 or anti-TCR alpha/beta monoclonal antibodies produced significantly fewer oocysts than controls following primary infection with both E. tenella and E. acervulina. Additionally, anti-CD8 treatment abrogated resistance to challenge infections. CD8-depleted chickens may exhibit decreased oocyst production following primary infection due to a lack of CD8+ lymphocytes to serve as transporting cells for sporozoites. The abrogation of resistance to secondary infection in CD8- and TCR alpha/beta-depleted chickens suggests that these cells are necessary for the development of protective immunity to coccidia.