|Dalloul, R - UNIV. OF MARYLAND|
|Shellem, T - UNIV. OF MARYLAND|
|Doerr, J - UNIV. OF MARYLAND|
Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: April 11, 2002
Publication Date: N/A
Interpretive Summary: Intestinal parasitism is a major stress factor that can lead to malnutrition and lowered performance and production efficiency of livestock and poultry. Coccidiosis, an intestinal infection caused by intracellular protozoan parasites belonging to several different species of Eimeria, costs the poultry industry more than $600 million in annual losses. Infection with coccidia parasites seriously impairs the growth and feed utilization of livestock and poultry. New method to control chicken coccidiosis is needed since current strategy is not efficient. On the basis of new findings that suggest an important role of vitamins on host immune response, ARS scientists, in collaboration with scientists at University of Maryland investigated the role of vitamin A in avian coccidiosis. The results indicate that vitamin A deficiency contributes to the enhance disease susceptibility to coccidiosis and decreased cell- mediated immune response to parasites in chickens, Therefore, this study indicate the importance of nutrient dietary supplementation such as vitamin A in poultry breeding to enhance host innate immunity against enteric parasites.
Technical Abstract: The effect of vitamin A (VitA) deficiency on the host intestinal immune response and the disease susceptibility to coccidiosis were investigated in broiler chickens following oral infection with Eimeria acervulina (EA). Day-old male broilers were fed milo-soybean mal diets either with 8000 IU VitA/kg feed (CONT) or without added VitA (A-DEF). At 25 d, a group of randomly selected birds from each treatment was inoculated orally with EA sporulated oocysts. Concanacalin A (ConA)-induced spleen lymphocyte proliferation was tested using MTT colorimetric assay. Upon challenge, VitA-deficient chickens showed lower CD4+IEL than CONT. Following EA infection, CD8+IEL increased in the CONT group whereas no change was found in IEL of A-DEF birds. A higher number of EA oocysts was recovered from A- DEF birds than from CONT (9.2x10 vs. 5.4x10, respectively; P<0.05). Serum samples taken 10 d post challenge showed higher antibody level against a recombinant coccidial antigen in A-DEF birds than in CONT birds. A-Def birds showed depressed ConA-induced lymphoproliferation response and produced lower serum interferon-gamma than CONT. These data show that VitA deficiency compromised local immune defenses of challenged birds, as reflected in lymphocyte profiles oocyst shedding, and interferon-gamma in A-DEF birds.