Submitted to: Journal Of Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: November 13, 1996
Publication Date: N/A
Interpretive Summary: Control of coccidiosis in the American poultry industry is usually through prophylactic addition of anticoccidial drugs to the feed. However, emergence of drug resistant strains of coccidia has decreased the effectiveness of this control and increased the potential for economic losses. New control methods are being sought. Because losses due to coccidiosis are generally associated with inflammatory responses, a greater understanding of these responses should lead to the development of new control measures. Nitric oxide (NO), a multipotent bioregulatory molecule, is a recognized product of the inflammatory response in vertebrates, but little is known about its generation or function during coccidia infections in chickens. In these experiments plasma levels of nitrite plus nitrate ions, stable metabolites of NO, were found to increase with increasing dose of Eimeria tenella and this increase was significant at 5 and 7 days post inoculation (PI). Treatment of infected chickens with aminoguanidine, a drug which inhibits NO synthesis, did not exacerbate infection as might be expected if NO were toxic to the parasite. It did decrease cecal bleeding, suggesting NO production enhances the hemorrhage associated with E. tenella infections.
Technical Abstract: The objective of this study was to determine if nitric oxide (NO) is produced during a primary infection with Eimeria tenella, a protozoan parasite of chicken ceca. Plasma levels of NO2- plus NO3-, stable metabolites of NO, were measured at various times post inoculation (PI) with various doses of parasite. Inoculation with 5 X 10,000 and 1 X 1,000,000 but not 1 X 1,000 oocysts/chick significantly increased plasma NO2-plus NO3- at 7 days PI. In chickens inoculated with 5 X 10,000 oocysts, significant increases in plasma NO2- plus NO3- occurred at 5 and 7 but not 3 days PI. Daily i.p. administration of aminoguanidine (inhibitor of induced NO synthase) during the period of infection, did not lower the increases in plasma NO2- plus NO3- at days 5 and 7 PI, and did not affect the degree of colonization of the cecal tissue by the parasite, but did cause the ceca to appear less swollen and filled with blood at days 5 and 7 PI as compared with ceca from untreated chickens. Hemorrhage is a major pathological manifestation of E. tenella infections, associated with the disruption of the cecal mucosa by the developing parasite. The results of this experiment are consistent with the hypothesis that an aminoguanidine-inhibitable NO synthase, perhaps in the vascular endothelium of the cecal blood vessels, may contribute to hemorrhage by causing vasodilation.