Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: September 30, 1997
Publication Date: N/A
Interpretive Summary: Parasitic infections elicit inflammatory responses from the invaded host that may include production of metabolites that are toxic to the parasite. Nitric oxide (NO) is one such metabolite. In some parasitic diseases, host resistance can be correlated positively wih the amount of NO produced, which can be assessed by measuring plasma levels of stable NO metabolites, nitrite and nitrate ions. It is not known whether NO is toxic to Eimeria tenella, an economically important coccidian parasite of chickens, or whether its production during infection can account for host resistance. We have found that a resistant inbred chicken strain, SC, apparently produces larger amounts of NO than a susceptible strain, TK, and is more sensitive to treatment with inhibitors of induced nitric oxide synthase (iNOS, the enzyme responsible for NO biosynthesis) than the TK strain, suggesting, on the one hand, that NO production may play an important role in resistance to E. tenella infection. On the other hand, the SC strain yields higher outputs of the coccidian oocysts during primary infection compared to the TK strain suggesting that the NO produced may not be effective in killing the parasite. These results indicate that resistance to coccidia infection is complex and probably involves additional reactions of the chicken immune system.
Studies were carried out to assess the importance of nitric oxide (NO) production in vivo to resistance to Eimeria tenella. The SC strain produced higher plasma levels of nitrite + nitrate (stable metabolites of NO) in response to primary infection than did the TK strain. The SC strain was also more responsive in reduction of plasma nitrite + nitrate and increased doocyst output during treatment of primary infections with inhibitors of induced nitric oxide synthase. However the SC strain, regardless of drug treatments, consistently yielded higher oocyst outputs than the TK strain during primary infection, indicating it could be susceptible to a higher parasite burden. On the other hand, the SC strain seems to develop immunity more rapidly than the TK strain, yielding smaller oocyst outputs after challenge infection. These results indicate that NO production during primary E. tenella infection may be only one of several immune responses, and may not be the main anticoccidial effector.