The effects of varying levels of cimetidine (N"-cyano-N-methyl-N'-(2-[(5-methylimidazol-4-yl)methylthio]-ethyl ) guanidine) on Eimeria acervulina (duodenal coccidiosis)-induced changes in gain, efficiency, duodenal pH, and liver copper concentration of chicks were investigated. In a preliminary trial, gain, efficiency, and duodenal pH were significantly reduced in chicks inoculated one time with 1 X 10(6) sporulated oocysts. Dietary addition of 121 ppm monensin (2-[5-ethyltetrahydro-5-[tetrahydro-3-methyl-5-[tetrahydro-6-hydro xy-6- (hydroxymethyl)-3,5-dimethyl-2H-pyran-2-yl]-2-furyl]-2-furyl]-9-hydroxy- beta-methoxy-alpha, gamma, 2,8-tetramethyl-1,6-dioxaspiro[4.5]decane-7-butyric acid) prevented these coccidiosis-induced aberrations. In subsequent trials, growth rate, feed efficiency, and duodenal pH were reduced by E. acervulina infection, but were unaffected (P greater than 0.10) by dietary addition of 0.01% cimetidine. Linear depressions (P less than 0.05) in gain and efficiency, however, were observed from 0.05 and 0.10% cimetidine additions. Dietary addition of 500 ppm copper increased liver copper levels thirtyfold (P less than 0.01) after 2 weeks. Significant coccidiosis X copper interactions were detected in gain, efficiency, duodenal pH reduction, and liver copper elevation of chicks repeatedly inoculated with 4 X 10(5) sporulated E. acervulina oocysts. Coccidiosis increased liver copper levels (P less than 0.01) of chicks fed excess copper an additional threefold compared with uninfected chicks fed excess copper. Dietary additions of 0.01, 0.05 or 0.10% cimetidine were ineffective in preventing coccidiosis-associated performance and duodenal pH depressions as well as the coccidiosis-induced liver copper elevation. Apparently, host response to cimetidine is minor in comparison to effects of coccidia on duodenal pH. Increased copper solubility at low duodenal pH may explain high tissue copper levels and enhanced copper toxicity due to coccidiosis.