| Coccidiosis, caused by intestinal protozoan parasites of genus Eimeria, continues to be one of the most widespread and economically important diseases in commercial poultry production. A series of four experiments were conducted to evaluate the interrelationships of Eimeria acervulina infection and amino acid (AA) nutrition in broiler chickens. In Experiment 1, growth performance, apparent ileal digestibility (AID) of AA, and plasma concentrations of AA, carotenoids, and alpha1-acid glycoprotein, an acute-phase protein, were evaluated in broilers inoculated with graded doses of E. acervulina oocysts. With the exception of Trp and Gly, AID of all AA decreased linearly or quadratically with increasing infection dose. The greatest reductions were observed for Cys, Ala, Val, Ser, and Thr. Plasma AA levels generally did not correspond with reductions in AID, with decreases observed for Arg, Tyr, Gln, and Asn and increases observed for Lys, Leu, Ile, Val, Pro, and Orn. Plasma alpha1-acid glycoprotein of broilers was not influenced by E. acervulina infection. In Experiment 2, the effects of supplementing copper, which can influence nutrient utilization, in diets of varying in AA density (low and high) on growth performance, apparent metabolizable energy, nutrient digestibility, and plasma carotenoids were evaluated in broiler chicks infected with E. acervulina. Growth performance of broilers fed the high AA density diets was improved compared with those fed low AA density diets. Copper supplementation generally improved pre-inoculation feed intake and weight gain of broilers fed low AA density diets. Eimeria infection markedly reduced plasma carotenoids, growth performance, apparent metabolizable energy, and nutrient digestibility of broilers, with little influence of dietary AA density or copper supplementation. Various interactions among AA density, copper supplementation, and infection status were observed for AID of AA. Experiment 3 included 2 separate trials that were conducted to determine if E. acervulina infection affected the potential for individual AA to become limiting in low crude protein diets fed to broilers, as indicated by growth performance, plasma carotenoids, and gene expression of intestinal cytokines during the acute and recovery phases of infection. A low crude protein diet that adequately supported broiler growth and allowed flexibility to formulate large reductions in individual AA concentrations was validated. Broilers were then fed the validated diet with equal (40%) reductions in individual or pairs of metabolically-related AA (Met + Cys, Lys, Thr, Val, Ile, Arg, Phe + Tyr, and Gly + Ser). The impact of E. acervulina on growth performance varied among the dietary groups, but the overall relative ranking of growth responses to AA reductions was similar for infected and uninfected birds. Intestinal cytokine responses to E. acervulina were not influenced by any of the dietary AA reductions. Experiment 4 evaluated the effects of feeding high (1.23% digestible) or low (0.74% digestible) Arg diets during the acute and recovery phases of E. acervulina infection on broiler growth and plasma levels of carotenoids, AA, urea, and nitric oxide, an important molecule in the immune response to Eimeria infection for which Arg is the key substrate. Plasma ratios of Arg:Lys indicated that dietary reduction of Arg induced antagonism between these two AA, regardless of infection status. In contrast to Experiment 1, plasma levels of both Arg and Lys of birds fed the high Arg diet were increased with infection, but the relatively larger increase in Lys led to a lower plasma Arg:Lys ratio for infected birds. Infection had minimal effects on plasma levels of these AA in birds fed the low Arg diet. Dietary Arg reduction did not inhibit the large E. acervulina-induced increase in plasma nitric oxide for birds at peak infection, but did affect plasma nitric oxide at lower levels observed is uninfected birds and in infected birds after recovery. Overall, this research demonstrates that E. acervulina-induced losses in broiler growth performance extend beyond reduced AA digestibility and identifies potential inefficiencies in AA metabolism that arise during coccidiosis. |
