Submitted to: Avian Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 13, 2001
Publication Date: N/A
Interpretive Summary: Coccidiosis causes significant economic losses in the poultry industry by reducing weight gains and feed efficiency. The conventional treatment for coccidiosis involves the use of chemicals applied as feed additives. However, drug resistant has become wide spread reducing the efficacy of chemotherapy. Recently the use of attenuated live vaccines coupled with chemotherapy has been effective in reducing losses to coccidia. It is clear that effective control in the future will be by a combination of chemotherapy and vaccine tailored to the particular needs of the producer. In order to effectively implement these strategies producers will need new methods to evaluate impact of coccidiosis on poultry growth. The current research address this issue by determining the mechanisms associated with muscle loss during coccidiosis infection in turkeys. Muscle catabolism was assessed by measuring plasma and muscle levels of an amino acid, 3-methyl histidine, that is indicative of breast muscle breakdown. These results indicated muscle breakdown was correlated with intensity and duration of infection. Experiments with uninfected turkeys that were fed same amount of feed indicated that decreased appetite caused by coccidiosis is only a responsible for muscle catabolism and decrease in weight gain. This method may form the basis for assessing impact of coccidiosis during poultry production
Technical Abstract: To assess muscle breakdown during avian coccidiosis, the level of the non- metabolizable amino acid 3-methyl-histidine (3MH) was determined in muscle and plasma from turkey poults infected with an Eimeria. The effect of levels of parasitism were evaluated at 6 days post inoculation (DPI) in birds receiving 2.5 x 104, 1 x 105 or 2 x 105 oocysts each. The changes in n3MH levels during recovery from acute infection were assessed at 6-29 DPI in animals given 1.9 x 105 oocysts per bird. In some experiments uninoculated birds given the same amount of feed as infected bird pair-fed) were used to determine the effect of feed deprivation on weight loss and 3MH levels. The 3MH levels of plasma and muscle were determined by high pressure liquid chromatography after derivatization with fluorescamine. Weight gains, breast muscle weight, dry weight of muscle, PCV and gross lesion scores were also determined. Infected birds had significantly elevated plasma and muscle 3MH at 6 DPI following a single dose of Eimeria oocysts. The plasma and muscle 3MH returned to control levels after 14 DPI. The 3MH levels increased with increasing dose of oocysts. Plasma and muscle 3MH levels were significantly elevated in pair-fed birds but 3MH levels in infected birds were incrased by 30% over pair-fed birds. The results suggested that muscle breakdown, as assessed by plasma and muscle levels of 3MH, increased during the acute stage of Eimeria infection in turkey poults. The underlying causes for this muscle break down probably involves in part a physiological response to decreased feed intake related to anorexia during the acute phase of infection. However, decreased feed intake account for only 70% of increase in 3MH suggesting another mechanism is responsible in part for increases in muscle catabolism.