Coccidiosis: effects of high environmental temperatures on anticoccidial protection.
In a series of nine experiments birds subjected to heat-stress showed decreases of 9 to 61 percent in feed intake. In only one of these experiments, involving E. acervulina and monensin, was there sufficient reduction of anticoccidial intake to partially nullify effects of drug protection. In this case, a 40 percent decrease in monensin intake resulted in significantly higher lesion scores (1.9 vs. 1.0) (P less than or equal to 0.05) in birds maintained at 32 C. for days 1 to 7 postinfection (P.I.) compared to controls maintained at 20C. No other failures due to heat stress occurred with this anticoccidial in three other trials with E. acervulina or or five trials involving E. tenella infection. In one experiment E. tenella coccidiosis (lesion scores 0.7 vs. 1.1) was more severe in the cool environment than in birds under heat-stress from 2 to 7 days P.I. Similarly, less severe lesions of E tenella (0.4 vs. 0.8) occurred during heat-stress (32 C) than in controls maintained at 11 C. in zoalene-fed and unmedicated control birds. No differences in lesion scores occurred in birds in hot versus cool room environments in two experiments involving sulfaquinoxaline or one with robenidene and E. tenella infection. E tenella lesions inunmedicated controls were significantly more severe in the cool than the hot environment in one experiment. Results from these experiments suggest that decreases in feed and anticoccidial intake during heat-stress could seldom be the cause of coccidiosis breaks under field conditions.
D000818:Animals; D002645:Chickens; D003048:Coccidiosis / Q000188:drug therapy / Q000662:veterinary*; D006358:Hot Temperature; D008297:Male; D008985:Monensin / Q000627:therapeutic use; D011201:Poultry Diseases / Q000188:drug therapy*
D008985:Monensin