PubMed · 7383005
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S B Guss. 1980. Practical parasite control.. https://pubmed.ncbi.nlm.nih.gov/7383005/
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Culture of neuroblastoma cells in a medium of low-thiamine concentration (6 nM) and in the presence of the transport inhibitor amprolium leads to the appearance of overt signs of necrosis; i.e., the chromatin condenses in dark patches, the oxygen consumption decreases, mitochondria are uncoupled, and their cristae are disorganized. Glutamate formed from glutamine is no longer oxidized and accumulates, suggesting that the thiamine diphosphate-dependent alpha-ketoglutarate dehydrogenase activity is impaired. When thiamine (10 microM) is added to the cells, the O2 consumption increases, respiratory control is restored, and normal cell and mitochondrial morphology is recovered within 1 h. Succinate, which is oxidized via the thiamine diphosphate-independent succinate dehydrogenase, is also able to restore a normal O2 consumption (with respiratory control) in digitonin-permeabilized thiamine-deficient cells. Our results therefore suggest that the slowing of the citric acid cycle is the main cause of the biochemical lesion induced by thiamine deficiency as observed in Wernicke's encephalopathy.
Two trials were conducted to evaluate the effects of feeding various anticoccidial products to turkeys to 8 wk and then growing to market age (16 wk for hens and 20 wk for toms). Anticoccidials evaluated in the first trial included amprolium at 187.5 mg/kg for 0 to 4 wk and 125 mg/kg for 4 to 8 wk; butynorate at 375 mg/kg for 0 to 8 wk; monensin at both 60 (MON-60) and 100 mg/kg for 0 to 8 wk; zoalene at 187.5 mg/kg for 0 to 4 wk and 125 mg/kg for 4 to 8 wk; and halofuginone at 3 mg/kg for 0 to 8 wk. In the second trial, MON-60 was replaced by a combination of sulfadimethoxine (62.5 mg/kg) plus ormetoprim (37.5 mg/kg) for 0 to 8 wk. In each trial each treatment was fed to four pens of 16 hens and four pens of 12 toms. Several of the anticoccidials significantly influenced the weight of both hens and toms by producing lower weights at the end of the 8-wk feeding period than birds in other treatments. However, after removal of the anticoccidials, compensatory gains were observed in almost every instance. Significant effects of previous anticoccidial feeding were noted on body weight of hens at 16 wk but not on weights of toms at 20 wk.
Two trials were conducted to compare the efficacy of currently approved anticoccidials for turkeys against challenge using a field isolate of mixed Eimeria species; E. adenoides, E. gallopavonis, and E. meleagrimitis. Poults in wire-floored cages were fed unmedicated diets from day-old to 3 wk of age. Diets were supplemented with either amprolium (AMP, 125 mg/kg), butynorate (BUT, 375 mg/kg), monensin (MON-60, 60 mg/kg; MON-100, 100 mg/kg), halofuginone (HAL; 3 mg/kg), zoalene (ZOA; 125 mg/kg), or sulfadimethoxine plus ormetoprim (SUL + ORM, 62.5 mg/kg and 37.5 mg/kg, respectively). After 2 days on the test diets, poults were individually weighed and inoculated with sporulated coccidial oocysts from the field isolate. Total fecal collections were obtained for Days 0 to 5 and 6 to 10 to estimate oocyst output. At 10 days postinoculation, the birds were individually weighed and killed to determine severity of intestinal lesions. The HAL and MON were most effective and AMP, ZOA, and SUL + ORM were least effective in maintaining weight and in reducing the severity of intestinal lesions. All the coccidiostats tested reduced oocyst passage, but poults fed HAL produced fewer oocysts. The results demonstrated differences in efficacy among anticoccidials with the more recently approved drugs providing the best protection against coccidiosis.