Amprolium

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Abstract
The coccidiostat, amprolium [1-(4-amino-2-n-propyl-5-pyrimidinylmethyl)-2-picolinium chloride · hydrochloride], when fed in the diet at 2,000 ppm or more to laying hens, produced lowered feed intake, decreased rate of lay, increased embryo mortality, and lowered chick viability at hatch. Associated with the subnormal hatches were markedly depressed free thiamine concentrations in the yolk, in some instances to barely detectable amounts. All of the adverse effects were counteracted by oral or parenteral administration of thiamine, which in turn, also elevated yolk thiamine concentrations. The latter route of administration was more effective in counteracting 4,000 ppm of amprolium in the diet. An injection of 50 to 100 μg of the vitamin was required as compared with the 1 to 10 mg ingested via the daily intake of 100 gm of diet containing 10 to 100 ppm of supplemental thiamine, respectively. High concentrations of amprolium in yolks had no adverse effect on the hatch, and as much as 20,000 ppm of amprolium in the diet were tolerated by the hen provided sufficient thiamine was administered. A reduction in food intake comparable to that caused by the feeding of amprolium produced similar losses in rate of lay. Amprolium increased embryo mortality during the first 7 days of incubation, during the later stage of incubation, and at hatch. Pair-feeding experiments revealed that inanition accounted for the higher embryo mortality during the first 7 days of incubation. In view of the lack of toxicity of amprolium per se, and the ability of thiamine to counteract the adverse reproductive effects, the symptomatology attributed to feeding high concentrations of amprolium to laying hens is considered reflective of an induced thiamine deficiency.