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Eimeria tenella sporozoites were incubated in the presence of 3 different [14C]-labeled sugars; D-glucose, 2-deoxy-D-glucose and 3-O-methyl-D-glucose. The initial velocity, Vi, of uptake of D-glucose and 2-deoxy-D-glucose was similar, 41 micrograms/10(10) sporozoites/min and 46 micrograms/10(10) sporozoites/min, respectively; whereas that for 3-O-methyl-D-glucose was significantly lower, 17 micrograms/10(10) sporozoites/min. Initial velocity studies also revealed that glucose uptake was a saturable event, with an apparent KT of 20 mM and an apparent Vmax of 312 micrograms/10(10) sporozoites/min. Uptake was unaffected by exogenous sodium levels or the presence of ouabain. However, 0.1 mM phloretin significantly inhibited glucose uptake. Thus, it would appear that E. tenella sporozoites possess a Na-independent, phloretin-sensitive, carrier-mediated monosaccharide-transport system.

Extracellular Eimeria tenella sporozoites exposed to 1.0 ,ug/ml monensin at 40 C had an accelerated rate of sodium influx as well as an increased rubidium uptake that was inhibited by the cardiac glycoside, ouabain. These results suggested the presence of a functional (Na+-K+)-ATPase and its stimulation by monensin. Under the same conditions, sporozoite ATP concentrations declined, lactate production increased and the rate of amylopectin utilization was enhanced. Exposure to monensin also appeared to stimulate the rate of sporozoite glycolysis. The results of this study demonstrated that the cidal effect of monensin on extracellular sporozoites was caused by the capability of the ionophore to act as a transmembrane sodium carrier. The polyether, ionophorous antibiotic, mo- nensin, is an effective anticoccidial agent and has been used extensively for the control of coccid- iosis for more than a decade. Despite its wide use the precise anticoccidial mode of action of this drug is not understood. Smith and Strout (1979) provided evidence that the polyether ionophores are accumulated by free (extracellular) Eimeria tenella sporo- zoites. Later, Smith et al. (1981) demonstrated that this uptake may reduce the number of spo- rozoites capable of invading host cells and may deny the initiation of first generation schizogony for those that do penetrate. In this same study it was shown that monensin may also express a lethal activity against the extracellular sporo- zoite. More recently Long and Jeffers (1982) pre- sented evidence that the merozoites are subject to a similar fate. Thus it appears that the free, invasive stages of the coccidia are susceptible to an anticoccidial activity of monensin. These findings show the utility of a readily available model system, the free sporozoite, for the study of the specific anticoccidial mode of action of the ionophorous antibiotics. In the present study we examined the influence of monensin on sodium and rubidium (as a po