The role of gamont entry into erythrocytes in the specificity of Hepatozoon species (Apicomplexa: Adeleida) for their frog hosts.

Hepatozoon species are apicomplexan parasites that infect blood cells and viscera of terrestrial vertebrates. One species, Hepatozoon clamatae, primarily infects green frogs, Rana clamitans , whereas another, Hepatozoon catesbianae, primarily infects bullfrogs, Rana catesbeiana , although both species of parasite are capable of infecting either species of frog. The aim of this study was to determine whether the basis for this partial host specificity is manifested at the gamont, or intraerythrocytic, stage of the parasite's life cycle. Blood was drawn from infected frogs and treated in vitro with a saline solution to induce intracellular gamonts to emerge from host erythrocytes. This treated blood was added to in vitro samples of uninfected blood of green frogs and bullfrogs. After 1 hr, samples were analyzed to determine the level of re-entry of the parasites into uninfected erythrocytes. Results obtained using multiple combinations of donor and recipient frogs indicate that extracellular gamonts of both parasite species do not exhibit preference for erythrocytes of 1 frog species over those of another. These results suggest that the basis for the observed host specificity is not determined at the gamont stage and is more likely dependent on another stage in the parasite life cycle.

Experimental transmission of Hepatozoon clamatae (Apicomplexa: Adeleida) to the wood frog, Rana sylvatica, and to the mosquito Culex pipiens.

Hepatozoon clamatae naturally infects the erythrocytes of green frogs (Rana clamitans), bullfrogs (Rana catesbeiana), and northern leopard frogs (Rana pipiens) in northeastern North America and uses the mosquito Culex territans as a definitive host. In this study, we show that the wood frog, Rana sylvatica, supports merogonic development, but not gamogonic development, of this protozoan parasite, and that the mosquito Culex pipiens serves as an experimental definitive host for sporogonic development. Two wood frogs were each force-fed Cx. territans, containing oocysts of H. clamatae in their Malpighian tubules, which had fed on blood of infected green frogs 30 days previously. Free merozoites were observed in 1 wood frog 35 days after inoculation, but intraerythrocytic gamonts were not observed. Fifteen Cx. pipiens were fed on a mixture of infected frog blood and physiological saline. Thirty days after blood feeding, 2 mosquitoes were infected with oocysts of H. clamatae, whereas the other 13 mosquitoes either were negative for infection or had died. The observed absence of gamogonic development of this parasite in wood frogs are discussed in light of previous records of host specificity of Hepatozoon species for their anuran hosts, and the importance of Cx. pipiens as an additional definitive host for H. clamatae.