Heramita salmonis, the causative agent of hexamitiasis in salmonoid fishes, is endemic in most trout and salmon hatcheries throughout North America. The etiologic agent, a protozoan flagellate, ostensibly causes cellular damage in the caecal mucosa of afflicted fishes. It is also believed that heavy infections may interfere with normal growth by direct competition with the host for available nutrients in the intestinal tract. While the role of this supposed pathogen is relatively unclear, its presence in test fishes at this laboratory has caused considerable concern during the conduct of controlled nutritional studies.

Although McNeil et al (1941) showed that the incidence of Hexamita infections is widespread, hexamitiasis appears to be commercially important only in turkeys (Almquist and Johnson, 1951) and fish (Davis, 1953).

Very little has been reported on the protozoacidal effects of various drugs on the Hexamita infections in fish (Fish and McKernan, 1940; Smith and Quistorff, 1940; and Nelson, 1941). The most widely used chemotherapeutic agents are p-carbamidobenzene arsonic acid (carbarsone) and mild mercurous chloride (calomel). Initial attempts at this laboratory to control the parasite in infected fish populations using these two drugs at the recommended concentrations demonstrated that the former was erratic in effectiveness and the latter was toxic and produced loss in fish weight. The present study, therefore, was undertaken to find more effective therapeutic agents which would be palatable, non-toxic, and still effectively eradicate the protozoan from fish.