The effect of experimental infection with the poisoning fluke, Nanophyetus salmincola, on five species, including three subspecies, of salmonid was studied. The estimated numbers of cercariae that killed in 24 hr 50% of kokanee (Oncorhynchus nerka), Montana black-spotted cutthroat trout (Salmo clarki lewisi), Atlantic salmon (S. salar), coho salmon (0. kisutch), rainbow trout (S. gairdneri), and coastal cutthroat trout (S. clarki clarki), all between 30 and 37 mm in fork length, were 58, 74, 110, 200, 295, and 430, respectively. This range in sensitivity of the different species of to the parasite was correlated with the natural duration of the host-parasite relationships. The symptomatic, gross, and histopathologic changes associated with penetration and migration of N. salmincola cercariae in the above trout and salmon species and in Lahontan cutthroat trout (S. clarki henshawi) are described. Penetration and migration of cercariae in were studied. Parasites were found inside fin rays and blood vessels, and were present in internal organs within 1 hr after epidermal penetration. Evidence for the pathogenicity of the poisoning fluke, Nanophyetus salmincola, to is inconclusive. Ward and Mueller (1926) examined brook trout fry that had died in an Oregon hatchery during a severe epizootic. The were heavily infected with encysted metacercariae of a digenetic trematode later identified as N. salmincola. The above authors believed that the parasites were the cause of the losses. They found a direct relationship between the degree of popeye (exophthalmia) and the number of parasites in the optic nerves. Simms et al. (1931a, b) believed that could tolerate large numbers of parasites; e.g., they found 14,062 parasites in an apparently healthy naturally infected cutthroat trout 4.6 inches long. Simms (1933) reported heavy N. salmincola infections in young rainbow and brook trout that were dying in an Oregon hatchery. Exophthalmia was obReceived for publication 7 October 1966. * This investigation was supported in part by Public Health Service Research Grant 5 R01 AI 06599-02, from the NIAID. Technical Paper No. 2199, Oregon Agricultural Experiment Station. A contribution from the Pacific Cooperative Water Pollution and Fisheries Research Laboratories. This study is part of a thesis submitted by the senior author to the Graduate School of Oregon State University in partial fulfillment of the requirements for the degree of Master of Science. The work was carried out at the Marine Science Center, Oregon State University, Newport, Oregon. served in many of the fish. Simms (1933) also found heavy infections in apparently healthy from streams and hatcheries. He reported that there were no deaths or signs of infection in young rainbow and brook trout that had heavy infections after laboratory exposure to infected snails. Shaw et al. (1934) exposed young rainbow and brook trout, approximately 2 inches long, to infected snails. The remained in good condition for periods up to 90 days even though some of the were exposed for 55 days to snails and were heavily parasitized. Bennington (1951) and Bennington and Pratt (1960) concluded, on the basis of results from laboratory experiments in which and infected snails were placed together in aquaria, that the parasite is pathogenic. In these experiments, 12 chinook salmon, two dace, one sculpin, and two goldfish died 6 to 24 hr after exposure to infected snails. Bennington (1951) stated that the parasite may be quite pathogenic to young fish during the season of low water in streams having high populations of infected snails. Farrell and Lloyd (1962) reported that rainbow trout were killed after laboratory exposure to infected snails. They stated that the degree of pathogenicity was directly proportional to the rate of accumulation of cercariae by fish. All of the above studies were concerned with approximately 24-hr mortalities of fish. There is no information on long-term mortality of infected with N. salmincola. Regarding the symptomatic, gross, and histo-