Glochidiosis of salmonid fishes. III. Comparative susceptibility to natural infection with Margaritifera margaritifera (L.) (Pelecypoda: Margaritanidae) and associated histopathology.

TLDR: The results of a study on the comparative susceptibility of salmonid fishes to natural infections with M. margaritifera and on development of the parasites in these fish and the associated histopathology are reported.

Abstract: The comparative susceptibility of 4 species of salmonid fishes, 30.5 to 87.0 mm in fork length, to the glochidia of the freshwater mussel (Margaritifera margaritifera) was determined by examination of 594 caged and 178 uncaged (native) fish for infection. Of the caged fish, 99% of the chinook salmon (Oncorhynchus tshawytscha), 75% of the coho salmon (Oncorhynchus kisutch), 88% of the cutthroat trout (Salmo clarki), and 95% of the steelhead trout (Salmo gairdneri) were infected. There was a similar relationship in infection incidence in the native fish species. Mean infection intensities in the caged and native fish were: 446 and 399 for chinook salmon, 8 and 24 for coho salmon, and 72 and 88 for steelhead trout, respectively, and 212 for caged cutthroat trout (native juvenile trout were not captured). Glochidia completed development in mussels in the Siletz River, Oregon, in 13 days at an average water temperature of 12.8 C. They were released by these mussels from 13 May to 15 June 1971. During development in fish, the parasites increased in length by 500% from an initial size of 70 to 75 tum. Encysted parasites occurred in the gill filaments, arches, rakers, and occasionally in the pseudobranchs of all fish species; but most were in the lamellae of the filaments. Initially, the cyst walls were approximately 15 tLm in thickness, but as the parasites increased in size the exposed part of the wall became thinner. Up to 15 lamellae may be fused to the wall. Except for lamellae "grasped" by the parasites, blood apparently continued to flow through capillaries of the fused lamellae, but these lamellae, except the outermost ones, probably no longer functioned in respiration. Parasites encysted on the sides of gill filaments restricted blood flow by "pinching" the arterioles. Large encysted parasites on the lamellae increased the physiological dead space in the water flow. Clubbing of the filaments resulted when large parasites were located distally. These pathological changes in heavy infections may result in early death of fish by asphyxiation. In less heavy infections, the invading or exiting parasites may provide portals of entry for fungi, and delayed mortality may occur from secondary infection. The first two papers in this series reported on the comparative susceptibility of salmonid fishes to experimental infection with Margaritifera margaritifera (Meyers and Millemann, 1977) and on tissue reactions of coho (Oncorhynchus kisutch) and chinook salmon (Oncorhynchus tshawytscha) to experimental infections (Fustish and Millemann, 1977). This paper reports the results of a study on the comparative susceptibility of salmonid fishes to natural infections with M. margaritifera and on development of the parasites in these fish and the associated histopathology. Some observations on relationship of temperature and development of glochidia in mussels are also reported. Received for publication 13 May 1977. * Technical Paper No. 4558, Oregon Agricultural Experiment Station. t U.S. Environmental Protection Agency, Region X, 1200 6th Avenue, Seattle, Washington 98101. t Environmental Sciences Division, Oak Ridge National Laboratory, P.O. Box X, Oak Ridge, Tennessee 37830. MATERIALS AND METHODS