Glochidiosis of Salmonid Fishes. III. Comparative Susceptibility to Natural Infection with Margaritifera margaritifera (L.) (Pelecypoda: Margaritanidae) and Associated Histopathology

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 µm. 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 µm 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.