|Abstract or Summary
- Glochidial development in freshwater mussels (Mararitifera margaritifera) located in the Siletz River, Oregon, was completed in 13 days at an average water temperature of 12.8 C. Glochidia were released by these mussels for 33 days, May 13 to June 15, 1971. The comparative susceptibility of four species of salmonid
fishes, 30.5 to 87.0 mm in fork length, to glochidiosis was determined by examination of 343 caged and 177 free-swimming (native) fish for infection. Of the caged fish, 99% of the chinook salmon (Oncorhynchus tshawytscha), 75% of the coho salmon (O. kisutch), 88% of the cutthroat trout (Salmo clarki), and 95% of the steelhead trout (S. 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 trout were not captured). This is the first detailed description of the metamorphosis of M. margaritifera glochidia in fish and the associated histopathology. Invading glochidia, which were 70 by 75 μ [micro meters] in size, increased in length by 500% during metamorphosis. Encysted glochidia occurred on the gill filaments, arches, rakers, and occasionally on the pseudobranchs of all fish species; however, most were on the lamellae of the filaments. Initially, the encysted glochidia have uneven walls approximately 15 μ [micro meters] in thickness, but as the parasite increases in size the outer wall, i.e., the part of the cyst that is not embedded in and surrounded by gill lamellae, becomes thinner. Also, approximately 15 gill lamellae may become fused to the wall. Except for the lamella grasped by the glochidium, blood apparently continues to flow through the capillaries of the fused lamellae. However, these
lamellae apparently can no longer function in respiration, except for the outermost lamella. Parasites encysted on the side of the gill filament restrict blood flow by pinching the filamental arteries. Large cysts on the lamellae increased the physiological dead space in the water flow. Clubbing of the filaments results when large cysts are located near the distal end of the filament. These pathological changes in heavy infections may result in immediate death of the fish by asphyxiation. In less heavy infections, delayed mortality occurs due to secondary infection with fungi, probably Saprolegnia sp. The invading or exiting glochidia may provide portals of entry for the fungi.