Either simultaneous or separate dietary deficiencies of vitamin E and selenium in Atlantic salmon during first 4 weeks of feeding caused twice the mortality shown in fish fed both supplemental vitamin E (0.5 IU/g dry diet) and selenium (0.1 mug/g). Subsequent dietary repletion with both vitamin E and selenium significantly reduced mortality during the following 2 weeks. Larger salmon (0.9 g initial mean weight), with vitamin E deficiency with or without selenium resulted in the following deficiency signs: extreme anemia, pale gills, anisocytosis, poikilocytosis, elevated plasma protein, exudative diathesis, dermal depigmentation, in vitro ascorbic acid-stimulated peroxidation in hepatic microsomes, yellow-orange liver color, yellow-brown intestinal contents, enlarged gall bladder distended with dark green bile, low vitamin E in carcass and hepatic tissue, muscular dystrophy, increased carcass fat and water, and a response to handling characterized by a transitory fainting with interruption in swimming. A deficiency of dietary selenium suppressed plasma glutathione peroxidase activity. Supplemental selenium with vitamin E significantly increased tocopherol activity in hepatic, but not carcass tissues. Supplements of both vitamin E and selenium were necessary to prevent muscular dystrophy.
Larval oysters were experimentally infected with isolates of pure cultures of marine Vibrio sp. These animals were studied live, histologically, with the immunofluorescent test and with electron microscopy. All inoculated groups, but no control groups, demonstrated decreased growth and/or high mortality.One bacterial isolate attached preferentially to larval shell and destroyed mantle tissue as it grew along the internal surface of the shell. Phagocytes consumed invading bacterial cells but were ultimately overwhelmed by the infection.The second bacterial isolate caused velar damage in young larvae that remained active. In these larvae, the velar cells became detached or internally disorganized and lost their rectractor muscle insertions. In more advanced larvae, detachment of absorptive cells of the digestive gland was the earliest change observed and seemed to result from attachment of bacterial antigens to the cell surface. In both younger and more advanced larvae, food cycling and nutrient utilization were disrupted early in the disease process. The older larvae showed a general atrophy.Clinical signs such as mantle cell detachment could be detected early in the disease. Other clinical observations and the immunofluorescent test were also useful in the early diagnosis of vibriosis in larval oysters.Key words: vibriosis, larval oysters, Crassostrea virginica, histology, electron microscopy, ultrastructure, immunofluorescence, oyster hatcheryDes larves d'huîtres ont été infectées expérimentalement par des isolats de cultures pures de Vibrio sp. marins. Ces animaux furent étudiés en vie, histologiquement, à l'aide du test d'immunofluorescence et enfin au microscope électronique. Tous les groupes inoculés, mais non les groupes témoins, accusent un déclin de croissance et/ou une mortalité élevée.
Mass mortalities of wild, captive and cultured scallops have been frequently reported. The cailses of such mortalities and population fluctuations have not been established. A review of specific diseases of scallops is presented and the following newly reported diseases are discussed. Odostomia spp. and Polydora spp. are important predators and shell inhabitants of captive and cultured scallops. Rickettsial infections in the bay scallop are reported. Bacterial infections, especially vibriosis, are common in cultured scallop larvae. Protozoan infections and fouling are common and may be pathogenic. These include algal infections of mantle tissue, environmental dinoflagellate blooms (e.g., Prorocentrum spp.), renal coccidia, Hexamita spp., trichodina‐like organisms, and others. A variety of helminth parasites, especially in adductor muscle tissues, are of public health importance. Fouling organisms are common in captive and cultured populations. Sabellaria vulgaris, a polychaete, is an important lethal fouling agent for wild bay scallops.
Motile scallops differ from many other bivalves by their anatomical and physiological predisposition to traumatic injuries, fouling and predation.
Specific diseases can be most readily observed in captive and cultured populations, increasing our understanding of diseases of wild stock and young larval and juvenile stages.
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