Comparative histopathology of epizootic salmonid virus diseases
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Geology topics
Publications and source records attributed to W. T. Yasutake.
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Abstract not available.
No abstract available.
The occurrence of infectious pancreatic necrosis in rainbow trout (Salmo gairdneri), brook trout (Salvelinus fontinalis), and cutthroat trout (Salmo clarki) has been experimentally authenticated for the first time in the western United States. The cutthroat trout represents a new host. Brook trout fin tissue culture inoculated with bacteria-free filtrate from the diseased fish tissue showed marked degenerative changes after 24 hours. Chinook salmon (Oncorhynchus tshawytscha), kokanee (O. nerka), and silver salmon (O. kisutch) were not susceptible to the virus when inoculated. Histologically, extensive pancreatic necrosis was observed in the original and experimental materials, but striated muscle hyalinization was detected only in the original material.
Fish pathology and its role in fish culture were brought into prominence in the spring of 1960 by the disclosure of a high incidence of hepatomas in hatchery-reared rainbow trout. The current problem came to light as the result of a routine inspection of live trout shipments at a California border fish-disease checking station. This service is performed by personnel of the California Department of Fish and Game to preclude the introduction or further spread of communicable fish diseases into California watersheds. Collaborative studies which followed revealed the nationwide distribution of the disease. This unusual disease soon attracted the attention of the Bureau of Sport Fisheries and Wildlife, the Food and Drug Administration, Public Health Service, and several western State health and conservation agencies.
Heramita salmonis , the causative agent of hexamitiasis in salmonoid fishes, is endemic in most trout and salmon hatcheries throughout North America. The etiologic agent, a protozoan flagellate, ostensibly causes cellular damage in the caecal mucosa of afflicted fishes. It is also believed that heavy infections may interfere with normal growth by direct competition with the host for available nutrients in the intestinal tract. While the role of this supposed pathogen is relatively unclear, its presence in test fishes at this laboratory has caused considerable concern during the conduct of controlled nutritional studies. Although McNeil et al (1941) showed that the incidence of Hexamita infections is widespread, hexamitiasis appears to be commercially important only in turkeys (Almquist and Johnson, 1951) and fish (Davis, 1953). Very little has been reported on the protozoacidal effects of various drugs on the Hexamita infections in fish (Fish and McKernan, 1940; Smith and Quistorff, 1940; and Nelson, 1941). The most widely used chemotherapeutic agents are p-carbamidobenzene arsonic acid (carbarsone) and mild mercurous chloride (calomel). Initial attempts at this laboratory to control the parasite in infected fish populations using these two drugs at the recommended concentrations demonstrated that the former was erratic in effectiveness and the latter was toxic and produced loss in fish weight. The present study, therefore, was undertaken to find more effective therapeutic agents which would be palatable, non-toxic, and still effectively eradicate the protozoan from fish.
In a study of coho salmon ( Oncorhynchus kisutch ), the gross chemical and histological changes occurring over a 14-month period spent in fresh water were determined. The determinations were made at 3-month intervals on: 1) hatchery-reared fish, 2) fish hatchery-reared for 3, 6, 9, and 12 months and then planted in a controlled stream for the remainder of the period; and 3) an indigenous group of wild fish in this stream. Wild fish showed high incidence of tissue damage from spinose hairs of the moth larva, Halisidota argentata. Hatchery fish were similarly affected with the severity and incidence of lesions varying directly with the time of exposure of the larvae in the wild environment. Both groups of fish were heavily parasitized by sporozoan organisms in the kidney and spinal cord. Kidney disease appeared in both wild and planted hatchery fish. The gross chemical composition of hatchery fish transformed rapidly after planting to that of the wild fish. Although the initial rate of fat loss is essentially constant for all hatchery groups after planting, fish that were hatchery reared for 9 to 12 months did not complete the transformation to the wild-type body composition by the time of downstream migration at 14 months.
Salmonids reared under artificial conditions show marked consistent differences in body composition in comparison with wild salmonids. Protein and mineral levels are lower and lipid values are higher in hatchery fish than in wild fish. As the period of artificial rearing is increased, these differences become more extreme. In hatchery fish, there is generally more microscopically visible fat in the liver and viscera than in these organs in wild fish although extremes are seen in both groups. In young hatchery fish and in wild fish, there is no correlation between fat deposition in the liver and in the pancreas, but in older hatchery fish, both of these organs are fatty and there is a simultaneous increase in total body lipid. In wild fish, ceroid deposition is greater, suggesting that the fatty acids are more highly unsaturated. There is little difference in disease incidence between the two groups, but parasitism is more pronounced in wild fish. The significant variables between wild and artificially produced fish appear to be limited to diet and environment. From the factors discussed above, diet alone is probably the most important single factor in producing the changes observed in body composition.
In 69 production diets fed to hatchery salmonids, there was a wide variation in the ingredients of the diets and in their content of protein, fat, carbohydrate and ash. There was a close correlation between the body composition of hatchery-raised fish and the composition of the diets fed. The data indicated, however, that differences in hatchery management, such as level of feeding, were also important contributing factors in producing the observed body composition of hatchery fish. Wild fish had a markedly different body composition characterized by a much lower level of fat and relatively higher protein and mineral content The effect on survival of differences in body composition between wild and hatchery fish is discussed. There is a clearly defined need for additional research on the nutritional requirements of salmonids, the relationship between body composition and ability to survive, and for quality control in hatchery nutrition.
Adverse effects from the medication of fish diseases with sulfonamides have been reported by several workers. A decreased growth rate (Gutsell and Snieszko 1949, Snieszko and Wood 1955), the production of drug resistant strains of pathogens (Snieszko 1952), sterility and kidney damage (Wood et al., 1955), and mortalities (Johnson and Brice 1953) have been described. Recently, increased mortalities and tissue damage were observed in young silver salmon after a single day's treatment with sulfamethazine. Subsequently an attempt to reproduce the conditions experimentally was made. The purpose of this paper is to describe the pathology of acute sulfamethazine toxicity and to discuss certain factors of possible importance in the etiology of losses among fish treated with sulfonamides.
During the histological examination of a group of wild and hatchery salmonids undescribed sporazoans were frequently observed. This was not unexpected, since Myxosporidia are typical fish parasites (Kudo, 1920). Myxidium were observed in kidney tubules, Cholromyxum in glomeruli, and Myxobous in the spinal cord and on epidermal scales. The present paper will deal with the description and indentification of these unclassified Myxosporodia.
In the summer of 1952, Snieszko and Griffin (1955) diagnosed kidney disease in brook trout from the Fish and Wildlife Service's station at Berlin, New Hampshire. During the examination of these fish, a peculiar lesion was observed in the vicinity of the gastric caeca. In very advanced cases, hard, glistening, white masses of tissue bearing a striking resemblance to mature testes often filled the abdominal cavity. In the initial examinations, the material was actually mistaken for normal testicular tissue. Subsequently, it was recognized as an entirely aberrant, proliferating tumor-like mass.
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Rucker et al., (1953) described a disease of sockeye salmon ( O ncorhynchus nerka ) of possible viral etiology. First seen in Washington in 1951 with relatively minor losses, the disease recurred in 1952 killing over two million fingerling salmon with a mortality rate of 91.5 percent (Watson, 1954). In 1953, the disease was present in every sockeye salmon hatchery in the state. Rucker, Watson and their associates have demonstrated that the disease is infectious, caused by a serially-transmissible and filterable agent, and specific for one species of fish. Watson et al., (1956) have described the hematology of infected salmon. The present paper deals with the histopathology of the disease.
During the histological examination of a collection of wild and hatchery salmonids, a peculiar foreign body was occasionally observed in various organs, particularly in the viscera. These objects, usually accompanied by a focal inflammation, were observed in 10 of 75 samples of wild trout and salmon collected in Oregon and Washington and were believed to represent an unknown type of parasitism. Their identity remained obscure until a massive concentration was observed in the tissues of wild coho salmon, ( Oncorhynchus kisutch ), from Minter Creek on the Olympic peninsula of Washington and in hatchery coho salmon from the Minter Creek Biological Station. The distribution of the structures suggested the intestinal tract as a point of origin. Subsequent stomach examinations revealed small, partially digested insect fragments with many long, spine-covered hairs. The insects were identified as second or third instars of the lepidopteran larvae, Halisidota argentata Packard. The spine-covered hairs penetrated the stomach wall and produced the observed lesions by working in an apparent porcupine quill-fashion throughout the body of the fish. The pathology of the Minter Creek salmon was sufficiently extensive to merit a description of the condition for the benefit of other workers who may encounter this rather unusual phenomenon and confuse it with an actual parasitic infection.
Since the original description of ceroid in rats, many papers have appeared on the etiology and characteristics of this pigment. It was first seen as a yellow, granular pigment in hematoxylin and eosin sections of the cirrhotic livers of choline deficient rats. The pigment was more fully characterized by Endicott and Lillie, and additional stainging reactions were summarized recently by Lillie. The pigment is sudanophilic in paraffin sections, acid-fast, basophilic, isotropic, iron negative, and highly resistant to solution in water, alcohol, fat solvents, and dilute aqueous acids and alkalis. It is stained by Mallory's hemofuscin stain and Weigert's myelin stain. It reduces osmium tetraoxide and diamine silver carbonate but not ferric ferricyanide. The Gmelin reactions for bile pigments is negative. It has a greenish yellow fluorescence at 3650-3660 Å. It is Schiff positive with or without antecedent diastase digestion after performic or periodic acid oxidation.