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Biomedical subjects

T R Meyers

Publications and source records attributed to T R Meyers.

16 recordsLinked to original sources
PubMed1998

Viral hemorrhagic septicemia virus, Ichthyophonus hoferi, and other causes of morbidity in Pacific herring Clupea pallasi spawning in Prince William Sound, Alaska, USA.

Pacific herring Clupea pallasi populations in Prince William Sound, Alaska, USA, declined from an estimated 9.8 x 10(7) kg in 1992 to 1.5 x 10(7) kg in 1994. To determine the role of disease in population decline, 233 Pacific herring from Prince William Sound were subjected to complete necropsy during April 1994. The North American strain of viral hemorrhagic septicemia virus (VHSV) was isolated from 11 of 233 fish (4.7%). VHSV was significantly related to myocardial mineralization, hepatocellular necrosis, submucosal gastritis, and meningoencephalitis. Ichthyophonus hoferi infected 62 of 212 (29%) fish. I. hoferi infections were associated with severe, disseminated, granulomatous inflammation and with increased levels of plasma creatine phosphokinase (CPK) and aspartate aminotransferase (AST). I. hoferi prevalence in 1994 was more than double that of most previous years (1989 to 1993). Plasma chemistry values significantly greater (p < 0.01) in males than females included albumin, total protein, cholesterol, chloride, glucose, and potassium; only alkaline phosphatase was significantly greater in females. Hypoalbuminemia was relatively common in postspawning females; other risk factors included VHSV and moderate or severe focal skin reddening. Pacific herring had more than 10 species of parasites, but they were not associated with significant lesions. Two of the parasites have not previously been described: a renal intraductal myxosporean (11% prevalence) and an intestinal coccidian (91% prevalence). Transmission electron microscopy of a solitary mesenteric lesion revealed viral particles consistent with lymphocystis virus. No fish had viral erythrocytic necrosis (VEN). Prevalence of external gross lesions and major parasites was not related to fish age, and fish that were year-lings at the time of the 1989 'Exxon Valdez' oil spill (1988 year class) had no evidence of increased disease prevalence.

Aging↗
PubMed1991

Preliminary results on the seasonality and life cycle of the parasitic dinoflagellate causing bitter crab disease in Alaskan tanner crabs (Chionoecetes bairdi).

Tanner crabs (Chionoecetes bairdi) from the Sullivan Island area of southeast Alaska were sampled for 1 year to determine the prevalence and intensity of the parasitic dinoflagellate which causes bitter crab disease (BCD). The prevalence and intensity of infection were the greatest in the summer, declined in the fall and winter, and increased again in the spring. A possible relationship between softer, newer shells and higher levels of parasitism was also observed. In vivo transmission studies in the laboratory suggested there are several morphologically different forms of the vegetative cell of the BCD dinoflagellate which occur prior to sporulation of the parasite. In addition, it appears that both the two spore types produced by the parasite are infectious by injection and that there is no ploidy difference between the two spore types and the vegetative cell, suggesting that the two spore types may not represent separate sexes.

Animals↗
PubMed1991

Coccidia, X-cell pseudotumors and Ichthyophonus sp. infections in walleye pollock (Theregra chalcogramma) from Auke Bay, Alaska.

One hundred twenty-five walleye pollock (Theragra chalcogramma) were collected from Auke Bay, Alaska (USA) in 1985 and examined for histologic evidence of disease-causing infectious agents in 1987. A Goussia sp.-like coccidium was found in the kidney tubules of 75% and an Eimeria sp.-like coccidium was found in the intestine of 18% of the fish examined. The kidney coccidium was associated with sloughing of the tubular epithelium, peritubular fibrosis and granuloma formation. The intestinal coccidium was associated with severe tissue displacement and inflammation. In addition, X-cell pseudotumors were observed in the pseudobranchs (4%), and the fungus Ichthyophonus sp. was observed in the kidney, intestine or brain of 2% of the pollock.

Animals↗
PubMed1987

Morphological and biochemical properties of four members of a novel group of reoviruses isolated from aquatic animals.

The morphological, biochemical and growth characteristics of four members of the Reoviridae, three from the fish hosts, golden shiner (Notemigonus crysoleucas), chum salmon (Oncorhynchus keta) and channel catfish (Ictalurus punctatus) and one from American oyster (Crassostrea virginica), were compared. Electron microscopy of negatively stained virions revealed icosahedral particles approximately 75 nm in diameter composed of a double capsid. Complete particles had buoyant densities in CsCl of 1.34 to 1.36 g/ml. The viruses replicated well in several fish cell lines, forming plaque-like syncytia in monolayer cultures. Each virus could be distinguished by the range of cell lines supporting its growth. Polyacrylamide gel electrophoresis showed that the genome of each virus was composed of 11 segments of dsRNA distributed among three size classes. There were three large, three medium and five small segments in each genome and each isolate had a unique electropherotype. The segments ranged from 2.5 X 10(6) to 0.31 X 10(6) mol. wt. with a total genome of approximately 15 X 10(6) mol. wt. Analysis by SDS-PAGE revealed that each virus had five major structural proteins. There were two large polypeptides of approximately 135,000 and 125,000 mol. wt., one medium size polypeptide of 70,000 mol. wt. and two small polypeptides of 45,000 and 34,000 mol. wt. Of the major structural proteins, those of approximately 70,000 and 34,000 mol. wt. were consistently present in the highest concentrations. Minor virion proteins were detected but were not characterized. These four viruses, isolated from aquatic animals, were unlike viruses of the six established genera of the Reoviridae.

Animals↗
PubMed1985

Hepatocarcinogenicity of benzo[a]pyrene to rainbow trout by dietary exposure and intraperitoneal injection.

The influence of benzo[a]pyrene [(BP) CAS: 50-32-8] on the induction of certain enzymes within the hepatic mixed-function oxidase (MFO) system and its potential carcinogenicity were examined in rainbow trout (Salmo gairdneri). Nine-week feeding trials were performed with 500 and 1,000 ppm BP to determine trout tolerance to BP. Levels of MFO enzymes, including ethoxyresorufin-O-deethylase (EROD), ethoxycoumarin-O-deethylase (ECOD), benzo[a]pyrene monooxygenase (BPMO), and cytochrome P450 were measured during this time. An 18-month feeding trial of a 1,000-ppm BP dose was initiated in duplicate groups of 100 fingerling rainbow trout. Samples of trout were killed at 6, 12, and 18 months for gross and histologic examination of the internal organs for neoplasms. A group of fifty 10-month-old rainbow trout were given 12 monthly ip injections of 1 mg BP in 0.4 ml propylene glycol (PG), and comparable controls were given PG injections only. The trout were held for an additional 6 months, killed at age 28 months, and examined as in the dietary study. Mean MFO enzyme levels of EROD, ECOD, BPMO, and cytochrome P450 were significantly (P less than .001) elevated, showing dose- and time-response relationships when compared to MFO enzyme levels in control fish. Twelve months after BP exposure was initiated, 15% of the BP-fed fish had histologically confirmed neoplasms of the liver. After 18 months the incidence increased to 25%. No evidence of neoplasia was observed in control fish. BP injected ip resulted in a 50% incidence of hepatocellular neoplasms and in a fibrosarcoma of the liver and papillary adenomas of the swim bladder in 1 fish. These results indicate that BP is a potent inducer of selected hepatic MFO enzymes and establish, for the first time, the hepatocarcinogenicity of BP in an aquatic species.

Adenocarcinoma↗
PubMed1984

Histological progression of hepatic neoplasia in rainbow trout (Salmo gairdneri).

The histological progression of hepatic neoplasia has not been as systematically studied in rainbow trout as it has been in rodents. Two putative preneoplastic lesions have been identified, the eosinophilic focus and the basophilic focus, but whether these correspond to similar lesions in rodent livers is not known. Preneoplastic liver lesions in rodents have been extensively characterized histochemically, but adaptation of these techniques to trout livers has not always been successful. Eosinophilic foci consist of hypertrophied cells, enlarged atypical nuclei, and dense glycogen-free cytoplasm. Mitotic figures are also occasionally seen. Usually, these foci have been infiltrated and at least partially destroyed by inflammatory cells, largely lymphocytes. In some liver sections, eosinophilic foci are intact and occasionally an eosinophilic-basophilic transformation can be seen. However, most often basophilic foci appear independently, surrounded by normal hepatocytes, with no indication of a prior eosinophilic stage. The cells of basophilic foci are similar to those of carcinomas: intensely basophilic, mitotically active, devoid of glycogen, and grouped into cords several cells in thickness. These nodules may appropriately be referred to as carcinomas in situ, because the only distinguishing characteristic is the size of the lesion. Attempts at differentiation between benign and malignant liver lesions appear arbitrary. We believe the best classification of the neoplastic liver lesion in trout is a hepatocellular carcinoma because the potential for malignant behavior always exists and, with sufficient time, can often be histologically demonstrated. We have also described our experience with the characteristics of other liver lesions associated with hepatocarcinogenesis.

Adenocarcinoma↗
PubMed1984

A limited epizootic of neuroblastoma in coho salmon reared in chlorinated-dechlorinated water.

During the 1976-77 brood year, approximately 12 cases of neuroblastoma were observed in a captive group of 100,000 fingerling coho salmon (Oncorhynchus kisutch) reared in a commercial hatchery. The tumors were large, occurring in the skeletal muscle near the dorsal fin causing conspicuous bulging of the overlying integument. Tumors examined from 3 fish each consisted of neuroblasts in trabecular patterns interspersed by glial fibrillar material and linear cavities resembling central neural canals lined by ependyma-like cells. Ganglion-like cells also were apparent morphologically and by special stain. Cancer of the tumor was characterized by an abundance of mitotic figures with occasional abnormal divisions, local invasion of normal tissues, and potentially metastatic tumor cell aggregates in organ vasculature. The etiology of this tumor may have been related to mutagenic-carcinogenic halogenated compounds possibly formed in the hatchery water supply during continuous chlorination of incoming river water.

Animals↗
PubMed1984

Rainbow trout embryos: advantages and limitations for carcinogenesis research.

Rainbow trout embryos are sensitive to the initiation of neoplasms in various tissues by brief exposures to solutions of water-soluble carcinogens. This characteristic was first demonstrated with the sparingly soluble liver carcinogen, aflatoxin B1 (AFB1). A 30-minute exposure of 21-day-old embryos (embryos hatch in 24-25 days at 12 degrees C) to a 0.5-ppm aqueous solution of AFB1 will result in approximately 65 of the survivors having at least 1 liver tumor, 1 year after treatment. The embryos are responsive to both AFB1 dose and the length of exposure and become increasingly sensitive with increased embryonic age. We have used rainbow trout embryos to demonstrate the hepatocarcinogenicity of other aflatoxin metabolites and precursors; aflatoxicol, aflatoxin G1, versicolorin A, and sterigmatocystin. In addition to mycotoxins, trout embryos are sensitive to several nitrosamine hepatocarcinogens including: dimethylnitrosamine, diethylnitrosamine, nitrosopyrrolidine, and 2,6-dimethylnitrosomorpholine. However, with the highly water-soluble nitrosamines, longer exposure time (up to 24 hr) are required. It is generally accepted that each of the above-named carcinogens requires metabolic activation to the ultimate carcinogenic form. This provides indirect evidence that the trout embryo is capable of cytochrome P-450-mediated metabolism. Finally, trout embryos are sensitive to the direct-acting carcinogen, N-methyl-N'-nitro-N-nitrosoguanidine. This compound produces tumors of the liver, stomach, kidney, and swim bladder, and a pronounced female-to-male sex reversal. Results to date have shown that the trout embryo is a sensitive, convenient, and economical whole animal model system with many distinct advantages for carcinogen testing and research.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Effect of cyclopropenoid fatty acids on the hepatic microsomal mixed-function-oxidase system and aflatoxin metabolism in rabbits.

Male New Zealand weanling rabbits were fed a diet containing 0.25% cyclopropenoid fatty acids for 28 days. Compared with the controls, the rabbits given cyclopropenoid fatty acids showed retarded growth, some moderate liver histological damage, altered hepatic mixed-function-oxidase activities and minor variations in vitro [14C]aflatoxin B1 metabolism. In in vitro assays the major hepatic metabolite of aflatoxin B1 (AFB1) was aflatoxicol (AFL) and the major AFL metabolite was AFB1. Minor amounts of aflatoxin M1 and a metabolite believed to be AFL-M1 were formed. The similarity of this AFB1 metabolite pattern to that in rainbow trout, taken together with the apparent absence of AFB1 detoxification products is consistent with the sensitivity of both species to the acute effects of AFB1.

Aflatoxin B1↗
PubMed1980

Glochidiosis of salmonid fishes. IV. Humoral and tissue responses of coho and chinook salmon to experimental infection with Margaritifera margaritifera (L.) (Pelecypoda: Margaritanidae).

Coho salmon (Oncorhynchus kisutch) are more resistant than chinook salmon (O. tshawytscha) to experimental infection with the glochidia of the freshwater mussel Margaritifera margaritifera. Histological sections of gills from coho salmon 16 hr postinfection (p.i.) showed that parasite encystment either did not occur or had progressed incompletely, which accounted for the loss of many glochidia from the gills. The remaining encysted glochidia were sloughed within 2 days (p.i.) by a well-developed hyperplasia. On chinook salmon, the parasites developed normally with no sloughing or hyperplasia. Analysis of blood samples taken from coho salmon at intervals during the infection showed significant increases in hematocrit, hemoglobin, the mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), and leukocyte numbers when compared with control fish. In infected chinook salmon only the hematocrit, erythrocyte numbers, and MCV increased while the MCHC decreased. Total plasma protein increased in coho salmon but decreased in chinook salmon during infection. Glochidial antibodies were demonstrated in the blood plasma of coho and chinook salmon 8 to 12 wk p.i. Fewer glochidia attached to the excised gills of coho salmon than to the gills of chinook salmon. Also, the in vitro survival time of parasites in mucus and plasma from coho salmon was less than in the same chinook salmon fluids.

Animals↗
PubMed1977

Glochidiosis of salmonid fishes. I. Comparative susceptibility to experimental infection with Margaritifera margaritifera (L.) (Pelecypoda: Margaritanidae).

This is the first report on the susceptibility of salmonid fishes to infection with the glochidia of the freshwater mussel Margaritifera margaritifera using known numbers of parasites under controlled conditions. The relative susceptibility of six species of salmonid fish, 20 to 80 mm in total length, to glochidiosis was determined by exposing fish individually to different numbers of parasites and plotting mortalities against these exposure levels at 70 days postexposure and also against the numbers of parasites recovered from fish 48 hr postinfection. The 70-day interpolated LE50 values (exposure concentrations of glochidia that killed 50% of the fish) for kokanee salmon (Oncorhynchus nerka kennerlyi), cutthroat trout (Salmo clarki), Atlantic salmon (S. salar), steelhead trout (S. gairdneri) and coho salmon (O. kisutch) were 17,500, 29,000, 35,000, 57,000, and 105,000, respectively. Chinook salmon (O. tshawytscha) was the most susceptible species. The LE50 values could not be estimated even at the lowest exposure levels because mortalities were too high. On the basis of the LE50 value, coho salmon was the most resistant species.

Animals↗
PubMed1977

Henneguya sp. (Cnidospora:Myxosporida) parasitic in the heart of the bluefish, Pomatomus saltatrix.

A myxosporidan parasite, Henneguya sp., was discovered in the bulbus and truncus arteriosus of bluefish, Pomatomus saltatrix. Infected fish were captured from the Atlantic Ocean near Montauk Point, Long Island, New York, Raritan Bay, New Jersey, and Chesapeake Bay, Maryland. Comparative features of mature spores showed that they were similar to those of Henneguya sebasta Moser and Love 1975, from the bulbus arteriosus of seven species of California rockfish, Sebastes. Studies on growth stages of the parasite from both host species are necessary before a definite identification of the bluefish parasite can be made.

Age Factors↗