Richard E. Wolke

Preliminary evaluation of the use of macrophage aggregates (MA) as fish health monitors

Discrete, round to ovoid macrophage aggregations (MA) containing pigment are commonly found widely distr ibuted in the spleen, l i ve r , and kidney of the higher te leos t i i (Agius 1980). These cel lu lar aggregations have been variously named (Grove 1968), most recently melano-macrophage centers (MMC) by Roberts (1975). The la t ter author, El l ls (1974), and Ferguson (1976) have suggested that MA have analogies to the germinal centers of homeotherms.

The use of fluorescent microspheres in the study of piscine macrophage aggregate kinetics

The kinetics of piscine liver, spleen, and kidney macrophage aggregate formation was studied in Carassius auratus using the sequential interperitoneal injection of fluorescent green and yellow microspheres. This study indicates that 1. macrophages migrating to or forming new aggregates move randomly throughout the aggregate mass and do not simply increase aggregate size by a laminating process (layer upon layer), 2. macrophages apparently form new aggregates and migrate to existing aggregates simultaneously, and 3. macrophage aggregates form in greater number and more rapidly in the spleen and kidney than in the liver.

Absence of overt toxicity from feeding the flavonol, quercetin, to rainbow trout (Salmo gairdneri)

The toxicity of the plant flavonol, quercetin, to rainbow trout (Salmo gairdneri) was investigated. Quercetin, which had been confirmed to be mutagenic in the Ames Salmonella/mammalian microsome test, was fed to trout at levels of 1 or 5% in the diet for 8 months. Survival, growth and feed conversion efficiency, selected haematological parameters and the relative weights of heart, liver and spleen were unaffected by the ingestion of quercetin, and there were no histopathological changes in any of the tissues examined.

The cellular immune response of rainbow trout (Salmogairdneri Richardson) to sheep red blood cells

Abstract The cellular immune response of rainbow trout, Salmo gairdneri, to sheep erythrocytes was investigated. Both the primary and secondary responses were measured using the migration inhibition factor (MIF), antigen-binding (ABC), and plaque-forming cell (PFC) assays. These immune function assays provide measures of both T and B cell activity. The kinetics of these three responses at 16°C were determined by sampling fish over an 18 day period for the primary response and a ten day period for the secondary response. The peak MIF response occurred two days after injection, while the primary peak PFC reponse was observed 14 days post-injection. Two ABC peaks were observed in the primary response, one at four days and one at ten days after injection. In the secondary response the peak ABC response was observed four days and the peak PFC response six days post-inoculation. The possible interrelationships of the various cell populations are discussed.

Acute toxicity of platinum to coho salmon (Oncorhynchus kisutch)

Abstract The effects of short-term exposure to tetravalent platinum on survival, opercular movement and post-treatment growth of coho salmon fry (Oncorhynchus kisutch) was investigated. Employing a static water acute toxicity bioassay with platinum as PtCl 4 2HCl·6 H 2 O, at 8.5±0.2°C, and a water hardness of 55.9±3.5 mg l. −1 (as CaCo 3 ), the 24, 48, and 96-h LC 50 values were 15.5, 5.2, and 2.5 mg Pt 4+ l. −1 respectively. Rates of opercular movement for fish exposed to platinum increased with increasing concentrations to a level of 1.0 mg l. −1 . No further significant increases were evident above this level. Hypoactivity of fish exposed to 0.3 mg l. −1 and higher was evident during the acute toxicity bioassay and much of the post-treatment study. Post-treatment rate of growth for fish exposed to sublethal concentration of platinum for 96 h was less than that of the controls. All organs examined histopathologically were within normal ranges with the exception of the gills and olfactory organ. Lesions in fish exposed to concentration of 0.3 mg l. −1 and higher were characterized by branchial epithelial hypertrophy and hyperplasia, and necrosis of olfactory epithelial cells.