Here I quantitatively review the literature on how fish gill morphology is affected by chemical and physical irritants in the surrounding water (e.g. various toxicants, extremes of temperature or p...

Fish Gill Structural Changes Induced by Toxicants and Other Irritants: A Statistical Review

Infectious diseases of fishes occur when susceptible fishes are exposed to virulent pathogens under certain environmental stress conditions. Very little research has been carried out to show the effect of pollution on outbreaks of infectious diseases of fishes. Therefore, examples taken from the literature were selected and reviewed to show the coincidence of infectious diseases with stress caused by temperature, eutrophication, sewage, metabolic products of fishes, industrial pollution, and pesticides.

The effects of environmental stress on outbreaks of infectious diseases of fishes

: Interest in the toxicity of tin compounds dates to the early 1800's when investigators demonstrated that inorganic tin compounds produced muscular weakness, loss of pain sensation, and immobility in dogs (Reiter and Ruppert 1984; Idemudia and McMillan 198Gb). In man, organotins can be assimilated by inhalation, absorption through the skin, and from food and drinking water (Zuckerman et al. 1978). The first documented case of organotin poisoning of humans was in 1880 when workers complained of headaches, general weakness, nausea, and diarrhea after exposure to triethyltin acetate vapors (Reiter and Ruppert 1984). Renewed interest in the toxicity of organotin compounds resulted from a medical tragedy in France in 1954. Stalinon, a proprietary compound of diethyltin diiodide plus linoic acid used to treat furuncles and other skin infections, caused 217 poisonings and 111 deaths (Piver 1973; Duncan 1980; Idemudia and McMillan 198Gb). The identified toxic components in Stalinon were triethyltin contaminants; victims received a total dose of 3 grams over a 6- to 8-week period. Symptoms included constant severe headache, rapid weight loss, vomiting, urine retention, vertigo, hypothermia, abdominal pain, and visual and psychic disturbances. Some of the more severely affected patients had convulsions. Death usually occurred in coma or from respiratory or cardiac failure. In survivors, headaches and diminished visual acuity remained for at least 4 years.

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Tin Hazards to Fish, Wildlife, and Invertebrates: A Synoptic Review.

We have tried to draw attention to an increasing body of evidence (from several publications) that parasites of fish might be useful indicators of pollution. Several types of pollutants, including domestic sewage, pesticides, polychlorinated biphenyls, heavy metals, pulp and paper effluents, petroleum aromatic hydrocarbons, acid rain, and others, are known to affect aquatic animals. Many of the latter are parasitized and, under natural environmental conditions, most fish parasites are believed to cause little or no harm. However, chronic exposure to pollutants over a period of time causes biochemical, physiological and behavioural host changes that ultimately can influence the prevalence and intensity of parasitism. Some of these changes include host nutrition, growth and reproduction. Macroscopic lesions might not always be apparent, but subtle disorders in several specific tissues and organs might occur. Pollutants might promote increased parasitism in aquatic animals, especially fish, by impairing the host's immune response or favouring the survival and reproduction of the intermediate hosts. Alternatively, decreased parasitism might ensue through toxicity of the pollutant to free-living stages and intermediate hosts or by alteration of the host's physiology. Experimental studies indicate that the numbers of ectoparasites such as trichodinid ciliates and monogeneans increase significantly on the gills following exposure to a pollutant, and this is supported by field data on other ciliates and monogeneans where evidence of pollution has been clearly demonstrated. There is also evidence that endoparasitic protozoons, such as myxozoons, microsporans and haematozoons, all of which are capable of proliferating in their hosts, increase substantially in prevalence and intensity when interacting with pollutants. The period of patency might also be prolonged in haematozoan infections. Most reports of pollution effects on endoparasites suggest increased parasitism in fish hosts. This also applies to fish living in areas which receive thermal effluents. Parasites might in turn enhance their hosts' susceptibility to pollutants, and information in support of this view is accumulating. Finally, immunosuppression represents one of the underlying mechanisms influencing increased parasitism. Thus, while published information suggests more than a casual connection between fish parasites and pollution, further research is needed to establish the cause-and-effect relationship and at the same time take cognizance of histopathological effects of the toxic agents and their concentrations in water. Areas for future research are recommended.

Influence of pollution on parasites of aquatic animals.

Zinc Hazards to Fish, Wildlife, and Invertebrates: A Synoptic Review

Acute heavy metal toxicity to fish has been attributed to the coagulation or precipitation of mucus on the gills and/or to cytological damage to the gills The physiological mechanism of death by either of the above causes is related to a breakdown in gas exchange at the gills This study of acute zinc toxicity to rainbow trout (Salmo gairdneri) supports an earlier hypothesis that modification of the gas exchange process at the gills creates hypoxia at the tissue level Tissue hypoxia appears to be a major physiological change preceding death once the gas exchange process at the gills is no longer sufficient to supply the oxygen requirements of the fish

Alma H. Jones

Papers

Acute Zinc Toxicity to Rainbow Trout (Salmo gairdneri): Confirmation of the Hypothesis that Death is Related to Tissue Hypoxia