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Adv Parasitol. 1991;30:201-38.

Influence of pollution on parasites of aquatic animals.

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  • 1Department of Biology and Ocean Sciences Centre, Memorial University of Newfoundland, St John's, Canada.


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.

[PubMed - indexed for MEDLINE]
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