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Mercury is an extremely toxic element; however only occasional poisoning cases have been reported. It has been used in the past as the active ingredient in ointments, parasiticidals, antiseptics, disinfectants, diuretics, and fungicides. Mercury can be a source of environmental contamination when present in seed dressing fungicides, anti-slime fungicides in pulp and paper industries, by-products of burning coal, mine tailings, and wastes from chlorine-alkali industries. Whatever the source, mercury finds its way into water sources and accumulates in fish and fish-eating animals. Inorganic mercury which enters a water source is readily converted to methyl mercury by aquatic microorganisms and accumulates in the tissues of fish. In Michigan, the bald eagle, great blue heron, common loon, mink, otter, common merganser (possible), and common goldeneye (possible) have been poisoned by mercury as a result of ingestion of mercury contaminated fish. Waterfowl may be exposed to chronic low levels of mercury present as an environmental contaminant. Mercury, which is eliminated from the female via egg laying, has been reported to cause abnormal egg laying behavior, impaired reproduction, slowed duckling growth, and altered duckling behavior in mallard ducks. Occasionally seed eating birds are affected by mercury toxicity after feeding on mercury fungicide treated seed.
Ingested mercury is rapidly absorbed by the intestinal tract and stored in the kidney and liver. Once absorbed, mercury is slowly eliminated in the urine, feces, saliva, sweat and milk.
Clinical Signs and Pathology
Depending upon the amount of mercury ingested, the clinical signs can either be peracute, acute, or chronic. Ingestion of large amounts of mercury results in almost immediate death due to heart attack. Symptoms of acute poisoning include severe abdominal pains, vomiting and diarrhea. The
intestinal mucosa is destroyed and if the animal survives this first stage, hemorrhagic gastroenteritis is followed by ulcerative colitis with destruction of the kidney tubules. Chronic exposure results in soreness, swelling, bleeding and ulceration of the gums, tongue and oral mucosa with anemia, edema, and body wasting ending in death. Chronic mercury poisoning may be accompanied by mental disturbances due to degeneration of nerve tracts and may result in blindness, weakness, incoordination, and coma.
Mercury poisoning is suspected from clinical signs and history of exposure to mercury contamination. Definitive diagnosis can be made by detection of high levels of mercury in the stomach contents, kidneys, and/or liver.
Absorption from the gut is so rapid that treatment of wildlife is usually not practical. When treatment is possible, the stomach should be emptied, and milk or raw egg white given to precipitate the mercury. Dimercaprol (BAL) is the treatment of choice accompanied by the administration of large amounts of intravenous fluids to prevent dehydration.
Control and Significance
Control of mercury poisoning in wildlife is aimed at reducing the presence of mercury as an environmental contaminant. Humans are susceptible to the toxic effects of mercury and have been poisoned due to the consumption of mercury contaminated fish and shellfish. Although wildlife deaths due to mercury poisoning are rare, there is a possibility that mercury may reduce populations by decreasing reproductive efficiency.
For questions about wildlife diseases, please contact the Michigan DNR Wildlife Disease Laboratory.