Mercury exists in a variety of organic and inorganic forms. The replacement of commercial mercurial compounds, including antiseptics (eg, mercurochrome), diuretics, and fungicides by other agents has decreased the likelihood of mercurial toxicosis. However, the increased use of button batteries with various amounts of mercury and other heavy metals poses a significant ingestion hazard. Exposure to environmental sources of organic methylmercury in the meat of predator species also exists.
These include the volatile elemental form of mercury (used in thermometers) and the salted forms (mercuric chloride [sublimate] and mercurous chloride [calomel]). Large button batteries and chewed or split/broken disk batteries are potential sources of mercury. Mercury button batteries may contain 15–50% mercuric oxide. Ingested inorganic mercury is poorly absorbed (10–35%) and relatively low in toxicity. Although rare, inhaled inorganic mercury is rapidly absorbed and highly toxic.
Large amounts of inorganic mercurials are corrosive and produce vomiting, diarrhea, and colic. Renal damage also occurs, with polydipsia and anuria in severe cases. In rare cases of chronic inorganic mercurial poisoning, the CNS effects resemble those of organic mercury poisoning. Mercury vapor from elemental mercury produces corrosive bronchitis and interstitial pneumonia and, if not fatal, leads to neurologic signs.
Inorganic mercury is converted to the organic alkyl forms, methylmercury and ethylmercury, by microorganisms in the sediment of rivers, lakes, and seas. Animals at the top of food chains (tuna, trout, seals, polar bears) bioaccumulate methylmercury above levels found in their environment. Marine life accumulates the most toxic form, methylmercury; therefore, fish (especially larger and older animals) must be monitored for contamination. There are reports of commercial cat food causing severe neurologic disturbances in cats fed an exclusive tuna diet for 7–11 mo. The body is also capable of forming organic mercury from inorganic forms.
The organic mercurials are well absorbed via all routes and bioaccumulate in the brain, kidneys, and muscle. Aryl mercurials (eg, phenylmercury fungicide) are slightly less toxic and less prone to bioaccumulation. Animals poisoned by organic mercury exhibit CNS stimulation and locomotor abnormalities after a lengthy latent period (weeks). Signs may include blindness, excitation, abnormal behavior and chewing, incoordination, and convulsions. The nervous system of young animals is especially vulnerable during development, as mercury affects cell migration and division. Cats show hindleg rigidity, hypermetria, cerebellar ataxia, and tremors. Mercury is also a mutagen, teratogen, and carcinogen, and is embryocidal. Differential diagnoses include conditions with tremors and ataxia as predominant signs, such as poisoning with metals and insecticides, cerebellar lesions due to trauma, or feline parvovirus.
After the ingestion of inorganic mercury, the major targets of toxicity are the GI tract and the kidneys. The CNS is primarily affected with organic mercury poisoning. Ingestion of inorganic mercury results in inflammation and necrosis, particularly in the glandular stomach, plus renal tubular damage. Tubular effects range from cellular degeneration to widespread necrosis. The neurologic changes with organic mercury occur primarily in the cerebellum and the cortex. Histologic lesions include degeneration of neurons and perivascular cuffing in the cerebrocortical gray matter, cerebellar atrophy of the granular layer, and damage to Purkinje cells.
Laboratory diagnosis must differentiate between normal concentrations of mercury in tissue (especially whole blood, kidney, and brain) and feed (<1 mg/kg dry basis). Urinary mercury best determines inorganic mercury exposure, while blood levels are best in organic mercury exposure. Levels that are even slightly elevated may be significant in young animals. Mercury levels must be interpreted along with history, clinical signs, and lesions.
Treatment and Control
Emesis and activated charcoal (1–3 g/kg, PO) are very effective at reducing absorption. Oral administration of sodium thiosulfate (1 g/kg) to bind mercury still in the gut and antioxidants, especially vitamin E, may be beneficial.
Chelation therapy is recommended after acute oral ingestion or urinary mercury is detected. The chelator dimercaprol (3 mg/kg body wt, IM, every 4 hr for the first 2 days, qid on the third day, and bid for the next 10 days or until recovery is complete) has been beneficial. When available, the water soluble, less toxic analog of dimercaprol, 2,3-dimercaptosuccinic acid, is the chelator of choice for organic mercury poisoning. Penicillamine (15–50 mg/kg, PO) may be used only after the gut is free of ingested mercury and renal function has been established. Neurologic signs may be irreversible once they develop.
Last full review/revision March 2012 by Herman J. Boermans, DVM, MSc, PhD