Mercury Poisoning in Animals - Toxicology - MSD Veterinary Manual (2023)

The physical, chemical, and kinetic properties of the various forms of mercury play an important role in influencing clinical manifestations, the extent and type of lesions, and the distribution of mercury in tissues. Organic forms of mercury, mainly methylmercury, are lipid soluble and well absorbed orally. Consequently, bioaccumulation in tissues such as the brain, kidney, and fetus is extensive. Methylmercury disrupts metabolic activity, causing degeneration and necrosis in many tissues, although the brain and fetus are more susceptible.

In the brain, neuronal degeneration and perivascular cuffing in the cerebrocortical gray matter are histologically evident. Cerebellar atrophy or hypoplasia and Purkinje cell degeneration are seen. Encephalomalacia, loss of myelin, and necrosis of axons may also be evident.

Methylmercury is mutagenic, carcinogenic, embryotoxic, and a potent teratogen. Inorganic forms of mercury, including elemental mercury, are absorbed shortly after skin contact. Elemental mercury vapors are inhaled and rapidly absorbed. This highly toxic form of mercury causes corrosive bronchitis and interstitial pneumonia. All forms of mercury cross the placenta. Inorganic forms of mercury bind to sulfhydryl groups in enzymes and other thiol-containing molecules, such as cysteine ​​and glutathione. Tissues rich in these components, such as the renal cortex, accumulate appreciable levels of mercury. Inorganic forms of mercury are cytotoxic and highly corrosive. Consequently, these forms of mercury cause severe inflammation, ulceration, and tissue necrosis in the gastrointestinal tract. Pale and swollen kidneys, manifesting histologically as tubular necrosis and interstitial nephritis, are consistent findings.

Inhalation of corrosive elemental mercury vapors in high concentrations causes severe breathlessness and respiratory problems, which are often fatal. Neurological manifestations may eventually develop at lower exposure levels. Due to its corrosive nature, inorganic mercury mainly causes gastrointestinal symptoms including anorexia, stomatitis, pharyngitis, vomiting, diarrhea, pain; and shock, dyspnea, and dehydration. With high exposure, death often occurs within hours. Surviving animals may have eczema, skin keratinization, anuria, polydipsia, hematuria, or melena. Neurological manifestations, including CNS depression or excitation, similar to those seen in organic mercury poisoning, may develop after chronic exposure. Depending on the level of exposure to organic mercury compounds such as methylmercury, it may take days for clinical manifestations to develop. Since these compounds are not corrosive, there are no gastrointestinal symptoms.

Common neurologic manifestations include blindness, ataxia, incoordination, tremors, abnormal behavior, hypermetria, nystagmus (feline), and tonic-clonic seizures. Advanced cases can be characterized by depression, anorexia, proprioceptive disorders, total blindness, paralysis with high mortality.

The developing nervous system of young animals is particularly vulnerable to organic mercury exposure and often manifests as cerebellar ataxia associated with cerebellar hypoplasia and death.

The significant variation in the clinical manifestations associated with the different forms of mercury and the duration of exposure underscores the need for repeat tissue analysis. Because inorganic forms of mercury are excreted in the urine, urinary mercury concentrations are the most reliable indicator of exposure. In contrast, organic mercury compounds that bioaccumulate in soft tissue are best evaluated in liver, kidney, or brain tissue.

For most animal species, blood, kidney, brain, and dietary mercury concentrations of < 0.1 mg/kg (ww) are considered normal. If poisoning is suspected, concentrations >6 mg/kg (blood), 10 mg/kg (kidneys), 0.5 mg/kg (brain), and 4 mg/kg (food, dry weight) support a diagnosis of poisoning. mercury. In general, the kidney is considered the most useful tissue for diagnosis. Concentrations in all tissues can be significantly higher after chronic exposure. Marine mammals and fish often contain significantly elevated levels of mercury that may not be associated with clinical disease (compared to ruminants or domesticated species); however, they can be a potential source of exposure for the most vulnerable species, particularly the fetus or younger animals.

Other tests, including those that detect proteinuria, azotemia, or nonregenerative anemia, may provide useful evidence in diagnosing mercury poisoning. Diagnosis can be made on the basis of analysis of tissue samples with appropriate histopathologic and clinicopathologic evidence, history, and clinical signs.

Because the neurological and kidney damage resulting from mercury poisoning is irreversible, treatment may be ineffective. Consequently, the prognosis for a full recovery is very poor. In food-producing animals, the significant accumulation of mercury in food-producing tissues and its profound effects on reproduction limit treatment options. Euthanasia and proper disposal is recommended in consultation with regulatory authorities.

In veterinary patients for whom treatment is indicated, oral administration of activated charcoal (1 to 3 g/kg) and sodium thiosulfate (0.5 to 1 g/kg) binds mercury and limits absorption. Vitamin E and selenium, which are antioxidants, can limit oxidative damage. Chelation therapy may be helpful if treatment is started soon after exposure, before nephrotoxic effects become severe. The fat-soluble chelator dimercaprol (3 mg/kg body weight, IM, every 4 hours for 2 days, followed by 4 times daily for 3 days, and twice daily for 10 days) may be beneficial. For organic mercury poisoning, 2,3-dimercaptosuccinic acid (10 mg/kg orally three times daily for 10 days) has been shown to be effective in dogs. With successful decontamination of the gastrointestinal tract, administration of penicillamine (50 to 100 mg/kg per day orally for 2 weeks) may reduce clinical symptoms. Limiting consumption of mercury-contaminated foods, such as fish products or water, will reduce exposure.

The World Health Organization and many countries have established comprehensive guidelines that reflect the serious nature of mercury poisoning for humans and animals. The water guidelines in most countries for mercury are 0.001 mg/l and 0.003 mg/l for humans and animals, respectively.