Mercury Poisoning in Animals

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

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

Methylmercury is mutagenic, carcinogenic, embryotoxic, and highly teratogenic. The inorganic forms of mercury, including elemental mercury, are poorly absorbed after skin exposure. Elemental mercury vapors are inhaled and rapidly absorbed. This highly toxic form of mercury produces 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 notable concentrations of mercury. Inorganic forms of mercury are cytotoxic and highly corrosive. Consequently, these forms of mercury cause severe inflammation, ulcers, and tissue necrosis in the gastrointestinal tract. Pale, swollen kidneys manifested histologically as tubular necrosis and interstitial nephritis are consistent findings.

The inhalation of corrosive elemental mercury vapors at high concentrations produces severe dyspnea and compromised respiratory function that is usually fatal. Neurologic manifestations may eventually develop at lower levels of exposure. Due to the its corrosive nature, inorganic mercury produces primarily gastrointestinal signs, including anorexia, stomatitis, pharyngitis, vomiting, diarrhea, pain; as well as shock, dyspnea, and dehydration. Death often occurs within hours at high levels of exposure. Animals that survive may exhibit eczema, skin keratinization, anuria, polydipsia, hematuria, or melena. Neurologic manifestations, including CNS depression or excitation similar to that which occurs in cases of organic mercury poisoning, may develop after chronic exposure. Depending on the level of exposure to organic mercury compounds such as methylmercury, clinical manifestations may take days to develop. Because these compounds are not corrosive, gastrointestinal signs do not occur.

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

The nervous system of young, developing animals is particularly susceptible to organic mercury exposure, and is frequently manifested as cerebellar ataxia associated with cerebellar hypoplasia and death.

• Tentative diagnosis is based on clinical signs; confirmed by analysis of tissue samples (eg, kidney) to determine mercury content

• Measurement of urinary mercury concentration can confirm exposure to inorganic mercury compounds

The considerable variation associated with the clinical manifestations related to the various forms of mercury and the duration of exposure underscores the need for repeated tissue analyses. 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, which bioaccumulate in soft tissues, are most appropriately assessed in liver, kidney, or brain tissues.

In most species, blood, kidney, brain, and feed concentrations of mercury < 0.1 mg/kg (wet wt) are considered normal. When poisoning is suspected, concentrations >6 mg/kg (blood), 10 mg/kg (kidney), 0.5 mg/kg (brain), and 4 mg/kg (feed, dry wt) are consistent with a diagnosis of mercury poisoning. Generally, the kidney is considered to be the most useful tissue diagnostically. Concentrations in all tissues may be substantially higher after chronic exposure. Marine mammals and fish often contain substantially increased concentrations of mercury that may not be associated with clinical disease (vs for ruminant or companion animal species); however, they may be a potential source of exposure for more susceptible species, particularly the fetus or younger animals.

Other tests, including to detect proteinuria, azotemia, or a nonregenerative anemia, may provide useful evidence to support a diagnosis of mercury poisoning. The diagnosis may be made on the basis of analysis of tissue specimens with appropriate histopathologic and clinical pathologic testing, history, and clinical signs.

Differential diagnoses may include conditions that produce gastrointestinal distress, renal disease, or neurologic dysfunction manifested by tremors, ataxia, or convulsions. Metals such as lead, arsenic, thallium, or cadmium; insecticides, including organophosphate, carbamate, or organochlorine compounds; oxalates; vitamin D; and mycotoxins such as T-2 toxin or thiamine deficiency should be considered. Infectious diseases, including hog cholera, erysipelas, and feline parvovirus, may resemble mercury poisoning.

• Because degenerative changes are permanent and there are serious food safety concerns associated with mercury poisoning, treatment is highly discouraged

• Efforts to reduce exposure via food or water sources are important

Because the neurologic and renal damage resulting from mercury poisoning is irreversible, treatment may be ineffective. Consequently, the prognosis for a complete recovery is very poor. In food-producing animals, considerable mercury accumulation in tissues intended as food and profound effects on reproduction limit treatment options. Euthanasia and appropriate disposal, in consultation with regulatory officials, is recommended.

In veterinary patients in which treatment is indicated, oral administration of activated charcoal (1–3 g/kg) and sodium thiosulfate (0.5–1 g/kg) will bind mercury and limit absorption. Vitamin E and selenium, which are antioxidants, may limit oxidative damage. Chelation therapy may be useful if treatment is started soon after exposure, before nephrotoxic effects become severe. The lipid-soluble chelator dimercaprol (3 mg/kg body wt, IM, every 4 hours for 2 days, followed by four times on day 3 and twice-a-day treatment for 10 days) may be beneficial. For organic mercury poisoning, 2.3-dimercaptosuccinic acid (10 mg/kg, by mouth, three times a day for 10 days) has been useful in dogs. If gastrointestinal tract decontamination has been successful, administration of penicillamine (50–100 mg/kg per day, by mouth, for 2 weeks) may reduce clinical signs. Limiting the consumption of mercury-contaminated food such as fish products or water will reduce exposure.

Comprehensive guidelines reflecting the serious nature of the mercury poisoning have been established internationally by the World Health Organization and many countries 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.

• Environmental Protection Agency: Basic Information about Mercury