Overview of Mercury Poisoning

By Barry R. Blakley, DVM, PhD, Department of Veterinary Biomedical Sciences, Western College of
Veterinary Medicine, University of Saskatchewan

Last full review/revision Dec 2013 | Content last modified Dec 2013

Historically, mercury poisoning was a common occurrence in both human and animal populations. The
replacement of mercury products used for medicinal, agricultural, or industrial purposes has resulted in
a decline in acute and chronic poisoning, although many wildlife species remain at risk. Predator species
considered to be near the top of the food chain, such as fish, seals, polar bears, and various bird species,
bioaccumulate significant quantities of mercury from dietary sources. Commercial fish products such as
tuna have been associated with chronic poisoning in human and animal (cats) populations. Mercury
exists in a variety of chemical forms, including elemental mercury (eg, thermometers, light bulbs),
inorganic mercurial (mercuric or mercurous) salts (eg, batteries, latex paints), and organic mercury (aryl,
methyl, or ethyl). Fossil fuels represent an important environmental source of mercury. In the
environment, inorganic forms of mercury are converted to methylmercury under anaerobic conditions
in the sediment of most water bodies. Similar conversions may also occur in the body.

Pathogenesis:

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 is 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 dermal 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 significant concentrations of mercury. Inorganic forms of mercury are cytotoxic
and highly corrosive. Consequently, these forms of mercury cause severe inflammation, ulcers, and
direct tissue necrosis in the GI tract. Pale, swollen kidneys manifested histologically by tubular necrosis
and interstitial nephritis are consistent findings.
Clinical Findings:

The inhalation of corrosive elemental mercury vapors that produces severe dyspnea and compromised
respiratory function is usually fatal at high levels of exposure. Neurologic manifestations may eventually
develop if exposure is not excessive. Inorganic mercury, related to its corrosive nature, produces
primarily GI manifestations, including colic, anorexia, stomatitis, pharyngitis, vomiting, diarrhea, shock,
dyspnea, and dehydration. Death often occurs within hours at high levels of exposure. Animals that
survive may exhibit eczema, skin keratinization, anuria, polydypsia, hematuria, or melena. Neurologic
manifestations, including CNS depression or excitation similar to that which occurs in organic mercury
poisoning, may develop after chronic exposure. Depending on the level of exposure to organic mercury
compounds such as methylmercury, clinical manifestations may require days to develop. Because these
compounds are not corrosive, GI signs are not seen. Neurologic manifestations that predominate
include blindness, ataxia, incoordination, tremors, abnormal behavior, hypermetria, nystagmus (cats),
and tonic-clonic convulsions. Advanced stages may be characterized by depression, anorexia,
proprioceptive defects, total blindness, paralysis, and high mortality. The nervous system of young,
developing animals is particularly susceptible to organic mercury exposure, which is frequently
manifested by cerebellar ataxia and death.

Diagnosis:

The considerable variation associated with the clinical manifestations related to the form of mercury
and the duration of exposure accentuates the need for multiple 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 the liver, kidney, or brain tissues. In most species, blood, kidney, brain, and
feed concentrations of mercury <0.1 mg/kg (wet weight) are considered normal. In poisoned species,
concentrations >6 mg/kg (blood), 10 mg/kg (kidney), 0.5 mg/kg (brain), and 4 mg/kg (feed, dry weight)
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 (as such concentrations would be associated in
traditional livestock or companion animal species), but they may be a potential source of exposure for
more susceptible species, particularly the fetus or younger animals. Other measurements, including the
presence of 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 tissue analysis in
association with appropriate histopathology, clinical pathology, clinical manifestations, and history.
Differential diagnoses may include conditions that produce GI disturbances, 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; or mycotoxins such as T-2 toxin should be considered. Infectious diseases, including hog
cholera, erysipelas, and feline parvovirus, may resemble mercury poisoning.

Treatment and Control:

Because the neurologic and renal damage is irreversible, treatment alternatives may be ineffective.
Consequently, the prognosis for a complete recovery is very poor. In food-producing animals, significant
mercury accumulation in edible tissues and profound effects on reproduction limit treatment options.
Euthanasia and disposal, in consultation with regulatory officials, is recommended. 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 hr for 2 days, followed by
qid treatment on day 3 and bid treatment for 10 days) may be beneficial. For organic mercury poisoning,
2.3-dimercaptosuccinic acid (10 mg/kg, PO, tid for 10 days) has been useful in dogs. If the GI tract has
been decontaminated for mercury, administration of penicillamine (50–100 mg/kg/day, PO, for 2 wk)
may reduce clinical signs.