Poisoning associated with various forms of mercury has decreased in recent years. Chronic exposure of fish and wildlife species related to environmental bioaccumulation of mercury remains a concern. In domestic species, clinical signs of involvement of the nervous, gastrointestinal, respiratory, and reproductive tracts are typical and are influenced by the mode, dose, and duration of exposure. The diagnosis can be confirmed on the basis of the clinical picture, histopathologic findings, and the results of tissue analysis for mercury concentration. Because tissue damage is permanent and food safety implications are important factors, treatment options may be limited and are often not recommended.
Historically, mercury poisoning has been a common occurrence in both humans and animals. The replacement of mercury products used for medical, agricultural or industrial purposes with alternatives has led to a decrease in cases of acute and chronic poisoning; although many species of wildlife remain in danger of extinction. Predatory species near the top of the food chain, such as fish, seals, polar bears, and several species of birds, bioaccumulate significant amounts of mercury from food sources. Commercial fish foods, such as tuna, have been linked to chronic poisoning in humans and cats.
Mercury exists in a variety of chemical forms, including elemental mercury (eg, thermometers, light bulbs), inorganic mercury salts (mercury(II) or mercury(II) salts (eg, batteries, paint latex) and organic mercury (aryl, methyl, or ethyl). Fossil fuels are a major environmental source of mercury. In the environment, inorganic forms of mercury are converted to methylmercury in the sediment of most bodies of water under anaerobic conditions Similar conversions can also occur in the body.
Pathogenesis of mercury poisoning in animals
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.
Clinical Findings of Mercury Poisoning in Animals
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.
Diagnosis of mercury poisoning in animals
The preliminary diagnosis is based on clinical signs; confirmed by analysis of tissue samples (eg kidney) for mercury content
Measurement of mercury concentration in urine can confirm exposure to inorganic mercury compounds(Video) Hitting the Target (Part 2): Clinical Examples of Therapeutic Drug Monitoring
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.
Differential diagnosisthey may include conditions that cause gastrointestinal upset, kidney disease, or neurological dysfunction manifested by tremors, ataxia, or seizures. metals likelead Lead poisoning in animals Lead poisoning in mammals and birds is characterized by neurological disorders, gastrointestinal disorders, hematological abnormalities, immunosuppression, infertility and renal disease...read more ,Arsenic Overview of Arsenic Poisoning in Animals The chemical element arsenic (symbol As, atomic number 33) is a nonmetal or semimetal in Group V on the periodic table. It is often referred to as metallic arsenic and for toxicological reasons... read more , such as cadmium;insecticides General description of insecticidal and acaricidal (organic) toxicosis in animals Insecticides are any substance or mixture of substances designed to prevent, destroy, repel or mitigate insects. Likewise, acaricides are substances that can destroy mites. A chemist can... read more , includingorganophosphates Organophosphate Toxicosis in Animals Organophosphates (OPs) are derivatives of phosphoric or phosphonic acid. There are currently hundreds of OP compounds in use, and they have replaced the banned organochlorine compounds...read more ,carbamato Carbamate poisoning in animals Carbamates are esters of carbamic acid. Unlike organophosphates (OPs), carbamates are not structurally complex. The amount of carbamates used today exceeds that of the OPs because carbamates... read more , or organochlorine compounds; oxalates; Vitamin D; ANDmycotoxin Overview of Mycotoxicosis in Animals For a discussion of mycotoxicosis in poultry, see Mycotoxicosis in Poultry. Acute or chronic toxicosis in animals can result from contact with food or bedding contaminated with toxins that are produced...read more such as T-2 toxin or thiamine deficiency should be considered. infectious diseases, includinghog cholera classic swine fever ,erisipel Erysipelothrix rhusiopathiae-Infection , Yfeline Parvovirus Panleucopenia felina , can resemble mercury poisoning.
Treatment and control of mercury poisoning in animals
Because the degenerative changes are permanent and there are serious food safety concerns associated with mercury poisoning, treatment is strongly discouraged.(Video) Sheep Pox and Goat Pox Information meeting // 22 November 2022 (English)
Efforts to reduce exposure through food or water sources are important
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.
Although cases of mercury poisoning in animals have decreased, bioaccumulation and food safety concerns related to mercury intake remain a priority worldwide.
The lack of generally effective treatment options with poor prognosis is a worldwide concern.(Video) Clinical Management of metabolic and nutritional diseases by Dr. S.Sivaraman #Sheepfarming
Testing the treatment in food-producing animals is not recommended due to potential human exposure.
For more information
Government of Canada:Mercury in the food chain
Information system for risk assessment:Formal Summary of Mercury Toxicity
World Health Organization:Water Quality Guidelines(Video) 30 FREE Online Resources For Veterinary Students, Veterinarians & Veterinary nurses - Vet Websites
Environmental protection agency:Basic information about Mercury
The EPA has established a limit of 2 parts per billion (ppb) of allowable mercury of drinking water. The Food and Drug Administration (FDA) has set a maximum permissible level of 1 part of methylmercury in a million parts of seafood (1 ppm).What is mercury toxicity in animals? ›
Clinical Findings of Mercury Poisoning in Animals
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.
Blood mercury levels above 100 ng/mL have been reported to be associated with clear signs of mercury poisoning in some individuals (e.g., poor muscle coordination, tingling and numbness in fingers and toes).What is the best test for mercury toxicity? ›
Your healthcare provider may recommend a urine test (most common), fecal, or blood test for mercury poisoning from fillings. Amalgam fillings and methylmercury (organic mercury), often found in seafood products, are the top sources of mercury that can lead to mercury poisoning.What is the guide number for mercury? ›
|CAS Number||UN/NA Number||DOT Hazard Label|
|NIOSH Pocket Guide||International Chem Safety Card|
|Mercury compounds [except (organo) alkyls] (as Hg)||MERCURY|
- difficulty sleeping.
- impaired sensations.
- muscle weakness and twitching.
- emotional changes (mood swings, irritability, nervousness)
- kidney damage.
- breathing difficulties.
Regardless, dogs, like other animals, are susceptible to mercury toxicity. A dose of 500 micrograms/day is acutely toxic to dogs and leads to rapid illness and death. Clinical signs of mercury poisoning include gastrointestinal ulcerations and hemorrhaging, kidney damage, and neurological damage.What is the treatment drug for mercury poisoning? ›
This is the drug of choice for the treatment of acute inorganic mercury toxicity. It is the preferred chelator for mercury salts. Dimercaprol is administered intramuscularly every 4 hours, mixed in a peanut oil base.
Small amounts of mercury are often present in blood, primarily due to variable amounts of methylmercury in the diet. Typical levels of total mercury in blood range up to about 5 micrograms/Liter (mcg /L).How much mercury is needed to cause harm? ›
Mild, subclinical signs of central nervous system toxicity can be seen in workers exposed to an elemental mercury level in the air of 20 μg/m3 or more for several years. Kidney effects have been reported, ranging from increased protein in the urine to kidney failure.