MERCURY TOXICITY

MERCURY TOXICITY

Epidemiology

Sources of poison

§                  Contamination of herbage and water by mercurial effluents from the metallurgy.

§                 Accidental ingestion of seeds treated with mercurial fungicides (viz., phenyl-, methyl- and ethyl- mercury compounds) and seed dressings. The commonest agent used is a dust of 5.25% methoxy-ethyl mercury silicate. Methylmercury dicyandiamide is also used. Treated seed is usually not harmful if it comprises only 10% of the ration and must be fed in large amounts for long periods before clinical illness occurs. A single feeding even of large amounts of grain thought to be incapable of causing mercury poisoning in ruminants but a fatal case has been reported in horse.

§                  Inadvertent use of mercurial ointments for skin lesions (common in dogs/cats due to licking of wounds). The continued administration of a strong mercuric ointment to horses can cause poisoning by inhalation of mercury vapor by cattle in the same stable.

Forms of Mercury

            Inorganic mercurials

§     Elemental mercury (liquid)

§     Mercuric chloride (sublimate)

§     Mercurous chloride (Calome: antiseptic, skin creams)

§     Mercurochrome (antiseptic)

o        Organic mercurials

§     Methyl / ethyl mercury: Accumulates in marine fish (Biomagnification) –                                Minamata disease and Nigata disease in Japan.

§     Mercurial effluents from industries – Minamata bay / Nigata bay – Plankton algae – Mercurials in fish (Biomagnification: about 300 fold or more) – consumption of fish by people – Disease (locomotor disturbances / abnormal gait).

§     Phenyl mercury: Fungicide (seed dressings): Nervous disorders.

Occurrence

            Mercury poisoning is rare in farm animals and occurs almost exclusively as a result of accidental feeding of grain treated with organic mercurial compounds used as antifungal agents.

Risk factors

            Sensitivity to mercury poisoning varies between species, toxicosis occurring in cattle on an average daily intake of mercury, in organic mercury form, of 10 mg/kg per day, while toxic effects are only obtained in sheep with intakes of 17.4 mg/kg body weight per day. In horses, feeding inorganic mercury @ 0.4 mg/kg body weight produces only mild signs of poisoning, and feeding methylmercury chloride (10 g over 10 weeks) causes serious illness including exudative dermatitis, renal insuffiency and degenerative neuropathy.

            The toxicity also depends on the solubility of mercurial compounds and susceptibility of animals. Cattle are highly susceptible.

Etiology

ª      Mercuric chloride and Mercuric biniodide – highly poisonous;

o   Toxic dose     for cattle & horses: 8 g.

for sheep: 4 g.

ª      Mercury is a cumulative poison because of its slow excretion from the intestines and kidney.

ª      Organic mercury taken regularly in the diet @ 1 mg/kg causes chronic poisoning in pigs. A level of 6 mg/kg causes deaths in pigs within 5 days.

Toxicokinetics

©      Elemental mercury is not absorbed from GIT.

©      Mercury vapour is lipid soluble, gets absorbed through inhalation, and oxidized to mercuric ions, which bind with plasma proteins.

©      Unconverted elemental mercury enters CNS and causes neuronal damage.

©      Inorganic mercurials are only slightly absorbed (2%) from GIT.

©      Organic mercurials are highly absorbed from GIT (up to 90%) and get distributed all over the body, including CNS.

©      Mercury is slowly excreted through faeces and urine.

Toxicodynamics

¨      Mercury is mutagen, teratogen, carcinogen and embryocidal.

¨      The mechanism of toxicosis is similar to that of arsenic.

¨      Even at low concentrations Hg is capable of inactivating –SH containing compounds.

¨      Hg_(i) cause coagulation of the alimentary mucosa, causing rapid development of gastroenteritis. Animals that survive GI disorder and absorb Hg may show signs of damage to peripheral capillaries especially those at the sites where mercury is excreted, in the kidney (nephrosis), colon (colitis) and mouth (stomatitis). Hg_(i) cause renal tubular necrosis and hepatotoxicty.

¨      Hg_(o)  in small doses liberate their mercury slowly into tissues and cause degenerative changes in brain and peripheral nerves and in kidney.

¨      In some cases of phenylmercuric acetate poisoning there are extensive subcutaneous haemorrhages and a bleeding tendency and the animals die suddenly.

¨      With larger doses there is stasis of the GI tract, and doses of 0.23 g/kg body weight there is general collapse.

¨      Methyl mercury also interacts with –SH groups in DNA and RNA and alters their structural integrity.

Clinical signs

Acute:

Nervous signs (excitement, tremors, convulsions and depression).

GI disturbances (gastroenteritis, bloody diarrhoea, vomiting with blood and dehydration).

Death occurs within a few hours due to shock and dehydration.

In less acute cases – salivation, a fetid breath and anorexia accompany the gastroenteritis and the animal survives for several days. There is oliguria, an increase in heart and respiratory rates and in some cases posterior paralysis. Convulsions occur in the final stages.

Chronic:

            Incoordination, altered gait, stumbling, head-pressing, muscle spasms, blood in urine/faeces, pale mucosae, epistaxis, nervous signs are more common in mongastrics than in ruminants.

            The common form of the disease is chronic mercurialism where small amounts of mercury are ingested over long periods. There is depression, anorexia, emaciation, and a stiff stilted gait which may progress to paresis. Alopecia, scabby lesions around the anus and vulva, pruritus, petechiation and tenderness of the gums and shedding of teeth are accompanied by chronic diarrhoea, weakness, incoordination and convulsions.

            In pigs: Hg_(o) causes blindness, staggering, continuous walking and inability to eat

although the appetite appears to be good.

            Cattle poisoned in the above way evidence staggering gait, standing on tiptoe and paresis. The animals lie down most of the time but appear normal in other respects, often eating well. Clinical signs may not develop until 30 days after feeding is commenced.

            Cattle poisoned experimentally show marked nervous signs including incoordination, head-pressing, muscle tremor with twitching of the eyelids, tetanus-like spasms on stimulation, excessive salivation, recumbency and inability to eat or drink. These are followed by tonic-clonic convulsions with opisthotonus.

Clinical pathology

            Hg can be detected at highest levels than normal in the blood, faeces and urine of affected animals and in the toxic source material.

            Among the earliest and most accurate indicators of nephrotoxicity due to Hg intoxication are the urinary concentrations of alkaline phosphatase and gamma-gultamyl transpeptidase.

Lesions

Acute: Severe gastroenteritis with oedema; hyperaemia and petechiation of the alimentary mucosa; liver and kidney are swollen; lungs are congested and            show multiple

haemorrhages; catarrhal stomatitis.

Microsopically – degenerative changes in the renal tubules.

Chronic: Hg_(o) – degenerative changes in nerve cells in the cortex of cerebrum, brainstem and spinal cord. These include neuronal necrosis, neuronophagia, cortical vacuolation and gliosis.

            Hg reaches its greatest concentration in kidney and this tissue should be submitted for assay. Levels of 100 mg/kg may be present in the kidney of the animals poisoned with Hg_(i). With chronic Hg_(o) poisoning in swine levels of Hg up to 2000 mg/kg may be present in the kidney.

Diagnosis

            Acute mercury poisoning is rare but should be suspected in animals which are exposed to Hg_(i) compounds and which show signs of gastroenteritis and nephritis. When there are nervous signs the syndrome resembles poisoning by lead or arsenic. Pigs poisoned by Hg_(o) compounds resemble those poisoned by As_(o) preparations.

Treatment

            Acute:            Large amounts of coagulable protein such as eggs should be given by mouth immediately, followed by gastric lavage with Saturated Sod. Bicarbonate sol. In dogs and cats / mild purgatives to facilitate removal from the gut before digestion and absorption occur.

            Rx with Sodium thiosulphate as described in As poisoning is recommended.

            BAL can be used but has the same limitations here as in As poisoning, and delay in treatment of any sort is likely to be fatal. Inj. of BAL (6.5 mg/kg body wt.) should be given every 4 hours. [BAL – 3 mg/kg in every 4 hr. on first 2 days, every 6 hr. on third day and every 12 hr. for next 10 days or until recovery].

            D-penicillamine: 15-50 mg/kg orally.

            Supportive treatment includes astringents given orally to control the gastroenteritis and fluids given parenterally to correct the dehydration.

Control

            Seed grains dusted with mercury compounds should not be fed to animals but the practice is reasonably safe if only small amounts are used.

Public health importance

            A matter of vital interest in chronic poisoning by Hg_(o) is the use of the meat from such animals for human consumption. The question of Hg excretion into milk also arises but very little appears to be excreted in this way.