Page 1123 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

1098 CHAPTER 10

VetBooks.ir MERCURY POISONING MONENSIN

Mercury toxicity is a rare cause of neurological dis-
feed additive for its growth-promoting and coccidio-
ease in horses. Organic fungicides used to treat seed Monensin is an ionophore antibiotic that is used as a
grain and inorganic mercury found in blistering static effects in cattle and poultry, respectively. The
agents are both hazardous and accessible to horses. primary action of monensin is selective transport of
The toxico-kinetics of elemental, organic and inor- sodium and potassium ions between the intracellu-
ganic mercury are distinctly different, with a var- lar and extracellular spaces. It is thought that toxicity
ied effect on the target organ of toxicosis. Chronic results from abnormal levels of potassium or calcium
exposure to elemental mercury vapour causes CNS within the cell, leading to cell death. The heart is the
dysfunction, but this type of toxicosis is unlikely. primary organ of toxicity. Horses are the domestic
The organic mercurial compounds, such as methyl animals most sensitive to monensin toxicosis, with
mercury, are neurotoxic to central and peripheral an LD50 of 2–3 mg/kg. Inadvertent consumption has
nerves. Inorganic mercury salts are corrosive to the resulted in several syndromes of toxicity, which are
GI tract and the absorbed fraction is nephrotoxic. dose related. Peracute toxicity may result in progres-
This is the most common type of toxicosis reported sive severe haemoconcentration, hypovolaemic shock
and has been associated with ingestion of blistering and death within a few hours of ingestion. These cases
compounds. are commonly found dead. The acute form results
in ataxia, progressive muscle weakness, tachycardia,
UREA AND NON-PROTEIN hypotension, dyspnoea, polyuria, anorexia, abdominal
NITROGEN SOURCES pain and intermittent profuse sweating. These cases
may show signs for 1–4 days before death. Horses
Urea has been used as a non-protein nitrogen source surviving sublethal doses show signs of unthriftiness,
for adult horses, but it has no advantage over more decreased athletic performance and cardiac failure.
common sources. Horses are not as efficient in the Cardiac arrhythmias and pleural and pericardial effu-
utilisation of urea as cattle, although toxicity is sion may also be seen. Clinicopathological findings
unlikely because urea is absorbed by the GI tract are not pathognomonic and toxicity should be sus-
and excreted in urine before reaching the hindgut, pected on the basis of clinical signs and exposure to
where it is hydrolysed by the microbial population contaminated feed. As the LD50 is so low for horses,
to ammonia. Horses are more susceptible to toxi- feed contamination may not be immediately apparent.
cosis by the ingestion of ammonium salts, which There is no specific antidote for monensin. Early
can occur following accidental exposure. The lethal and aggressive treatment with fluids to combat hae-
dose of urea when ingested orally is 4 g/kg and the moconcentration and hypovolaemic shock is war-
lethal dose of ammonium salts is about 1.5 g/kg ranted in patients with known ingestion. Correction
when ingested orally. Clinical signs are confined of acid–base and electrolyte abnormalities is essen-
to the nervous system, with muscle tremors, inco- tial. The use of mineral oil and activated charcoal to
ordination and weakness. Death is the result of evacuate the bowel and decrease absorption, respec-
ammonia intoxication. The exact mechanism of tively, is also warranted.
ammonia toxicosis is not known, but is thought to There are two important treatment contraindi-
involve inhibition of the citric acid cycle. Animals cations in horses that have ingested monensin. The
that die of ammonia toxicosis exhibit no character- first is that digitalis glycosides should never be used
istic lesions. Clinical signs and history may be use- acutely in affected horses, as they have been shown to
ful in establishing a diagnosis. Blood ammonia may be synergistic with monensin and immediately fatal
be evaluated, but many factors influence the levels to cardiac cells. The second is that calcium should
found and results should be interpreted with cau- not be administered to acutely affected horses,
tion. Treatment with lactulose (200 ml p/o or per because it can be irritating to an injured myocardium
rectum q4–6 h) may be attempted. and the hypocalcaemia that is seen is transitory, with