Ionophores:
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Key Point #1
Ionophores were the first toxins discussed. These are found in pelleted food for ruminants, or calf milk replacer. The lecturer focused mainly on equine toxicity, but toxicity has been reported in dogs, and general principles of patient management apply to dogs as well.
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Key Point #2
Ionophores are classed as carboxylic polyether antibiotics, and they disrupt the cation concentration gradient in certain ruminal microorganisms, negatively affecting their metabolism. This includes coccidia as well as certain gram positive bacteria. Shifting the ruminal microorganism population leads to cattle being able to utilise feed more efficiently with less waste products such as lactic acid, acetic acid and methane being produced.
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Key Point #3
Monensin, one commonly used ionophore, has a mean LD in dogs of 6 mg/kg and is also toxic to horses, cats and poultry. About 550 mg is enough to kill approx 50% of horses that ingest it, and in horses, effects are predominantly cardiotoxic, with myocardial necrosis occurring. Signs include sweating, arrhythmia, tachycardia, atrial fibrillation, and acute death. Diarrhoea, weakness, depression and signs of colic are also common. As well as decreased electrolyte levels (Na+, Cl-, Mg2+), glucosuria is common.
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Key Point #4
Treatments used include emptying the stomach via stomach tube and dosing with activated charcoal and mineral oil. Iv fluids are indicated for hypotensive shock and some vets use vitamin E to attempt to protect the heart muscle. An echocardiogram can reveal the extent of myocardial necrosis if the patient survives, but this may not estimate risk of sudden death very accurately.
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Key Point #5
Horses may die weeks later from myocardial fibrosis. This also means when horses have recovered from an acute episode of toxicity that they cannot even be ridden casually, due to the risk of death from myocardial fibrosis and sudden fatal arrhythmia. They may go on to develop congestive heart failure or suffer sudden death.
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Key Point #6
It is important that horses not be allowed to eat feed intended for other animals, and even feed intended for poultry can poison horses, as they are extremely sensitive to ionophore toxicity. The toxin affects cardiac and skeletal muscle, as well as possibly liver and kidney. The lethal dose of monensin in horses is 2-3 mg/kg and of salinomycin it is 0.6 mg/kg
Sodium monofluoroacetate (1080)
This is a toxin we see occasionally in Australia, although not as much as in previous years as alternative baits are being used more now.
It was interesting to hear the seizures described as “waxing and waning” with almost normal behaviour in between. This has not been my experience in the couple of cases I have seen and almost invariably in case reports in the Australian Veterinary Journal cases are reported as progressing from nervous or anxious to agitated, then frenzied, behaviour such as screaming and running in circles, to seizures, paddling and convulsions, collapse and death.
Treated animals are kept under general anaesthesia until they can be recovered without seizure activity.
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Supportive care measures described include the use of
1. intravenous fluids
2. sodium bicarbonate continuous infusion
3. calcium gluconate continuous infusions. Evidence suggests hypocalcaemia contributes to fluoroacetate toxicity, therefore correction of low calcium has been recommended
4. acetamide (10% in 5% dextrose - used in people in Australia
5. gastric lavage to remove toxin in the GI tract
6. activated charcoal to bind enteric toxin -
Measures to control CNS and muscular activity include
1. Levetiracetam - up to 60 mg/kg – 1st choice for many toxins
2. Methocarbamol 100-200 mg/kg iv may be used for significant toxicosis -
Other possible treatments may include:
1. peritoneal dialysis
2. neurotransmitter modulators
3. 4-methylpyrazole -
Ethanol has been described as a treatment, presumably to utilise ethanol as an acetate donor, but the lecturer has only seen studies in mice, and one study in dogs.
A study in 1951 showed benefit to using ethanol and acetate (or either, but together had synergistic effect as an antidote) but only when given immediately after the poison. When given to dogs 30 minutes after poisoning no benefit was seen. Clinically this is unlikely to be much use to us.
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Barbiturate use has been studied in the context of 1080 poisoning. In one study, barbiturates were beneficial 30 min or 3 hours after poisoning, and the effectiveness of barbiturate therapy was dependent on the dose of 1080 received. At a 1080 dose 2x LD50 all dogs survived (both times). At 4x LD50 80% and 17% of dogs survived. At 30 min after 6x LD50 no dogs survived.
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It is important that horses not be allowed to eat feed intended for other animals, and even feed intended for poultry can poison horses, as they are extremely sensitive to ionophore toxicity. The toxin affects cardiac and skeletal muscle, as well as possibly liver and kidney. The lethal dose of monensin in horses is 2-3 mg/kg and of salinomycin it is 0.6 mg/kg
