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Chlorate toxicosis
History: Two 700-800 pound castrated-male Angus calves,
reportedly about 1 year old, were submitted to the Heeke ADDL
in late summer for a legal necropsy. The owner reported waking
up that morning to find 10 dead animals (out of a herd of
16). Affected animals included weaned grass-fed calves and
mature cows. Five of the dead were lying next to the water
trough; the remainder were scattered over a 10-acre pasture.
The owner had seen no previous signs of illness or unusual
behavior in the herd. The animals were housed in an open pasture
composed of fescue and other grasses, and had access to woods.
Water came from three separate ponds, two of which were spring-fed.
One pond drained a piece of pasture and roadside that had
been sprayed by the county on the previous day with a product
allegedly similar to Roundup herbicide. All animals had been
given a multivalent vaccine for blackleg at three months of
age. No other vaccines or treatments had been given to the
herd.
Gross Findings: The only gross lesion in either animal was
a muddy-brown discoloration of the blood and body tissues
(methemoglobinemia).
Preliminary laboratory findings: A drop of clear ocular
fluid from both calves was placed on a white ceramic spot
dish and mixed with one drop of diphenylamine reagent. A dark
blue color immediately developed, suggesting the presence
of nitrate in the ocular fluid. A presumptive diagnosis of
nitrate toxicosis was made.
Preliminary follow-up: The owner was contacted that afternoon
and told to search for a source of nitrate. Possible sources
would include nitrate accumulating plants (sorghum or sudan
grass, green corn silage), spilled concentrated fertilizer,
or possibly runoff from a manure pit or fertilizer storage
bin into drinking water. The owner reported that the pasture
had no known sources of nitrate, but he did find that the
cattle had broken into an old storage shed at the back of
the pasture and an old rusted 1- pound can of white granular
material was present on the floor of that shed. The can had
been broken open and the white granular material had been
scattered over the floor. It appeared that the cattle had
licked the can and the white material. The owner did not know
what the material was, but did not think it looked like fertilizer.
A sample of this white material was submitted to the lab for
analysis. The cattle were locked out of the shed.
Toxicology Findings: The white granular material was composed
of irregular white crystals measuring 1-2 mm in diameter,
and had no detectable odor. It was easily dissolved in water,
producing a clear solution. In qualitative colorimetric analysis,
the material reacted identically to sodium chlorate.
Discussion: Chlorate toxicosis has been reported in cows,
sheep, horses, chickens, dogs and humans. It occurs rarely
in southern Indiana, and is usually caused by accidental consumption
of sodium chlorate or potassium chlorate. It apparently has
a "salty" taste that cattle crave. (I did not taste
the material myself.) Before the advent of modern herbicides
these compounds were frequently used in southern Indiana to
kill Johnson grass, and old forgotten bags or canisters of
the material can still be found in many old farm buildings.
Chlorate toxicosis also occurs in pet animals and young children
by accidental consumption of match heads (potassium chlorate).
Like nitrate, chlorate is a potent oxidizing agent that converts
hemoglobin to methemoglobin. Clinical signs of chlorate toxicosis
reportedly include methemoglobinemia, ataxia, prostration,
purgation, hematuria and hemoglobinuria. Death occurs very
rapidly and is the usual outcome as treatment is very difficult.
Unlike nitrate toxicosis, methylene blue treatment of chlorate
toxicosis is often disappointing because chlorate also denatures
glucose-6-phosphate dehydrogenase. (The antidotal effect of
methylene blue depends on NADPH produced by glucose-6-phosphate
dehydrogenase.) In addition to methylene blue treatment (4
mg/kg in dogs, 10-15 mg/kg in cattle), treatment should also
include gastric lavage and vitamin C (20 mg/kg).
Some veterinarians and county agents keep diphenylamine reagent
on hand to monitor nitrate levels in silage corn. The diphenylamine
reaction is a useful qualitative benchtop test that can make
a rapid and timely diagnosis of nitrate poisoning. Because
chlorate reacts similarly to nitrate in a number of chemical
reactions including the diphenylamine reaction, it can be
confused with nitrate toxicosis. Chlorate toxicosis should
be considered as a differential diagnosis in cases of suspected
nitrate toxicosis where no nitrate source can be found.
- by Duane Murphy, Pathologist,
Heeke ADDL
References
1. Beasley VR, Dorman DC, Fikes JD, Diana SG,: 1994, A systems
affected approach to veterinary toxicology: Reference notes
for toxicology VB 320, University of Illinois, pp 767-768.
2. Gregory DG, Miller S, Whaley MW: 1993, Chlorate toxicosis
in a group of swine. J Vet Diag Inves 5: 494-496.
3. Murphy DA: 1999, Use of diphenylamine reagent as an on-site
quick test for nitrate toxicosis. 42nd Annual Meeting of the
American Association of Veterinary Laboratory Diagnosticians,
p 32 (abstract)
4. Steffen C, Wetzel E: 1993, Chlorate poisoning: Mechanisms
of toxicity. Toxicology 84: 217-231.
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