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Winter 2002 Newsletter

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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


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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406 S. University
West Lafayette, IN 47907
Phone: 765-494-7440
Fax: 765-494-9181

11367 E. Purdue Farm Road
Dubois, IN 47527
Phone: (812) 678-3401
Fax: (812) 678-3412

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