Chlorate poisoning in beef cattle

Abstract

A disease syndrome characterized by hemolysis, methemoglobinemia, methemoglobinuria, and death was observed in a herd of purebred Limousin beef cattle grazing on pasture in November in Alberta. Improper disposal of the nonselective herbicide, sodium chlorate, was identified as the causal agent. Highly variable blood methemoglobin levels reflected differences in herbicide consumption.

During the month of November in west-central Alberta, a producer of purebred Limousin discovered 5 dead cattle in a group of 45 animals. The dead cattle were randomly distributed in a quarter section pasture containing trees and gently rolling hills. Two additional cattle were clinically affected: the 1st animal was a mature lactating cow. Her head was lowered, apparently pressing her nose in the snow. She was reluctant to move and exhibited signs of dyspnea. There was evidence of blood stained material from the nares and melena in the rectal discharge. Dark brown urine dribbled from the vulva. The cow was in good body condition and afebrile. Death occurred within minutes after examination. The 2nd cow was affected in a similar fashion.

Further investigation indicated that the producer had been hauling reclaimed soil from around underground fuel storage tanks to fill low areas in the pasture. The soil had been tested prior to removal for hydrocarbon contaminants. Contamination of soil material was not evident. The ditches bordering the pastures had been sprayed with herbicides suspected to contain picloran (Tordon; Dow AgroSciences, Sarnia, Ontario) and 2–4-D. Neither product, at high levels of exposure, produces a clinical syndrome similar to the present case. An abandoned yard site located centrally in the pasture contained an old house and several other buildings. Closer inspection revealed the presence of several batteries on the ground and in one of the sheds. In the shed, several metal pesticide containers with painted labels obscured by rust and corrosion were found. On the wooden floor, several kilograms of a white crystalline substance was readily apparent. There was no labeled container to identify the substance. An old pump was also present in the shed. Manure on the floor indicated that cattle had access to the shed. The door had been knocked down; possibly by the cattle. While on this pasture, the cattle had not been given salt or mineral supplements.

Case description

Postmortem examination of the 1st animal indicated the presence of brown discoloration of many tissues, including the sclera, mucous membranes, and blood. The spleen was not engorged. The liver and kidney appeared black. Red-brown fluid was present in the peritoneal, pericardial, and plural cavities. Similar fluid was also dripping from the nares. Melena was present in the rectum. Froth was present in the airways and lungs. A diagnosis of hemoglobinuric nephrosis was made by the diagnostic laboratory, based on pathological examination.

Blood, liver, and kidney tissue samples were collected from dead and moribund animals for further analysis. Extensive hemolysis and methemoglobinemia was detected in all blood samples by Prairie Diagnostic Services at the Western College of Veterinary Medicine. The methemoglobinemia detected in the blood samples was highly variable, ranging from 3.7% to 71.6% (1% to 3% normal). Methemoglobinuria was also detected in urine samples.

Metal analysis of the liver from 1 animal indicated that magnesium (6.36 mol/kg, wet weight (ww); normal range, 4.11 to 10.3 mmol/kg), zinc (898 μmol/kg, ww; normal range, 383 to 1530 μmol/kg), molybdenum (11.5 μmol/kg, ww; normal range, 1.46 to 14.6 μmol/kg) and iron (5.34 mmol/1kg, ww; normal range, 0.81 to 5.37 mmol/kg) concentrations were normal. The copper (187.3 μmol/kg, ww; normal range, 393.5 to 1574 μmol/kg) and manganese (34.6 μmol/kg, ww; normal range, 36.4 to 109.2 μmol/kg) concentrations were marginal. The white crystalline powder was submitted to Enviro-Test Laboratories in Edmonton. Chemical analysis indicated that the substance was 95.6% sodium chlorate.

Clinically affected cattle were treated with penicillin (Pen Aqueous; Rafter Products, Calgary, Alberta, 66 000 IU/kg bodyweight (BW), IM and methylene blue (Wiler-PCCA, London, Ontario), 1 mg/kg BW, IV, after examination. Within 10 min of treatment, some alleviation of the dyspnea was evident.

Based upon the data collected, a presumptive diagnosis of chlorate poisoning was made. The cattle had ingested varying quantities of the herbicide, sodium chlorate, resulting in intra-vascular hemolysis, methemoglobinemia, methemoglobinuria, and death. Sufficient quantities of the chlorate herbicide were present in the shed to kill many cattle. For a large animal, at least 500 g of the herbicide must be consumed to cause death.

Discussion

Sodium chlorate has been used for many years as a nonselective herbicide or defoliant. Chemically, chlorates are strong oxidizing agents that have the potential to react violently with many organic chemicals (1,2). Cattle must consume at least 1 g/kg BW for it to be fatal. Methemoglobin production and gastrointestinal disturbances may occur at levels exceeding 0.1 g/kg BW, and 0.06 g/kg BW, respectively. The saline taste of the herbicide is attractive to cattle, often resulting in the consumption of large lethal quantities (3). The use of sodium chlorate as a herbicide has declined in recent years. Consequently, poisoning in cattle is a rare occurrence. Historical reports have documented the clinical syndrome in cattle (4,5). Cattle typically die within 24 h of exposure. The syndrome is characterized by abdominal pain, anorexia, diarrhea, salivation, cyanosis, dyspnea, methemoglobinemia, hematuria, intravascular hemolysis, “tarry” discharge from the nostrils, anus, or vulva, and, possibly, terminal convulsions (1,3,4,6). Postmortem examination of dead animals frequently describes the presence of dark chocolate discoloration of tissues, erosions or inflammation of the gastrointestinal tract, and nephritis and blood-stained urine (1,3,4,6). Similar manifestations have been observed in humans (7).

Mortality observed in livestock populations exhibiting few clinical manifestations prior to death often present a distinct diagnostic challenge. In the present case, methemoglobinuria, methemoglobinemia, and hemolysis were consistent and distinctive abnormalities present in the affected animals. A limited number of agents are known to produce these abnormalities. Historical evidence presented early in the investigation did not clearly suggest a specific etiologic agent. Early concerns about the possibility of an anthrax outbreak, which were ultimately deemed to be unfounded, hampered the initial diagnostic investigation. Delays associated with the anthrax investigation precluded the opportunity to analyze tissues for chlorates. The chlorate ion is rapidly decomposed subsequent to death. Methemoglobin production was an obvious and consistent blood abnormality that was apparent without laboratory analysis.

Nitrate poisoning is a frequent cause of methemoglobin production. High nitrate-containing feed or nitrate fertilizers are common sources (8). In the present case, nitrate poisoning was suspected initially as a possible cause, since the cattle were grazing on a frozen pasture. The presence of hemolysis and methemoglobinuria, which are not associated with nitrate poisoning, indicated that this etiology was unlikely. Nitrate poisoning is often associated with the consumption of plants or contaminated feed or water. The ingestion of nitrates in this situation would be relatively consistent from animal to animal. Consequently, the levels of methemoglobin would exhibit limited variability. In the present case, extreme variation in the levels of methemoglobin suggested that the source of the oxidizing agent was unlikely associated with the feed or water.

Methemoglobin formation and hemolytic anemia are also associated with chronic copper poisoning (8). The marginal levels of copper in the liver indicated that copper toxicosis was not responsible for the syndrome. Other agents, including zinc, phenothiazine, onions, Brassica spp., or saponin-containing plants produce a hemolytic anemia, but methemoglobin formation is not observed (8). These etiologies were, therefore, unlikely. Red maple trees (Acer rubrum) produce a syndrome similar to that of chlorate poisoning, which is characterized by hemoglobinuria, hemoglobinemia, anemia, icterus, and mild methemoglobin production. The pasture, upon careful inspection, was not populated by these distinctly, characteristic trees.

A tentative diagnosis of chlorate poisoning can be made with a systematic evaluation of the blood and tissue abnormalities to assess the oxidative damage. In blood samples, methemoglobinemia, hemoglobinemia, Heinz body formation, a normochronic normocytic anemia, and hyperkalemia generated by the oxidative and hemolytic processes are typically present (1,4,7,8). The outstanding observation present at necropsy is the darkened chocolate brown discoloration of tissues (1,4). Nephrotoxic changes and urine abnormalities associated with the impact of hemolytic debris on renal function are often present (4,7). Inflammation and erosion throughout the gastrointestinal tract reflect the oxidative and irritant properties of chlorates (2,4,7).

In addition to the blood abnormalities, analysis of the gastrointestinal contents for sodium chlorate or sodium chloride may provide supporting diagnostic evidence (1,3,6). The oxidative damage induced by chlorate exposure continues after death (4). The chlorate anion appears to function as a catalyst, resulting in continued hemolysis and methemoglobin formation. Consequently, virtually complete hemolysis and 100% methemoglobin production is often observed, if there is a delay in sample analysis. Other agents, such as copper or nitrate, which also induce methemoglobin formation, are not associated with continued oxidative damage after death. The oxidative processes with these agents ceases with the death of the animal. In the live animal, the continuous oxidative damage, therefore, will have a negative impact on the prognosis, which is typically poor for chlorate poisoning (2).

Food safety and tissue residues of chlorate are a concern in surviving cattle. The majority of the chlorate is excreted unchanged in the urine within 48 h (4). In the environment, decomposition of the chlorate occurs in about 1 wk (2). The limited persistence of chlorate in the animal and in the environment virtually eliminates public health and environmental concerns. Elaborate decontamination procedures are not required. The administration of an adsorbant soon after exposure may be beneficial, although the additional stress of handling severely compromised animals may, in fact, result in more fatalities.

There are conflicting reports concerning the treatment of affected cattle. Sodium thiosulfate and methylene blue are considered by some investigators to be ineffective (4,6,7). Methylene blue and antibiotic treatment in the present case appeared to produce some improvement. The transient favorable response to methylene blue may have reduced the methemoglobin level, resulting in less dyspnea but continued hemolysis ultimately causing the death of the animal. Antibiotics were viewed as beneficial by one investigator (6), although no basis for the conclusion was stated. In reality, once extensive hemolysis and oxidative damage have occurred, treatment is unlikely to be effective. Therapeutic intervention may be beneficial only in mildly affected cattle. Gastric lavage may also improve the prognosis, if this treatment is initiated soon after exposure and prior to absorption, or before the oxidative damage has become extensive (1). In human poisonings, the extent of hemolysis and renal failure, as well as the development of disseminated intravascular coagulation (DIC), influences the course of the clinical syndrome and ultimately the prognosis (7). The development of DIC has not been reported in domestic animals.

In a dry protected environment such as an abandoned shed, chlorate compounds will retain oxidizing properties for extended periods of time. Since chlorates are highly combustible when mixed with a variety of organic or inorganic chemicals (2), great care should be taken during chemical cleanup. It would be prudent to consult with decontamination specialists prior to the decommissioning operation in the shed.

Historically, chlorate poisonings in cattle have been associated with excessive application of the herbicide, malicious poisoning, mistaken use as a salt supplement or careless disposal (1,2). Recently, the oral administration of chlorates has been shown to reduce levels of Escherichia coli and Salmonella typhimurium in the gastrointestinal tract of livestock (9,10). No acute poisoning has been associated with this supplementation practice. Under recommended treatment levels in the drinking water, the dose of the chlorate ion is unlikely to exceed 0.2 mg/kg BW. Therefore, the potential for poisoning is related exclusively to calculation errors or inappropriate disposal of the chlorate product. The opportunity for misuse of sodium chlorate in drinking water to control the levels of pathogenic bacteria in livestock may cause a resurgence of this infrequent toxicosis. CVJ