CASE REPORT AN OUTBREAK OF ORGANOPHOSPHATE POISONING (THIMET) IN CATTLE W. S. PUGH'
History
The owner had purchased 48 head of Hereford heifers (300-500 lbs) to establish a cowcalf herd. Twenty-three of these were purchased from stockyards four weeks previous to the poisoning; one week later, eight others were acquired locally and 17 Western heifers arrived tvo weeks previous to the poisoning. The cattle were housed in a pole barn with a large dirt yard where the animals were allowed to run. The cattle were fed from a dirt floor manger and initially received hay but had been changed to a ration of 350 lbs of corn silage, three bales of hay and 30 lbs of ground corn chop for one week. The first distressed animal was found by the owner who said he thought "the heifer had something caught in her throat." He passed a stomach tube but found no obstruction. The next morning the -heifer was dead. She had chewed the wood on the manger before death. On post mortem examination, the rumen was full, the intestines were filled with a greencoloured fluid and petechial hemorrhages were seen in the lower trachea. The carcass had the odour of "turnips". When quizzed about the odour, the owner was unable to identify it. Two weeks previously, another heifer had been found recumbent; she was salivating, exhibiting muscular tremors, was completely anorexic, had diarrhea and a temperature of 95°F. The heifer was force fed and stood after two weeks of recumbency (H. W. Cooper, Forest, Ontario).
able to rise; her temperature was 103°F. A tentative diagnosis of a typical infectious
thrombomeningoencephalitis (ITEME) was Twenty-six other animals were affected over the next six days. Clinical signs included: protrusion of the tongue, excessive salivation, respiratory dyspnea, extension of the tail, dribbling urine and staggering. Muscular tremors made.
were observed first in the shoulders and forelimbs and then progressed posteriorly over the whole body. The heifers could run for only a
short distance when they would then collapse and had considerable difficulty rising. Eventually, they went into sternal and then lateral recumbency due to paresis of the legs. The condition was always progressive; the heifers in lateral recumbency became dull, appeared cyanotic and finally would die. The pupils of both eyes were constricted. The course of the illness usually lasted from 15 minutes to one hour. Three animals exhibited temperatures between 103°F and 104°F, while the remainder had normal temperatures. Some of the animals had diarrhea but this seemed to be more prevalent in the last few animals which were sick.
Morbidity and Mortality Twenty-six animals were treated for the condition and of these, 14 died. All animals that were found recumbent and unable to rise died; those that were treated earlier in the condition survived. The number of heifers which were affected and died on each day of the outbreak were as follows:
Clinical Findings While doing the post mortem examination on the original heifer, two other heifers were noticed ill. The first one acted "lazy" and Number of heifers which died would rise only when prodded. She knuckled Day while walking, dribbled urine, had a high Thursday 1* stepping gait and staggered as she walked. Friday 1 Muscular tremors were also obvious and her Saturday 3 temperature was 101.5°F. Sunday 2 The second heifer was in sternal recum- Monday 4 bency, lethargic, salivating, dyspneic and un- Tuesday 2 Wednesday 2 * 'P.O. Box 728, Forest, Ontario NON 1JO. *animal found dead by owner 56 CAN. VET. JOUR., vol. 16, no. 2, February, 1975
POISONING
Gross Pathology
Tissue Calf C Calf A Calf B Two animals were submitted to the Veterinary Services Laboratory, Huron Park, On- Perirenal Fat 0.004 ppm 0.26 ppm 0.15 ppm tario. At necropsy, both animals showed pe- Liver 0.021 ppm 0.008 ppm techial hemorrhages on the tracheal mucosa; Kidney 0.002 ppm 0.038 ppm the larynx and peri-laryngeal and pharyngeal Brain 0.025 ppm 0.19 ppm Limit of detection 0.002 ppm. soft tissues were edematous, swollen and hyperemic; the lungs were congested but no pneumonia was present. A fecal flotation reThe contaminated dirt removed from the vealed a 1+ infestation of gastrointestinal manger contained 1200 ppm phorate. helminths and a 2+ infestation of Nematodirus species. Diagnosis A second submission was made the followA diagnosis of organophosphate poisoning ing day to the same laboratory and a necropsy (Thimet Phorate) was made based on clinical revealed petechial and ecchymotic hemor- signs, toxicology, history and response to treatrhages; the rumen contained rancid smelling ment. The laboratory findings suggested that contents and a chemical rumenitis and reticuli- a subclinical infectious bovine rhinotracheitis tis were present; the small intestines contained (IBR) was present as well as rumenitis and mucopurulent material and petechial hemor- parasitism. rhages were seen on their serosal surfaces; the kidneys were friable and mushy; Trichuris Treatment species were seen in the colon. Initial treatment was symptomatic as the Two heifers were submitted to the Vet- tentative diagnosis was infectious thromboemerinary Services Laboratory, Guelph, Ontario. bolic meningoencephalitis. The heifers were Gross post mortem findings were atelectasis of given 2.5 g of chloramphenicol1 and 1 g thiathe lungs and a small area of hemorrhage on min hydrochloride2 intravenously and 40 mg the serosal surface of the bladder of Calf A. of atropine sulfate3 subcutaneously. Calf B had extensive submucosal (agonal) When the tentative diagnosis of organophoshemorrhages in the trachea and epicardium. phate poisoning was made, the animals were The lungs were collapsed and congested; the then treated with atropine sulfate, 0.25 mg/kg intestines were flaccid and contained a copious every five hours (1). The heifers were immeamount of watery-green fluid. Hemorrhages diately treated when first signs were seen and were present in the perirenal fat; the brain was those which were recumbent failed to respond swollen and edematous and the meningeal but all those found ill before they became reveins were markedly congested. cumbent responded and recovered quickly. Histopathology Discussion There was marked pulmonary edema and The diagnosis in this case was made in two congestion with atelectasis of alveoli. There principal ways. The animals were treated with were hemorrhages in the submucosa of the atropine sulfate subcutaneously merely as trachea. The glomerular epithelial cells of the symptomatic treatment. The heifers responded kidney had vacuolated cytoplasm. Many of the rapidly and in five minutes breathed easier, nuclei of the tufts were pyknotic. There was ceased salivating and became alert again. Sectubular nephrosis. The hepatocytes showed ondly, with further history, it was learned from (fatty infiltration) vacuolation. The meningeal a neighbour that he and the owner had cleaned and parenchymal capillaries of the brain were up a broken bag of insecticide along one wall engorged with blood. of the barn. This was the same location as part of the manger. The insecticide was found to Bacteriology be Thimet Phorate (Cyanamide).4 This comClostridium spp. were isolated from the pound was described as having the smell of intestines, both in pure culture and in combination with E. coli. Intestinal contents were IRogarmycine - 200, Rogar/STB, London, Oninjected intramuscularly into mice and they died within 48 hours and clostridial species tario. 2Thiamine hydrochloride, W. E. Saunders Ltd., were recovered from the injected legs. London, Ontario.
3Atropine sulfate, Ormond Supplies, Hamilton, Ontario.
Toxicology The results of the toxicological examination for Thimet Phorate are as follows:
4Thimet Phorate, Cyanamid of Canada Ltd., Montreal, Quebec. 57
CANADIAN VhltRINARY JOURNAL
turnips - an odour that was noted on the first post mortem. The area was immediately fenced and subsequently only three animals had to be treated for organophosphate poisoning. The manger and the area immediately in front of the manger were dug out to a depth of two feet and polyethylene was placed on the bottom and the area refilled with gravel. Thimet Phorate is an organophosphate of the same toxicity as parathion (4). The maximum nontoxic dose tested in one study was 0.1 mg/kg when fed by the oral route, and the minimum toxic dose found orally was 0.25 mg/kg (3). This chemical is poisonous by skin contact, inhalation and ingestion. With the dirt sample from the manger heavily contaminated and the heifers being fed from the ground, the route of poisoning would be both inhalation and ingestion. The fact that the outbreak did not occur for two weeks after the last animals arrived at the feedlot is due to cumulative effect of the organophosphates by progressive inhibition of cholinesterase (2). Higher levels of Thimet could possibly be found in some of the remaining heifers. In feeding trials with lindane, it was found that feeding nontoxic levels of lindane produced higher levels of lindane in animal fat than animals deliberately poisoned by higher levels (3). This is of significance as tissue levels of the heifers will affect their marketability. From a communication with H. S. Funnell of the Laboratory of Toxicology, Ontario Ministry of Agriculture and Food, it was learned that the allowable tolerance of Thimet in food is zero. Thimet is also relatively insoluble in both aqueous media and lipids although slightly more soluble in the latter. Therefore, once an animal has been exposed to it, it will probably remain in the fat depot for some time. Subcutaneous fat analysis will have to be done on these animals before the meat can be consumed. The atropine sulfate used on these animals controls or abolishes only the muscarinic but not the nicotinic-like effects. It is interesting to note that while transporting two carcasses to a laboratory, the owner placed the contaminated dirt sample in the cab of the pick-up truck and ten hours after the
58
two hour journey, his wife, who had accompanied him to the laboratory, began to show signs of organophosphate poisoning. She had a numbness of the left side of her face and body; she vomited and her pupils were dilated. She also had difficulty getting her breath and said her throat was full of mucus. Treatment of the poisoning with atropine alleviated all symptoms in 12 hours and she was released from hospital several days later. The route of absorption, in this case, was through inhalation as she had not handled the sample and it was contained in a polyethylene bread wrapper. The potency of this group of insecticides needs to be re-emphasized to all groups of people in agriculture. In this case, 14 valuable animals were lost due to a broken bag of Thimet that was "thought" to be thoroughly cleaned up. If the potency of these chemicals was understood, would this have happened? The package has many warnings on it but many fail to read these. Whose responsibility is it? Summary
The clinical, pathological and toxicological findings (Thimet Phorate) of organophosphate poisoning in a beef herd are described. Resume L'auteur decrit les observations cliniques, pathologiques et toxicologiques relatives A des cas d'empoisonnement par un organophosphate (Thimet Phorate) qui se sont produits dans un troupeau de bovins de boucherie. References 1. BLOOD, D. C. and J. A. HENDERSON. Veterinary Medicine, 3rd Edition. p. 804. London: Bailliere, Tindall and Cassell. 1968. 2. GARNER'S Veterinary Toxicology, 2nd Edition. pp. 242-257. London: Bailliere, Tindall and Cassell. 1963.
3. GIBBONS, W. J., E. J. CATCoTT and J. F.
SMITHCORS. Bovine Medicine and Surgery. pp. 271-283. Wheaton, Illinois: American Veterinary Publications. 1970. 4. Guide to Chemicals used in Crop Protection. Publication 1093. Canada Department of Agriculture. 1968.
History
The owner had purchased 48 head of Hereford heifers (300-500 lbs) to establish a cowcalf herd. Twenty-three of these were purchased from stockyards four weeks previous to the poisoning; one week later, eight others were acquired locally and 17 Western heifers arrived tvo weeks previous to the poisoning. The cattle were housed in a pole barn with a large dirt yard where the animals were allowed to run. The cattle were fed from a dirt floor manger and initially received hay but had been changed to a ration of 350 lbs of corn silage, three bales of hay and 30 lbs of ground corn chop for one week. The first distressed animal was found by the owner who said he thought "the heifer had something caught in her throat." He passed a stomach tube but found no obstruction. The next morning the -heifer was dead. She had chewed the wood on the manger before death. On post mortem examination, the rumen was full, the intestines were filled with a greencoloured fluid and petechial hemorrhages were seen in the lower trachea. The carcass had the odour of "turnips". When quizzed about the odour, the owner was unable to identify it. Two weeks previously, another heifer had been found recumbent; she was salivating, exhibiting muscular tremors, was completely anorexic, had diarrhea and a temperature of 95°F. The heifer was force fed and stood after two weeks of recumbency (H. W. Cooper, Forest, Ontario).
able to rise; her temperature was 103°F. A tentative diagnosis of a typical infectious
thrombomeningoencephalitis (ITEME) was Twenty-six other animals were affected over the next six days. Clinical signs included: protrusion of the tongue, excessive salivation, respiratory dyspnea, extension of the tail, dribbling urine and staggering. Muscular tremors made.
were observed first in the shoulders and forelimbs and then progressed posteriorly over the whole body. The heifers could run for only a
short distance when they would then collapse and had considerable difficulty rising. Eventually, they went into sternal and then lateral recumbency due to paresis of the legs. The condition was always progressive; the heifers in lateral recumbency became dull, appeared cyanotic and finally would die. The pupils of both eyes were constricted. The course of the illness usually lasted from 15 minutes to one hour. Three animals exhibited temperatures between 103°F and 104°F, while the remainder had normal temperatures. Some of the animals had diarrhea but this seemed to be more prevalent in the last few animals which were sick.
Morbidity and Mortality Twenty-six animals were treated for the condition and of these, 14 died. All animals that were found recumbent and unable to rise died; those that were treated earlier in the condition survived. The number of heifers which were affected and died on each day of the outbreak were as follows:
Clinical Findings While doing the post mortem examination on the original heifer, two other heifers were noticed ill. The first one acted "lazy" and Number of heifers which died would rise only when prodded. She knuckled Day while walking, dribbled urine, had a high Thursday 1* stepping gait and staggered as she walked. Friday 1 Muscular tremors were also obvious and her Saturday 3 temperature was 101.5°F. Sunday 2 The second heifer was in sternal recum- Monday 4 bency, lethargic, salivating, dyspneic and un- Tuesday 2 Wednesday 2 * 'P.O. Box 728, Forest, Ontario NON 1JO. *animal found dead by owner 56 CAN. VET. JOUR., vol. 16, no. 2, February, 1975
POISONING
Gross Pathology
Tissue Calf C Calf A Calf B Two animals were submitted to the Veterinary Services Laboratory, Huron Park, On- Perirenal Fat 0.004 ppm 0.26 ppm 0.15 ppm tario. At necropsy, both animals showed pe- Liver 0.021 ppm 0.008 ppm techial hemorrhages on the tracheal mucosa; Kidney 0.002 ppm 0.038 ppm the larynx and peri-laryngeal and pharyngeal Brain 0.025 ppm 0.19 ppm Limit of detection 0.002 ppm. soft tissues were edematous, swollen and hyperemic; the lungs were congested but no pneumonia was present. A fecal flotation reThe contaminated dirt removed from the vealed a 1+ infestation of gastrointestinal manger contained 1200 ppm phorate. helminths and a 2+ infestation of Nematodirus species. Diagnosis A second submission was made the followA diagnosis of organophosphate poisoning ing day to the same laboratory and a necropsy (Thimet Phorate) was made based on clinical revealed petechial and ecchymotic hemor- signs, toxicology, history and response to treatrhages; the rumen contained rancid smelling ment. The laboratory findings suggested that contents and a chemical rumenitis and reticuli- a subclinical infectious bovine rhinotracheitis tis were present; the small intestines contained (IBR) was present as well as rumenitis and mucopurulent material and petechial hemor- parasitism. rhages were seen on their serosal surfaces; the kidneys were friable and mushy; Trichuris Treatment species were seen in the colon. Initial treatment was symptomatic as the Two heifers were submitted to the Vet- tentative diagnosis was infectious thromboemerinary Services Laboratory, Guelph, Ontario. bolic meningoencephalitis. The heifers were Gross post mortem findings were atelectasis of given 2.5 g of chloramphenicol1 and 1 g thiathe lungs and a small area of hemorrhage on min hydrochloride2 intravenously and 40 mg the serosal surface of the bladder of Calf A. of atropine sulfate3 subcutaneously. Calf B had extensive submucosal (agonal) When the tentative diagnosis of organophoshemorrhages in the trachea and epicardium. phate poisoning was made, the animals were The lungs were collapsed and congested; the then treated with atropine sulfate, 0.25 mg/kg intestines were flaccid and contained a copious every five hours (1). The heifers were immeamount of watery-green fluid. Hemorrhages diately treated when first signs were seen and were present in the perirenal fat; the brain was those which were recumbent failed to respond swollen and edematous and the meningeal but all those found ill before they became reveins were markedly congested. cumbent responded and recovered quickly. Histopathology Discussion There was marked pulmonary edema and The diagnosis in this case was made in two congestion with atelectasis of alveoli. There principal ways. The animals were treated with were hemorrhages in the submucosa of the atropine sulfate subcutaneously merely as trachea. The glomerular epithelial cells of the symptomatic treatment. The heifers responded kidney had vacuolated cytoplasm. Many of the rapidly and in five minutes breathed easier, nuclei of the tufts were pyknotic. There was ceased salivating and became alert again. Sectubular nephrosis. The hepatocytes showed ondly, with further history, it was learned from (fatty infiltration) vacuolation. The meningeal a neighbour that he and the owner had cleaned and parenchymal capillaries of the brain were up a broken bag of insecticide along one wall engorged with blood. of the barn. This was the same location as part of the manger. The insecticide was found to Bacteriology be Thimet Phorate (Cyanamide).4 This comClostridium spp. were isolated from the pound was described as having the smell of intestines, both in pure culture and in combination with E. coli. Intestinal contents were IRogarmycine - 200, Rogar/STB, London, Oninjected intramuscularly into mice and they died within 48 hours and clostridial species tario. 2Thiamine hydrochloride, W. E. Saunders Ltd., were recovered from the injected legs. London, Ontario.
3Atropine sulfate, Ormond Supplies, Hamilton, Ontario.
Toxicology The results of the toxicological examination for Thimet Phorate are as follows:
4Thimet Phorate, Cyanamid of Canada Ltd., Montreal, Quebec. 57
CANADIAN VhltRINARY JOURNAL
turnips - an odour that was noted on the first post mortem. The area was immediately fenced and subsequently only three animals had to be treated for organophosphate poisoning. The manger and the area immediately in front of the manger were dug out to a depth of two feet and polyethylene was placed on the bottom and the area refilled with gravel. Thimet Phorate is an organophosphate of the same toxicity as parathion (4). The maximum nontoxic dose tested in one study was 0.1 mg/kg when fed by the oral route, and the minimum toxic dose found orally was 0.25 mg/kg (3). This chemical is poisonous by skin contact, inhalation and ingestion. With the dirt sample from the manger heavily contaminated and the heifers being fed from the ground, the route of poisoning would be both inhalation and ingestion. The fact that the outbreak did not occur for two weeks after the last animals arrived at the feedlot is due to cumulative effect of the organophosphates by progressive inhibition of cholinesterase (2). Higher levels of Thimet could possibly be found in some of the remaining heifers. In feeding trials with lindane, it was found that feeding nontoxic levels of lindane produced higher levels of lindane in animal fat than animals deliberately poisoned by higher levels (3). This is of significance as tissue levels of the heifers will affect their marketability. From a communication with H. S. Funnell of the Laboratory of Toxicology, Ontario Ministry of Agriculture and Food, it was learned that the allowable tolerance of Thimet in food is zero. Thimet is also relatively insoluble in both aqueous media and lipids although slightly more soluble in the latter. Therefore, once an animal has been exposed to it, it will probably remain in the fat depot for some time. Subcutaneous fat analysis will have to be done on these animals before the meat can be consumed. The atropine sulfate used on these animals controls or abolishes only the muscarinic but not the nicotinic-like effects. It is interesting to note that while transporting two carcasses to a laboratory, the owner placed the contaminated dirt sample in the cab of the pick-up truck and ten hours after the
58
two hour journey, his wife, who had accompanied him to the laboratory, began to show signs of organophosphate poisoning. She had a numbness of the left side of her face and body; she vomited and her pupils were dilated. She also had difficulty getting her breath and said her throat was full of mucus. Treatment of the poisoning with atropine alleviated all symptoms in 12 hours and she was released from hospital several days later. The route of absorption, in this case, was through inhalation as she had not handled the sample and it was contained in a polyethylene bread wrapper. The potency of this group of insecticides needs to be re-emphasized to all groups of people in agriculture. In this case, 14 valuable animals were lost due to a broken bag of Thimet that was "thought" to be thoroughly cleaned up. If the potency of these chemicals was understood, would this have happened? The package has many warnings on it but many fail to read these. Whose responsibility is it? Summary
The clinical, pathological and toxicological findings (Thimet Phorate) of organophosphate poisoning in a beef herd are described. Resume L'auteur decrit les observations cliniques, pathologiques et toxicologiques relatives A des cas d'empoisonnement par un organophosphate (Thimet Phorate) qui se sont produits dans un troupeau de bovins de boucherie. References 1. BLOOD, D. C. and J. A. HENDERSON. Veterinary Medicine, 3rd Edition. p. 804. London: Bailliere, Tindall and Cassell. 1968. 2. GARNER'S Veterinary Toxicology, 2nd Edition. pp. 242-257. London: Bailliere, Tindall and Cassell. 1963.
3. GIBBONS, W. J., E. J. CATCoTT and J. F.
SMITHCORS. Bovine Medicine and Surgery. pp. 271-283. Wheaton, Illinois: American Veterinary Publications. 1970. 4. Guide to Chemicals used in Crop Protection. Publication 1093. Canada Department of Agriculture. 1968.
