CASE REPORT SULPHUR POISONING IN CATTLE R. J. JULIAN AND K. B. Introduction Sulphur, usually mixed with lard or oil, has been used topically on livestock for the treatment of fungal and parasitic skin infections for many years. Sulphur has also been used orally as a tonic and for skin conditions in man and animals. Recent reports from Russia indicate that feeding sulphur to cattle is an effective method of prevention and treatment of ringworm (3, 4). This case report describes poisoning in a group of young cattle given sulphur orally by their owner as a treatment for ringworm.
HARRISON*
Post-mortem Examination The seventh animal to die was presented for examination. The carcass was dehydrated, and the viscera were severely congested. Specific lesions were found only in the digestive tract. There was a pronounced odour of hydrogen sulphide when the rumen was opened. Much of the rumen mucosa appeared normal and well preserved; however, severe changes were present in the wall of the dorsal sac of the rumen above the level of ingesta. In this area, the mucosa was pale with a rough, caseous appearance and was tightly adherent. The wall was discoloured, hard, and thickened with
edema and hemorrhage. Multiple large and small ulcers and erosions were present in the History Twenty yearling heifers had been raised in a abomasum and upper duodenum. Granules of yard and open shed all winter. Several were sulphur were found in the ingesta on the floor thin and had rough, scurfy skin with an of the rumen and abomasum. occasional grey ringworm-like plaque. One Histopathological examination of the more morning in April of 1970, the twenty heifers severely affected parts of the rumen wall rewere offered and shortly thereafter consumed vealed necrosis of the mucosa, extreme thicken12 pounds of sulphur mixed with ground corn. ing of the submucosal connective tissue with Two heifers were found dead that afternoon, fibrin and edema, fibrin thrombi in the vessels and two more died each day for the following of the submucosa, and prominent vasculitis of three days. Four died over the next five days, large and small vessels with fibrinoid necrosis making a total mortality of 12 (60%). of blood vessel walls and with large numbers of neutrophils around blood vessels and in the blood vessel walls. The reaction extended into the muscularis with infiltration of neutrophils Clinical Examination Six of the ten affected animals seen alive had between muscle fibres and an inflammatory exurespiratory distress and laboured breathing. date made up of fibrin and neutrophils between There was a pronounced odour of hydrogen the circular and longitudinal muscle layers. sulphide on their breath. The animals appeared Thrombosis and vasculitis were also evident depressed and were unaware of their surround- within the muscle layers. Hemorrhage was ings or of being handled. All ten sick animals present under the serosa. Similar but less severe were mildly to moderately ataxic. Even though lesions were present in the affected areas of the they appeared dull, occasional muscle-twitching abomasum. Special stains did not reveal fungal was present and colicky pain was obvious with elements in the tissues or thrombosed blood the animals treading, switching, and getting up vessels. and down. Severe watery diarrhea occurred within a few hours, but animals surviving more Discussion than 48 hours became dehydrated and constiMortality in a group of heifers fed sulphur pated. Ataxia progressed to recumbency with under similar circumstances in which six of 40 coma occurring prior to death. All animals young feeder cattle died acutely, followed by which showed signs died. further mortality over the next week or so has been reported previously in Ontario (1). In that *Veterinary Services Laboratory, Ontario Min- report, death was attributed to the effects of istry of Agriculture and Food, Brighton, Ontario hydrogen sulphide gas formed in the digestive (Julian) and Roslin, Ontario (Harrison). tract. as
CAN. VET. JOUR., vol. 16, no. 1, January, 1975
POISONING
Since sulphur is relatively non-toxic in its been involved in the death of animals that surcrystalline form, it would appear that the vived more than two or three days.
damage to the tissues and death of the animals may be caused by one or more of several products which may be produced in the digestive tract: Hydrogen sulphide gas, which is particularly toxic to the respiratory and central nervous systems, producing histotoxic anoxia; hydrogen sulphide in solution is relatively nontoxic, but the sulphide portion produces a cathartic action in the intestine (2); sulphur dioxide gas which is a powerful irritant particularly in the respiratory tract (2) and which, in the case described, may have produced the lesion above the level of the ingesta in the rumen. (Sulphur dioxide gas produces sulphurous acid when dissolved in water, such as on moist mucous membranes. When dissolved in the ingesta of the rumen, it would be neutralized); pentathionic acid which may be the product responsible for the therapeutic activity and the keratolytic property of sulphur and which has been shown to have germicidal and fungicidal activity (2). Morbidity and mortality in the animals described here and in the outbreak described previously (1) were likely due to the combined activity of these products. The acute deaths were likely due to the action of the hydrogen sulphide on the respiratory or central nervous system following inhalation or absorption of hydrogen sulphide gas from the rumen, or possibly to absorption of hydrogen sulphide and production of. sulphhemoglobinemia. Later mortality may have been due to dehydration from diarrhea. Damage to the digestive tract and the severe colic may have been caused by sulphur dioxide (sulphurous acid) or pentathionic acid and this may have
Summary A case of sulphur poisoning is described in which 12 of 20 cattle died following the feeding of sulphur. Respiratory distress and abdominal pain were the prominent signs. Examination of one animal revealed vasculitis and necrosis of the rumen and abomasal wall. The possible toxic effects of sulphur are discussed. Resume L'auteur decrit un cas d'empoisonnement par le soufre, attribuable a une medication orale avec cet element et qui causa la mort de 12 des 20 taures d'un troupeau. Des difficultes respiratoires et de la douleur abdominale constituaient les principaux signes cliniques. L'examen histologique des tissus d'une de ces taures revela des l6sions de vasculite et de necrose au sein de la paroi du rumen et de la caillette. L'auteur commente aussi les effets toxiques possibles du soufre. References 1. COUGHLIN, C. L. Hydrogen sulphide poisoning in cattle. Can. J. comp. Med. 8: 111-113. 1944. 2. GOODMAN, L. S. and A. GILMAN. The Pharmacological Basis of Therapeutics. 4th Edition, Section XII, Chapter 50, pp. 1057-1058. Toronto: Collier-MacMillan Canada Ltd. 1970. 3. KusHAREv, A. V. and E. T. Popov. The treatment and prevention of ringworm in cattle by feeding sulphur. Problemy Veterinarnoi Sanitarii 42: 115-118. 1972. (Abs. Vet. Bull. 43: No. 2883. 1973) 4. MAL'TSEV, V. S. Treatment and prevention of ringworm in cattle by feeding sulphur. Problemy Veterinarnoi Sanitarii 42: 119-122. 1972. (Abs. Vet. Bull. 43: No. 3407. 1973)
ABSTRACT The differences between cattle which develop "shipping fever" and those which do not. R. G. Thomson, S. Chander, M. L. Fox and M. Savan (Dept. Path., Ont. Vet. Coll., Guelph, Ontario).
killed after sampling and the extent of their pulmonary lesions assessed. The parameters measured previously could then be compared between those which had extensive, moderate or minimal pulmonary lesions. Animals with pneumonia had higher body temperatures, plasma fibrinogen levels, mean colony counts of P. hemolytica in their nasal flora but lower serum antibody levels to P. hemolytica than those without pneumonia. Some parameters were related to the extent of pilmonary lesions.
Over a period of several years range cattle were brought from Western Canada, sampled for varying periods after arrival and either resold or killed. Parameters assessed were bacterial nasal flora, serum antibody to P. hemolytica and PI-3 virus, nasal antibody to P. hemolytica and PI-3 virus, body temperature, plasma fibrinogen, in some cases leukocyte counts and plasma cortisol. Fifty animals were
Research Rostrum of the Twenty-sixth Canadian Veterinary Medical Association Annual Convention, Guelph, Ontario 1974. 29
HARRISON*
Post-mortem Examination The seventh animal to die was presented for examination. The carcass was dehydrated, and the viscera were severely congested. Specific lesions were found only in the digestive tract. There was a pronounced odour of hydrogen sulphide when the rumen was opened. Much of the rumen mucosa appeared normal and well preserved; however, severe changes were present in the wall of the dorsal sac of the rumen above the level of ingesta. In this area, the mucosa was pale with a rough, caseous appearance and was tightly adherent. The wall was discoloured, hard, and thickened with
edema and hemorrhage. Multiple large and small ulcers and erosions were present in the History Twenty yearling heifers had been raised in a abomasum and upper duodenum. Granules of yard and open shed all winter. Several were sulphur were found in the ingesta on the floor thin and had rough, scurfy skin with an of the rumen and abomasum. occasional grey ringworm-like plaque. One Histopathological examination of the more morning in April of 1970, the twenty heifers severely affected parts of the rumen wall rewere offered and shortly thereafter consumed vealed necrosis of the mucosa, extreme thicken12 pounds of sulphur mixed with ground corn. ing of the submucosal connective tissue with Two heifers were found dead that afternoon, fibrin and edema, fibrin thrombi in the vessels and two more died each day for the following of the submucosa, and prominent vasculitis of three days. Four died over the next five days, large and small vessels with fibrinoid necrosis making a total mortality of 12 (60%). of blood vessel walls and with large numbers of neutrophils around blood vessels and in the blood vessel walls. The reaction extended into the muscularis with infiltration of neutrophils Clinical Examination Six of the ten affected animals seen alive had between muscle fibres and an inflammatory exurespiratory distress and laboured breathing. date made up of fibrin and neutrophils between There was a pronounced odour of hydrogen the circular and longitudinal muscle layers. sulphide on their breath. The animals appeared Thrombosis and vasculitis were also evident depressed and were unaware of their surround- within the muscle layers. Hemorrhage was ings or of being handled. All ten sick animals present under the serosa. Similar but less severe were mildly to moderately ataxic. Even though lesions were present in the affected areas of the they appeared dull, occasional muscle-twitching abomasum. Special stains did not reveal fungal was present and colicky pain was obvious with elements in the tissues or thrombosed blood the animals treading, switching, and getting up vessels. and down. Severe watery diarrhea occurred within a few hours, but animals surviving more Discussion than 48 hours became dehydrated and constiMortality in a group of heifers fed sulphur pated. Ataxia progressed to recumbency with under similar circumstances in which six of 40 coma occurring prior to death. All animals young feeder cattle died acutely, followed by which showed signs died. further mortality over the next week or so has been reported previously in Ontario (1). In that *Veterinary Services Laboratory, Ontario Min- report, death was attributed to the effects of istry of Agriculture and Food, Brighton, Ontario hydrogen sulphide gas formed in the digestive (Julian) and Roslin, Ontario (Harrison). tract. as
CAN. VET. JOUR., vol. 16, no. 1, January, 1975
POISONING
Since sulphur is relatively non-toxic in its been involved in the death of animals that surcrystalline form, it would appear that the vived more than two or three days.
damage to the tissues and death of the animals may be caused by one or more of several products which may be produced in the digestive tract: Hydrogen sulphide gas, which is particularly toxic to the respiratory and central nervous systems, producing histotoxic anoxia; hydrogen sulphide in solution is relatively nontoxic, but the sulphide portion produces a cathartic action in the intestine (2); sulphur dioxide gas which is a powerful irritant particularly in the respiratory tract (2) and which, in the case described, may have produced the lesion above the level of the ingesta in the rumen. (Sulphur dioxide gas produces sulphurous acid when dissolved in water, such as on moist mucous membranes. When dissolved in the ingesta of the rumen, it would be neutralized); pentathionic acid which may be the product responsible for the therapeutic activity and the keratolytic property of sulphur and which has been shown to have germicidal and fungicidal activity (2). Morbidity and mortality in the animals described here and in the outbreak described previously (1) were likely due to the combined activity of these products. The acute deaths were likely due to the action of the hydrogen sulphide on the respiratory or central nervous system following inhalation or absorption of hydrogen sulphide gas from the rumen, or possibly to absorption of hydrogen sulphide and production of. sulphhemoglobinemia. Later mortality may have been due to dehydration from diarrhea. Damage to the digestive tract and the severe colic may have been caused by sulphur dioxide (sulphurous acid) or pentathionic acid and this may have
Summary A case of sulphur poisoning is described in which 12 of 20 cattle died following the feeding of sulphur. Respiratory distress and abdominal pain were the prominent signs. Examination of one animal revealed vasculitis and necrosis of the rumen and abomasal wall. The possible toxic effects of sulphur are discussed. Resume L'auteur decrit un cas d'empoisonnement par le soufre, attribuable a une medication orale avec cet element et qui causa la mort de 12 des 20 taures d'un troupeau. Des difficultes respiratoires et de la douleur abdominale constituaient les principaux signes cliniques. L'examen histologique des tissus d'une de ces taures revela des l6sions de vasculite et de necrose au sein de la paroi du rumen et de la caillette. L'auteur commente aussi les effets toxiques possibles du soufre. References 1. COUGHLIN, C. L. Hydrogen sulphide poisoning in cattle. Can. J. comp. Med. 8: 111-113. 1944. 2. GOODMAN, L. S. and A. GILMAN. The Pharmacological Basis of Therapeutics. 4th Edition, Section XII, Chapter 50, pp. 1057-1058. Toronto: Collier-MacMillan Canada Ltd. 1970. 3. KusHAREv, A. V. and E. T. Popov. The treatment and prevention of ringworm in cattle by feeding sulphur. Problemy Veterinarnoi Sanitarii 42: 115-118. 1972. (Abs. Vet. Bull. 43: No. 2883. 1973) 4. MAL'TSEV, V. S. Treatment and prevention of ringworm in cattle by feeding sulphur. Problemy Veterinarnoi Sanitarii 42: 119-122. 1972. (Abs. Vet. Bull. 43: No. 3407. 1973)
ABSTRACT The differences between cattle which develop "shipping fever" and those which do not. R. G. Thomson, S. Chander, M. L. Fox and M. Savan (Dept. Path., Ont. Vet. Coll., Guelph, Ontario).
killed after sampling and the extent of their pulmonary lesions assessed. The parameters measured previously could then be compared between those which had extensive, moderate or minimal pulmonary lesions. Animals with pneumonia had higher body temperatures, plasma fibrinogen levels, mean colony counts of P. hemolytica in their nasal flora but lower serum antibody levels to P. hemolytica than those without pneumonia. Some parameters were related to the extent of pilmonary lesions.
Over a period of several years range cattle were brought from Western Canada, sampled for varying periods after arrival and either resold or killed. Parameters assessed were bacterial nasal flora, serum antibody to P. hemolytica and PI-3 virus, nasal antibody to P. hemolytica and PI-3 virus, body temperature, plasma fibrinogen, in some cases leukocyte counts and plasma cortisol. Fifty animals were
Research Rostrum of the Twenty-sixth Canadian Veterinary Medical Association Annual Convention, Guelph, Ontario 1974. 29
