CASE REPORT SNAKEBITE IN THE HORSE W. E. FITZGERALD, B.V.Sc. Veterinary Clinical Centre, Werribee, Victoria, 3030 Introduction
There is very little information available on snakebite in the horse. This report describes in detail 4 cases of snakebite in horses seen within this Werribee practice area. The diagnosis was circumstantial in 2 of these cases, but confirmed in the other 2. case Nistories Case 1 During October 1973, a 9-month-old male hack in generally poor condition was kept tethered in long dry grass beside a suburban railway line. This terrain was considered to be ideal cover for snakes. The owner observed that the horse had suddenly become staggery and anorectic. When examined, he was recumbent and appeared depressed but would readily rise if disturbed. The recumbency was apparently voluntary. He was sweating moderately and when standing was twitching and restless. Antibiotic and antihistamine therapy was instituted. Antivenene was not used because of cost and the mildness of clinical signs, considered to be due to non-lethal envenomation. Good nursing was advised as it was considered that recovery might be prolonged. The following day his clinical condition had deteriorated slightly, however recovery occurred gradually over the following week. Clinical pathology of blood taken at the initial examination revealed a low haematocrit value but normal total and differential white cell counts. Plasma Creatine Phosphokinase (CPK) was estimated (Table 1). Case 2 During November a 3-year-old Thoroughbred gelding was agisted on a property near a small town within the Werribee shire. It was sharing a 25 ha grassy paddock with 3 other horses when it was observed to be slightly lame on the right foreleg. The next morning he was found to be in lateral recumbency and was depressed and sweating. On examination, the pupils were dilated and fixed, he was unable to stand and there was no muscle tone, although some cutaneous twitching was evident. The pulse was barely detectable and the heart rate was 60 per min and weak. Respiration was slow and shallow, and gastrointestinal activity depressed. Although the weather and environment were favourable for snake activity? Australian Vererinary Journal, Vol. 51, January, 1975
a thorough search of the patient failed to locate fang punctures. Clinical pathology on blood produced results paralleling those of Case 1. Because of the poor prognosis the horse was treated symptomatically, but died that evening. Case 3 A 4-month-old Standardbred colt and its mother had recently been moved onto a stubble paddock. Fences constructed of stone and piles of stones surrounding some trees provided a good environment for snakes. One hot January morning the owner observed the foal to be normal but 2 hours later he was staggering and trembling. Although at the time of the veterinary examination these signs were very pronounced, he still took flight when approached. When finally caught he was sweating profusely and was very shaky, making it necessary to cast him for examination and treatment. Fixed mydriasis was present and the eyelids appeared half-closed. Fang punctures were located on the mucous membrane of his upper lip. 3000 IU of Tiger snake antivenene, 5 % dextrose in normal saline, and Ringer’s lactate solution were given intravenously. He was also treated with antihistamines? antibiotics and tetanus antitoxin. The clinical signs had greatly abated by that evening and an uneventful recovery followed over the next 2 days. Case 4
Although the weather during April had been cold and wet, the preceding few days were warm and fine. A number of Clydesdale foals had been drenched and left in a small yard overnight. The
next morning a 7-month-old filly was found to be sweating and trembling violently. She was standing when examined. The clinical signs were sugTABLE 1 Clinical Pathology of Blood in Cases of Snakebite+ in Horses Cases
1
2
3
Haematocrit (%) Haemolysist Creatine phosphokinase (mU/rnl)
29 nil 244
28 nil 181
49
nil 540
*Presumed tiger snake in each case. ?As judged by unaided eye.
37
gestive of snakebite and fang punctures were found on the mucous membrane of the upper lip. It was necessary to cast her to carry out treatment, which was the same as in Case 3. It was found that on conclusion of the infusion the venepuncture continued to bleed for a prolonged time. She was revisited later in the afternoon, by which time improvement was marked, mydriasis was less pronounced and a positive pupillary light reflex was present. Although the initial improvement was rapid, full recovery was not complete for several more days. Tiger snakes had been numerous around the property all summer and it was demonstrated that they were still active when a 75 cm tiger snake was killed on the day that the filly had been bitten. Henry (1935) reported a confirmed case in which a military horse was bitten on a leg by a tiger snake. The progression of clinical signs was not rapid; 12 hours after the bite the horse was weak, trembling and had impaired vision. It was noted that the trembling greatly abated when the animal lay down. The horse’s temperature, pulse and respiration rate remained normal. Syrnptomatic treatment was to no avail and it was necessary to destroy the horse on the fourth day. A series of cases has been reported in Queensland, the most common species involved being the brown snake, Demansia textilis (Pascoe 1974). By far the most common snake species in this Werribee practice area is the tiger snake, Notechis scutatus. Its venom is strongly neurotoxic, moderately coagulant and weakly haemolytic and cytotoxic (Trinca 1959; Hungerford 1967; Trinca 1971). Many factors affect the rate of onset and severity of clinical signs. A bite may be rendered ineffective by thick skin, interposition of hair, or merely by a poor purchase for the discharge of venom at the site. The venom gland may be relatively empty following a recent meal, or even due to moulting or season of the year. On the other hand, a tiger snake is an active and pugnacious opponent when provoked and may bite repeatedly (Trinca 1959; Trinca 1971). The following general clinical pattern was observed in the 4 reported cases. Pronounced pupillary dilation, negative pupillary light reflex and a positive eye preservation reflex, were constant features. Drooping of the eyelids was observed only as a response to bright sunlight. Trembling was a most obvious sign in the standing patient. In the fully recumbent horse muscle tone was very low and only some cutaneous twitching was still apparent; that is,
paralysis was advanced. A noteworthy manifestation associated with this trembling in the early stages was an apparent restlessness. During this stage it was sometimes impossible to get the horse to stand still. It would lie down suddenly, almost as though it had colic and would then relax. This restlessness, along with the trembling, reappeared as soon as the horse got to its feet again. Mental alertness was not depressed until the syndrome was very advanced, as it was in Case 2 . Sweating was pronounced in all 4 cases. Temperature, pulse rate and respiration rate remained within normal limits; however, if stressed or excited the pulse and respiration rates would alter markedly. Although the haematocrit of the horse in Case 2 was unaccountably low, the haemograms were within normal limits. No haemolysis was detected in any of the cases. A low to moderate degree of muscle damage was evidenced by a slightly elevated plasma CPK and was attributed to the cytopathic component of the venom. In the 2 confirmed cases the fang marks were on the upper lip, suggesting that the inquisitive horse approached the snake with its muzzle. These punctures, present on the mucous membrane, showed no signs of inflammation and were therefore difficult to find. Bites on haired skin would be very difficult to locate. Supportive treatment was aimed at restoring energy, fluid and electrolyte balance, and preventing secondary sequelae. The prolonged clotting time noted in Case 4 was not observed in any of the other cases. A search of the records at the Veterinary Clinical Centre, Werribee, produced 4 other cases in horses of illness which was diagnosed as snakebite on the grounds of clinical signs and on the probability that snakes were active in the environment. Two cases had clinical signs very much like those described and recovered after receiving 3000 IU of tiger snake antivenene. Another exhibited acute signs, consistent with snakebite, as described, but quickly became recumbent and died in spite of antivenene treatment. This horse’s haemogram was normal but its plasma CPK was 2360 mU/ml. Histopathologically there were areas of acute muscular degeneration that were consistent with snakebite. There were no other significant lesions. The fourth involved a mare which very suddenly became recumbent and unwilling to rise. She was showing the syndrome attributable to snakebite but was also rolling. The next day she was showing signs of acute colic, At post-mortem examination, torsion of the bowel, muscular degeneration and fang marks on a leg
38
Australian Veterinary fournul, Vol. 51, January, 1975
Discussion
were found. It would seem that the intestinal accident was a sequela to the snakebite. Summary
Four cases of snakebite in horses are presented. Diagnosis was made on clinical signs in all, plus fang punctures in 2 cases. Tiger snake antivenene was used in the treatment of 2 patients and these recovered rapidly. Of the 2 in which antivenene was not used, 1 severely affected horse died. The clinical signs which were observed were those of progressive general paralysis and were entirely referable to the neurotoxic component of the venom.
Austrciliuri Veterinary Journul, Vol. 51. January, 1975
References Henry, M. (1935)-Aust. vet. I. 11: 39. Hungerford, T. G. (1967&"Diseases of Livestock". Angus and Robertson; 6th Ed., Melbourne. Pascoe, R. R. (1974)-Aust. vet. Ass. Conference Handbook, 50: 91. Seddon, H. R. (1968)-"Diseases of Domestic Animals in Australia". Cwlth Aust. Dep. HIth Sew. Publ. No. 7 (revised by H. E. Albiston). Cwlth Gov. Printer, Canberra. Trinca, G. F. (1959)-Proc. Aust. vet. Ass. (Vic. Div.j 17: 81. Trinca, J. C. ( 1 9 7 1 j C . S . L . Veterinary Handbook". 2nd edn, Commonwealth Serum Laboratories, Melbourne. (Received f o r publication 30 May 1974)
39
There is very little information available on snakebite in the horse. This report describes in detail 4 cases of snakebite in horses seen within this Werribee practice area. The diagnosis was circumstantial in 2 of these cases, but confirmed in the other 2. case Nistories Case 1 During October 1973, a 9-month-old male hack in generally poor condition was kept tethered in long dry grass beside a suburban railway line. This terrain was considered to be ideal cover for snakes. The owner observed that the horse had suddenly become staggery and anorectic. When examined, he was recumbent and appeared depressed but would readily rise if disturbed. The recumbency was apparently voluntary. He was sweating moderately and when standing was twitching and restless. Antibiotic and antihistamine therapy was instituted. Antivenene was not used because of cost and the mildness of clinical signs, considered to be due to non-lethal envenomation. Good nursing was advised as it was considered that recovery might be prolonged. The following day his clinical condition had deteriorated slightly, however recovery occurred gradually over the following week. Clinical pathology of blood taken at the initial examination revealed a low haematocrit value but normal total and differential white cell counts. Plasma Creatine Phosphokinase (CPK) was estimated (Table 1). Case 2 During November a 3-year-old Thoroughbred gelding was agisted on a property near a small town within the Werribee shire. It was sharing a 25 ha grassy paddock with 3 other horses when it was observed to be slightly lame on the right foreleg. The next morning he was found to be in lateral recumbency and was depressed and sweating. On examination, the pupils were dilated and fixed, he was unable to stand and there was no muscle tone, although some cutaneous twitching was evident. The pulse was barely detectable and the heart rate was 60 per min and weak. Respiration was slow and shallow, and gastrointestinal activity depressed. Although the weather and environment were favourable for snake activity? Australian Vererinary Journal, Vol. 51, January, 1975
a thorough search of the patient failed to locate fang punctures. Clinical pathology on blood produced results paralleling those of Case 1. Because of the poor prognosis the horse was treated symptomatically, but died that evening. Case 3 A 4-month-old Standardbred colt and its mother had recently been moved onto a stubble paddock. Fences constructed of stone and piles of stones surrounding some trees provided a good environment for snakes. One hot January morning the owner observed the foal to be normal but 2 hours later he was staggering and trembling. Although at the time of the veterinary examination these signs were very pronounced, he still took flight when approached. When finally caught he was sweating profusely and was very shaky, making it necessary to cast him for examination and treatment. Fixed mydriasis was present and the eyelids appeared half-closed. Fang punctures were located on the mucous membrane of his upper lip. 3000 IU of Tiger snake antivenene, 5 % dextrose in normal saline, and Ringer’s lactate solution were given intravenously. He was also treated with antihistamines? antibiotics and tetanus antitoxin. The clinical signs had greatly abated by that evening and an uneventful recovery followed over the next 2 days. Case 4
Although the weather during April had been cold and wet, the preceding few days were warm and fine. A number of Clydesdale foals had been drenched and left in a small yard overnight. The
next morning a 7-month-old filly was found to be sweating and trembling violently. She was standing when examined. The clinical signs were sugTABLE 1 Clinical Pathology of Blood in Cases of Snakebite+ in Horses Cases
1
2
3
Haematocrit (%) Haemolysist Creatine phosphokinase (mU/rnl)
29 nil 244
28 nil 181
49
nil 540
*Presumed tiger snake in each case. ?As judged by unaided eye.
37
gestive of snakebite and fang punctures were found on the mucous membrane of the upper lip. It was necessary to cast her to carry out treatment, which was the same as in Case 3. It was found that on conclusion of the infusion the venepuncture continued to bleed for a prolonged time. She was revisited later in the afternoon, by which time improvement was marked, mydriasis was less pronounced and a positive pupillary light reflex was present. Although the initial improvement was rapid, full recovery was not complete for several more days. Tiger snakes had been numerous around the property all summer and it was demonstrated that they were still active when a 75 cm tiger snake was killed on the day that the filly had been bitten. Henry (1935) reported a confirmed case in which a military horse was bitten on a leg by a tiger snake. The progression of clinical signs was not rapid; 12 hours after the bite the horse was weak, trembling and had impaired vision. It was noted that the trembling greatly abated when the animal lay down. The horse’s temperature, pulse and respiration rate remained normal. Syrnptomatic treatment was to no avail and it was necessary to destroy the horse on the fourth day. A series of cases has been reported in Queensland, the most common species involved being the brown snake, Demansia textilis (Pascoe 1974). By far the most common snake species in this Werribee practice area is the tiger snake, Notechis scutatus. Its venom is strongly neurotoxic, moderately coagulant and weakly haemolytic and cytotoxic (Trinca 1959; Hungerford 1967; Trinca 1971). Many factors affect the rate of onset and severity of clinical signs. A bite may be rendered ineffective by thick skin, interposition of hair, or merely by a poor purchase for the discharge of venom at the site. The venom gland may be relatively empty following a recent meal, or even due to moulting or season of the year. On the other hand, a tiger snake is an active and pugnacious opponent when provoked and may bite repeatedly (Trinca 1959; Trinca 1971). The following general clinical pattern was observed in the 4 reported cases. Pronounced pupillary dilation, negative pupillary light reflex and a positive eye preservation reflex, were constant features. Drooping of the eyelids was observed only as a response to bright sunlight. Trembling was a most obvious sign in the standing patient. In the fully recumbent horse muscle tone was very low and only some cutaneous twitching was still apparent; that is,
paralysis was advanced. A noteworthy manifestation associated with this trembling in the early stages was an apparent restlessness. During this stage it was sometimes impossible to get the horse to stand still. It would lie down suddenly, almost as though it had colic and would then relax. This restlessness, along with the trembling, reappeared as soon as the horse got to its feet again. Mental alertness was not depressed until the syndrome was very advanced, as it was in Case 2 . Sweating was pronounced in all 4 cases. Temperature, pulse rate and respiration rate remained within normal limits; however, if stressed or excited the pulse and respiration rates would alter markedly. Although the haematocrit of the horse in Case 2 was unaccountably low, the haemograms were within normal limits. No haemolysis was detected in any of the cases. A low to moderate degree of muscle damage was evidenced by a slightly elevated plasma CPK and was attributed to the cytopathic component of the venom. In the 2 confirmed cases the fang marks were on the upper lip, suggesting that the inquisitive horse approached the snake with its muzzle. These punctures, present on the mucous membrane, showed no signs of inflammation and were therefore difficult to find. Bites on haired skin would be very difficult to locate. Supportive treatment was aimed at restoring energy, fluid and electrolyte balance, and preventing secondary sequelae. The prolonged clotting time noted in Case 4 was not observed in any of the other cases. A search of the records at the Veterinary Clinical Centre, Werribee, produced 4 other cases in horses of illness which was diagnosed as snakebite on the grounds of clinical signs and on the probability that snakes were active in the environment. Two cases had clinical signs very much like those described and recovered after receiving 3000 IU of tiger snake antivenene. Another exhibited acute signs, consistent with snakebite, as described, but quickly became recumbent and died in spite of antivenene treatment. This horse’s haemogram was normal but its plasma CPK was 2360 mU/ml. Histopathologically there were areas of acute muscular degeneration that were consistent with snakebite. There were no other significant lesions. The fourth involved a mare which very suddenly became recumbent and unwilling to rise. She was showing the syndrome attributable to snakebite but was also rolling. The next day she was showing signs of acute colic, At post-mortem examination, torsion of the bowel, muscular degeneration and fang marks on a leg
38
Australian Veterinary fournul, Vol. 51, January, 1975
Discussion
were found. It would seem that the intestinal accident was a sequela to the snakebite. Summary
Four cases of snakebite in horses are presented. Diagnosis was made on clinical signs in all, plus fang punctures in 2 cases. Tiger snake antivenene was used in the treatment of 2 patients and these recovered rapidly. Of the 2 in which antivenene was not used, 1 severely affected horse died. The clinical signs which were observed were those of progressive general paralysis and were entirely referable to the neurotoxic component of the venom.
Austrciliuri Veterinary Journul, Vol. 51. January, 1975
References Henry, M. (1935)-Aust. vet. I. 11: 39. Hungerford, T. G. (1967&"Diseases of Livestock". Angus and Robertson; 6th Ed., Melbourne. Pascoe, R. R. (1974)-Aust. vet. Ass. Conference Handbook, 50: 91. Seddon, H. R. (1968)-"Diseases of Domestic Animals in Australia". Cwlth Aust. Dep. HIth Sew. Publ. No. 7 (revised by H. E. Albiston). Cwlth Gov. Printer, Canberra. Trinca, G. F. (1959)-Proc. Aust. vet. Ass. (Vic. Div.j 17: 81. Trinca, J. C. ( 1 9 7 1 j C . S . L . Veterinary Handbook". 2nd edn, Commonwealth Serum Laboratories, Melbourne. (Received f o r publication 30 May 1974)
39
