CASE REPORT AN OUTBREAK OF SWAZNSONA POISONING IN HORSES B. M. ~'SULLIVAN*, and J. A. GOODWIN? SUMMARY: On 6 properties in south-western Queensland an outbreak of nervous disease occurred in horses due to ingestion of Swainsona (Darling pea). Loss of condition, depression, hyperaesthesia and hyperexcitability were seen in affected horses. At autopsy of 2 horses generalised cytoplasmic vacuolation was seen in the neurones of the central nervous system and in the liver, adrenal and thyroid. The clinical and pathological features were similar to those described in horses suffering from Swainsona poisoning in Australia and Astragalus and Oxytropis in North America.
Introduction
head lowered or walking slowly in circles. The clinical signs of nervous system damage increased and by mid-July the mare was markedly incoordinated and when persuaded to move would plunge forward and fall. Hyperaesthesia to touch was marked and at a needle prick the mare would rear and fall. Access to Swainsona was denied to the mare, but after 10 days, when no improvement was seen, she was killed and a post-mortem examination was carried out. The foal was transported to the laboratory and History and Clinical Signs on arrival was in poor condition and markedly During floods in February 1976 in south- depressed, standing for long periods with head western Queensland large areas of land which are lowered, eyes closed and apparently unaware of usually flood-free were covered by water and its surroundings. It could be approached and subsequently Swainsona flourished on land on touched without response but attempts to restrain which it does not normally grow. On a number the foal provoked violent struggling which reof properties the horse paddocks were involved sulted in its falling to the ground and continuing and many horses were exposed to unusually large to struggle until it regained its feet. Vision was stands of Swainsona during the autumn and poor and the pupillary eye reflex was absent. winter of 1976. Specimens of S . brachycarpa, The head was held partly ventro-flexed with mild S. galegifolia and S. luteola from 2 properties tonic contraction of the cervical musculature. were identified by the Government Botanist. When its head was raised the foal exhibited an In June, some horses with access to Swain- exaggerated tonic neck reflex, lifting both foresona were noticed to be losing condition and to limbs off the ground and rearing backwards. The be depressed when undisturbed. However, when foal could urehend pasture by snatching at it and an attempt was made to drive or ride affected pulling with slow, deliberate chewing but with horses they became unmanageable, rearing and little evidence of swallowing. It was not ataxic plunging and often falling. Apparent addiction of while walking or grazing and although it had irhorses to Swainsonu was observed with affected regular vertical head nodding it showed no loss animals selectively grazing the plant. Twenty- of balance or wide based stance. Autopsy of the four horses were known to be affected on 6 foal was carried out 12 days after removal from access to Swainsona. properties. On one of these properties 6 of 10 horses were Pathology affected and 2 of them, a 3-year-old mare and its No macroscopic lesions were seen at autopsy 6-month-old foal, were closely observed and in either horse. Histologically the significant lesion autopsies performed. Four of the affected horses in both horses was widespread foamy vacuolation had been introduced to the property early in of the cytoplasm of neurones throughout the May. The mare was found in mid-June in an spinal cord and brain. The neurones in the nuclei emaciated condition, alternately standing with its of the brainstem were most severely affected. Vacuoles were also present in hepatocytes, in the *Animal Research Institute, Yeerongpilly, Queensland, 4105. tQueensland Deparlment of Primary Industries, Goondiwindi, cells of the zona fasciculata of the adrenal and in Queensland, 4390.
Poisoning of sheep and cattle with Swainsonu, or Darling pea, has been known for many years and the clinical signs and pathology have been described (Hartley and Kater 1965, Laws and Anson 1968). In 1971 Hartley and Gibson described Swainsonu poisoning in an orphan foal on a property where cattle were affected. This report describes an outbreak of nervous disease in horses attributable to ingestion of Swainsona.
446
Austrulian Vefcrinury Journul, Vol. 53, September, 1977
follicular epithelium of the thyroid but were not liver, adrenal and thyroid but the neurones of the central nervous system were severely affected. found in the cells of the kidney or lymph nodes. Examination of blood smears from both horses Haematological examination was carried out only at the time of autopsy did not show any vacuo- at autopsy and vacuolation of circulating lympholation of lymphocytes as was described in cattle, cytes was not seen. This was consistent with the sheep and guinea pigs by Huxtable and Gibson findings of Huxtable and Gibson (1970) in cattle, sheep and guinea pigs in which vacuoles (1970). disappeared from the circulating lymphocytes Discussion The clinical and pathological features of the within 10 days of being denied access to Swaindisease in the horses described are similar in sona. Horses in the area have access to some Swuinmost respects to those of Swainsonu poisoning of cattle and sheep and of the foal described by sona in most years but it was only after flooding Hartley and Gibson ( 1971). They are also similar of the higher country that exposure to extensive to those of horses suffering from poisoning by stands of the plant occurred and they became locoweed (Astrugalus and Oxytropis) in North affected by it. Some of the most severely affected America (Oehme et al 1968; James and Van horses had been recently introduced to the area Kampen 1971; Harries et a1 1972). Horses suffer- and being unfamiliar with Swainsonu may have ing from either locoweed or Darling pea toxicity grazed it more freely and become addicted to the suffer loss of condition and depression but be- plant. come excited when handled. At autopsy they have References cytoplasmic vacuolation of neurones in the Harries, W. N., Baker, F. P. and Johnston, A. (1972)central nervous system and similar changes in the Can. vet. 1. 13: 141. parenchymatous cells of other organs. Hartley, W. J. and Gibson, A. J. (1971)-Aust. vet. J . 47: 300. James et a1 (1970) have described the clinical Hartley, W. J. and Kater, J. C. (1965)-Ausr. vet. 3. similarities and comparative pathology of Astra41: 107. Huxtable, C. R. and Gibson, A. (1970)-Aust. vet. 3. galus and Swuinsona poisoning in sheep. 46: 446. James and Van Kampen (1971) found that 1 James, L. F. and Van Kampen, K. R. (1971)--1. Am. month after the cessation of ingestion of Astruvet. med. Ass. 158: 614. galus nearly all evidence of cytoplasmic vacuo- James, L. F., Van Kampen, K. R. and Hartley, W. J. (1970)--Path. vet. 7: 116. lation had disappeared from the parenchymatous Laws, L. and Anson, R. B. (1968)-Aust. vet. 3. 44: organs but it persisted in the neurones of the 447. central nervous system. In the 2 horses examined Oehme, F. W., Bailie, W. E. and Hulbert, L. C. (1968) -4.Am. vet. med. Ass. 152: 271. here 10 and 12 days after being deprived access to Swainsona, mild vacuolation was present in the (Received tor publication 14 October 1976)
Australian Veterinary Journal, Vol. 5 3 , September, 1977
447
Introduction
head lowered or walking slowly in circles. The clinical signs of nervous system damage increased and by mid-July the mare was markedly incoordinated and when persuaded to move would plunge forward and fall. Hyperaesthesia to touch was marked and at a needle prick the mare would rear and fall. Access to Swainsona was denied to the mare, but after 10 days, when no improvement was seen, she was killed and a post-mortem examination was carried out. The foal was transported to the laboratory and History and Clinical Signs on arrival was in poor condition and markedly During floods in February 1976 in south- depressed, standing for long periods with head western Queensland large areas of land which are lowered, eyes closed and apparently unaware of usually flood-free were covered by water and its surroundings. It could be approached and subsequently Swainsona flourished on land on touched without response but attempts to restrain which it does not normally grow. On a number the foal provoked violent struggling which reof properties the horse paddocks were involved sulted in its falling to the ground and continuing and many horses were exposed to unusually large to struggle until it regained its feet. Vision was stands of Swainsona during the autumn and poor and the pupillary eye reflex was absent. winter of 1976. Specimens of S . brachycarpa, The head was held partly ventro-flexed with mild S. galegifolia and S. luteola from 2 properties tonic contraction of the cervical musculature. were identified by the Government Botanist. When its head was raised the foal exhibited an In June, some horses with access to Swain- exaggerated tonic neck reflex, lifting both foresona were noticed to be losing condition and to limbs off the ground and rearing backwards. The be depressed when undisturbed. However, when foal could urehend pasture by snatching at it and an attempt was made to drive or ride affected pulling with slow, deliberate chewing but with horses they became unmanageable, rearing and little evidence of swallowing. It was not ataxic plunging and often falling. Apparent addiction of while walking or grazing and although it had irhorses to Swainsonu was observed with affected regular vertical head nodding it showed no loss animals selectively grazing the plant. Twenty- of balance or wide based stance. Autopsy of the four horses were known to be affected on 6 foal was carried out 12 days after removal from access to Swainsona. properties. On one of these properties 6 of 10 horses were Pathology affected and 2 of them, a 3-year-old mare and its No macroscopic lesions were seen at autopsy 6-month-old foal, were closely observed and in either horse. Histologically the significant lesion autopsies performed. Four of the affected horses in both horses was widespread foamy vacuolation had been introduced to the property early in of the cytoplasm of neurones throughout the May. The mare was found in mid-June in an spinal cord and brain. The neurones in the nuclei emaciated condition, alternately standing with its of the brainstem were most severely affected. Vacuoles were also present in hepatocytes, in the *Animal Research Institute, Yeerongpilly, Queensland, 4105. tQueensland Deparlment of Primary Industries, Goondiwindi, cells of the zona fasciculata of the adrenal and in Queensland, 4390.
Poisoning of sheep and cattle with Swainsonu, or Darling pea, has been known for many years and the clinical signs and pathology have been described (Hartley and Kater 1965, Laws and Anson 1968). In 1971 Hartley and Gibson described Swainsonu poisoning in an orphan foal on a property where cattle were affected. This report describes an outbreak of nervous disease in horses attributable to ingestion of Swainsona.
446
Austrulian Vefcrinury Journul, Vol. 53, September, 1977
follicular epithelium of the thyroid but were not liver, adrenal and thyroid but the neurones of the central nervous system were severely affected. found in the cells of the kidney or lymph nodes. Examination of blood smears from both horses Haematological examination was carried out only at the time of autopsy did not show any vacuo- at autopsy and vacuolation of circulating lympholation of lymphocytes as was described in cattle, cytes was not seen. This was consistent with the sheep and guinea pigs by Huxtable and Gibson findings of Huxtable and Gibson (1970) in cattle, sheep and guinea pigs in which vacuoles (1970). disappeared from the circulating lymphocytes Discussion The clinical and pathological features of the within 10 days of being denied access to Swaindisease in the horses described are similar in sona. Horses in the area have access to some Swuinmost respects to those of Swainsonu poisoning of cattle and sheep and of the foal described by sona in most years but it was only after flooding Hartley and Gibson ( 1971). They are also similar of the higher country that exposure to extensive to those of horses suffering from poisoning by stands of the plant occurred and they became locoweed (Astrugalus and Oxytropis) in North affected by it. Some of the most severely affected America (Oehme et al 1968; James and Van horses had been recently introduced to the area Kampen 1971; Harries et a1 1972). Horses suffer- and being unfamiliar with Swainsonu may have ing from either locoweed or Darling pea toxicity grazed it more freely and become addicted to the suffer loss of condition and depression but be- plant. come excited when handled. At autopsy they have References cytoplasmic vacuolation of neurones in the Harries, W. N., Baker, F. P. and Johnston, A. (1972)central nervous system and similar changes in the Can. vet. 1. 13: 141. parenchymatous cells of other organs. Hartley, W. J. and Gibson, A. J. (1971)-Aust. vet. J . 47: 300. James et a1 (1970) have described the clinical Hartley, W. J. and Kater, J. C. (1965)-Ausr. vet. 3. similarities and comparative pathology of Astra41: 107. Huxtable, C. R. and Gibson, A. (1970)-Aust. vet. 3. galus and Swuinsona poisoning in sheep. 46: 446. James and Van Kampen (1971) found that 1 James, L. F. and Van Kampen, K. R. (1971)--1. Am. month after the cessation of ingestion of Astruvet. med. Ass. 158: 614. galus nearly all evidence of cytoplasmic vacuo- James, L. F., Van Kampen, K. R. and Hartley, W. J. (1970)--Path. vet. 7: 116. lation had disappeared from the parenchymatous Laws, L. and Anson, R. B. (1968)-Aust. vet. 3. 44: organs but it persisted in the neurones of the 447. central nervous system. In the 2 horses examined Oehme, F. W., Bailie, W. E. and Hulbert, L. C. (1968) -4.Am. vet. med. Ass. 152: 271. here 10 and 12 days after being deprived access to Swainsona, mild vacuolation was present in the (Received tor publication 14 October 1976)
Australian Veterinary Journal, Vol. 5 3 , September, 1977
447
