Intravenous inoculation produced a three-fold increase in pulmonary arterial pressure within 100 seconds at a dose of 400 fig, (4pgIkg). Oral dosing with simplexin reproduced the range of signs characteristic of St. George disease, including inappetence, weight loss, jugular distention, and submandibular oedema. H. B. ROBERTS, B.V.Sc. T. J. McCLURE. B.V.Sc.. Ph.D. Department of Veterinary Medicine, University of Sydney, Camden, New South Wales 2570. E. RITCHIE, D.Sc. W. C. TAYLOR, D.Sc. P. W. FREEMAN, Ph.D Department of Organic Chemistry, University of Sydney, Sydney, New South Wales 2006. 23 December 1974
References Clark, I. A. (197l)-Aust. vet. J . 47: 123. Clark, I. A. (1973kRes. vet. Sci. 14: 341. Hegnauer, R. (1973)-“Chemotaxonomie der Pflanzen”, vol. 6, p 512. (Birkhaiiser, Basel and Stuttgart, 1973.) McClure, T. J . and Farrow, B. R. H. (1971)-Aust. vet. J . 47: 100. Ohigashi, H., Katsumata, H., Kawazu, K., Koshimizu, K. and Mitsui, T. (1974)-Agr. biol. Chem. 38: 1093. Roberts, H. B. and Healy, P. J. (1971)-Aust. vef. J . 47: 123. Ronlh, A. and Wickberg, B. (1970)--Tetrahedron Letters, p 4261. Sakata, K., Kawazu, K. and Mitsui, T. (1971bAgr. biol. Chem. 35: 1084; 2113. Scout, G. H., Balkenhol, W. G., Poling, M. and Hickernell, G. L. ( 1 9 7 0 t J . Am. chem. SOC. 92: 1070.
ENZOOTI’C CALCINOSIS OF CATTLE IN PAPUA NEW GUINEA There appear to be no reports of any cattle diseases in Australia or Papua New Guinea characterised by a general metastatic mineralisation of the soft tissues. This letter reports the presence of a cattle disease in Papua New Guinea which closely resembles the disease “Enteque seco” in Argentina, “Enzootic Calcinosis” in Europe and “Naalehu Disease” in Hawaii. So far the disease has been only reported from the Bulolo Valley, where the cattle are introduced as weaners and kept in pine plantations until almost two years old and then fattened on nearby improved pasture. The disease is known to have been present for at least 3 years. The prevalence of the clinical disease is approximately 10% of the herd and it has been seen in all age groups. However, cattle bred on the property are reported not to show clinical symptoms of the disease. The predominant age group affected have been the introduced weaner cattle and clinical symptoms appear 6-8 weeks after the weaned cattle have been running in the pine plantations. The typical clinical symptqms as described by Worker and Carillo (1967) and Dirksen et a1 (1971) were present, consisting of rapid wasting, contraction of the tendons which result in the cattle standing on their toes, “tucked-up’’ abdomen, stiff gait and hyper-excitability. In severely affected cattle, serum calcium and serum inorganic phosphorus are increased. Post-mortem examination revealed the characteristic metastatic mineralisation of soft tissue which include the epicardium, particularly the left ventricle and atrium, the bicuspid value resulting in increased thickness, chordae tendineae which become hypertrophied and the aorta. The internal surface of the aorta appeared dense!y corregated and intermingled are irregular bone-like deposits. which were commonly present at the thoracic/abdominal junction. At the terminal bifurcation of the aorta and scattered along the abdominal aorta were dense orange coloured plaques. The caudal extremity of the diaphragmatic lobes of the lungs were often emphysematous owing to trapped air due to the cavernous bone-like structures - the cut surface of the lung was honeycombed and firm. The fore and hind leg tendons also appeared to be mineralised. The carpal and tarsal joints had deep erosions of their articular surfaces. Microscopically dense baso326
philic material may be observed in the tunica intima of the affected vascular tree and occasional cartilaginous deposits may be observed in the tunica media. The alveolar septa was thickened and mineralised. Chemical analysis of the lesions revealed deposits of calcium and inorganic phosphorus, The condition is initially seen in the young cattle and if they are removed from the toxic pasture a t the first signs of the disease, they recover. However, chronic cases of the disease only partially recover and then only after an extended period of time. Solanurn malacoxylon has been shown to cause the disease in Argentina (Worker and Carillo 1967), but this plant is not thought to be present in Papua New Guinea nor Australia. Another plant may be involved in Papua New Guinea, as Dirksen et a1 (1974) has shown that in Europe the disease is caused by Trisetum flavescens. Attempts are currently being made to identify the toxic agent. The metastatic mineralisation of soft tissues is similar to that found in hypervitaminosis D. There is one report by Seawright and Watt (1971) which.may suggest that the toxic principle may be in Australia, as they describe a “pumice stone lung” which is one of the characteristics of the disease and is identical to the lesions found in affected cattle from Papua New Guinea. It is not known whether they examined the cardio-vascular system of the affected animals. J . W. COPLAND, B.V.Sc. Veterinary Laboratory, P.O. Box 6372, Boroko, Papua New Guinea 13 December 1974
References Dirksen, G., Plank, P., Simon, U., Hanichen, T., Daniel, P. and Speif, A. (1974)-Dtsch. tierarztl. Wschr. 80: 565-588. Dirksen, G., Plank, P., Dammrich and Hanichen, T. (1971)-Vet. med. Rev. 213: 207. Seawright, A. A. and Watt, D. A. (1971)-Aust. vet. 1. 47: 612. Worker, N. A. and Carillo, B. J. (1967)-Nature, Lond. 215: 72. Australian Veterinary Journal, Vol. 51. Jone, 1975
References Clark, I. A. (197l)-Aust. vet. J . 47: 123. Clark, I. A. (1973kRes. vet. Sci. 14: 341. Hegnauer, R. (1973)-“Chemotaxonomie der Pflanzen”, vol. 6, p 512. (Birkhaiiser, Basel and Stuttgart, 1973.) McClure, T. J . and Farrow, B. R. H. (1971)-Aust. vet. J . 47: 100. Ohigashi, H., Katsumata, H., Kawazu, K., Koshimizu, K. and Mitsui, T. (1974)-Agr. biol. Chem. 38: 1093. Roberts, H. B. and Healy, P. J. (1971)-Aust. vef. J . 47: 123. Ronlh, A. and Wickberg, B. (1970)--Tetrahedron Letters, p 4261. Sakata, K., Kawazu, K. and Mitsui, T. (1971bAgr. biol. Chem. 35: 1084; 2113. Scout, G. H., Balkenhol, W. G., Poling, M. and Hickernell, G. L. ( 1 9 7 0 t J . Am. chem. SOC. 92: 1070.
ENZOOTI’C CALCINOSIS OF CATTLE IN PAPUA NEW GUINEA There appear to be no reports of any cattle diseases in Australia or Papua New Guinea characterised by a general metastatic mineralisation of the soft tissues. This letter reports the presence of a cattle disease in Papua New Guinea which closely resembles the disease “Enteque seco” in Argentina, “Enzootic Calcinosis” in Europe and “Naalehu Disease” in Hawaii. So far the disease has been only reported from the Bulolo Valley, where the cattle are introduced as weaners and kept in pine plantations until almost two years old and then fattened on nearby improved pasture. The disease is known to have been present for at least 3 years. The prevalence of the clinical disease is approximately 10% of the herd and it has been seen in all age groups. However, cattle bred on the property are reported not to show clinical symptoms of the disease. The predominant age group affected have been the introduced weaner cattle and clinical symptoms appear 6-8 weeks after the weaned cattle have been running in the pine plantations. The typical clinical symptqms as described by Worker and Carillo (1967) and Dirksen et a1 (1971) were present, consisting of rapid wasting, contraction of the tendons which result in the cattle standing on their toes, “tucked-up’’ abdomen, stiff gait and hyper-excitability. In severely affected cattle, serum calcium and serum inorganic phosphorus are increased. Post-mortem examination revealed the characteristic metastatic mineralisation of soft tissue which include the epicardium, particularly the left ventricle and atrium, the bicuspid value resulting in increased thickness, chordae tendineae which become hypertrophied and the aorta. The internal surface of the aorta appeared dense!y corregated and intermingled are irregular bone-like deposits. which were commonly present at the thoracic/abdominal junction. At the terminal bifurcation of the aorta and scattered along the abdominal aorta were dense orange coloured plaques. The caudal extremity of the diaphragmatic lobes of the lungs were often emphysematous owing to trapped air due to the cavernous bone-like structures - the cut surface of the lung was honeycombed and firm. The fore and hind leg tendons also appeared to be mineralised. The carpal and tarsal joints had deep erosions of their articular surfaces. Microscopically dense baso326
philic material may be observed in the tunica intima of the affected vascular tree and occasional cartilaginous deposits may be observed in the tunica media. The alveolar septa was thickened and mineralised. Chemical analysis of the lesions revealed deposits of calcium and inorganic phosphorus, The condition is initially seen in the young cattle and if they are removed from the toxic pasture a t the first signs of the disease, they recover. However, chronic cases of the disease only partially recover and then only after an extended period of time. Solanurn malacoxylon has been shown to cause the disease in Argentina (Worker and Carillo 1967), but this plant is not thought to be present in Papua New Guinea nor Australia. Another plant may be involved in Papua New Guinea, as Dirksen et a1 (1974) has shown that in Europe the disease is caused by Trisetum flavescens. Attempts are currently being made to identify the toxic agent. The metastatic mineralisation of soft tissues is similar to that found in hypervitaminosis D. There is one report by Seawright and Watt (1971) which.may suggest that the toxic principle may be in Australia, as they describe a “pumice stone lung” which is one of the characteristics of the disease and is identical to the lesions found in affected cattle from Papua New Guinea. It is not known whether they examined the cardio-vascular system of the affected animals. J . W. COPLAND, B.V.Sc. Veterinary Laboratory, P.O. Box 6372, Boroko, Papua New Guinea 13 December 1974
References Dirksen, G., Plank, P., Simon, U., Hanichen, T., Daniel, P. and Speif, A. (1974)-Dtsch. tierarztl. Wschr. 80: 565-588. Dirksen, G., Plank, P., Dammrich and Hanichen, T. (1971)-Vet. med. Rev. 213: 207. Seawright, A. A. and Watt, D. A. (1971)-Aust. vet. 1. 47: 612. Worker, N. A. and Carillo, B. J. (1967)-Nature, Lond. 215: 72. Australian Veterinary Journal, Vol. 51. Jone, 1975
