POSSIBLE PENTACHLOROPHENOL POISONING IN CATS Pentachlorophenol (PCP)* is used for the treatment of timber prior to, saw milling, to prevent fungal infection. Dieldrin is also occasionally used as an insecticide. PCP and dieldrin can be absorbed through the intact skin and deaths in people working with PCP have been reported (Gordon 1956; Barnes 1957). A series of sudden deaths in colonies of laboratory and zoo animals and cats has been tentatively traced to dieldrin in contaminated sawdust (Anon 1977). Schipper (1961) has shown that wood preservatives containing PCP may be extremely toxic to young pigs, the toxicity decreasing with age. Harrison (1959), working with sheep and calves, stated that chemical analysis of blood and urine from live animals or liver and stomach contents from fatal cases, together with the suspected poisonous material, would furnish sufficient evidence to confirm or eliminate PCP as the cause of poisoning. This letter records PCP poisoning as the possible cause of death in 3 cats (2 Siamese, 1 Abysinnian) from a cattery near Perth. The owners used pine shavings as bedding for their horse loose boxes and decided to use this material for litter in their cattery. Three days after delivery of a new consignment of shavings, which were used in 14 cat litter trays, a male redpoint Siamese was found lying comatose in its cage. Clinical and pathological examinations revealed icterus with markedly elevated serum glutamic-oxaloacetic transaminase and glutamic-pyruvic transaminase levels. The cat died despite supportive fluid and corticosteroid therapy. Post-mortem examination confirmed a generalised icterus with markedly swollen liver. The only significant microscopic lesions were diffuse vacuolar degeneration of hepatocytes and periportal haemorrhage in the liver. N o significant bacteria were isolated from heart blood, liver, lung and intestinal content nor any viruses from fresh lung tissue. Toxicological examination of liver and kidney for arsenic and lead proved negative for this and subsequent dead cats. The cat food (a proprietary mince for pets) was examined for aflatoxins with negative results. Eight more cats became ill within 7 days after exposure to the new wood-shavings litter and were presented with similar clinical signs, which included hyperaesthesia and apparently severe abdominal pain. Two of these cats died with similar post-mortem and laboratory findings. The others gradually recovered with extensive supportive therapy. Five cats remained apparently healthy. Since 8 cats which were not exposed to the new woodshavings litter showed no signs of illness at the cattery, a possibility of PCP or dieldrin poisoning was considered and "Pentabrite" (sodium pentachlorphenate JoOg/l) Terra Trading Co.. Perth.
various samples analysed at the Government Chemical Laboratories, Perth (Table I). The levels of dieldrin and DDT metabolites in the samples were low and could possibly be due to residues in the cat food. The levels of PCP in the liver. kidney and stomach contents presumably were due to contact with wood-shavings litter and circumstantial evidence indicates PCP poisoning to be the cause of death. N o published figures on the toxic levels of PCP in cats were available. R. L. PEET, G. MacDONALD, Department of Agriculture, Jarrah Road, South Perth, Western Australia, 6151. A . KEEFE, 9 Lyall Street, Belmont, Western Australia, 6104. 19August 1977
References
Anon. (1977)-New Scientist 74: 233.
Barnes, J. M . (1957)-1n Advances in Pest Control Research, Vol. 1 , Interscience, New York. Gordon, D. C. (1956)--Med. J . Aust. 2: 43, 485. Harrison, D. L. (1959)-N.Z. vet. J . 7 : 89. Schipper, I. A. (1961)-Am. J . vet. Res. 22: 401.
TABLE 1 Results of Chemical Analysis of Sam les f r o m Cats with Suspected Penrachlorophenof Poisoning Cat No.
Sample
DDT and PentaDieldrin M e t a b e chloromg/kg lites phenol mg/kg mg/kg
1 1
Liver and kidney Stomach and contents
0.01 0.04
2 2
Liver Stomach contents
0.02 0.03
3 3
-
Kidney Liver Wood shavings
* * *
0.02
~~~
1.4
0.15
1 .o
0.06 0.15
9 .o 10.0
* * *
24.0 20.0
~~~
470.0
Not examined.
SPINAL NEMATODIASIS OF THE DOG ASSOCIATED WITH ANCYLOSTOMA CANZNUM Attention has recently been drawn to the occurrence of cerebrospinal nematodiasis in young dogs infected with the rodent lungworm Angiostrongylus canronensis in southern Queensland (Mason et a/ 1976). Thirteen cases between the ages of 6 and 14 weeks occurred during the summer months and were characterised by pain and ascending ataxia and paresis. Focal granulomata were observed in the brain and all levels of the spinal cord and occasionally nematode larvae could be identified. In one case dissection yielded immature adults. This letter is prompted by the diagnosis of a similar clinical case but of different aetiology. A 12-week-old cocker spaniel was presented with clinical neurological signs. The owners reported loss of balance for several days and at examination torticollis and pain on flexion of the neck were very evident. One week later there was posterior paresis and constant pain, which progressed to quadriplegia.and death over the following
week. Radiographs of the spinal column, total and differential white cell count and erythrocyte sedimentation rate were normal. The outstanding clinical feature throughout the course of the disease was pain. Autopsy showed lesions in the cervical spinal cord only which was submitted for laboratory examination. About 2 cm of the mid-cervical cord showed severe meningeal and deep tissue haemorrhage. Transection at levels from the cervical to sacral regions showed no other lesions. A young adult female Ancylostoma caninum was dissected out from the haemorrhagic cord. The parasite measured 10 mm in length, 0.41 mm wide at the oesophagus and contained a few nonembryonated eggs in utero. Microscopically haemorrhagic and necrotic tracks in the cervical cord were found to lead from the subarachnoid space to the central grey matter. Blood vessels in the vicinity showed endothelial swelling and a sometimes intense lymphoid and
,6002
AusrrcJiun Veterinary Journal, Vol. 53, December, 1977
plasma cell reaction around them. There was scattered degenerative swelling of neuronal bodies and fibres and general swelling of neuroglial cells. Three Ancylostorna species have been identified in dogs and cats in coastal north Queensland, A. caninurn, A. brasiliensis and A. cubaeforrne (Setasuban and Waddell 1973). The prevalence of A. caninurn is particularly high in the dog. Skinpenetrating larvae migrate via the blood during their life-cycle while those ingested usually develop directly in the intestine (Okoshi and Murata 1968) and only occasionally invade other organs. Aherrant migration of A. caninurn and other nematodes, particularly ascarids, is a common phenomenon in abnormal hosts. Invasion of the central nervous system and ocular tissues of mice and man by larvae of Toxocara canis is well known (Kelly 1977) and Sprent (1955) reviewed apparently rare involvement of the central nervous system in other species of animals by members of the Strongyloidea. A. caninurn have been recovered in experimental infections from various organs of the rat (Matsusaki 1950), mice and guinea pigs (Nichols 1956). In the latter species up to half of the larvae were located in the brain, severe damage to the nervous system resulting in death as early as 6 days post-infection. No ocular involvement was found with mice injected per 0 s (Olsen et a1 1972) and only a small percentage were recovered from the brain or cord. In none of these cases of aberrant ancylostomiasis was there any development of the larvae beyond the third-stage although Nichols (1956) reported a slight increase in size. The present case appears to be an example in which partial maturity of the nematode was achieved and a critical anatomical structure affected in the normal host, circum-
stances that hitherto have not been recorded with this genus of parasite. The prevalence of ancylostomiasis in Queensland suggests that cerebrospinal nematodiasis in dogs may be commoner than is realised. T. D. BUICK, 378 Mulgrave Road, Cairns, Queensland, 4870 R. S. F. CAMPBELL, G. W. HUTCHINSON, Department of Tropical Veterinary Science, James Cook University, Townsville, Queensland, 481 1 17October 1977
References Kelly, J. D. (1977)--Cunine Pararirofogy, Vet. Rev. No. 17, University of Sydney Post-graduate Foundation in Veterinary Science, Sydney. Mason, K. V., Prescott, C. W., Kelly, W. R. and Waddell, A. H. (1976)-Aust. vet. 1. 52: 295. Matsusaki, G. (1950)-Yokoham Med. BuCf. 2: 154. Nichols, R. L. (19561.4. Pararif. 42: 363. Okoshi, S . and Murata, Y . (1968)--Iap. J . vet. Sci. 43.
Olsen, L. J., Beechie, R. A. and Beechie, B. J. (1972)J . Parasit. 58: 639. Setasuban, P. and Waddell, A. H. (1973)-Ausf. vet. J . 4 9 110. Sprent, J. F. A. (1955)-ParaSifology 46: 31.
PERINATAL FOAL MORTALITY ASSOCIATED WlTH A HERPESVIRUS Equine herpesvirus I (EHV 1) has been recognised in Australia for a number of years; however in contrast to overseas experience the association of EHVl with clinical abortion or neonatal foal mortality has not been reported. On 16 September, 1977 one 3-day-old foal, from a thoroughbred stud in the Camden district, died with severe respiratory distress. On the basis of histopathological examination i t was subsequently diagnosed to have herpesvirus infection. Prior to 24 October I977 90 mares have foaled and 22 foals have died associated with the infection. Foals either were stillborn or were weak and soon developed severe respiratory signs, or were normal at birth and developcd respiratory symptoms I8 to 24 hours later. Foals that were examined while still alive showed elevated temperatures, heart and respiratory rates. Ausculation of the thorax revealed increased bronchial sounds and fine sibilant rales. Despite the use of antibiotics, diuretics, corticosteroids, oxygen therapy and assisted positive pressure ventilation all foals died. Blood from a number of foals showed that thcy were severely leucopaenic with total white blood cell counts often less than 3,00O/pI. They were invariably neutropaenic but lymphopaenia was not a constant feature. Autopsy showed grossly enlarged lungs that were very firm, oedematous and purple in colour. Some had only a few scattered aerated lobules. Other lungs showod a greater degree of aeration and moderate to sevcre ocdema and congestion. Fluid and haeniorrhagic striations were noted in the trachea and bronchi. Excessive fluid was not found in either the thoracic or abdominal cavities. The spleefi \\a( marginally enlarged and the lymphoid follicles were ofrcn more prominent. Hepatic lesions were not seen.
Ausfralian Veterinary Journal, Vol. 53, December, 1977
Histopathology of lung showed a moderate to severe alveolar oedema with congestion and collapse associated with a slight to moderate acute necrotising bronchitis with a few to many eosinophilic intranuclear inclusions in bronchiolar epithelium. A herpesvirus was isolated from 10 foals in dog kidney cell culture and identified by electron microscopy. This centre has also identified herpesvirus infection of a still born foal from the Oberon district. Now that the disease has been identified in 3 geographical areas in New South Wales further outbreaks would be anticipated. A detailed report will be published in a subsequent issue of the Australian Veterinary Journal. R. J . DIXON, W. J . HARTLEY, D. R. HUTCHINS. E. E. LEPHERD, Department of Veterinary Clinical Studies, University of Sydney, Camden, New South Wales, 2570. CAROLINE FEILEN, R . F. JONES, DARlA N. LOVE, MARGARET SABINE, ANNE L. WELLS, Department of Veterinary Pathology, Unibersity o f Sydney, 'Sydney, New South Wales, 2006. I4 November 1977.
603
various samples analysed at the Government Chemical Laboratories, Perth (Table I). The levels of dieldrin and DDT metabolites in the samples were low and could possibly be due to residues in the cat food. The levels of PCP in the liver. kidney and stomach contents presumably were due to contact with wood-shavings litter and circumstantial evidence indicates PCP poisoning to be the cause of death. N o published figures on the toxic levels of PCP in cats were available. R. L. PEET, G. MacDONALD, Department of Agriculture, Jarrah Road, South Perth, Western Australia, 6151. A . KEEFE, 9 Lyall Street, Belmont, Western Australia, 6104. 19August 1977
References
Anon. (1977)-New Scientist 74: 233.
Barnes, J. M . (1957)-1n Advances in Pest Control Research, Vol. 1 , Interscience, New York. Gordon, D. C. (1956)--Med. J . Aust. 2: 43, 485. Harrison, D. L. (1959)-N.Z. vet. J . 7 : 89. Schipper, I. A. (1961)-Am. J . vet. Res. 22: 401.
TABLE 1 Results of Chemical Analysis of Sam les f r o m Cats with Suspected Penrachlorophenof Poisoning Cat No.
Sample
DDT and PentaDieldrin M e t a b e chloromg/kg lites phenol mg/kg mg/kg
1 1
Liver and kidney Stomach and contents
0.01 0.04
2 2
Liver Stomach contents
0.02 0.03
3 3
-
Kidney Liver Wood shavings
* * *
0.02
~~~
1.4
0.15
1 .o
0.06 0.15
9 .o 10.0
* * *
24.0 20.0
~~~
470.0
Not examined.
SPINAL NEMATODIASIS OF THE DOG ASSOCIATED WITH ANCYLOSTOMA CANZNUM Attention has recently been drawn to the occurrence of cerebrospinal nematodiasis in young dogs infected with the rodent lungworm Angiostrongylus canronensis in southern Queensland (Mason et a/ 1976). Thirteen cases between the ages of 6 and 14 weeks occurred during the summer months and were characterised by pain and ascending ataxia and paresis. Focal granulomata were observed in the brain and all levels of the spinal cord and occasionally nematode larvae could be identified. In one case dissection yielded immature adults. This letter is prompted by the diagnosis of a similar clinical case but of different aetiology. A 12-week-old cocker spaniel was presented with clinical neurological signs. The owners reported loss of balance for several days and at examination torticollis and pain on flexion of the neck were very evident. One week later there was posterior paresis and constant pain, which progressed to quadriplegia.and death over the following
week. Radiographs of the spinal column, total and differential white cell count and erythrocyte sedimentation rate were normal. The outstanding clinical feature throughout the course of the disease was pain. Autopsy showed lesions in the cervical spinal cord only which was submitted for laboratory examination. About 2 cm of the mid-cervical cord showed severe meningeal and deep tissue haemorrhage. Transection at levels from the cervical to sacral regions showed no other lesions. A young adult female Ancylostoma caninum was dissected out from the haemorrhagic cord. The parasite measured 10 mm in length, 0.41 mm wide at the oesophagus and contained a few nonembryonated eggs in utero. Microscopically haemorrhagic and necrotic tracks in the cervical cord were found to lead from the subarachnoid space to the central grey matter. Blood vessels in the vicinity showed endothelial swelling and a sometimes intense lymphoid and
,6002
AusrrcJiun Veterinary Journal, Vol. 53, December, 1977
plasma cell reaction around them. There was scattered degenerative swelling of neuronal bodies and fibres and general swelling of neuroglial cells. Three Ancylostorna species have been identified in dogs and cats in coastal north Queensland, A. caninurn, A. brasiliensis and A. cubaeforrne (Setasuban and Waddell 1973). The prevalence of A. caninurn is particularly high in the dog. Skinpenetrating larvae migrate via the blood during their life-cycle while those ingested usually develop directly in the intestine (Okoshi and Murata 1968) and only occasionally invade other organs. Aherrant migration of A. caninurn and other nematodes, particularly ascarids, is a common phenomenon in abnormal hosts. Invasion of the central nervous system and ocular tissues of mice and man by larvae of Toxocara canis is well known (Kelly 1977) and Sprent (1955) reviewed apparently rare involvement of the central nervous system in other species of animals by members of the Strongyloidea. A. caninurn have been recovered in experimental infections from various organs of the rat (Matsusaki 1950), mice and guinea pigs (Nichols 1956). In the latter species up to half of the larvae were located in the brain, severe damage to the nervous system resulting in death as early as 6 days post-infection. No ocular involvement was found with mice injected per 0 s (Olsen et a1 1972) and only a small percentage were recovered from the brain or cord. In none of these cases of aberrant ancylostomiasis was there any development of the larvae beyond the third-stage although Nichols (1956) reported a slight increase in size. The present case appears to be an example in which partial maturity of the nematode was achieved and a critical anatomical structure affected in the normal host, circum-
stances that hitherto have not been recorded with this genus of parasite. The prevalence of ancylostomiasis in Queensland suggests that cerebrospinal nematodiasis in dogs may be commoner than is realised. T. D. BUICK, 378 Mulgrave Road, Cairns, Queensland, 4870 R. S. F. CAMPBELL, G. W. HUTCHINSON, Department of Tropical Veterinary Science, James Cook University, Townsville, Queensland, 481 1 17October 1977
References Kelly, J. D. (1977)--Cunine Pararirofogy, Vet. Rev. No. 17, University of Sydney Post-graduate Foundation in Veterinary Science, Sydney. Mason, K. V., Prescott, C. W., Kelly, W. R. and Waddell, A. H. (1976)-Aust. vet. 1. 52: 295. Matsusaki, G. (1950)-Yokoham Med. BuCf. 2: 154. Nichols, R. L. (19561.4. Pararif. 42: 363. Okoshi, S . and Murata, Y . (1968)--Iap. J . vet. Sci. 43.
Olsen, L. J., Beechie, R. A. and Beechie, B. J. (1972)J . Parasit. 58: 639. Setasuban, P. and Waddell, A. H. (1973)-Ausf. vet. J . 4 9 110. Sprent, J. F. A. (1955)-ParaSifology 46: 31.
PERINATAL FOAL MORTALITY ASSOCIATED WlTH A HERPESVIRUS Equine herpesvirus I (EHV 1) has been recognised in Australia for a number of years; however in contrast to overseas experience the association of EHVl with clinical abortion or neonatal foal mortality has not been reported. On 16 September, 1977 one 3-day-old foal, from a thoroughbred stud in the Camden district, died with severe respiratory distress. On the basis of histopathological examination i t was subsequently diagnosed to have herpesvirus infection. Prior to 24 October I977 90 mares have foaled and 22 foals have died associated with the infection. Foals either were stillborn or were weak and soon developed severe respiratory signs, or were normal at birth and developcd respiratory symptoms I8 to 24 hours later. Foals that were examined while still alive showed elevated temperatures, heart and respiratory rates. Ausculation of the thorax revealed increased bronchial sounds and fine sibilant rales. Despite the use of antibiotics, diuretics, corticosteroids, oxygen therapy and assisted positive pressure ventilation all foals died. Blood from a number of foals showed that thcy were severely leucopaenic with total white blood cell counts often less than 3,00O/pI. They were invariably neutropaenic but lymphopaenia was not a constant feature. Autopsy showed grossly enlarged lungs that were very firm, oedematous and purple in colour. Some had only a few scattered aerated lobules. Other lungs showod a greater degree of aeration and moderate to sevcre ocdema and congestion. Fluid and haeniorrhagic striations were noted in the trachea and bronchi. Excessive fluid was not found in either the thoracic or abdominal cavities. The spleefi \\a( marginally enlarged and the lymphoid follicles were ofrcn more prominent. Hepatic lesions were not seen.
Ausfralian Veterinary Journal, Vol. 53, December, 1977
Histopathology of lung showed a moderate to severe alveolar oedema with congestion and collapse associated with a slight to moderate acute necrotising bronchitis with a few to many eosinophilic intranuclear inclusions in bronchiolar epithelium. A herpesvirus was isolated from 10 foals in dog kidney cell culture and identified by electron microscopy. This centre has also identified herpesvirus infection of a still born foal from the Oberon district. Now that the disease has been identified in 3 geographical areas in New South Wales further outbreaks would be anticipated. A detailed report will be published in a subsequent issue of the Australian Veterinary Journal. R. J . DIXON, W. J . HARTLEY, D. R. HUTCHINS. E. E. LEPHERD, Department of Veterinary Clinical Studies, University of Sydney, Camden, New South Wales, 2570. CAROLINE FEILEN, R . F. JONES, DARlA N. LOVE, MARGARET SABINE, ANNE L. WELLS, Department of Veterinary Pathology, Unibersity o f Sydney, 'Sydney, New South Wales, 2006. I4 November 1977.
603
