It will be seen from the table that of the seventy lesions examined, 54 were found to be due t o tuberculosis (77.1%), 1 1 were due to actinobacillosis and 3 due to actinomycosis. That is, 20% of all lesions were due to lesions characterised by ray or club formations. In addition we found one carcinoma and one bacterial granuloma. It has been well established that fluorescence acid fast microscopy yields a greater percentage of acid fast positive smears than the Ziehl-Neelson method (Koch and Cote 1965). In our series it was 1.5 times more effective than the Zrehl-Neelson method, revealing tubercle bacilli in 78% of tuberculous lesions. Tammemagi el a1 (1973) examined 650 lesions which had been diagnosed macroscopically at abattoirs as tuberculous. On histological examination 515 of these were considered to be tuberculosis and 67 actinobacillosis. A further 8 1 specimens were submitted with an undecided macroscopic diagnosis; 15 of these were diagnosed histologically as tuberculosis and 50 as actinobacillosis. If these two groups are combined we have 731 lesions, 530 of which were diagnosed as tuberculosis (72.6%) and 117 were diagnosed as actinobacillosis (16.0%). These results in general agree with our own. The crush preparation technique does not identify tuberculous or Corynebacterium lesions or neoplasms, but rather allows a proportion of lesions to be eliminated from the differential diagnosis. The technique appears to be as reliable as histological examination in differentiating lesions with ray or club formations from lesions of tuberculosis. Our results and those of
Tammemagi et a1 (1973) indicate that use of the technique at the abattoir would reduce the number of lesions sent for laboratory diagnosis by 5 2 0 % . We would like to express our appreciation t o Mr W. A. Royal for his guidance and encouragement and for the provision of laboratory facilities and to Professor J. Francis for his assistance in the preparation of the material for publication. We are indebted to those inspectors of the Department of Primary Industry who assisted us considerably by collecting the lesions. P. L. YOUNG, B.V.Sc., B.Sc., Q.D.A.H., P. R. KAHLER, B.V.Sc., Q.D.A., A. E. MARTIN, B.V.Sc., P. FIELD, B.V.Sc. Faculty of Veterinary Science, University of Queensland, St. Lucia, Queensland, 4067 27 May I974 References Barton, M. D. (1972)-N.S.W. vet. Proc. 8: 21. Cruickshank, R. ( 1965)-''Medical Microbiology", 1 lth edn, E. & S. Livingstone Ltd, Edinburgh. Hotchi, M. and Schwarz, J. (1972)-Arch. Path. 93: 392. Koch, M . L. and Cote, R. A. (1965)-Arn. rev. resp. Dis. 91: 283. Shahan, M. S . and Davis, C. L. (1942)-Am. J . vet. Res. 3: 321. Tammemagi, L., Simmons, G. C., Kelman, R., and Hall, W. T. K. (1973)-Aust. vet. J. 49: 507. Truant, J. P., Brett, W. A., Thomas, W. (1962)-Henry Ford Hosp. med. Bull. 10: 287.
AN OUTBREAK OF GANGRENOUS CELLULITIS CAUSED BY ,CLOSTRZDlUM SEPTICUM IN A BROILER FLOCK some birds were swollen with skin broken over the foot Gangrenous cellulitis in poultry has been reported in Australian flocks (Hungerford 1969); however, the pads. Feathers from the affected areas pulled out easily. On post mortem, marked gaseous cellulitis and bloody causative organism was not identified. The condition serosanguinous exudate was seen in the affected areas, has been regarded as a mixed Staphylococcusparticularly in the region of the flanks. The cellulitis Clostridium perfringens infection, often occurring as a sequel t o fowl pox lesions; CI. septicurn, Cl. novyi and varied from unilateral to bilateral and was accompanied CI. sordellii have also been implicated in the disease by inflammation of the adjacent muscles. The livers of (Hungerford 1969; Gerdon 1973). This paper reports affected birds were dark and congested. Pa!e bone an outbreak of gangrenous cellulitis caused by CI. marrow was seen in some birds. Smears of the liver lesions and serosanguinous fluid septicurn in an Australian broiler flock. of 12 affected birds revealed numerous Gram-positive Three groups of 20,000 broiler chickens hatched rod-shaped oragnisms ( 0 . 4 - 0 . 6 ~wide) occurring in long from eggs from a multi-age breeding farm were raised from day-old in 3 separate sheds in which the litter was filaments (12-25p). No growth occurred aerobiyally, 12 months old. Sheds 1 and 2 were hatched and but in anaerobic culture of the livers and serosanguinous delivered to the farm from the same hatchery 3 days exudates at 24 hours a continuous spreading film of prior to those in Shed 3. The farm had no previous growth formed on the surface of blood agar plates. In a Gram stain the cells were Gram-positive rods 0 . 4 - 0 . 6 ~ history of this disease. x 2-6p, arranged singly, in pairs, and short chains: after At 5 t weeks of age a sudden increase in mortality occurred in one shed ( 3 ) as compared with mortalities 48 hours an oval subterminal spore, slightly wider than the bacilli, was formed. In old cultures (3-4 days) the in the other two sheds ( 1 & 2, Table 1 ) . The dead rods stained gram-negative. birds were distributed throughout the shed and were En cooked meat medium at 37°C for 2 days, gas well grown for their age. Affected birds, both male and production and pink discoloration of the meat with no female, were off their feed and water, listless, showed ataxia and were sitting with drooping heads. The birds digestion occurred. Acid and gas were produced from exhibited marked incoordination in movement. Mor- glucose, lactose, maltose and salicin, but not in mannibidity in the flock was low, and sick birds were found to1 or sucrose. Litmus milk turned acid and clotted with gas production in 3 days. The isolate was identionly with difficulty. The other 2 sheds remained free of fied as Clostridium septicurn. Staphylococcus aztreus this disease. was not isolated, and appeared not to be implicated in On external examination areas devoid of feathers were seen on wings, back, legs and abdomen. The skin on the disease. In vitro the CI. septicum culture was susceptible to these areas was necrotic with blood-tinged exudate over the surface. There was crepitation under the skin, par- the antibiotics chloramphenicol ( 1Opg) and penicillin (1.5 units), but was resistant t o tetracycline ( l o p g ) , ticularly over the abdomen. The shanks and feet of 106
Australian Veterinary Journal, Vol. 51, February, 1975
streptomycin (lo&, erythromycin (10pg) and sulphafurazole (lOOpg), using Multodisks 30H*. The disease outbreak was not reported to the laboratory until 3 days after the onset of mortality. This coincided with a change in feed source to all 3 sheds 2 days prior t o the onset of mortality in Shed 3, due to unavailability of the normal feed. A tentative diagnosis of gangrenous cellulitis based on post mortem lesions and bacterial smears was made, and flock treatment with chloramphenicol via the drinking water at the rate of 35 mg/bird/day was commenced. After 4 days administration of chloramphenicol the mortality rate remained high, therefore the feed was replaced by that from the original source, supplemented with penicillin for 5 days at a level of 220 g/tonne of feed, and the chloramphenicol medication was discontinued. When the penicillin treatment was finished the mortality had returned to the level prior to the outbreak, and no further lesions of gangrenous cellulitis were present in dead birds. ‘Oxoid, Distributed by Abbott Laboratories, Sydney.
It appears that the birds in Shed 3 may have been more susceptible to disease than those in Sheds 1 and 2, the nutritional stress of a change in feed triggering off the Clostridium septicum infection. Although the fall in death rate may have been a normal pattern unaffected by antibiotic treatment, and following the return to the original source of feed, it is possible due to the in vitro susceptibility of the organism to chloramphenicol and penicillin that the antibiotic treatments were effective, the initial lag in response being due to sick birds not drinking and therefore not receiving the full therapeutic dose. B. S. BAINS, B.V.Sc. MARGARET A. MacKENZIE, M.Sc. Provincial Traders R y Ltd, Box 10, P.O., Morningside, Queensland, 4170 14 August 1974 Referenem -. _ _ .- .-..Gerdon, D. (1973)-Av. Dis. 17: 205. Huneerford. T. G. ( 1969)-‘‘Diseases of Poultry” 4th ed;. An& and Robertson, Sydney.
ACUTE COPPER POISONING IN CAlTLE In a case report by Mylrea and Byrne (1974) information was given on an outbreak of acute copper poisoning in Aberdeen Angus calves, involving the use of a commercial copper preparation.* The dose rate used gave a range from 0.8 to 3.6 mg Cu/kg body weight. At the present time this product is only registered for use by stockowners in sheep. However, it is widely used by veterinarians in large animal practice as an ethical presentation for cattle. At the dose rates used in such situations there have been no signs of toxicity. The therapeutic ratio of copper injections is probably narrow, dependent t o a large degree on the existing comer _ _ status of the animal. The exaerimental dose rate ‘“CUJEC’ T ~ m qVaccine Laboratory (Australia) pty Ltd, Dandenonh, Victona.
currently under investigation is 0.24 mg Cu/kg as a maximum level, with a maximum dose of 90 mg Cu for an animal of 375 kg or over. This means that the dose rate reported by Mylrea and Byrne (1974) provided at least 3 times, and possibly up to 12 times, the maximum therapeutic dose. The acute toxicity was therefore entirely due to a gross overdosage, as stated by the authors (Mylrea and Byrne 1974). G. A. REED, B.V.Sc., Dip.Agr.Extn., Tasman Vaccine Laboratory (Australia) Pty Ltd, P.O. Box 347, Dandenong, Victoria, 3175 6 November 1971 Ref ereuce Mylrea, p. J., Byrne, D. T. (1974)-Aust. vet. J . , 50: 169.
DEATH DUE TO RUPTURE OF THE ORIGIN OF THE GASTROCNEMIUS MUSCLES IN A FILLY In mid-December 1972, the owner reported that a on the left leg showed that a similar injury had thoroughbred filly was walking with difficulty due to occurred. Very large clots of blood were associated the hind legs being far forward under the body. The with the torn muscle ends. This accounted for the pale mucous membranes and the lack of blood in the filly walked for only 50 metres, then lay down, rolling abdominal vessels. from side to side, and died before she could be examThe group of fillies t o which this one belonged ined clinically. An autopsy was carried out. The filly was in good should have been stabled a month previously, but due condition, the mucous membranes of the eyes and mouth to shortage of stable accommodation they were still were very pale and the hind legs were greatly swollen, being heavily grain fed in the paddock. They had been particularly between the hock and the stifle joints. There observed on a number of occasions to be playing, was a small aneurysm in the anterior mesenteric artery with occasional rearing in the air during play. It seems and only a small quantity of blood was noted in the likely then, that during a rearing episode, this particular aorta and mesenteric vessels. On both hind legs, a filly may have either reared too high and collapsed backwards onto her gastrocnemius muscles, or may massive area of subcutaneous haemorrhage had occurred from the extra abdominal section of the internal iliac have been pushed back onto it by another filly. Once rupture of the muscle origins occurred, haemorrhage artery to half way down each cannon bone. Similar types of haemorrhage have been observed would be marked, leading to death from anaemia. R. R. PASCOE, M.V.Sc., F.R.C.V.S., M.A.C.V.Sc. with fractured femurs but dissection of the right leg showed the bones to be intact. Dissection of muscle Oakey, Queensland, 4401. mass then showed a complete tearing of both heads of 21 August 1974 the gastrocnemius muscle from their origins. Dissection Australian Veterinary Journal, Vol. 51, February, 1975
107
Tammemagi et a1 (1973) indicate that use of the technique at the abattoir would reduce the number of lesions sent for laboratory diagnosis by 5 2 0 % . We would like to express our appreciation t o Mr W. A. Royal for his guidance and encouragement and for the provision of laboratory facilities and to Professor J. Francis for his assistance in the preparation of the material for publication. We are indebted to those inspectors of the Department of Primary Industry who assisted us considerably by collecting the lesions. P. L. YOUNG, B.V.Sc., B.Sc., Q.D.A.H., P. R. KAHLER, B.V.Sc., Q.D.A., A. E. MARTIN, B.V.Sc., P. FIELD, B.V.Sc. Faculty of Veterinary Science, University of Queensland, St. Lucia, Queensland, 4067 27 May I974 References Barton, M. D. (1972)-N.S.W. vet. Proc. 8: 21. Cruickshank, R. ( 1965)-''Medical Microbiology", 1 lth edn, E. & S. Livingstone Ltd, Edinburgh. Hotchi, M. and Schwarz, J. (1972)-Arch. Path. 93: 392. Koch, M . L. and Cote, R. A. (1965)-Arn. rev. resp. Dis. 91: 283. Shahan, M. S . and Davis, C. L. (1942)-Am. J . vet. Res. 3: 321. Tammemagi, L., Simmons, G. C., Kelman, R., and Hall, W. T. K. (1973)-Aust. vet. J. 49: 507. Truant, J. P., Brett, W. A., Thomas, W. (1962)-Henry Ford Hosp. med. Bull. 10: 287.
AN OUTBREAK OF GANGRENOUS CELLULITIS CAUSED BY ,CLOSTRZDlUM SEPTICUM IN A BROILER FLOCK some birds were swollen with skin broken over the foot Gangrenous cellulitis in poultry has been reported in Australian flocks (Hungerford 1969); however, the pads. Feathers from the affected areas pulled out easily. On post mortem, marked gaseous cellulitis and bloody causative organism was not identified. The condition serosanguinous exudate was seen in the affected areas, has been regarded as a mixed Staphylococcusparticularly in the region of the flanks. The cellulitis Clostridium perfringens infection, often occurring as a sequel t o fowl pox lesions; CI. septicurn, Cl. novyi and varied from unilateral to bilateral and was accompanied CI. sordellii have also been implicated in the disease by inflammation of the adjacent muscles. The livers of (Hungerford 1969; Gerdon 1973). This paper reports affected birds were dark and congested. Pa!e bone an outbreak of gangrenous cellulitis caused by CI. marrow was seen in some birds. Smears of the liver lesions and serosanguinous fluid septicurn in an Australian broiler flock. of 12 affected birds revealed numerous Gram-positive Three groups of 20,000 broiler chickens hatched rod-shaped oragnisms ( 0 . 4 - 0 . 6 ~wide) occurring in long from eggs from a multi-age breeding farm were raised from day-old in 3 separate sheds in which the litter was filaments (12-25p). No growth occurred aerobiyally, 12 months old. Sheds 1 and 2 were hatched and but in anaerobic culture of the livers and serosanguinous delivered to the farm from the same hatchery 3 days exudates at 24 hours a continuous spreading film of prior to those in Shed 3. The farm had no previous growth formed on the surface of blood agar plates. In a Gram stain the cells were Gram-positive rods 0 . 4 - 0 . 6 ~ history of this disease. x 2-6p, arranged singly, in pairs, and short chains: after At 5 t weeks of age a sudden increase in mortality occurred in one shed ( 3 ) as compared with mortalities 48 hours an oval subterminal spore, slightly wider than the bacilli, was formed. In old cultures (3-4 days) the in the other two sheds ( 1 & 2, Table 1 ) . The dead rods stained gram-negative. birds were distributed throughout the shed and were En cooked meat medium at 37°C for 2 days, gas well grown for their age. Affected birds, both male and production and pink discoloration of the meat with no female, were off their feed and water, listless, showed ataxia and were sitting with drooping heads. The birds digestion occurred. Acid and gas were produced from exhibited marked incoordination in movement. Mor- glucose, lactose, maltose and salicin, but not in mannibidity in the flock was low, and sick birds were found to1 or sucrose. Litmus milk turned acid and clotted with gas production in 3 days. The isolate was identionly with difficulty. The other 2 sheds remained free of fied as Clostridium septicurn. Staphylococcus aztreus this disease. was not isolated, and appeared not to be implicated in On external examination areas devoid of feathers were seen on wings, back, legs and abdomen. The skin on the disease. In vitro the CI. septicum culture was susceptible to these areas was necrotic with blood-tinged exudate over the surface. There was crepitation under the skin, par- the antibiotics chloramphenicol ( 1Opg) and penicillin (1.5 units), but was resistant t o tetracycline ( l o p g ) , ticularly over the abdomen. The shanks and feet of 106
Australian Veterinary Journal, Vol. 51, February, 1975
streptomycin (lo&, erythromycin (10pg) and sulphafurazole (lOOpg), using Multodisks 30H*. The disease outbreak was not reported to the laboratory until 3 days after the onset of mortality. This coincided with a change in feed source to all 3 sheds 2 days prior t o the onset of mortality in Shed 3, due to unavailability of the normal feed. A tentative diagnosis of gangrenous cellulitis based on post mortem lesions and bacterial smears was made, and flock treatment with chloramphenicol via the drinking water at the rate of 35 mg/bird/day was commenced. After 4 days administration of chloramphenicol the mortality rate remained high, therefore the feed was replaced by that from the original source, supplemented with penicillin for 5 days at a level of 220 g/tonne of feed, and the chloramphenicol medication was discontinued. When the penicillin treatment was finished the mortality had returned to the level prior to the outbreak, and no further lesions of gangrenous cellulitis were present in dead birds. ‘Oxoid, Distributed by Abbott Laboratories, Sydney.
It appears that the birds in Shed 3 may have been more susceptible to disease than those in Sheds 1 and 2, the nutritional stress of a change in feed triggering off the Clostridium septicum infection. Although the fall in death rate may have been a normal pattern unaffected by antibiotic treatment, and following the return to the original source of feed, it is possible due to the in vitro susceptibility of the organism to chloramphenicol and penicillin that the antibiotic treatments were effective, the initial lag in response being due to sick birds not drinking and therefore not receiving the full therapeutic dose. B. S. BAINS, B.V.Sc. MARGARET A. MacKENZIE, M.Sc. Provincial Traders R y Ltd, Box 10, P.O., Morningside, Queensland, 4170 14 August 1974 Referenem -. _ _ .- .-..Gerdon, D. (1973)-Av. Dis. 17: 205. Huneerford. T. G. ( 1969)-‘‘Diseases of Poultry” 4th ed;. An& and Robertson, Sydney.
ACUTE COPPER POISONING IN CAlTLE In a case report by Mylrea and Byrne (1974) information was given on an outbreak of acute copper poisoning in Aberdeen Angus calves, involving the use of a commercial copper preparation.* The dose rate used gave a range from 0.8 to 3.6 mg Cu/kg body weight. At the present time this product is only registered for use by stockowners in sheep. However, it is widely used by veterinarians in large animal practice as an ethical presentation for cattle. At the dose rates used in such situations there have been no signs of toxicity. The therapeutic ratio of copper injections is probably narrow, dependent t o a large degree on the existing comer _ _ status of the animal. The exaerimental dose rate ‘“CUJEC’ T ~ m qVaccine Laboratory (Australia) pty Ltd, Dandenonh, Victona.
currently under investigation is 0.24 mg Cu/kg as a maximum level, with a maximum dose of 90 mg Cu for an animal of 375 kg or over. This means that the dose rate reported by Mylrea and Byrne (1974) provided at least 3 times, and possibly up to 12 times, the maximum therapeutic dose. The acute toxicity was therefore entirely due to a gross overdosage, as stated by the authors (Mylrea and Byrne 1974). G. A. REED, B.V.Sc., Dip.Agr.Extn., Tasman Vaccine Laboratory (Australia) Pty Ltd, P.O. Box 347, Dandenong, Victoria, 3175 6 November 1971 Ref ereuce Mylrea, p. J., Byrne, D. T. (1974)-Aust. vet. J . , 50: 169.
DEATH DUE TO RUPTURE OF THE ORIGIN OF THE GASTROCNEMIUS MUSCLES IN A FILLY In mid-December 1972, the owner reported that a on the left leg showed that a similar injury had thoroughbred filly was walking with difficulty due to occurred. Very large clots of blood were associated the hind legs being far forward under the body. The with the torn muscle ends. This accounted for the pale mucous membranes and the lack of blood in the filly walked for only 50 metres, then lay down, rolling abdominal vessels. from side to side, and died before she could be examThe group of fillies t o which this one belonged ined clinically. An autopsy was carried out. The filly was in good should have been stabled a month previously, but due condition, the mucous membranes of the eyes and mouth to shortage of stable accommodation they were still were very pale and the hind legs were greatly swollen, being heavily grain fed in the paddock. They had been particularly between the hock and the stifle joints. There observed on a number of occasions to be playing, was a small aneurysm in the anterior mesenteric artery with occasional rearing in the air during play. It seems and only a small quantity of blood was noted in the likely then, that during a rearing episode, this particular aorta and mesenteric vessels. On both hind legs, a filly may have either reared too high and collapsed backwards onto her gastrocnemius muscles, or may massive area of subcutaneous haemorrhage had occurred from the extra abdominal section of the internal iliac have been pushed back onto it by another filly. Once rupture of the muscle origins occurred, haemorrhage artery to half way down each cannon bone. Similar types of haemorrhage have been observed would be marked, leading to death from anaemia. R. R. PASCOE, M.V.Sc., F.R.C.V.S., M.A.C.V.Sc. with fractured femurs but dissection of the right leg showed the bones to be intact. Dissection of muscle Oakey, Queensland, 4401. mass then showed a complete tearing of both heads of 21 August 1974 the gastrocnemius muscle from their origins. Dissection Australian Veterinary Journal, Vol. 51, February, 1975
107
