(Papema and Alves de Matos 1984). Rickettsia1cell bodies can be large (similar to elongated cells) or small, whereas chlamydia are highly pleomorphic, the morphology dependant on the stage of the development cycle. In neither sample of fiigeriing barramundi was the epitheliocystis infection associated withdisease. This sibling group of fish are the only ones in which epitheliocystishas been detected in 3 years of diagnostic examinations of sea-cage reared barramundi in northern Queensland. It appears the infection is benign and of very low prevalence.
References Bradley TM, Newcomer CE and Maxwell KO (1988) D b Aquar Org 4 9 Hoffman GL, Dunbar CE. Wolf K and ZwiUenberg LO (1969) Antonie van Leeuwenhoek 35:146 Krieg NR and Holt JF (editors) (1984) Bergey's Manual of Sysfemafic Bacteriology Vol 1, Williams and Wilkins, Baltimore Langdon JS, Elliot K and Mackay B (1991) Awl Vef J68244 Papema I (1fl7) Aquaculture 10169 Papema I and Alves de Matos AP (1984) J Fish Dis 7: 137 Papema I and Sabnai I (1980) In FLrh Diseases, Third COPRAQ Session edited by Ahne W, Springer-Verlag, Berlin Papema1,SabnaiIandZachaIyA (1981)JFishDis4:459
(Acceptedfor publication 25 February 1992)
Pasteurella multocida septicaemia in pigs Department of Agriculture, Regional Veterinary Laboratory, PO Box 388, Benalla, Victoria 3672 10 High Street, Seymour, Victoria 3660
JT MACKIE M BARTON JKETTLEWELL
Pasteurella rnultocida is often isolated from pneumonic lungs in pigs, where it is usually considered a secondary pathogen (Buddle 1985; Farrington 1986; Muirhead 1987). The primary septicaemic form of pasteurellosis is rare in pigs (Edwards 1959; MurtyandKaushik 1965; Dungworth 1985; Verma 1988). There are at least 2 unpublished Australian reports of sudden death in pigs associated with P rnultocida (Buddle 1985; L Sims,personal communication). Five serotypes (A, B, D, E and F) of P rnultocida are recognised on the basis of capsular antigens (Carter 1984; Rimler and Rhoades 1987). Serotype A, and to a lesser extent serotype D, are associated with pneumonic pasteurellosis in pigs, while toxigenic strains of serotype D are associated with atrophic rhinitis (de Jong el a1 1980; Rutter and Rojas 1982) and have been isolated from pigs in Australia with atrophic rhinitis (Mercy et a1 1986). Serotype B was the cause of septicaemicpasteurellosis in pigs in India reported by Murty and Kaushik (1965) and Verma (1988), and serotype B has been isolated from pigs in Australia (Carter 1975). Haemorrhagic septicaemia of cattle, caused by serotypes B and E, has not been reported in Australia (Geering and Forman 1987). This report describes an episode of sudden death in pigs associated with isolation of P rnultocida serotype D. On 1 May, 1989 on a 15-sow piggery near Seymour, Victoria, 3 of 70 grower pigs, between 14 to 22 weeks of age, were found dead at morning feed time. No abnormalities were noted by the owner the previous day, though it is possible that subtle changes in behaviour may have been missed. Over the following 24 h a
TerramycinU Injectable [email protected]
,Pfizer Agricare Pty Ltd, West Ryde, New South Wales
Australian VeterinaryAssociation Vol. 69, No. 9, September 1992
further 7 growers were lethargic and had rectal temperatures of 40.0 to 41.SoC.These 7 pigs were treated with a single intramuscular injection of long-acting oxytetracycline*. Within 48 h of treatment the 7 affected grower pigs appeared normal and rectal temperatures were < 39.5"C. No further deaths or clinical signs were observed. No clinical signs of atrophicrhinitis, such as snout deformities or bloody nasal discharges were noted in any pigs by the owner, either before the deaths occurred or subsequently. The 3 pigs that were found dead were necropsied at the laboratory about 7 h later. There was swelling of the pharyngeal region and blue discolouration of the skin, particularly over the ears and ventral abdomen. The lungs were congested and oedematous and there was generalised congestion of abdominal viscera and the meninges. Fibrin was present in the peritoneal and pleural cavities. No joint lesions were apparent. The nasal turbinates were not examined. Portions of liver, lung, spleen, kidney, heart and brain from the 3 pigs were fixed in phosphate buffered 10% formalin and processed routinely for histopathology. Microscopic lesions were consistent with widespread vascular damage. In the liver there were thrombi in portal vessels and multifocal necrosis of the parenchyma associated with aggregation of neutrophils. Other changes in the liver included diffuse congestion, aggregations of inflammatory cells (predominantly neutrophils) within sinusoids,infiltration of some portal areas by neutrophils. hypertrophy of Kupffer cells and the presence of fibrin and neutrophils over the capsule. In the lung, there was diffuse congestion, thickening and hypercellularity of alveolar walls with numerous leucocytes in alveolar capillaries. There were small foci of necrosis and occasionalthrombosed blood vessels within alveolar walls. Alveoli contained a moderate amount of protein-rich exudate. Fibrin and neutrophilswere present over the visceralpleura. In blood vessels of the meninges and brain there was marked diffuse congestion, hypertrophy of endothelial cells, mild hypercellularity of some vessel walls and necrosis of the wall of an occasional vessel. Some vessels were thrombosed. In the spleen there was diffuse congestion, depletion of lymphoid tissue and fibrin and neutrophils were present over the capsule. In the kidney there was marked, diffuse congestion. Numerous colonies of gram-negativebacteria were present in blood vessels in the lung, brain, renal glomeruli and renal interstitiurn.Occasional bacterial colonies were present throughout the other tissues. Samples of liver, lung and spleen and swabs of the peritoneal and pleural cavity of all 3 pigs were cultured directly onto 7% sheep blood agar with aStaphylococcuraureus nurse colony and MacConkey agar, and incubated under 5% C02 at 37OC. P multocida was isolated in pure growth or as the predominant organism from d l samples and swabs. The isolate was identified as serotype D using the acriflavine test (Carter and Subronto 1973)and was identified as non-toxigenic by an agarose overlay method using bovine turbinate cells (Eamens et a1 1988). Streptococcus sub and Actinobacillus pleuropneumonia were not isolated and selectiveculturefor Salmonella sp was negative. Selectivecultures for Haernophilusparasuis and Mycoplasma sp were not carried out. Organisms resembling Bacillus anthracis were not seen in smears of peripheral blood stained with polychrome methylene blue. There are few descriptions of the macroscopic lesions associated with septicaemicpasteurellosis in pigs and there appear to be no descriptions of the microscopic lesions. Edwards (1959) described an excess of blood-stained serousfluids, subcutaneous haemorrhagic oedema,patchy haemorrhagicconsolidationof the lungs and extensive epicardial haemorrhage in neonatal pigs. Murty and Kaushik (1965) described swelling of the pharyngeal region, diffuse bluish-red discolouration of the skin, congested and oedematous lungs, congested kidneys, petechial haemorrhages on serous membranes and subcutaneous tissues, haemorrhagic gastroenteritis and congested and oedematousmesenteric and mediastinal lymph nodes in pigs 3 to 6 months old. Dungworth (1985) described septicaemic disease without 227
distinctive lesions in adult pigs. P mulfocida is a common commensal in the nasopharynx of pigs puddle 1985). Factors contributing to the development of septicaemicdisease in pigs are not known.In cattle, septicaemic pasteurellosisis associated with stress factors including a change in diet or climate and poor body condition. In the case reported in this paper, stress factors that could be identified included changes in diet, temperature, levels of manure gases and ventilation, thoughdetailsof most of the changes are sketchy. On7 April 1989 (about 3 weeks before the deaths occurred) the grower ration was changed from a ration containing 17% crude protein to a ration containing 18% crude protein. On 20 April there was a change to warmer weather during which the mean maximum daily temperature at Mangalore 5 km away rose from 18.2 "C in the 7-day period before 20 April to 22.2"C in the 1l d a y period between 20 April and 30 April inclusive. After the change in ration and the onset of warmer days, the owner reported an apparent increase in the levels of the manure gases ammonia and hydrogen sulphide in the grower shed. In an attempt to improve the ventilationof the shed, the windows and doors were manually opened for extended periods during the day, but were closed completely at night because of the low minimum nightly temperatures. Ventilation within the shed was restricted by the walls of the pens in which the pigs were kept, in that 3 of the 4 walls of each pen were solid. Drainage of the pens was provided by way of flush channels, 80 cm deep. A diagnosis of septicaemia due to P multocida serotype D was made, based on the isolation of P multocida from a range of tissues from all 3 pigs, the absence of other bacteria that cause septicaemia, and the presence of multifocal thrombosis and necrosis in liver, lung and brain associated with gram-negative bacteria. Similarclinical and pathologicalfindings associatedwith isolation of P multocida serotype A have been observed at least once previously in Australia (L Sims, personal communication). We thank Dr G Eamens, Elizabeth Macarthur Agricultural Institute, Camden, for serotyping and toxigenicity testing of the P multocida isolate. The Bureau of Meteorology, Melbourne, kindly supplied the daily temperature data.
References Buddle JR (1985)Bacferial and Fungal Diseases of Pigs, Australian B u m u of Animal Health/Australian Government Publishing Service, Canberra (Animul Heulth in Australia, vol6) p 133 Carter GR (1975) In Direares ofswine, 4th edn, edited by Dunne HW and Leman AD, Iowa State University Press. Ames. p 621 Carter GR (1984) In Bergeys Manual of Systematic Bucferwlogy, Vol 1, edited by Krieg NR and Holt JG, Williams and Wilkins, Baltimore, p 552 Carter GR and Subronto P (1973)AmJ Vet Rar 34: 293 de Jong MF, Oei HL and Testenburg GJ (1980) Proc 6th Cong Int Pig Vet SOC, p 21 1 Dungworth DL (1985) In Pathology of Domestic Animals, Vol2,3rd edn, edited by Jubb KVF, Kennedy PC and PalmerN, AcademicPress,London, p 492 E m a s GJ, Kirkland PD, Turner MJ, Gardner IA, White MP and H o m i ~ k y CL(1988)Aurf Vef J65:120 Edwards BL (1959) Vet Rec 71: 208 Farrington DO (1986) In Diseuses of Swine, 6th edn,edited by Leman AD, Straw B, Mengeling WL, Penny RHC and Scholl E, Iowa State University Press,Ames, p 436 Geering WA and Forman AJ (1987) Exotic Direuses, Australian Bureau of Animal HealWAustralian Government Publishing Service. Canberra (AnirnalHeulth in Australia, vol9) p 122 Mercy AR,Salerian M, Lloyd JM,Richards RB and Robertson GM (1986) Aust Vet J 63: 256 Muimead MR (1987) In Pig Production, University of Sydney Post-graduate Committee in Veterinary Science, Proceedings No 95, p 567 Murty DK and Kaushik RK (1965) Vet Rec 7 7 41 1 Rimler RB and Rhoades KR (1987)J Clin Microbiol25: 615 Rutter JM and Rojas X (1982) Vet Rec 110: 531 Verma ND (1988) Vet Rec 123:63 (Accepted for publication 12 June 1992)
Flood plain staggers, a tunicaminyluracil toxicosis of cattle in northern New South Wales NSW Agriculture, CA BOURKE Regional Veterinary Laboratory, MJ CARRIGAN Agricultural Research and Veterinary Centre, Orange, New South Wales 2800 NSW Agriculture, Regional Veterinary Laboratory, Private Mail Bag, Armidale, New South Wales 2350
The tunicaminyluracil, tunicamycin, is the type compound of a group of toxic substances produced by soil-borne micro-organisms of the genera Streptomyces and Ciavibacter (Edgar et a1 1982; Jag0 et a1 1983; Frahn et a1 1984). Two naturally occurring tunicaminyluracil toxicoses have been recorded: annual rye grass toxicity in sheep and cattle (McIntosh et a1 1967; Berry and Wise 1975; Jag0 et a1 1983; Finnie and Jag0 1985). and water damaged wheat toxicity in pigs (Bourke 1987). In the former syndrome the toxic agent was called corynetoxin but it is a member of the tunicaminyluracil group. This contribution describes a new tunicaminyluracil toxicosis affectingcattle grazing pastures dominated by Agrostis avenacea (blown grass or blow away grass). In October 1990, cattle in the Bourke, Brewanina, Mungindi and Moree districts of north-west New South Wales, grazing flood plain pastures along major river systems, developed nervous signs, and many subsequently died. The following species made a sigmfkant contribution to the pasture mix in toxic paddocks: Agrostis sp (blow away grass), Panicum sp (Coolah grass), Pmpalidiurn sp (Warrego summer grass) andMarsilea sp (nardoo). Many farms with affected cattle had experiencedheavy flooding during the preceding winter, and consequently rotting vegetation was widespread at the start of the outbreak. The pasture in all toxic paddocks was dominated by Agrostis sp and this dominance continued throughout the period of pasture toxicity. A more detailed description of pasture composition, and related field matters, is presented in the paper of Davis, Curran, Hetherington, Norris, Wise, Seawright and Bryden (unpublished). The clinical signs displayedby affected cattle from 2 properties in the Bourke district, and 2 properties in the Moree district, were assessed at the commencementof the outbreak. They were recognised from the outset, by the authors, as those observed previously in animals affected by tunicaminyluracil toxicoses (McIntoshetal1967; Berry and Wise 1975; Bourke 1987).These signs were characterised by the presence of short periods of cerebral convulsions that ranged in severity from mild to severe. Affected cattle fell into lateral or sternal recumbency and displayed varying degrees of opisthotonus,nystagmus, eye rolling, disturbed consciousness, salivation, jaw champing, tetanic spasms, and limb paddling. If left alone many cases recovered, only to show the same nervous signs later on. These periods of cerebral convulsionscould be precipitated by either forced exercise or high ambient temperatures, and frequently resulted in death. Affected cattle also displayed signs of a cerebdlum dysfunction, including a wide-based stance, disturbed equilibrium, and thoracic limb hypermetria. Other signs observed were mild head tremors and muscle fasciculations. At necropsy the livers of affected cattle were usually pale and swollen. The lungs were frequently congested, and small epicardial
Australian VeferinaryAssociation Vol. 69, No. 9, September 1992