Enterotoxaemia in a foal due to Clostridium perfringens type A

Blaney BJ, Gartner RJW and McKenzie RA (1981b) - JAgric Sci. Comb 97: 639 Cavaye JM, Thompson PJM and Scattini WJ (1986) - Queensland DeDartment of Primary Industries Farmnote F3/Jan 86 Clewkt JF (1987) - Queensland Department of Primary Industries Press Release 29 June Groenendyk S and Seawright AA (1974) - Aust Ver J 50: 131 Hamilton NA (1984) - Queensland Department of Primary Industries Information Sheet McDonald W (1986) - New South Wales Department of Agriculture Agfact P2.5.21 McKenzie RA, Blaney BJ and Gartner RJW (1981a) - J Agric Sci, Cam&91: 69 McKenzie RA, Gartner RJW, Blaney BJ and Glanville RJ (1981b) Aust Vet J 57: 554 McKenzie RA and Schultz K (1983) - J Agric Sci, Comb 100: 249 McKenzie RA (1985) - in Plant Toxico/ogy.Edited by AA Seawright, MP Hegarty, LF James and RF Keeler, Queensland Poisonous Plants Committee, Brisbane p 150 Scattini WJ and Johnson B (1988) - Queensld Agric J 114 77 Walthall, JC and McKenzie RA (1976) - Aust Vet J 52: 11

(Accepted f o r publication 30 May 1988)

Enterotoxaemia in a foal due to Clostridium perfringens type A Oakey Veterinary Hospital, PO Box 2, Oakey, Queensland 4401

AJ DART RR PASCOE

Toowoomba Veterinary Laboratory, JA GIBSON BJ HARQueensland Department of Primary Industries, ROWER Tor St, Toowoomba, Queensland 4350 Of 5 toxigenic types of Clostridium perfringens (A, B, C, D and E) that cause enterotoxaemia in domestic animals, only a few cases of type B and type C enterotoxaemia have been described in foals (Dickie et al 1978; Nilo and Chalmers 1982; Olubunmi and Taylor 1985; Sims et a1 1985; Howard-Martin et a1 1986; Pearson 1986). This report describes a case of C . perfringens type A enterotoxaemia in a foal. A 2-day-old thoroughbred colt was admitted for examination at the Oakey Veterinary Hospital with haemorrhagic diarrhoea and severe abdominal pain. Birth had been uncomplicated and immediately after birth the umbilical stump was treated with a tincture of iodine and tetanus prophylaxis was administered. The mare had adequate amounts of colostrum, and for the first 36 h of life the foal was observed to be suckling normally. After this time, a yellow watery diarrhoea and signs of mild abdominal discomfort developed. The studmaster applied a muzzle to prevent nursing and administered a combination of 1.25g of sulphadimidine and 0.25g trimethToprim* combined with anti-diarrhoea powder via a stomach tube. The abdominal discomfort subsided and the foal's demeanour improved following an intravenous injection of 5Omg of flunixen megulaminet. Hydration was maintained throughout the day with 5OOml of balanced electrolyte solution$ administered by stomach tube every 2 h. During the day the consistency of the faeces changed to that of a thin red paste. Nine hours after the initial treatment the foal became acutely depressed then began to roll violently with severe abdominal pain. The foal's legs were cold to touch and it had become dehydrated. Upon arrival the foal's rectal temperature was 39.4"C, it was estimated to be approximately 10% dehydrated based on skin turgor, and had congested mucous membranes with a delayed capillary refill time. A catheter was inserted and fiied

into the cephalic vein, and a compound sodium lactate drip commenced. Two blood samples were found to be haeniolysed at the time of collection. The pain was not responsive to an intravenous injection of 5Omg of flunixen megulamine so the foal was prepared for abdominal surgery. After induction with 75mg xyzalines combined with 150mg ketaminel given intravenously, an endotracheal tube was passed and anaesthesia maintained using halothane in oxygen. The abdomen was prepared aseptically and the abdominal cavity opened via a ventral midline incision. There were diffuse patchy haemorrhages on the serosal surface of the entire small intestine and the mesenteric vessels were engorged with blood. The lumen of the small intestine was distended with gas and a foul smelling haemorrhagic fluid. There was no obvious intestinal displacement, so a sample of the contents was collected aseptically and the intestine was decompressed and replaced. Intraoperative therapy consisted of 50ml of equine gammaglobulin# and 18OOmg of benzyl penicillin intravenously combined with 15OOmg of procaine penicillin and 15Qmg of gentamycin sulphate injected intramuscularly. A total of 6 litres of compound sodium lactate was administered and fluid therapy maintained post-operatively. Recovery from anaesthesia was uneventful with no signs of abdominal paiin, and the mare and foal were separated into adjoining stables. Despite therapy the foal died 4 h after surgery. A post-mortem examination was performed 3 h after death. Approximately 600ml of serosanguinous fluid was found in the peritoneal cavity. The haemorrhage on the serosal surface of the small intestine was more extensive than at the time of surgery. Despite decompression during surgery, the lumen of the small intestine was again distended with gas and contained a foul smelling haemorrhagic fluid which extended down into the large intestine. The mucous membrane of the intestine from the pyloris to the ileocaecal valve appeared dark purple. The lungs were congested and the heart was pale with circular cream discolourations on the epicardium. Pieces of liver, kidney, lung, heart, caecum, colon and small intestine were fixed in 10% buffered neutral formalin, paraffin embedded and sectioned at 6p thick. Sections were stained with haematoxyin and eosin and Brown and Brenn's modification of Gram's stain. Histological lesions were confined to the gut, especially the small intestine. The necrosis of villi in the small intestine was uniform and extensive. Most of the epithelium, except for the crypt enterocytes, had sloughed. The denuded necrotic villi were outlined by a continuous layer of large Gram-positive bacilli consistent with Clostridiiz spp. (Figure 1). The serosa, submucosa and lamina proprial were severely hyperaemic, with areas of haemorrhage and emphysema. There was no significant infiltration by inflammatory cells. Lesions in sections of caecum and colon were similar but much less severe than those in the small intestine and the submucosa was oedematous rather than haemorrhagic or emphysematous. Smears of small intestinal contents stained with Gram, and collected during surgery, had a predominance of large Grampositive bacilli present. Pipettes of heart, kidney, small intestine, caecum and colon as well as the ante-mortem samlple of small intestinal contents were cultured anaerobically on 5% sheep blood agar and in cooked meat medium*. Samples,were also cultured aerobically on sheep blood agar, MacConkey agar and selective media for salmonallae. All plates were incubated at 37°C. A pure heavy growth of C. perfringens was isolated from anaerobic cultures of all intestinal samples and kidney. Low numbers of Echerichia coli and 01 streptococci were also isolated. No bacteria were isolated from the heart. C. perfringens was identified by its characteristic stormy fermentation reaction in litmus milk and the production of

5 Rompun", Bayer Australia Ltd, Botany, New South Wales

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Lectade", Beecham Veterinary Products, Dandenong, Victoria 3175

330

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1 Ketama@, Mavlab Pty Ltd, Rochedale, Queensland 41:23 # Equine Gammaglobulin", Commonwealth Serum Laborato-

ries, Parkville, Victoria 3025. Oxoid", Oxoid Limited, Victoria. Australian Veterinary Journal, Vol. 65, No. 10, October, 1988

pain no longer responsive to analgesia led to our decision to perform a laparotomy. Hindsight indicates that careful evaluation of the history and clinical signs combined with the haemolysed blood samples should have distinguished this disease process from an intussusception. Flemming (1985) suggests that treatment of calves with C. perfringens type A enterotoxaemia is not feasible because of high levels of a toxin causing severe intravascular haemolysis with death usually occurring within 12 h. Treatment of foals with C. perfringens type B or C enterotoxaemia has also been unrewarding. All foals on this stud farm were foaled in a different paddock and given a 3-day course of penicillin prophylactically following this incident; there have been no further deaths from enteritis. References Dickie CW, Klinkerman DL, and Petrie RJ (1978)-J A m Vet Med Ass 173: 306 Fleming S (1985)-In Veterinary Clinics of Nth A m Food An Prac 1: 509

Howard-Martin M, Morton RJ, Qualls CW and MacAllister CG (1986)--3 Am Vet Med Ass 189: 564 Niilo L, and Chalmers GA (1982)-Can Vet J 23: 299 Olubunmi PA and Tavlor DJ f1985k-Troa Vet 3: 28 Pearson EG, Hedstrom OR, Son R,'and Wedam J (1986)--J Am Vet Med Ass 188: 1309 Sims LD, Tzipori S, Hazard GH, and Carroll CL (1985)-Aust Vet J 6 2 : 194

(Accepted for publication 4 May 1988)

Rhodococcus equi infection in goats Figure 1. Small intestine with intact crypts (C) and necrotic villi (N) outlined by a layer of large Gram-positive bacilli (arrowed). Gram stain (Brown and Brenn's modification) X 400. acid from glucose, maltose, lactose and sucrose; it produced a double zone of haemolysis on sheep blood agar. The isolate was further identified as C. perfringens Type A by toxinahtitoxin neutralisation tests in mice. Diagnostic antisera" against C. Perfringens Types A, C and D were used to demonstrate CY toxin in supernatant fluid of cooked meat medium, filter. Intestinal contents sterilised by passing through a 0 . 2 ~ were not tested for CY toxin. C. perfringens type A is a Gram-positive spore forming anaerobic bacillus known to cause food poisoning in man, necrotic enteritis in chickens and diarrhoea in lambs, calves and piglets (Flemming 1985; Olubunmi and Taylor 1985). It has never previously been reported as a cause of enteritis in foals. It can be found in soil and in the normal flora of the intestinal tract of both man and animals. Abrupt changes in diet, high amounts of carbohydrate and protein in the small intestine contents, or damage to the intestinal mucosa have been thought to favour clostridial multiplication and toxin production in calves (Flemming 1985); their role in enterotoxaemia of foals has not been established. In this case the foal had a normal birth and no predisposing factors could be identified that might have precipitated disease other than possible stress caused by a storm when the foal was 12 h old. Foals with enteritis due to C. perfringens types B and C enteritis usually show a profuse haemorrhagic diarrhoea and severe abdominal pain in conjunction with the usual signs of a bacterial enteritis including dehydration and elevated temperature. The clinical history and signs on admission of our foal were similar to previous reports but it also developed acute depression and sudden circulatory collapse, combined with probable intravascular haemolysis. Profuse haemorrhagic diarrhoea and severe colic are rarely seen in young foals with eneritis, and when present, invariably indicate an intussusception. The clinical signs combined with

t Wellcome Diagnostics, Dartford, England Australian Veterinary Journal, Vol. 65, No. 10, October, 1988

New South Wales MJ CARRIGAN Department of Agriculture, Agricultural Research and Veterinary Centre, Forest Road, Orange, New South Wales 2800 New South Wales Department of Agriculture, Regional Veterinary Laboratory, Wagga Wagga, New South Wales 2650 Pastures Protection Board, Gundagai, New South Wales 2722

IJ LINKS

AG MORTON

Rhodococcus equi was first recognised as an animal pathogen in 1923 when it was isolated from the lungs of pneumonic foals (Magnusson 1923). Since then most of the recorded cases of R. equi infection have been in horses and pigs (Barton and Hughes 1980). It has also been isolated from suppurative lesions in cattle, buffalo, sheep, cats, koalas, reptiles, man (Barton and Hughes 1980) and deer (Carman and Hodges 1987). The only 2 reports of R. equi being isolated from lesions in goats are from India (Natarajan and Nilakantan 1974) and the United States of America (Whitford and Jones 1974). This report describes the necropsy and bacteriological findings of R. equi infection in 3 goats from different farms in Australia. Goat 1, an aged Saanen doe with a history of chronic weight loss, was presented for necropsy in an advanced state of decomposition. Multiple well encapsulated abscesses, 3 to 4mm in diameter, were found throughout the lungs and liver. These contained a very thick yellowish pus. Goat 2, a 2-year-old Saanen doe, was introduced onto a farm, 2 weeks prior to the appearance of clinical signs. The goat developed an abnormal posture which progressed to posterior paralysis despite treatment with antibiotics, antiinflammatory drugs and thiamine. It was presented for necropsy one week after clinical signs developed. The goat was bright and alert, and had hindlimb paralysis but was able to bear weight on its front legs. Frontlimb withdrawal and eye preservation reflexes were normal. At necropsy there was 33 1