EQUINE VETERINARY JOURNAL

159 TABLE I1

RESULTS O F SEROLOGICAL TESTS O F POSSIBLE DIAGNOSTIC SIGNIFICANCE

Ref.

1 1 RBPT

-

63 64 65 66

+ +

i-I

SAT

CFT i.u.

1/40 1/80 3/320 1/80

51.5 102.5 574.5 102.5

-1-1

1 1 AGT

4/20 2/20 4/20 4/20 4/20 ~

_

4/1280 2/80 3/160 3/2560 2/80

Clinical condition

Tendinitis Donkey, thickened ridge of tissue along withers Head shaking, poll evil Fistulous withers, Brircella isolated from pus Asthmatic condition

_

_

_ _ _ _ _ _ _ ~ ~ _ _ _ _ _ _ _

61 68 69 70

-

+ + +

-

3/20 4/160

36 328

4/20

4/1280 )

2/160 2/80

246 123

4/20 4/20

2/5120 ) No data 3/160 )

-

Not clinically affected

Expression of titres: In these tables, denominators of the fractions given indicate degree of dilution of the test serum, while numerators indicate the extent of agglutination or fixation at that dilution. Thus 4/10 indicates complete agglutination or fixation at a dilution of 1 in 10: 2/10 indicates 50 per cent agglutination, etc., at that dilution. Accepted for publication 21.4.71

CURYN€BACT€R/UM €QU/ INFECTI0N IN A THOROUGHBRED FOAL M. C . ROBERTS Department of Veterinary Medicine, University of Queensland, St. L ucia, Brisbane, Australia 4067 L. R. POLLEY Department of Veterinary Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, S7N OWO, Canada

The disease produced by Corynebacterium equi affects foals of 2 to 3 months of age or older, and is characterised by a suppurative bronchopneumonia, mediastinal lymphadenitis and occasional alimentary tract involvement. Of 61 foals with generalised infection autopsied at Newmarket in a 5 year period, only 4.9 per cent had C. equi infection (Platt, 1973), whilst in Dublin, the pathological incidence was 2-3 per cent of all diseased foals examined in 10 years (Farrelly, 1969). The disease has attracted little attention in the British Isles, the clinical incidence is unknown, and the diagnosis is invariably made retrospectively after the death or destruction of the foal. Undoubtedly there is a lack of familiarity with the condition amongst clinicians resulting in cases being misdiagnosed and remaining unrecognised. This report highlights some salient features of the disease, and indicates some additional procedures which might aid the clinical diagnosis. CLINICAL HISTORY When first examined, the subject, a well grown 4 month old Thoroughbred colt foal had a pyrexia (39.5"C), a bilateral serous oculonasal discharge without other upper respiratory symptoms, serous exudation around all coronets, and appeared less active than normal. Intravenous oxytetracycline administration marginally reduced the pyrexia, and lessened the nasal discharge although the foal remained listless and lost condition. Further antibiotic (ampicillin) and supportive therapy brought no improvement, and the foal was referred to the University of Bristol after a clinical course of 2 weeks. On admission, the foal, unthrifty and intensely lethargic, had a normal temperature and pulse rate, a slightly elevated respiratory rate, and no evidence of nasal discharge, lymphadenit is, coughing or sneezing. The coronets were unremarkable. Auscultation revealed harsh bronchial sounds and rilles but no areas of dullness or wheezing. Intestinal sounds were present and abdominal palpation elicited pain. The foal had little thirst or appetite, passed small hard faeces, was continuously grinding his teeth and moved reluctantly. Chloramphenicol, corticosteroids, parenteral and oral fluids were given daily without effect.

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The foal deteriorated rapidly and was destroyed on the third day after becoming severely dyspnoeic and distressed. A moderate polymorphonuclear leucocytosis on arrival (1 1.0 x 109/1)was more pronounced (18.2 x 109/1) with a left shift by day 3. Amino aspartate transferase (AAT) levels were not elevated. PATHOLOGY There was a pleural exudate, and the lungs, which were extensively consolidated and distorted by adhesions and multiple, small, thick-walled abscesses containing whitish creamy pus, showed severe bronchopneumonia. A large, thick-walled saccular structure, roughly ovoid in shape (25 x 20 x 20 cm) attached to the mesenteric side of the ileum adjacent to the ileocaecal junction (fig. l), contained a mixture of ingesta and purulent material and communicated with the ileal lumen via 2 irregular orifices. Peritoneal fluid was normal in volume and appearance. The hepatic, iliac and mesenteric lymph nodes were enlarged and oedematous, and the bronchial and cranial mediastinal lymph nodes were distinctly abscessed. Several renal cortical infarcts were present. C. equi was obtained in pure culture from a lung abscess, the pleural effusion and an hepatic lymph node, and was demonstrated within macrophages and extracellularly in Gram-stained sections of the lung and ileal sac wall.

Fig. 1. Large sacculur structure (S) attached to the ileum (1) at the ileo-caecal junction ( 1 4 3 .

DISCUSSION This case illustrates some of the clinical features, diagnostic problems, refractoriness to treatment, and pathological changes associated with this insidious disease. The intense depression and unthriftiness predominated throughout, but the respiratory signs were not severe until the final day. In particular the serous nasal discharge and pyrexia were transient, and there was no evidence of a soft cough or rattling respiratory noise (Bain, 1963). Alimentary dysfunction was not apparent despite the pain on abdominal palpation, and the size and location of the saccular structure. The role of C . equi in gastrointestinal disturbances is equivocal. The organism is considered a potential cause of acute and chronic diarrhoea in the older foal (Merritt, Bolton and Cimprich, 1975) whilst comparable findings of mesenteric abscessation, lymphadenitis, discrete ulceration and erosion of the small and large intestinal mucosae were not associated with dysfunction (Bain, 1963). Without experimental study, the mode of infection remains unresolved, although ingestion is the most likely route with intestinal lesions an essential feature, initial infection localising in solitary lymphoid follicles or Peyer’s patches followed by lymphoid or haematogenous spread. Attempts should be made to establish a clinical diagnosis in suspected cases of C. equi infection. Bacteriological examination of nasopharyngeal swabs, tracheal washings or pleural effusions, and possibly faeces would be useful. Thoracic radiography could determine the degree of pulmonary involvement. Unfortunately serological tests have proved unreliable as immunity appears to be more cellular than antibody mediated (Carter and Hylton, 1974). Tissue invasion and the subsequent progress of infection are governed by the foal’s immunological status. The age incidence coincides with the fall in maternally derived antibody and the attainment of active immunity; protein electrophoresis could indicate whether there is any defect in the foal’s immune capacity. ACKNOWLEDGEMENT The authors are grateful to Mr. J. Horlock of Leintwardine, Shropshire for referring the case to the Department of Veterinary Medicine, University of Bristol. REFERENCES Bain, A. (1963). Corynebacterium equi infections in the equine. Aust. vet. J. 39, 116-121. Carter, G. R. and Hylton, G. A. (1974). An indirect haemagglutination test for antibodies to Corynebacterium equi. Am. J. vet. Res. 35, 1393-1395. Farrelly, B. T. (1969). Corynebacterium equi infection in foals in Ireland. Irish vet. J. 23, 231-232. Merritt, A. M., Bolton, J. R. and Cimprich, R. (1975). Differential diagnosis of diarrhoea in horses over six months of age. J . S. Afr. vet. med. Ass. 46, 73-76. Platt, H. (1973). Septicaemia in the foal. A review of 61 cases. Br. vet. J. 129. 221-229. Accepted for publication 6.5.77

Corynebacterium equi infection in a thoroughbred foal.

EQUINE VETERINARY JOURNAL 159 TABLE I1 RESULTS O F SEROLOGICAL TESTS O F POSSIBLE DIAGNOSTIC SIGNIFICANCE Ref. 1 1 RBPT - 63 64 65 66 + + i-I...
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