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Erysipelothrix rhusiopathiae endocarditis
Journal of Infection
(1980) 2, 83-85
CASE REPORT
Erysipelothrix rhusiopathiae endocarditis N. Muirhead* and T. M. S. Reidt
*Aberdeen Royal Infirmary ~fLaboratory, City Hospital, Aberdeen
Summary We report a case of infective endocarditis due to chronic lymphatic leukaemia (CLL).
Erysipelothrix rhusiopathiae in a man
with
Introduction
Erysipelothrix rhusiopathiae infection in man usually causes self-limiting skin lesions which respond promptly to penicillin therapy (Beeson and McDermott, 1975). Endocarditis due to this organism is rare but published accounts (Heggers, Buddington and McAllister, 1974; Freland 1976) indicate that previously normal valves may be involved and the response to penicillin therapy is poor despite invariable in vitro sensitivity. Case report
A 53-year-old farmer presented in August 1978 with a three-month history of lassitude, night sweats, weight loss of 4.5 kg, polyarthralgia and slight exertional dyspnoea. Chronic lymphatic leukaemia had been diagnosed in 1971 and treated with a short course of chlorambucil. His haematological condition has remained stable thereafter apart from persistently low serum immunoglobulins (Igs). On admission he had a fever of 38.5°C, slight anaemia, and left axillary lymphadenopathy. He was sweating profusely. There were scaly erythematous patches on his left arm and right flank which his general practitioner had been treating as ringworm with oral griseofulvin. There was no finger clubbing or splinter haemorrhages. Pulse was 96/min, regular and collapsing, BP 134/72, with normal heart sounds and no murmurs. Abdominal examination Reprint requests to: T. M. S. Reid, Consultant Bacteriologist, City Hospital, Urquhart Road, Aberdeen.
0163-4453/80/010083+03 $01.00/0
© 1980 The British Society for the Study of Infection
84
N. Muirhead and T. M. S. Reid
revealed 5 cm of splenomegaly and the liver was just palpable. Examination was otherwise normal. During the next three days his temperature and sweats continued and he developed a progressive, early diastolic murmur at his left sternal edge with a late systolic apical murmur. Serial blood cultures grew Erysipelothrix rhusiopathiae sensitive to penicillin. The organism was identified by biochemical tests, growth on Packer' s medium (Packer, 1943) and by mouse intraperitoneal inoculation. Electrocardiogram and chest X-ray were normal. Echocardiography confirmed the presence of aortic regurgitation with some left ventricular enlargement. No vegetations were detected. Investigations showed: haemoglobin 12.1 g/dl, white cell count 14.7 × 109/1, 54 per cenl lymphocytes, 42 per cent polymorphs, 4 per cent monocytes, platelets 155 × 109/1, blood film-mild normochromic normocytic red cells with small mature lymphocytes. Biochemical screen was normal. Immunoglobin estimations: IgG 6.6g/1 (normal 7-18g/1), IgA 0.6g/1 (0.9,4.5 g/l), IgM I. 2 g/1 (0-6-2.8 g/l). The patient was treated with intravenous benzylpenicillin 12 mega units per day for two weeks. Oral therapy with phenoxymethylpenicillin 1 g 6-hourly and probenecid 500 mg 12-hourly was continued for a further three weeks. He became afebrile within 24 hours and has remained so. Six months later his murmurs were unchanged but there was no cardiac failure. The spleen was not palpable. The titre of anti-erysipelothrix antibody measured by the indirect immunofluorescent technique had fallen from 1:256 to 1:32. Comment
Our case illustrates many of the typical features of erysipelothrix endocarditis (Baird and Benn, 1975). The mortality in published series is high (around 30 per cent) Baird and Benn, 1975; Freland, 1976) despite invariable in vitro sensitivity to penicillin. Involvement of normal valves particularly aortic is found (Baird and Benn, 1975; Heggers, Buddington and McAllister, 1974) although in our case the presence of an undiagnosed congenital anomally, e.g. bicuspid aortic valve, cannot be excluded. Cutaneous erysipeloid was present in only 50 per cent of patients with endocarditis (Freland, 1976). The skin lesions in our patient were not typical but a diagnosis of ringworm was not substantiated by microscopy and culture of skin scrapings. Erysipelothrix rhusiopathiae is often dismissed as a skin contaminant when grown from blood culture (Heggers, Buddington and McAllister, 1974; McCarty and Bornstein, 1960). It is possible therefore that potentially fatal infection is more common than previously realised. Erysipelothrix endocarditis has not been recorded in the immunocompromised host (Freland, 1976; McCarty and Bornstein, 1960). However the secondary hypogammaglobulinaemia in our CLL patient may have predisposed him to systemic infection. Occupational exposure to animals or fish
Erysipelothrix rhusiopathiae endocarditis
85
frequently precedes infection (Heggers, B u d d i n g t o n and McAllister, 1974; M c C a r t y and Bornstein, 1960). It is important that Erysipelothrix rhusiopathiae should be considered a possible cause of infective endocarditis where the occupational history is relevant. (We are grateful to Professor W. Walker for permission to report this case.) References
Baird, P. J. and Benn, R. (1975). Erysipelothrix endocarditis. Medical Journal of Australia, 2, 743. Beeson, P. B. and McDermott W. (Editors). Textbook of Medicine, 14th Edition, W. B. Saunders and Company, London (1975), p. 368. Freland, C. (1976). Les infections h Erysipelothrix rhusiopathiae. Pathologie et Biologie, 25, 345. Heggers, J. P., Buddington, R. S. and McAllister, H. A. (1974). Erysipelothrix endocarditis diagnosis by fluorescence microscopy. Report of a case. American Journal of Clinical Pathology, 62, 803. McCarty, D. and Bornstein, S. (1960). Erysipelothrix endocarditis. Report on a septicaemic form of the erysipeloid of Rosenbach. American Journal of Clinical Pathology, 33, 39. Packer, R. A. (1943). The use of sodium azide and crystal violet in a selective medium for streptococci and Erysipelothrix rhusiopathiae. Journal of Bacteriology, 46, 343.
(1980) 2, 83-85
CASE REPORT
Erysipelothrix rhusiopathiae endocarditis N. Muirhead* and T. M. S. Reidt
*Aberdeen Royal Infirmary ~fLaboratory, City Hospital, Aberdeen
Summary We report a case of infective endocarditis due to chronic lymphatic leukaemia (CLL).
Erysipelothrix rhusiopathiae in a man
with
Introduction
Erysipelothrix rhusiopathiae infection in man usually causes self-limiting skin lesions which respond promptly to penicillin therapy (Beeson and McDermott, 1975). Endocarditis due to this organism is rare but published accounts (Heggers, Buddington and McAllister, 1974; Freland 1976) indicate that previously normal valves may be involved and the response to penicillin therapy is poor despite invariable in vitro sensitivity. Case report
A 53-year-old farmer presented in August 1978 with a three-month history of lassitude, night sweats, weight loss of 4.5 kg, polyarthralgia and slight exertional dyspnoea. Chronic lymphatic leukaemia had been diagnosed in 1971 and treated with a short course of chlorambucil. His haematological condition has remained stable thereafter apart from persistently low serum immunoglobulins (Igs). On admission he had a fever of 38.5°C, slight anaemia, and left axillary lymphadenopathy. He was sweating profusely. There were scaly erythematous patches on his left arm and right flank which his general practitioner had been treating as ringworm with oral griseofulvin. There was no finger clubbing or splinter haemorrhages. Pulse was 96/min, regular and collapsing, BP 134/72, with normal heart sounds and no murmurs. Abdominal examination Reprint requests to: T. M. S. Reid, Consultant Bacteriologist, City Hospital, Urquhart Road, Aberdeen.
0163-4453/80/010083+03 $01.00/0
© 1980 The British Society for the Study of Infection
84
N. Muirhead and T. M. S. Reid
revealed 5 cm of splenomegaly and the liver was just palpable. Examination was otherwise normal. During the next three days his temperature and sweats continued and he developed a progressive, early diastolic murmur at his left sternal edge with a late systolic apical murmur. Serial blood cultures grew Erysipelothrix rhusiopathiae sensitive to penicillin. The organism was identified by biochemical tests, growth on Packer' s medium (Packer, 1943) and by mouse intraperitoneal inoculation. Electrocardiogram and chest X-ray were normal. Echocardiography confirmed the presence of aortic regurgitation with some left ventricular enlargement. No vegetations were detected. Investigations showed: haemoglobin 12.1 g/dl, white cell count 14.7 × 109/1, 54 per cenl lymphocytes, 42 per cent polymorphs, 4 per cent monocytes, platelets 155 × 109/1, blood film-mild normochromic normocytic red cells with small mature lymphocytes. Biochemical screen was normal. Immunoglobin estimations: IgG 6.6g/1 (normal 7-18g/1), IgA 0.6g/1 (0.9,4.5 g/l), IgM I. 2 g/1 (0-6-2.8 g/l). The patient was treated with intravenous benzylpenicillin 12 mega units per day for two weeks. Oral therapy with phenoxymethylpenicillin 1 g 6-hourly and probenecid 500 mg 12-hourly was continued for a further three weeks. He became afebrile within 24 hours and has remained so. Six months later his murmurs were unchanged but there was no cardiac failure. The spleen was not palpable. The titre of anti-erysipelothrix antibody measured by the indirect immunofluorescent technique had fallen from 1:256 to 1:32. Comment
Our case illustrates many of the typical features of erysipelothrix endocarditis (Baird and Benn, 1975). The mortality in published series is high (around 30 per cent) Baird and Benn, 1975; Freland, 1976) despite invariable in vitro sensitivity to penicillin. Involvement of normal valves particularly aortic is found (Baird and Benn, 1975; Heggers, Buddington and McAllister, 1974) although in our case the presence of an undiagnosed congenital anomally, e.g. bicuspid aortic valve, cannot be excluded. Cutaneous erysipeloid was present in only 50 per cent of patients with endocarditis (Freland, 1976). The skin lesions in our patient were not typical but a diagnosis of ringworm was not substantiated by microscopy and culture of skin scrapings. Erysipelothrix rhusiopathiae is often dismissed as a skin contaminant when grown from blood culture (Heggers, Buddington and McAllister, 1974; McCarty and Bornstein, 1960). It is possible therefore that potentially fatal infection is more common than previously realised. Erysipelothrix endocarditis has not been recorded in the immunocompromised host (Freland, 1976; McCarty and Bornstein, 1960). However the secondary hypogammaglobulinaemia in our CLL patient may have predisposed him to systemic infection. Occupational exposure to animals or fish
Erysipelothrix rhusiopathiae endocarditis
85
frequently precedes infection (Heggers, B u d d i n g t o n and McAllister, 1974; M c C a r t y and Bornstein, 1960). It is important that Erysipelothrix rhusiopathiae should be considered a possible cause of infective endocarditis where the occupational history is relevant. (We are grateful to Professor W. Walker for permission to report this case.) References
Baird, P. J. and Benn, R. (1975). Erysipelothrix endocarditis. Medical Journal of Australia, 2, 743. Beeson, P. B. and McDermott W. (Editors). Textbook of Medicine, 14th Edition, W. B. Saunders and Company, London (1975), p. 368. Freland, C. (1976). Les infections h Erysipelothrix rhusiopathiae. Pathologie et Biologie, 25, 345. Heggers, J. P., Buddington, R. S. and McAllister, H. A. (1974). Erysipelothrix endocarditis diagnosis by fluorescence microscopy. Report of a case. American Journal of Clinical Pathology, 62, 803. McCarty, D. and Bornstein, S. (1960). Erysipelothrix endocarditis. Report on a septicaemic form of the erysipeloid of Rosenbach. American Journal of Clinical Pathology, 33, 39. Packer, R. A. (1943). The use of sodium azide and crystal violet in a selective medium for streptococci and Erysipelothrix rhusiopathiae. Journal of Bacteriology, 46, 343.