Letters to the Editor
II 5
24. Gallen IW, Ispahani P. Fulminant Capnocytophaga canimorus (DF-2) septicaemia. Lancet I99I; 337: 308. 25. Hantson P, Gautier PE, Verkemans MC et al. Fatal Capnocytophaga canimorus septicaemia in a previously healthy woman. Ann Emerg Med I99I; zo: 93-9426. Howell JM, Woodward GR. Precipitous hypotension in the emergency department caused by Capnocytophaga canimorus sp nov sepsis. Am ,7 Emerg Med I99o; 8:312-314 .
Group G p-haemolytic streptococcal vertebral osteomyelitis Accepted for publication 27 November I 9 9 I Sir, Vertebral osteomyelitis, which presents as a spondylo-discitis, is a rare but important cause of back pain. Staphylococci and mycobacteria are the c o m m o n e s t pathogens, 1 but isolation and identification of the responsible organism is essential if subsequent treatment is to be successful in eradicating the infection. We present a case which illustrates this point, as the organism isolated was not previously known to cause vertebral osteomyelitis. A 4o-year-old West African w o m a n was admitted for removal of a benign ovarian cyst. At this time she gave a history of back pain for the past 5 months which had been more severe during the previous Io days. T h e pain was exacerbated by m o v e m e n t but not relieved significantly by lying flat. T h e patient had also noticed general malaise, night sweats and a loss of one stone in weight, during the previous 2 months. On examination, a low-grade fever (37'5 °C) was present. T h e r e was marked tenderness over L3 to L5 vertebrae with sacrospinalis muscle spasm, and a virtually complete loss of spinal m o v e m e n t in all planes. X - r a y of the lumbar spine showed narrowing of the L 3 / 4 intervertebral joint space with adjacent bony destruction suggestive of an infective spondylo-discitis. Radioactive technetium and C T scans lent further support to this diagnosis. A full microbiological screen yielded no organism or source of infection and so a bone biopsy of the inferolateral aspect of L3 was performed. Culture of this yielded a pure growth of group G fl-haemolytic streptococcus ( G G S ) . Serological tests revealed normal titres of antistreptolysin O (ASO), a n t i - D N A a s e B (ADB), and group A-specific antihyaluronidase, but elevated groups C- and G-specific antihyaluronidase ( A H T C G ) (40 u n i t s / m l , normal range < Io units/ml). T h e G G S which we isolated tested positive for M protein capsular antigen and was identified as T type 7/320. T r e a t m e n t had been started with oral fucidin and Iv flucloxacillin but, following isolation of G G S , was changed to IV benzyl penicillin I2 million units/24 h ( M I C < 0"03 rag/l, M B C = 0"03 rag/l). T h e patient's condition subsequently improved, her back pain and pyrexia quickly resolved, and her E S R and C-Reactive protein (CRP) fell f r o m 74 m m / h and 40 mg/1 respectively to normal. T w o weeks later, she was c o m m e n c e d on oral antibiotics following an episode of penicillin allergy [(clindamycin 1.2 g / 2 4 h ( M I C < o'~2 mg/1, M B C = o.I2 mg/l)]. She was then mobilised while wearing a neofract plastic jacket. A further spinal X - r a y after antibiotic therapy for 3 months revealed bony healing with new bone formation. Unlike septic arthritis, osteomyelitis caused by G G S infection is extremely rare. T h e r e have been only two previous reports of it being caused by this organism 2' 3 and this is the first report of vertebral osteomyelitis caused by a G G S infection. We were unable to explain our patient's predisposition to serious infection by this organism: she was in good health, no p r i m a r y infective site was apparent, and there was no evidence of previous spinal pathology. Unusual virulence of the organism m a y
I I6
Letters to the Editor
therefore have been responsible, as suggested by the presence of M protein, a virulence factor rarely seen in G G S .
* Department of Rheumatology and t Public Health Laboratory, St George's Hospital Medical School, Blackshaw Road, London S W I 7 oQT, U.K.
J . H . Tobias* P . Y . C . Lee3; F . E . Bruckner*
References I. Norden CW. In: Mandell GL, Douglas RG, Bennett JE, Eds. Principles and practice of infectious disease. Edinburgh: Churchill Livingstone, 199o: 922-930. 2. Hess OM, Youssef S, Luthy R, Seigenthaler W. Rezidivierende Sepsis mit Streptokokken der Lancefield-Gruppe G. Schweiz Med Wochenschr 198o: IiO: 129-13o. 3- Vartian C, Lerner PI, Shales DM, Gopalkrishna KV. Infections due to Lancefield group G streptococci. Medicine 1985; 64: 75-88.
Staphylococcus lugdunensis e n d o c a r d i t i s Accepted for publication 19 December 1991 Sir, We wish to present another case of endocarditis caused by Staphylococcus lugdunensis, adding to those previously reported. 1-3 A 59-year-old carpenter presented to the Accident and E m e r g e n c y D e p a r t m e n t with a short history of chest pain. His past medical history included a mitral valve replacement for rheumatic heart disease 13 years before; since then he had remained well. Closer questioning revealed an influenza-like illness 3 months before admission since when he had noticed occasional night sweats and fever. H e had no focal central nervous system signs or s y m p t o m s but he described experiencing intermittent short episodes of strange thought processes during the previous few months. H e had undergone cautery for nose-bleeds I year before but had no other recent surgery and he had no skin lesions. Total dental clearance had been p e r f o r m e d prior to mitral valve replacement in 1977 . On initial examination he was afebrile, normotensive and had a collapsing pulse. H e had no cutaneous stigmata of endocarditis. Auscultation was consistent with a prosthetic mitral valve, and an aortic stenotic m u r m u r was heard. T h e r e was no evidence of incompetence in either valve. Investigation showed a slightly raised W B C count of 12"2 x lO9/1 (75 % neutrophils), haemoglobin concentration of I 1.3 g/dl, and E S R of 86 m m in the first hour. S e r u m biochemistry and a chest X - r a y were normal. Blood cultures yielded G r a m - p o s i t i v e cocci in clusters after 24 h in both bottles. An urgent echocardiogram showed mild aortic stenosis but no vegetations were seen. A working diagnosis of prosthetic valve endocarditis was made and treatment was started with flucloxacillin 2 g 4 hourly and gentamicin 80 m g 12 hourly after taking further blood for culture. All six blood culture bottles yielded staphylococci after 24 h. T h e organism was Staphaurex (Wellcome) and Staphylase (Oxoid) negative; it was also tube-coagulase and slide-coagulase negative using h u m a n plasma. Identification by A P I - s t a p h was Staphylococcus warneri. T h e organism was sensitive by disc-diffusion methods to methicillin, penicillin, fusidic acid, erythromycin, trimethoprim, gentarnicin, vancomycin, chloramphenicol and rifampicin. T h e minimal inhibitory and minimal bactericidal concentration of penicillin was found to be 0"03 mg/1. T h e flucloxacillin was therefore changed to benzyl penicillin 1.2 g 4 hourly. T h e organism was subsequently identified as S. lugdunensis by the delayed positive D N A s e , and positive ornithine decarboxylase test. 4
II 5
24. Gallen IW, Ispahani P. Fulminant Capnocytophaga canimorus (DF-2) septicaemia. Lancet I99I; 337: 308. 25. Hantson P, Gautier PE, Verkemans MC et al. Fatal Capnocytophaga canimorus septicaemia in a previously healthy woman. Ann Emerg Med I99I; zo: 93-9426. Howell JM, Woodward GR. Precipitous hypotension in the emergency department caused by Capnocytophaga canimorus sp nov sepsis. Am ,7 Emerg Med I99o; 8:312-314 .
Group G p-haemolytic streptococcal vertebral osteomyelitis Accepted for publication 27 November I 9 9 I Sir, Vertebral osteomyelitis, which presents as a spondylo-discitis, is a rare but important cause of back pain. Staphylococci and mycobacteria are the c o m m o n e s t pathogens, 1 but isolation and identification of the responsible organism is essential if subsequent treatment is to be successful in eradicating the infection. We present a case which illustrates this point, as the organism isolated was not previously known to cause vertebral osteomyelitis. A 4o-year-old West African w o m a n was admitted for removal of a benign ovarian cyst. At this time she gave a history of back pain for the past 5 months which had been more severe during the previous Io days. T h e pain was exacerbated by m o v e m e n t but not relieved significantly by lying flat. T h e patient had also noticed general malaise, night sweats and a loss of one stone in weight, during the previous 2 months. On examination, a low-grade fever (37'5 °C) was present. T h e r e was marked tenderness over L3 to L5 vertebrae with sacrospinalis muscle spasm, and a virtually complete loss of spinal m o v e m e n t in all planes. X - r a y of the lumbar spine showed narrowing of the L 3 / 4 intervertebral joint space with adjacent bony destruction suggestive of an infective spondylo-discitis. Radioactive technetium and C T scans lent further support to this diagnosis. A full microbiological screen yielded no organism or source of infection and so a bone biopsy of the inferolateral aspect of L3 was performed. Culture of this yielded a pure growth of group G fl-haemolytic streptococcus ( G G S ) . Serological tests revealed normal titres of antistreptolysin O (ASO), a n t i - D N A a s e B (ADB), and group A-specific antihyaluronidase, but elevated groups C- and G-specific antihyaluronidase ( A H T C G ) (40 u n i t s / m l , normal range < Io units/ml). T h e G G S which we isolated tested positive for M protein capsular antigen and was identified as T type 7/320. T r e a t m e n t had been started with oral fucidin and Iv flucloxacillin but, following isolation of G G S , was changed to IV benzyl penicillin I2 million units/24 h ( M I C < 0"03 rag/l, M B C = 0"03 rag/l). T h e patient's condition subsequently improved, her back pain and pyrexia quickly resolved, and her E S R and C-Reactive protein (CRP) fell f r o m 74 m m / h and 40 mg/1 respectively to normal. T w o weeks later, she was c o m m e n c e d on oral antibiotics following an episode of penicillin allergy [(clindamycin 1.2 g / 2 4 h ( M I C < o'~2 mg/1, M B C = o.I2 mg/l)]. She was then mobilised while wearing a neofract plastic jacket. A further spinal X - r a y after antibiotic therapy for 3 months revealed bony healing with new bone formation. Unlike septic arthritis, osteomyelitis caused by G G S infection is extremely rare. T h e r e have been only two previous reports of it being caused by this organism 2' 3 and this is the first report of vertebral osteomyelitis caused by a G G S infection. We were unable to explain our patient's predisposition to serious infection by this organism: she was in good health, no p r i m a r y infective site was apparent, and there was no evidence of previous spinal pathology. Unusual virulence of the organism m a y
I I6
Letters to the Editor
therefore have been responsible, as suggested by the presence of M protein, a virulence factor rarely seen in G G S .
* Department of Rheumatology and t Public Health Laboratory, St George's Hospital Medical School, Blackshaw Road, London S W I 7 oQT, U.K.
J . H . Tobias* P . Y . C . Lee3; F . E . Bruckner*
References I. Norden CW. In: Mandell GL, Douglas RG, Bennett JE, Eds. Principles and practice of infectious disease. Edinburgh: Churchill Livingstone, 199o: 922-930. 2. Hess OM, Youssef S, Luthy R, Seigenthaler W. Rezidivierende Sepsis mit Streptokokken der Lancefield-Gruppe G. Schweiz Med Wochenschr 198o: IiO: 129-13o. 3- Vartian C, Lerner PI, Shales DM, Gopalkrishna KV. Infections due to Lancefield group G streptococci. Medicine 1985; 64: 75-88.
Staphylococcus lugdunensis e n d o c a r d i t i s Accepted for publication 19 December 1991 Sir, We wish to present another case of endocarditis caused by Staphylococcus lugdunensis, adding to those previously reported. 1-3 A 59-year-old carpenter presented to the Accident and E m e r g e n c y D e p a r t m e n t with a short history of chest pain. His past medical history included a mitral valve replacement for rheumatic heart disease 13 years before; since then he had remained well. Closer questioning revealed an influenza-like illness 3 months before admission since when he had noticed occasional night sweats and fever. H e had no focal central nervous system signs or s y m p t o m s but he described experiencing intermittent short episodes of strange thought processes during the previous few months. H e had undergone cautery for nose-bleeds I year before but had no other recent surgery and he had no skin lesions. Total dental clearance had been p e r f o r m e d prior to mitral valve replacement in 1977 . On initial examination he was afebrile, normotensive and had a collapsing pulse. H e had no cutaneous stigmata of endocarditis. Auscultation was consistent with a prosthetic mitral valve, and an aortic stenotic m u r m u r was heard. T h e r e was no evidence of incompetence in either valve. Investigation showed a slightly raised W B C count of 12"2 x lO9/1 (75 % neutrophils), haemoglobin concentration of I 1.3 g/dl, and E S R of 86 m m in the first hour. S e r u m biochemistry and a chest X - r a y were normal. Blood cultures yielded G r a m - p o s i t i v e cocci in clusters after 24 h in both bottles. An urgent echocardiogram showed mild aortic stenosis but no vegetations were seen. A working diagnosis of prosthetic valve endocarditis was made and treatment was started with flucloxacillin 2 g 4 hourly and gentamicin 80 m g 12 hourly after taking further blood for culture. All six blood culture bottles yielded staphylococci after 24 h. T h e organism was Staphaurex (Wellcome) and Staphylase (Oxoid) negative; it was also tube-coagulase and slide-coagulase negative using h u m a n plasma. Identification by A P I - s t a p h was Staphylococcus warneri. T h e organism was sensitive by disc-diffusion methods to methicillin, penicillin, fusidic acid, erythromycin, trimethoprim, gentarnicin, vancomycin, chloramphenicol and rifampicin. T h e minimal inhibitory and minimal bactericidal concentration of penicillin was found to be 0"03 mg/1. T h e flucloxacillin was therefore changed to benzyl penicillin 1.2 g 4 hourly. T h e organism was subsequently identified as S. lugdunensis by the delayed positive D N A s e , and positive ornithine decarboxylase test. 4
