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Native Valve Endocarditis due to Streptococcus vestibularis and Streptococcus oralis
Journal of Infection (2002) 45: 39±41 doi:10.1053/jinf.2002.1004, available online at http://www.idealibrary.com on
Native Valve Endocarditis due to Streptococcus vestibularis and Streptococcus oralis Elif Doyuk², Oliver J. Ormerod and Ian C. J. W. Bowler* Department of Microbiology, Department of Cardiology, The John Radcliffe Hospital, Oxford Radcliffe Hospitals NHS Trust, Oxford OX3 9DU, UK Viridans streptococci are the commonest cause of native valve infective endocarditis (IE). The taxonomy of this group is evolving allowing new disease associations to be made. Streptococcus vestibularis is a recently described member of the viridans group, first isolated from the vestibular mucosa of the human oral cavity. It has rarely been associated with human disease. Streptococcus oralis, another member of the viridans group resident in the human oral cavity is a well known cause of IE and bacteraemia in neutropenic patients. We report the first case of native mitral valve endocarditis # 2002 The British Infection Society due to S. vestibularis in a patient with co-existing S. oralis endocarditis.
Introduction During the last two decades, the clinical spectrum of infective endocarditis (IE) has changed in several ways. The disease occurs in an older age group, more patients now have prosthetic valves, fewer patients have underlying rheumatic valve disease, new aetiological agents have been described, and diagnostic and surgical techniques have improved [1]. Viridans streptococci still cause most cases of IE, most often in patients with underlying valvular heart disease [2]. They form a significant part of the normal flora of the human oral cavity and are associated with several other disease conditions including dental caries, septicaemia in neutropenic patients, as well as purulent infections of oral and other sites [3]. Many members of the viridans family are known to be able to cause IE, including Streptococcus mitis, Streptococcus sangius, Streptococcus mutans, Streptococcus salivarius, Streptococcus gordoni, and Streptococcus oralis [4]. It is likely that other members of the viridans group are also able to cause IE but poorly defined taxonomy and difficulties in speciation prevent this
* Please address all correspondence to: I. C. J. W. Bowler, Department of Microbiology, Level 7, The John Radcliffe Hospital, Oxford Radcliffe Hospitals NHS Trust, Oxford OX3 9DU, UK. y Current address: Department of Clinical Bacteriology and Infectious Diseases, Osmangazi University Medical Faculty, 26040 Eskipehir, Turkey. 0163-4453/02/$35.00
association being made. Streptococcus vestibularis, a member of viridans group first isolated from the vestibular mucosa of the human oral cavity was not known to cause human disease until two cases of prosthetic valve IE were reported recently [5]. We describe a case of native valve IE due to this organism in a patient co-infected with S. oralis.
Case Report A 73-year-old female was admitted to hospital with a 4-month history of general malaise, weight loss, night sweats, breathless, and anorexia. Prior to this, she had been in good health. Her GP had noted `a leaky valve' 4 years previously but an echocardiogram had not been done. She had no other risk factors for endocarditis: she denied any symptoms referable to the teeth, gastrointestinal or urogenital tract, recent dental or abdominal surgery, or intravenous drug abuse. She was allergic to penicillin. She was taking atenolol 50 mg for mild hypertension. On physical examination she had a temperature of 37.2 C but no stigmata of endocarditis. A 4/6 pansystholic murmur was heard at the apex. Chest, abdominal and neuromuscular examination were normal except for reduced ankle reflexes. Chest radiography showed left ventricular dilatation. The full blood count showed anaemia (Hb:10.6 g/dL normocytic normochromic). Serum vitamin B12, folate, ferritin, and total iron binding capacity were normal but serum iron # 2002 The British Infection Society
40
E. Doyuk et al.
was low (5.0 mmol/l NR 11-30). Serum creatinine, electrolytes, liver and thyroid function tests were normal. The CRP was 55 mg/l, and ESR 38 mm/h. Blood cultures (6 sets, 12 bottles) grew a mixture of a non-haemolytic streptococcus (12 bottles) and an alpha haemolytic streptococcus (8 bottles). The nonhaemolytic organism, with MICs to penicillin and ceftriaxone of 0.023 mg/l and 0.016 mg/l respectively failed to identify (API Strep profile 5040010), but was confirmed as S. vestibularis by the Streptococcal Reference Laboratory at the Central Public Health Laboratory, Colindale. The alpha haemolytic organism identified as S. oralis (confirmed by the Reference Laboratory) with MICs to penicillin and ceftriaxone of 0.012 and 0.023 mg/l respectively. Both organisms were sensitive to vancomycin by comparative disc testing. Transthoracic echocardiography showed a dilated left ventricle with moderate impairment of left ventricular systolic function. The severely regurgitant mitral valve was prolapsed with a vegetation attached to the posterior leaflet. There were ruptured chordae. The left atrium was mildly dilated. No other complication of infective endocarditis was detected. Intravenous ceftriaxone 2 g daily and gentamicin 1 mg/kg tds were initiated. After two weeks of antibiotic therapy she remained ill with fluctuating fever and elevated CRP. Blood cultured 11 days into therapy was sterile. Physical examination was unchanged. A transoesophageal echocardiogram showed a perforation in the posterior mitral valve leaflet. It was assumed the fever was a reaction to the cephalosporin and her treatment was changed to vancomycin 500 mg bd which was continued for a further 4 weeks with an excellent clinical response. The patient was left with severe mitral regurgitation with left ventricular dilatation on echocardiography. She underwent uneventful mitral valve replacement 4 months after completing antibiotic therapy.
Discussion Clinical experience over past decade suggests that the incidence of polymicrobial IE has increased [1]. Patients with this condition have a mean age of 36.5 years and the male-to-female ratio is nearly 2 : 1. Many clinical studies suggest that polymicrobial IE is more common in intravenous drug users (IVDU). Our patient denied IVDU. Polymicrobial endocarditis has been reported to involve between 2 and 12 organisms in a variety of combinations. The most common were S. aureus and -heamolytic streptococci, Haemophilus species and
viridans streptococci, Pseudomonas species, and Candida species [1,6]. A review of the literature (Medline, using key words: IE and S. vestibularis and S. oralis, polymicrobial) failed to identify any case of IE due to S. vestibularis and S. oralis. Oral streptococci are among the most common causes of IE. In a recent survey of IE the most common species were S. sangius (31.9%), S. oralis (29.8%), and S. gordoni (12.7%) [7,8]. However, recent taxonomic studies of these microorganisms have resulted in the recognition of several new species as well as the redefinition of older ones. S. oralis is one of the newly described species within the viridans streptococci [9,10]. S. oralis produce extracellular dextran from sucrose and there is evidence to suggest that dextran promotes adhesion to thrombus in the rabbit endocarditis model. Little is known about potential pathogenic features of S. oralis that might be relevant to endocarditis, although the species has a significant glycosidase potential, including N-acetyl-neurominidase activity, and many plasma glycoproteins carry N-acetylneurominic acid groups. It may be that S. oralis grows more successfully in plasma or thrombotic vegetations than other species of oral streptococci [3,9]. Resistance in S. oralis in mediated by an altered penicillin binding protein 2B gene which is thought to have spread to or from S. pneumoniae, as the 16S rRNA sequences exhibit more than 99% sequence homology [7]. S. oralis is therefore a significant human pathogen which may have decreased susceptibility to penicillin. S. vestibularis is a member of the viridans streptococci first isolated from the vestibular mucosa of human oral cavity and described as a new species in 1988 [3]. S. vestibularis induces low level caries in gnotobiotic rats and is able to adhere to buccal epithelial cells [11]. The organism has been reported as the cause of two cases of prosthetic valve endocarditis [5]. Ours is the first description of native valve disease caused by S. vestibularis. The source of the organisms causing IE in this lady remain obscure. We assume the two organisms involved arose from the same unknown source because they share the same colonising niches in the mouth and gut. Her presentation and clinical course were typical of IE due to viridans streptococci despite the presence of two infecting organisms. As the taxonomy of the viridans group becomes better defined it is likely that novel disease associations will be made with the newly recognised species. In summary, we report a case of polymicrobial IE caused by S. vestibularis and S. oralis. To our knowledge this is first published report of native valve endocarditis due to S. vestibularis.
Native Valve Endocarditis
References 1 Baddour LM, Meyer J, Henry B. Polymicrobial infective endocarditis in the 1980s. Rev Infect Dis 1991; 13: 363±370. 2 Bayer AS, Scheld WM. Endocarditis and intravascular infections. In: Mandell GL, Bennett JE, Dolin R (eds). Principles and Practice of Infectious Diseases. New York, Churchill Livingstone 2000: pp. 857± 902. 3 Beighton D, Hardie JM, Whiley RA. A scheme for the identification of viridans streptococci isolated from cases of infective endocarditis. J Med Microbiol 1991; 35: 367±372. 4 Johnson CC, Tunkel AR. Viridans Streptococci and groups C and G streptococci. In: Mandell GL, Bennett JE, Dolin R (eds). Principles and Practice of Infectious Diseases. New York, Churchill Livingstone 2000: pp. 2167±2182. 5 Partridge SM. Prosthetic valve endocarditis due to Streptococcus vestibularis. J Infect 2000; 41: 284±285. 6 Sande MA, Lee BL, Mills J, Chambers III HF. Endocarditis in intravenous drug users. In: Kaye D (ed.) Infective Endocarditis New York, Raven Press, 1992: pp. 345±360.
41
7 Burnie JP, Brooks W, Donohoe M, Hodgetts S, AL-Ghamdi A, Matthews RC. Defining antibody targets in Streptococcus oralis infection. Infect Immun 1996; 64(5): 1600±1608. 8 Kennedy HF, Morrison D, Kaufmann ME et al. Origins of Staphylococcus epidermidis and Streptococcus oralis causing bacteremia in a bone marrow transplant patient. J Med Microbiol 2000; 49(4): 367±370. 9 Douglas CWI, Heath J, Hampton KK, Preston FE. Identity of viridans streptococci isolated from cases of infective endocarditis. J Med Microbiol 1993; 39: 179±182. 10 Jacobs JA, Stappers JL, Sels JP. Endocarditis due to Streptococcus oralis in a patient with a colon tumour. Eur J Clin Microbiol Infect Dis 1995; 14(6): 557±558. 11 Willcox MDP, Knox KW, Green RM, Drucker DB. An examination of strains of bacterium Streptococcus vestibularis for relative cariogenicity in gnotobiotic rats and adhesion in vitro. Arch Oral Biol 1991; 36(5): 327±333.
Native Valve Endocarditis due to Streptococcus vestibularis and Streptococcus oralis Elif Doyuk², Oliver J. Ormerod and Ian C. J. W. Bowler* Department of Microbiology, Department of Cardiology, The John Radcliffe Hospital, Oxford Radcliffe Hospitals NHS Trust, Oxford OX3 9DU, UK Viridans streptococci are the commonest cause of native valve infective endocarditis (IE). The taxonomy of this group is evolving allowing new disease associations to be made. Streptococcus vestibularis is a recently described member of the viridans group, first isolated from the vestibular mucosa of the human oral cavity. It has rarely been associated with human disease. Streptococcus oralis, another member of the viridans group resident in the human oral cavity is a well known cause of IE and bacteraemia in neutropenic patients. We report the first case of native mitral valve endocarditis # 2002 The British Infection Society due to S. vestibularis in a patient with co-existing S. oralis endocarditis.
Introduction During the last two decades, the clinical spectrum of infective endocarditis (IE) has changed in several ways. The disease occurs in an older age group, more patients now have prosthetic valves, fewer patients have underlying rheumatic valve disease, new aetiological agents have been described, and diagnostic and surgical techniques have improved [1]. Viridans streptococci still cause most cases of IE, most often in patients with underlying valvular heart disease [2]. They form a significant part of the normal flora of the human oral cavity and are associated with several other disease conditions including dental caries, septicaemia in neutropenic patients, as well as purulent infections of oral and other sites [3]. Many members of the viridans family are known to be able to cause IE, including Streptococcus mitis, Streptococcus sangius, Streptococcus mutans, Streptococcus salivarius, Streptococcus gordoni, and Streptococcus oralis [4]. It is likely that other members of the viridans group are also able to cause IE but poorly defined taxonomy and difficulties in speciation prevent this
* Please address all correspondence to: I. C. J. W. Bowler, Department of Microbiology, Level 7, The John Radcliffe Hospital, Oxford Radcliffe Hospitals NHS Trust, Oxford OX3 9DU, UK. y Current address: Department of Clinical Bacteriology and Infectious Diseases, Osmangazi University Medical Faculty, 26040 Eskipehir, Turkey. 0163-4453/02/$35.00
association being made. Streptococcus vestibularis, a member of viridans group first isolated from the vestibular mucosa of the human oral cavity was not known to cause human disease until two cases of prosthetic valve IE were reported recently [5]. We describe a case of native valve IE due to this organism in a patient co-infected with S. oralis.
Case Report A 73-year-old female was admitted to hospital with a 4-month history of general malaise, weight loss, night sweats, breathless, and anorexia. Prior to this, she had been in good health. Her GP had noted `a leaky valve' 4 years previously but an echocardiogram had not been done. She had no other risk factors for endocarditis: she denied any symptoms referable to the teeth, gastrointestinal or urogenital tract, recent dental or abdominal surgery, or intravenous drug abuse. She was allergic to penicillin. She was taking atenolol 50 mg for mild hypertension. On physical examination she had a temperature of 37.2 C but no stigmata of endocarditis. A 4/6 pansystholic murmur was heard at the apex. Chest, abdominal and neuromuscular examination were normal except for reduced ankle reflexes. Chest radiography showed left ventricular dilatation. The full blood count showed anaemia (Hb:10.6 g/dL normocytic normochromic). Serum vitamin B12, folate, ferritin, and total iron binding capacity were normal but serum iron # 2002 The British Infection Society
40
E. Doyuk et al.
was low (5.0 mmol/l NR 11-30). Serum creatinine, electrolytes, liver and thyroid function tests were normal. The CRP was 55 mg/l, and ESR 38 mm/h. Blood cultures (6 sets, 12 bottles) grew a mixture of a non-haemolytic streptococcus (12 bottles) and an alpha haemolytic streptococcus (8 bottles). The nonhaemolytic organism, with MICs to penicillin and ceftriaxone of 0.023 mg/l and 0.016 mg/l respectively failed to identify (API Strep profile 5040010), but was confirmed as S. vestibularis by the Streptococcal Reference Laboratory at the Central Public Health Laboratory, Colindale. The alpha haemolytic organism identified as S. oralis (confirmed by the Reference Laboratory) with MICs to penicillin and ceftriaxone of 0.012 and 0.023 mg/l respectively. Both organisms were sensitive to vancomycin by comparative disc testing. Transthoracic echocardiography showed a dilated left ventricle with moderate impairment of left ventricular systolic function. The severely regurgitant mitral valve was prolapsed with a vegetation attached to the posterior leaflet. There were ruptured chordae. The left atrium was mildly dilated. No other complication of infective endocarditis was detected. Intravenous ceftriaxone 2 g daily and gentamicin 1 mg/kg tds were initiated. After two weeks of antibiotic therapy she remained ill with fluctuating fever and elevated CRP. Blood cultured 11 days into therapy was sterile. Physical examination was unchanged. A transoesophageal echocardiogram showed a perforation in the posterior mitral valve leaflet. It was assumed the fever was a reaction to the cephalosporin and her treatment was changed to vancomycin 500 mg bd which was continued for a further 4 weeks with an excellent clinical response. The patient was left with severe mitral regurgitation with left ventricular dilatation on echocardiography. She underwent uneventful mitral valve replacement 4 months after completing antibiotic therapy.
Discussion Clinical experience over past decade suggests that the incidence of polymicrobial IE has increased [1]. Patients with this condition have a mean age of 36.5 years and the male-to-female ratio is nearly 2 : 1. Many clinical studies suggest that polymicrobial IE is more common in intravenous drug users (IVDU). Our patient denied IVDU. Polymicrobial endocarditis has been reported to involve between 2 and 12 organisms in a variety of combinations. The most common were S. aureus and -heamolytic streptococci, Haemophilus species and
viridans streptococci, Pseudomonas species, and Candida species [1,6]. A review of the literature (Medline, using key words: IE and S. vestibularis and S. oralis, polymicrobial) failed to identify any case of IE due to S. vestibularis and S. oralis. Oral streptococci are among the most common causes of IE. In a recent survey of IE the most common species were S. sangius (31.9%), S. oralis (29.8%), and S. gordoni (12.7%) [7,8]. However, recent taxonomic studies of these microorganisms have resulted in the recognition of several new species as well as the redefinition of older ones. S. oralis is one of the newly described species within the viridans streptococci [9,10]. S. oralis produce extracellular dextran from sucrose and there is evidence to suggest that dextran promotes adhesion to thrombus in the rabbit endocarditis model. Little is known about potential pathogenic features of S. oralis that might be relevant to endocarditis, although the species has a significant glycosidase potential, including N-acetyl-neurominidase activity, and many plasma glycoproteins carry N-acetylneurominic acid groups. It may be that S. oralis grows more successfully in plasma or thrombotic vegetations than other species of oral streptococci [3,9]. Resistance in S. oralis in mediated by an altered penicillin binding protein 2B gene which is thought to have spread to or from S. pneumoniae, as the 16S rRNA sequences exhibit more than 99% sequence homology [7]. S. oralis is therefore a significant human pathogen which may have decreased susceptibility to penicillin. S. vestibularis is a member of the viridans streptococci first isolated from the vestibular mucosa of human oral cavity and described as a new species in 1988 [3]. S. vestibularis induces low level caries in gnotobiotic rats and is able to adhere to buccal epithelial cells [11]. The organism has been reported as the cause of two cases of prosthetic valve endocarditis [5]. Ours is the first description of native valve disease caused by S. vestibularis. The source of the organisms causing IE in this lady remain obscure. We assume the two organisms involved arose from the same unknown source because they share the same colonising niches in the mouth and gut. Her presentation and clinical course were typical of IE due to viridans streptococci despite the presence of two infecting organisms. As the taxonomy of the viridans group becomes better defined it is likely that novel disease associations will be made with the newly recognised species. In summary, we report a case of polymicrobial IE caused by S. vestibularis and S. oralis. To our knowledge this is first published report of native valve endocarditis due to S. vestibularis.
Native Valve Endocarditis
References 1 Baddour LM, Meyer J, Henry B. Polymicrobial infective endocarditis in the 1980s. Rev Infect Dis 1991; 13: 363±370. 2 Bayer AS, Scheld WM. Endocarditis and intravascular infections. In: Mandell GL, Bennett JE, Dolin R (eds). Principles and Practice of Infectious Diseases. New York, Churchill Livingstone 2000: pp. 857± 902. 3 Beighton D, Hardie JM, Whiley RA. A scheme for the identification of viridans streptococci isolated from cases of infective endocarditis. J Med Microbiol 1991; 35: 367±372. 4 Johnson CC, Tunkel AR. Viridans Streptococci and groups C and G streptococci. In: Mandell GL, Bennett JE, Dolin R (eds). Principles and Practice of Infectious Diseases. New York, Churchill Livingstone 2000: pp. 2167±2182. 5 Partridge SM. Prosthetic valve endocarditis due to Streptococcus vestibularis. J Infect 2000; 41: 284±285. 6 Sande MA, Lee BL, Mills J, Chambers III HF. Endocarditis in intravenous drug users. In: Kaye D (ed.) Infective Endocarditis New York, Raven Press, 1992: pp. 345±360.
41
7 Burnie JP, Brooks W, Donohoe M, Hodgetts S, AL-Ghamdi A, Matthews RC. Defining antibody targets in Streptococcus oralis infection. Infect Immun 1996; 64(5): 1600±1608. 8 Kennedy HF, Morrison D, Kaufmann ME et al. Origins of Staphylococcus epidermidis and Streptococcus oralis causing bacteremia in a bone marrow transplant patient. J Med Microbiol 2000; 49(4): 367±370. 9 Douglas CWI, Heath J, Hampton KK, Preston FE. Identity of viridans streptococci isolated from cases of infective endocarditis. J Med Microbiol 1993; 39: 179±182. 10 Jacobs JA, Stappers JL, Sels JP. Endocarditis due to Streptococcus oralis in a patient with a colon tumour. Eur J Clin Microbiol Infect Dis 1995; 14(6): 557±558. 11 Willcox MDP, Knox KW, Green RM, Drucker DB. An examination of strains of bacterium Streptococcus vestibularis for relative cariogenicity in gnotobiotic rats and adhesion in vitro. Arch Oral Biol 1991; 36(5): 327±333.