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Case Report

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Endocarditis Caused by Stomatococcus mucilaginosus in an Immunocompetent Patient Christophe Rolland] and Frederic Wallet?, ‘Laboratoire de Biologie polyvalente, Centre hospitalier de Seclin, Seclin, France, ‘Laboratoire de Bacte’riologie, Hygidne, H6pital A. Calmette, CHRU de Lille, France

Introduction Stomatococcus mucilaginosus is a

gram-positive, coagulase-negative, encapsulated, non-spore-forming coc- cus considered part of the commensal flora of the oral cavity and the upper respiratory tract in humans (1). Although it appears to be a microorganism of low virulence, reported cases of S. mucilagi- nosus bacteremia have established the pathogenic potential of the organism, especially in immunocompromised patients or those with vascular foreign bodies (2,3). We present here the first case of spontaneously occurring endo- carditis due to S. mucilaginosus in an

Mailing Address: C. Rolland, M.D., Lubora- toire polyvalent du CH de Se&n, All&e des Mavronniers, 59471 Se&n, France. Tel.: 33-320.62.70.17. Fax: 33-320.62.75.03. E-mail: christophe.rolland@Och-seclinfr

immunocompetent patient with a healthy aortic valve.

Case report In September 2002, a 73-year-old

man was hospitalized in our medical unit because of general and prolonged asthenia, recent weight loss, and persis- tent biological inflammatory syndrome. The patient was treated for moderate hypercholesterolemia and was known to have controlled high blood pressure; he had suffered from a pulmonary embolism 4 years before. He had no history of valvular heart disease and had never had cardiac complaints. He had not received any antibiotics during the months before admission to the hos- pital, and he only reported oral dental caries without antibiotic protection 2 years before. Upon admission, physical examination of the patient revealed a temperature of 37.8”C and signs of car- diac insufficiency. Poor dentition and

oral hygiene were noted. No murmur was found on examination of the heart, nor were there any peripheral signs of endocarditis.

Laboratory tests revealed a white blood cell count of 9.8 x 109/1 with 76% polymorphonuclear leukocytes and 15% lymphocytes, an erythrocyte sedimen- tation rate of 112 mm/h, a C-reactive protein (CRP) of 93 mg/ml, and an inflammatory anemia (hemoglobin, 9 g/dl). An assessment of his immune system was performed: the level of immunoglobulins was normal (16.4 g/l), and the HIV serology was nega- tive. Renal function tests, urinalysis, and other routine laboratory tests were within normal limits. Three days after admission, his fever increased to 40°C. Before starting antibiotic treatment with ceftriaxone (2 g/day) and gentamicin (180 mg/day), four sets of blood cul- tures were obtained.

Clinical Microbiology Newsletter 26:5,2004 0 2004 Elsevier 0196.4399/00 (see frontmatter) 37

All blood cultures became positive in a BACTEC 9120 analyzer (Becton Dickinson Diagnostic System, Pont-de- Claix, France) with growth in aerobic and anaerobic bottles after 48 h of incu- bation. Direct examination of a Gram- stained smear revealed gram-positive cocci, 2 to 3 urn in diameter, arranged in small, irregular clusters and tetrads. The best bacterial growth on subculture was obtained on 5% blood agar and on chocolate agar after incubation at 37°C for 24 h under ambient atmospheric conditions; growth was poor on nutrient agar and only very small colonies grew on blood agar under anaerobic condi- tions. No growth was obtained on NaCl agar, indicating an intolerance of the organism to salt. Incubation with 7% COP did not significantly improve the culture growth. Colonies were small, mucoid, convex with regular borders, odorless, and slightly rubbery but were remarkable for strong adherence to the agar surface. The bacterium was non- hemolytic on 5% blood agar and non- pigmented. The catalase reaction was weakly positive, esculin hydrolysis was positive, coagulase reaction was nega- tive, and tests for oxidase and urease reactions were both negative. Biochem- ical identification of the isolate was per- formed by using an API ID 32 STAPH (bioMCrieux, Marcy l’Etoile, France) in accordance with the manufacturer’s instructions. The kit identified the iso- late as S. mucilaginosus (code number 063 135210; excellent identification, 99.9%).

Antibiotic susceptibility testing per- formed by the disk diffusion method (AB Bio-Rad, Marnes-la-Coquette, France) on Mueller-Hinton agar supple- mented with 5% horse blood revealed that the bacterium was susceptible to penicillin G, ampicillin, ceftriaxone, erythromycin, pristinamycin, vancomy- tin, and rifampin but was less suscepti- ble to trimethoprim-sulfamethoxazole, tetracycline, and aminoglycosides. MICs of P-lactam antibiotics were determined by the standard agar diffu- sion method by using Mueller-Hinton agar supplemented with 5% sheep blood and by Etest (AB Biodisk, Solna, Sweden). The MIC results were 0.032, 0.016, and 0.032 pg/ml for penicillin G, ampicillin, and ceftriaxone, respectively.

Because of the patient’s prolonged fever and the results of the blood cul-

ture, a transesophageal echocardiogra- phy was performed which revealed a pediculous vegetation (12 mm) on the aortic sigmoid valve, associated with a grade III aortic insufficiency. The ejec- tion fraction was decreased at 50%. These characteristics allowed a diagno- sis for this patient of an infective but poorly symptomatic endocarditis with bacteremia due to S. mucilaginosus. A further evaluation of the endocarditis included cerebral tomography and an EEG because of an episode of con- fusion during hospitalization, but the results were normal. Abdominal echog- raphy revealed the presence of three nodular liver lesions compatible with secondary abscesses. The antimicrobial treatment was modified, based upon the susceptibility of the organism, to include intravenous ceftriaxone (2 g/day) and intravenous, then oral, rifampin (600 mg x 2lday) for a period of 6 weeks. The patient became afebrile, and the CRP fell to 36 mg/l.

Discussion S. mucilaginosus is a gram-positive,

encapsulated, non-spore-forming coccus of the family Micrococcaceae, described as part of the normal flora of the mouth (1). We report here a case of infective endocarditis due to S, mucilaginosus occurring in a patient without preexist- ing valvular heart disease. The isolation of the bacterium in four consecutive sets of blood cultures before initiation of antibiotic treatment implicated it as the causative organism of the infective endocarditis. The patient’s poor dental hygiene and mucous lesions of the oral cavity are considered the most probable source of the bacteremia, with a secon- dary spread to the endocardium. Because phenotypic identification of S. mucila- ginosus can be difficult, in other cases the microorganism may have been mis- identified and confused with coagulase- negative staphylococci, micrococci, or streptococci. Therefore, its pathogenic potential may have been underestimated.

Our isolate was identified on the basis of its main distinctive character- istics, in accordance with the data of Coudron et al. (4) (strong adherence of the colonies to the agar surface, weakly positive catalase reactivity, and inability to grow on nutrient agar containing salt), and the identification was confirmed with a commercial identification

system. The antimicrobial susceptibility of our strain to penicillin G, ampicillin, ceftriaxone, rifampin, and vancomycin appears to be in agreement with the results reported in other communica- tions (2,3,5,6). However, relative resis- tance to penicillin G has been described and could have been due to recent anti- biotic exposure (7). The activity of aminoglycosides was more limited, as reported by other investigators (5?6).

S. mucilaginosus has previously been described as an opportunistic pathogen, but invasive disease caused by this organism appears to be described uncommonly in the literature. All pre- viously published studies have empha- sized that symptomatic bacteremia occurs in patients with underlying dis- eases, especially those with immuno- compromised states, such as severe neutropenia (2,3,8), or patients with vascular foreign bodies (2,9). In the same way, in six reported cases of endocarditis, patients had the following risk factors: history of intravenous drug abuse (4,7,10,11) and/or cardiac valve disease, e.g., presence of a prosthetic valve (4,7,10), mitral valve prolapse (12) or rheumatic carditis (9). Unlike these previous reports, we describe the first instance of spontaneous infective endocarditis due to S. mucilaginosus ocurring in a patient who did not pre- sent with classic risk factors. Finally, our observations suggest that the viru- lence of S. mucilaginosus may be under- estimated and that mucosal lesions of the oropharynx, as described in our patient, could represent a risk factor for endo- carditis due to this organism, even with- out any prior damage to cardiac valves.

References Bergan, T. and M. Kocur. 1982. Stomato- coccus mucilaginosus gen. nov., sp. nov., ep. rev., a member of the family Micrococcaceae. Int. J. Syst. Bacterial. 32:374-377. Ascher, D.P. et al. 1991. Infections due to Stomatococcus mucilaginosus: 10 cases and review. Rev. Infect. Dis. 13:1048-1052. McWhinney, PH. et al. 1992. Stomato- coccus mucilaginosus: an emerging pathogen in neutropenic patients. Clin. Infect. Dis. 14:641-646. Coudron, P.E. et al. 1987. Isolation of Stomatococcus mucilaginosus from drug user with endocardidtis. J. Clin. Microbial. 251359-1363.

38 0196.4399/00 (see frontmatter) 0 2004 Elsevier Clinical Microbiology Newsletter 26:5,2004

5. Kaufhold, A., R.R. Reinert, and W. Kern. 1992. Bacteriemia caused by Stomatococcus mucilaginosus: report of 7 cases and review of the literature. Infection 20213-220.

6. Von Eiff, C., M. Herrmann, and G. Peters 1995. Antimicrobial susceptibilities of Stomatococcus mucilaginosus and of Micrococcus spp. Antimicrob. Agents Chemother. 393268-270.

7. Pinsky, R.L., V. Piscitelli, and J.E. Patterson. 1989. Endocarditis caused by relatively penicillin-resist~t Stomato-

coccus mucilaginosus. J. Clin. Microbial. 27:215-216.

8. Zinner, S.H. 1999. Changing epidemi- ology of infections in patients with neutropenia and cancer: emphasis on gram-positive and resistant bacteria. Clin. Infect. Dis. 29:490-494.

9. Rubin, S.J., R.W. Lyons, andA.J. Murcia. 1978. Endocarditis associated with cardiac catheterization due to Micrococcus muci~aginosus incertae sedis. J. Clin, Microbial. 7:546-549.

10. Lazar, H.L., C. Sulis, and X. Hauser. 1988. Slomatococcus mucilaginosus prosthetic vaIve endocarditis. J. Thorac.

Cardiovasc. Surg. 95:940.

11. Relman, D.A., K. Ruoff, and M.J. Ferrano. 1987. Stomatococcus muci- laginosus in an intravenous drug abuser. J. Infect. Dis. 155:1080-1082.

12. Prag, J., E. Kjoller, and F. Espersen. 1985. S~omat5coccus mucilaginosus endocarditis. Eur. J. Clin. Microbial. 4:422-424.

Call for Submissions Case Reports

If your laboratory has isolated an uncommon organism, a common organism from an unusual patient, or an organism that presented a particular diagnostic challenge, why not share the information with your colleagues through the Clinical Microbiology Newsletter. The editors would like to receive interesting case reports from our readers for possible publication in the ~~s~ette~ Submitted case reports should contain (i) a brief clinical his- tory summ~izing the symptoms and course of the illness, (ii) a description of how the organism(s) was cultured and differentiated from closely associated organisms, and (iii) the results of sus- ceptibility tests for the isolate(s).

Letters Letters expressing opinions or

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accuracy of references, which should include complete publication informa- tion. References should be listed in the nu~eri~aZ order by which they occur throughout the text, numbered corzsec- utively, and cited in the text by these numbers. List the first author in a reference with last name followed by initials; list subsequent authors in the same reference with initials followed by last names. (Editors are always listed with initials followed by last names.) If there are more than three authors, include only the name of the first author followed by “et al.” Include abstracts, materials in press, personal communi- cations, and submitted material in the references section. Citations to personal communications must be accompanied by a letter from the person cited giving permission for the citation. Some typi- cal examples of references are listed below.

1. Petts, D.N. 1999. Evaluation of the

2.

3.

4.

6.

5.

Oxoid Dryspot streptococcal grouping kit for grouping beta-hemolytic strepto- cocci. J. Clin. Microbial. 37:255-257. Reich, K.A. and G.K. Schoolnik. 1996. ~alovib~n, secreted from the light organ symbiont Vibriofischeri, is a member of a new class of ADP-ribosyltransferases. J. Bacterial. 178209-215. Walls, J.J., K.M. Asanovich, and J.S. Dumler. 1998. Comparison of Ehrlichia equi and human granulocytic ehrlichiosis (HGE) agent strains for IFA serodiagnosis of HGE. C-208, p. 165. In Abstracts of the 98th General Meeting of the American Society for Microbiology 1998. ASM Press, Washington, DC. McGough, D.A. et al. 1994. Fungi and fungal infections, p. 1169-I 196. In R.D. McClatchey (ed.), Clinical laboratory medicine. Williams & Wilkins, Baltimore, MD. Bennish, M.L. 1994. Cholera: patho- physiology, clinical features, and treat- ment, p. 229-255. In I.K. Wachsmuth, PA. Blake, and 0. Olsvik (ed.), Vibrio cho~erae and cholera, molecular to global perspectives. ASM Press, Washington, D.C. Jones, T. Personal communication.

Address for Submissions Send the original typescript (double spaced, four copies), diskette, and any photographs and figures to:

Paul A. Granato, Ph.D. Dept. of Microbiology &

Immunology WH 2204 SUNY Upstate Medical University 750 E. Adams St. Syracuse, NY 13210 USA

Clinical Microbiology Newsletter 26:5,2004 0 2004 Elsevier 0196-4399/00 (see frDntmatter) 39