Endocarditis caused by Finegoldia magna (formerly Peptostreptococcus magnus): diagnosis depends on the blood culture system used

Endocarditis caused by Finegoldia magna (formerly Peptostreptococcus magnus): diagnosis depends on the blood culture system used

Diagnostic Microbiology and Infectious Disease 47 (2003) 359 –360 www.elsevier.com/locate/diagmicrobio Case report Endocarditis caused by Finegoldi...

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Diagnostic Microbiology and Infectious Disease 47 (2003) 359 –360

www.elsevier.com/locate/diagmicrobio

Case report

Endocarditis caused by Finegoldia magna (formerly Peptostreptococcus magnus): diagnosis depends on the blood culture system used Stefano Bassettia,*, Gerd Laifera, Gisela Goyb, Ursula Fluckigera, Reno Freib a

Division of Infectious Diseases, University Hospital Basel, Petersgraben 4, CH – 4031 Basel, Switzerland b Bacteriology Laboratory, University Hospital Basel, Petersgraben 4, CH – 4031 Basel, Switzerland Received 14 February 2003; received in revised form 10 April 2003

Abstract We present a patient with prosthetic valve endocarditis caused by Finegoldia magna (formerly Peptostreptococcus magnus). Blood cultures in the BacT/ALERT and BACTEC 9240 system were negative. We therefore tested different blood culture systems: F. magna grew in the SEPTI-CHEK BHI-S and in the ISOLATOR, but not in the BacT/ALERT system. © 2003 Elsevier Inc. All rights reserved.

1. Introduction Finegoldia magna (formerly Peptostreptococcus magnus) is part of the normal human mucocutaneous flora and is the most common Gram-positive anaerobic coccus isolated from clinical specimens (Murdoch, 1998). It is a relevant human pathogen causing soft tissue infections, septic arthritis, osteomyelitis, and has been isolated in a variety of cases with polymicrobial infection (Bourgault et al., 1980; Murdoch, 1998; Murdoch & Shah, 1999). Bacteremia due to F. magna is rare but has been reported notably following obstetric or gynecologic infections (Topiel & Simon, 1986). Only one case of native-valve endocarditis (Cofsky & Seligman, 1985) and three cases of prosthetic valve endocarditis caused by F. magna have been previously described (Poue¨dras et al., 1992; van der Vorm et al., 2000). In the native-valve endocarditis case, F. magna was recovered from blood samples cultivated in thioglycollate medium (growth of F. magna in three of three bottles) and in trypticase soy broth (growth in one of three bottles). On the contrary, all three patients more recently described with

S. B. was supported by grants from the University of Basel (Sonderprogramm zur Fo¨rderung des akademischen Nachwuchses) and from the Department of Internal Medicine, University Hospital Basel (VFWAWF). Presented at the Joint Annual Meeting of the Swiss Society of Infectious Diseases and the Swiss Society for Microbiology, Basel, Switzerland, March 6-7, 2003; Abstract P 106. * Corresponding author. Tel. ⫹41-61-265-25-25; fax: ⫹41-61-265-3198. E-mail address: [email protected] (S. Bassetti). 0732-8893/03/$ – see front matter © 2003 Elsevier Inc. All rights reserved. doi:10.1016/S0732-8893(03)00091-9

prosthetic valve endocarditis had negative blood cultures (remarkably, the two patients reported by van der Vorm et al. had several negative blood culture sets processed with both the BACTEC 9240 and the BacT/ALERT system).We report an additional case of prosthetic valve endocarditis due to F. magna and present the results of an assessment of the capability of different blood culture systems to detect F. magna. A 68-year-old man underwent implantation of a prosthetic aortic valve (Edwards MIRA) and venous single graft coronary bypass in September 2001 because of combined aortic stenosis with regurgitation, and coronary artery disease. The patient was discharged 11 days after surgery. On postoperative Day 13 he was admitted to another hospital because of fever (38.5°C). On physical examination a systolic murmur was present over the aortic area. Neither a diastolic murmur nor signs of heart failure were found. The surgery wounds were unremarkable. C-reactive-protein level (CRP) (67 mg/L; normal value ⬍ 10 mg/L) and platelet count (472 ⫻ 109/L) were increased, while the leukocyte count was normal (5.4 ⫻ 109/L). Blood cultures were drawn (BACTEC Plus aerobic/F and anaerobic/F bottles) and incubated in the BACTEC 9240 system, and an empiric therapy with vancomycin and amikacin was immediately started. Blood cultures yielded no growth (incubation for 14 days). The antibiotic therapy with vancomycin and amikacin was stopped after 5 days, and the patient discharged. Two months later a severe paravalvular leakage of the prosthetic aortic valve was seen on echocardiography. CRP was slightly elevated (21 mg/L), the leukocyte and

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platelet count was normal. Seven blood culture sets incubated in the BacT/ALERT system (FA and FN bottles), used at our hospital, remained negative despite incubation for 4 weeks followed by terminal subcultures. The patient underwent surgery for valve refixation. Operative findings included slushy aortic tissue, suspicious of infection. Biopsies of this aortic tissue were taken for culture, and the patient was empirically started on vancomycin, amikacin and rifampin. On Day 7 after surgery, biopsies of the aortic wall yielded Finegoldia magna grown in thioglycollate medium and anaerobically on Brucella blood agar. Biochemical identification (Rapid ID ANA II System, Remel Inc., Lenexa, KS) was confirmed by 16S rRNA gene sequencing. The antibiotic therapy was changed to penicillin (5 millions units i.v. q 6 h) plus metronidazole (500 mg i.v. q 8 h). After determination of MICs for the isolated F. magna (penicillin 0.06 mg/L, metronidazole 0.50 mg/L, ceftriaxone 4.0 mg/L; Etest, AB Biodisk, Solna, Sweden), metronidazole was stopped on postoperative Day 9, and penicillin continued for 6 weeks in total. The patient was then discharged and treated for a further 2 weeks with ceftriaxone 2 g i.v. qd. Several blood cultures drawn from this patient with F. magna prosthetic valve endocarditis and incubated in the BacT/ALERT (FA and FN bottles) and BACTEC 9240 system (BACTEC Plus aerobic/F and anaerobic/F bottles) were negative. We therefore compared different blood culture systems regarding their ability to detect F. magna. The F. magna isolate from the patient presented above, and another clinical F. magna isolate were used. An aerobic (FA) and an anaerobic (FN) bottle of the BacT/ALERT system (Organon Teknika Corp., Durham, NC), an ISOLATOR 10 tube (Oxoid Ltd., Hampshire, England), all containing 10 mL sheep blood, and a BBL SEPTI-CHEK BHI-S bottle (Becton Dickinson, Sparks, MD) were seeded with a bacterial inoculum adjusted to reach a final concentration of 103 colony-forming units (CFU) F. magna per ml. The final concentration was verified by immediate subculture of the inoculated bottles on blood agar: the concentration ranged between 1.2 ⫻ 102 CFU/ml (in a SEPTI-CHEK BHI-S bottle) and 3.4 ⫻ 103 CFU/ml (in an ISOLATOR tube). Blood culture systems were processed according to manufacturer’s recommendations. After 4 weeks incubation, no growth was detected in the BacT/ALERT FA and FN bottles. Also subcultures taken from the culture-negative bottles and incubated anaerobically for 10 days on Brucella blood agar with hemin and vitamin K1 (Becton

Dickinson, Meylan, France) were negative. On the contrary, F. magna growth was visible after 2 days of incubation in the SEPTI-CHEK BHI-S bottles, and subcultures yielded F. magna. Also with the ISOLATOR system, F. magna grew on blood agar plates after 2 days of anaerobic incubation. We demonstrated that F. magna does not grow in both FA and FN bottles of the BacT/ALERT system. This result is consistent with the observation made by van der Vorm et al. (van der Vorm et al., 2000). These authors showed that the anticoagulant sodium polyanethol sulfonate (SPS) could not account for this finding, because the F. magna isolates tested in their study were resistant to SPS. They also observed that F. magna does not grow readily in the BACTEC 9240 system and recommended the use of additional media, such as conventional thioglycollate medium, for blood cultures from patients with a suspected infection which may be caused by F. magna. Our results show that F. magna is detected by other validated blood culture systems, such as the SEPTI-CHEK BHI-S and the ISOLATOR system. In conclusion, the relevance of F. magna as a cause of bacteremia and endocarditis may be underestimated, since these bacteria are not detected by automated blood culture systems such as the BacT/ALERT system. Additional blood culture systems (SEPTI-CHEK BHI-S, ISOLATOR) or media (thioglycollate medium) should be used in particular in case of suspected prosthetic valve endocarditis. References Bourgault, A.-M., Rosenblatt, J. E., & Fitzgerald, R. H. (1980). Peptococcus magnus: a significant human pathogen. Ann Intern Med 93, 244 – 248. Cofsky, R. D., & Seligman, S. J. (1985). Peptococcus magnus endocarditis. South Med J 78, 361–362. Murdoch, D. A. (1998). Gram-positive anaerobic cocci. Clin Microbiol Rev 11, 81–120. Murdoch, D. A., & Shah, H. N. (1999). Reclassification of Peptostreptococcus magnus (Prevot 1933) Holdeman and Moore 1972 as Finegoldia magna comb. nov. and Peptostreptococcus micros (Prevot 1933) Smith 1957 as Micromonas micros comb. nov. Anaerobe 5, 555–559. Poue¨ dras, P., Donnio, P. Y., Sire, J. M., & Avril, J. L. (1992). Prosthetic valve endocarditis and paravalvular abscess caused by Peptostreptococcus magnus. Clin Infect Dis 15, 185. Topiel, M. S., & Simon, G. L. (1986). Peptococcaceae bacteremia. Diagn Microbiol Infect Dis 4, 109 –117. van der Vorm, E. C., Dondorp, A. M., van Ketel, R. J., & Dankert, J. (2000). Apparent culture-negative prosthetic valve endocarditis caused by Peptostreptococcus magnus. J Clin Microbiol 38, 4640 – 4642.