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Journal of Clinical Microbiology, February 2009, p. 503-504, Vol. 47, No. 2
0095-1137/09/$08.00+0 doi:10.1128/JCM.00707-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
| CASE REPORT |

Service de Microbiologie,1 Service de Cardiologie, AP-HP, Hôpital Européen Georges Pompidou, Paris, France,2 Université Paris Descartes, Faculté de Médecine, Paris, France,3 UMR S 872—Equipe 12, Laboratoire de Recherche Moléculaire sur les Antibiotiques, Centre de Recherche Biomédical des Cordeliers, Université Paris Descartes, and Université Pierre et Marie Curie, Paris, France4
Received 14 April 2008/ Returned for modification 16 October 2008/ Accepted 19 November 2008
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In 2007, a physical examination yielded no signs of IE. Sarcoidosis was quiescent under prednisolone treatment at 6 mg/day. The white blood cell count was 14.2 x 109 cells/liter (90% polymorphonuclear), and the C-reactive protein (CRP) level was 35.6 mg/liter (N, <10 mg/liter). Two out of three aerobic blood cultures, started at a 24-h interval in the absence of antibiotic treatment, were positive after 4 days, yielding a gram-negative bacillus with the same cultural characteristics, i.e., improvement of bacterial growth in medium supplemented with horse blood and the same antibiotic susceptibility and resistance profile as described above. TEE revealed a newly apparent moderate aortic regurgitation. The initial treatment was cefotaxime and gentamicin for 14 days. After 4 days, the patient became afebrile and her white blood cell count and CRP level dropped to 10.1 x 109 cells/liter and 12 mg/liter, respectively. A thoracoabdominal computed tomography scan and vertebral column magnetic resonance imaging were normal. 16S rRNA gene amplification and sequencing led to the identification of Pseudomonas stutzeri. Antibiotic therapy was changed to oral ciprofloxacin and doxycycline since the patient refused prolonged intravenous therapy. Cardiac surgery was not performed because of the high risk of death. After 16 months of treatment, the patient is in stable cardiac condition and the CRP level is below 15 mg/liter. The serum trough concentrations of ciprofloxacin and doxycycline were 1.1 and 2.4 mg/liter, respectively. Repeated blood cultures have been negative.
The isolate from 2003 was recovered and identified as P. stutzeri by the method described above. Analysis of the genomic fingerprints of both isolates, after random amplification by PCR (6), showed that they were highly related (Fig. 1).
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FIG. 1. DNA fragment banding pattern as visualized after acrylamide gel electrophoresis of PCR products obtained by random amplification of polymorphic DNA with three primers (A, B, and C [6]) and silver staining. Lanes: 1 and 2, control clinical strains of P. stutzeri; 3, P. stutzeri isolated in 2007; 4, P. stutzeri isolated in 2003; L, DNA ladder (the molecular sizes on the right are in base pairs).
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Recurrent IE due to the same microorganism is rare (ca. 3% of IE cases; 1, 4) and can be caused by relapse or reinfection, usually distinguished by a delay of recurrence of less or more than 6 months, respectively (4). However, a relapse after 9 months has been described (1). We report here a unique delay of 4 years for relapsing endocarditis proven by genomic strain analysis. Reinfection with the same P. stutzeri strain would have been highly improbable considering the genetic variability of this species (6) and in the absence of plausible exposure given the patient's lifestyle. We hypothesize that the moderate activity of cefotaxime against members of the family Pseudomonadaceae, reflected by the clinical improvement in 2003, possibly in conjunction with the particularly low virulence of the strain living in a dormant state, may explain the delayed relapse despite the presence of the mechanical valve. A prolonged follow-up is necessary to ensure the definite cure of this EI.
Published ahead of print on 3 December 2008. ![]()
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