S. Tubiana). y Bruno Hoen and Xavier Duval contributed equally. z The members of COMBAT study group are listed at the Acknowledgments section.
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Clinical Microbiology and Infectionj o u r n a l h o m e p a g e : w w w . c l i n i c a l m i c r o b i o l o g y a n d i n f e c t i o n . c o m
Streptococcus pneumoniae is an important cause of acute otitis media (AOM). The aim of this study was to evaluate trends in antibiotic resistance and circulating serotypes of pneumococci isolated from middle ear fluid of French children with AOM during the period 2001-2011, before and after the introduction of the PCV-7 (2003) and PCV-13 (2010) vaccines. Between 2001 and 2011 the French pneumococcal surveillance network analysed the antibiotic susceptibility of 6683 S. pneumoniae isolated from children with AOM, of which 1569 were serotyped. We observed a significant overall increase in antibiotic susceptibility. Respective resistance (I+R) rates in 2001 and 2011 were 76.9% and 57.3% for penicillin, 43.0% and 29.8% for amoxicillin, and 28.6% and 13.0% for cefotaxime. We also found a marked reduction in vaccine serotypes after PCV-7 implementation, from 63.0% in 2001 to 13.2% in 2011, while the incidence of the additional six serotypes included in PCV-13 increased during the same period, with a particularly high proportion of 19A isolates. The proportion of some non-PCV-13 serotypes also increased between 2001 and 2011, especially 15A and 23A. Before PCV-7 implementation, most (70.8%) penicillin non-susceptible pneumococci belonged to PCV-7 serotypes, whereas in 2011, 56.8% of penicillin non-susceptible pneumococci belonged to serotype 19A. Between 2001 and 2011, antibiotic resistance among pneumococci responsible for AOM in France fell markedly, and PCV-7 serotypes were replaced by non-PCV-7 serotypes, especially 19A. We are continuing to assess the impact of PCV-13, introduced in France in 2010, on pneumococcal serotype circulation and antibiotic resistance.
We report the first case of Enterococcus gallinarum endocarditis developing on normal native heart valves. Using phenotypic and molecular methods, a precise identification of this naturally vancomycin-resistant species allowed an optimal antibiotic therapy and the patient's recovery.
CASE REPORTA 62-year-old Vietnamese man was admitted to our hospital in January 2001 because of presumptive endocarditis. He had been living in France since 1952 and worked as a veterinarian. He had a background history of cholecystectomy, gastrectomy for bleeding gastric ulcer in 1965, brucellosis treated with tetracycline in 1967, and polycythemia. The patient did not report any hospitalization stay of more than 1 day (for therapeutic phlebotomy) since 1965. He had no previously damaged cardiac valves. He did not receive any antimicrobial treatment during the months before hospitalization, but in the first days of January, he was treated with roxithromycin (150 mg twice a day [b.i.d.]) and corticosteroids for a putative diagnosis of pneumonia. On 14 January 2001, he was admitted to a local hospital because of heart failure and persistent fever. The combination amoxicillin-clavulanic acid (1 g three times a day [t.i.d.]) was added to the regimen. On 17 January, the transthoracic echocardiography demonstrated the presence of mitral and aortic vegetations. Amoxicillin-clavulanic acid and roxithromycin were switched to cefotaxime (2 g t.i.d.) and gentamicin (100 mg b.i.d.) for presumably infective endocarditis. On the third day of the cefotaxime-gentamicin regimen, the patient required mechanical ventilation because of heart failure and was admitted to our hospital. Transoesophageal echocardiography demonstrated voluminous aortic vegetation with valvular destruction, prolapsus, and aortic regurgitation. There were also two mitral vegetations with mitral regurgitation. Because an Enterococcus species was isolated from two blood cultures, cefotaxime was switched to vancomycin (1 g b.i.d.). The patient underwent replacement of the mitral and aortic valves on 23 January.Based on the disk diffusion method (27), the strain was first reported as susceptible to ampicillin, erythromycin, vancomycin, teicoplanin, trimethoprim-sulfamethoxazole, and rifampin, but resistant to lincomycin. No high-level resistance to gentamicin was detected by a screening test on agar plates containing 500 g of gentamicin per ml. The bacteriological analysis of surgically removed valves obtained 18 h after the beginning of vancomycin therapy yielded growth of an enterococcal strain. Blood culture and valve isolates were identified as Enterococcus gallinarum by physiological and molecular methods (12) and had identical antibiotic susceptibility patterns. Strains grew on a 6-g/ml vancomycin agar plate, on bile esculin agar, were nonhemolytic on sheep blood agar, and were positive for Streptococcus group D antigen by latex agglutination (Slidex Strepto kit; bioMerieux, Marcy l'Etoile, France). They were identified as E. gallinarum by the API Rapid ID 32 Strep system (...
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