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-lactam Resistance, Serotype Distribution, and Genotypes of Meningitis-causing Streptococcus pneumoniae, Rio de Janeiro, Brazil

Barroso, David E. MD, PhD*; Godoy, Daniel BSc; Castiñeiras, Terezinha M. P. P. MD; Tulenko, Mary M. BSc§; Rebelo, Maria C. MSc; Harrison, Lee H. MD§

Pediatric Infectious Disease Journal:
doi: 10.1097/INF.0b013e31822f8a92
Original Studies

Background: Here, we report a laboratory-based study of Streptococcus pneumoniae recovered from patients with meningitis in Rio de Janeiro State, Brazil.

Methods: The aim of this study was to determine the evolution of β-lactam resistance, antimicrobial susceptibility pattern, serotypes, and genetic diversity of S. pneumoniae, isolated from meningitis patients between 2000 and 2008.

Results: A total of 264 S. pneumoniae recovered from patients between 2000 and 2008 were included. Susceptibility testing (E-test) of S. pneumoniae showed resistance to penicillin, ceftriaxone, oxacillin, cotrimoxazole, tetracycline, ofloxacin, erythromycin, chloramphenicol, and rifampicin. Penicillin resistance (PEN-R, minimal inhibitory concentration [MIC] ≥0.12 μg/mL) increased from 8% of isolates in 2000–2002, to 12% in 2003–2005, and to 20% in 2006–2008. Ceftriaxone resistance (MIC ≥1.0 μg/mL) was detected among some PEN-R isolates (13%) from 2004 onward. Within the PEN-R isolates, serotypes that are included in 10-valent pneumococcal conjugate vaccine predominated (90%), and resistance was detected mostly in isolates of serotypes 14 (61%), 23F (16%), 6B (10%), and 19F (3%). Multilocus sequence typing showed that 52% of the PEN-R isolates, and 89% of those with MICs ≥0.5 μg/mL, were sequence type (ST)-156 or single-locus variants of this ST (ST-557 or ST-4388); all of these isolates were serotype 14 and were assigned to the Spain9V-3 clone.

Conclusions: β-lactam resistance increased recently among cerebrospinal fluid isolates and was mainly due to the surge of the ST-4388, a previously undescribed gki single-locus variants of ST-156. Regional surveillance is shown to be essential to provide optimal antimicrobial therapy, monitor highly successful clones, and formulate adequate vaccination strategy.

Author Information

From the *Laboratory of Biochemical Systematics, Oswaldo Cruz Institute, FIOCRUZ, Rio de Janeiro, Brazil; †Department of Infectious Disease Epidemiology, Imperial College School of Medicine, London, United Kingdom; ‡Department of Preventive Medicine, Federal University School of Medicine, Rio de Janeiro, Brazil; §Infectious Diseases Epidemiology Research Unit, University of Pittsburgh School of Medicine and Graduate School of Public Health, Pittsburgh, PA; and ¶Central Laboratory Noel Nutels, State Department of Health, Rio de Janeiro, Brazil.

Accepted for publication July 25, 2011.

Presented in part at the 7th International Symposium on Pneumococci and Pneumococcal Diseases 2010, Tel Aviv, Israel.

Supported in part by a Fogarty International Center Global Infectious Diseases Research Training Program grant, National Institutes of Health, to the University of Pittsburgh (D43TW006592). L.H.H. receives research support and lecture fees from Sanofi Pasteur; lecture fees from Novartis Vaccines; and has served as a consultant to GlaxoSmithKline, Novartis Vaccines, Sanofi Pasteur, and Pfizer.

The authors have no other funding or conflicts of interest to disclose.

Address for correspondence: David E. Barroso, MD, PhD, Laboratory of Biochemical Systematics, Oswaldo Cruz Institute, FIOCRUZ, Av Brasil 4365, Rio de Janeiro, Brazil 21040-900. E-mail:

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© 2012 Lippincott Williams & Wilkins, Inc.