Background: Streptococcus agalactiae or group B Streptococcus (GBS) is an important pathogen in neonates and nonpregnant individuals. Epidemiological studies of GBS resistance to fluoroquinolones (FQs) in Latin America are scarce. This study aimed to determine the local prevalence of FQ resistance in the frame of a national, prospective multicenter study of invasive GBS infections and to investigate mechanisms of resistance, serotype distribution, and clonal relationships among resistant isolates. Methods: From July 2014 to July 2015, 162 invasive GBS isolates were collected from 86 health care centers in 32 Argentinean cities. All isolates were screened for FQ nonsusceptibility using a five-disc scheme: levofloxacin (LVX), ciprofloxacin, norfloxacin (NOR), ofloxacin, and pefloxacin (PF). LVX minimal inhibitory concentration (MIC) was determined by the agar dilution method. Sequencing of internal regions of gyrA and parC genes was performed. Capsular typing and genetic characterization of nonsusceptible isolates were assessed by latex agglutination, pulsed-field gel electrophoresis (PFGE), and multilocus sequence typing. Results: Twenty-four of one hundred sixty-two GBS isolates exhibited no inhibition zones to all tested FQs with an MIC range of 16-32 mg/L for LVX, and one isolate with MIC = 1 mg/L showed no inhibition zones around NOR and PF discs. In all resistant isolates, point mutations were detected in both genes. Serotype Ib was prevalent (88%). One PFGE type accounted for 84% of the FQ-resistant isolates and belonged to serotype Ib, sequence type 10. Conclusions: The prevalence of FQ resistance was 14.8% likely to be associated with dissemination of an ST10/serotype Ib clone. The unexpected high rate of resistance emphasizes the relevance for continuous surveillance of GBS epidemiology and antibiotic susceptibility.

Introduction: Streptococcus agalactiae (group B streptococcus, GBS) is a recognized urinary pathogen both in males and pregnant or non-pregnant women. Data regarding GBS serotypes recovered from urinary tract infections (UTIs) are scarce. The aim of this study was to describe the clinical and microbiological characteristics of UTIs caused by GBS in adult patients in Argentina. Methodology: A prospective multicenter study involving 86 centers was conducted in Argentina between July 1st, 2014 and June 30th, 2015. Antimicrobial susceptibility and serotype distribution of GBS isolated from the urinary tract of adult patients were determined. Susceptibility tests were performed by the disk diffusion and/or agar dilution methods. Epidemiological and clinical characteristics of the patients were considered to identify associated comorbilities. Results: Seven hundred and one GBS were sent to the reference laboratory in the above mentioned period, however, only 211 fulfilled our selection criteria (demographic data availability, underlying diseases reported, colony counts greater than 105 CFU/mL, single organism isolated from the urine sample). No penicillin-resistant GBS was found but fluoroquinolone resistance was high (12.8%), especially among GBS isolated from men and non-pregnant women. UTIs due to GBS were associated to underlying diseases in men and non-pregnant women, particularly diabetes mellitus. Most of the isolates showed serotypes Ia and III. Conclusions: GBS are still susceptible to penicillin but fluoroquinolone resistance is a growing concern, at least in Argentina. There are underlying conditions that could be associated to urinary infections caused by GBS.

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The aim of this report is to describe a rare case of necrotizing pneumonia due to group B Streptococcus serotype III in a relatively young male adult (48 years old) suffering from diabetes. The organism was isolated from his pleural fluid and was only resistant to tetracycline. The patient first received ceftazidime (2g/8h i.v.)+clindamycin (300mg/8h) for 18 days and then he was discharged home and orally treated with amoxicillin clavulanic acid (1g/12h) for 23 days with an uneventful evolution. As in the cases of invasive infection by Streptococcus pyogenes, clindamycin could prevent streptococcal toxic shock syndrome.