This study determined the antimicrobial susceptibilities of 186 clinical isolates of Nocardia spp. isolated in Gipuzkoa, northern Spain, between 1998 and 2009. Most isolates were recovered from respiratory samples, Nocardia nova, N. farcinica, N. cyriacigeorgica, N. abscessus, and N. carnea being the species most frequently isolated. Linezolid and amikacin were the only two antimicrobials to which all isolates were susceptible. The majority of N. flavorosea, N. carnea, and N. farcinica isolates were trimethoprim-sulfamethoxazole resistant.

Scedosporium prolificans infection was analyzed in 18 patients from whom the fungus was isolated during the period 1990-1999. Of these 18 patients, 12 had some predisposing factor and either unconfirmed infection or colonization, and 6 patients had confirmed disseminated infection: 4 patients with leukemia died, 1 patient with breast cancer who underwent autologous bone marrow transplantation survived, and 1 patient with advanced acquired immunodeficiency syndrome died, although the fungal infection did not seem to affect his clinical symptoms.

Streptococcus pneumoniae serotype 3, isolated from a penicillin-allergic patient and initially susceptible to fluoroquinolones, macrolides, lincosamides, quinupristin-dalfopristin, and telithromycin, became resistant to all these drugs during treatment. Mutations in the parC and gyrA and in the 23S rRNA and the ribosomal protein L22 genes were detected in the resistant isolates.

The aim of this study was to determine the prevalence and characteristics of non-fluoroquinolone (FQ)-susceptible Streptococcus pyogenes isolates and to study their mechanisms of resistance. We performed a prospective prevalence study with 468 isolates collected from 2005 to 2007 and a retrospective study that was based on the examination of existing data collected from 1999 to 2008. The retrospective study included data for isolates with high-level resistance (HR) to ciprofloxacin (MIC > 32 g/ml) (HR isolates) and isolates with the same emm types as those reported in the literature with low-level resistance (LR) to ciprofloxacin (MICs, 2 to 8 g/ml) (LR isolates, n ‫؍‬ 205). Genetic characterization of the isolates was performed by means of emm typing and multilocus sequence typing. The prevalence of LR ranged from 1.9% in 2005 to 30.8% in 2007. This increase was mainly due to the circulation of an emm6 subtype (emm6.4) that represented 77.1% of the LR isolates in 2007. Notably, another emm6 subtype, also detected in 2007 (emm6.37), showed coresistance to 14-and 15-membered macrolides mediated by the mefA gene. Only three HR isolates were detected (isolates emm68.1/ST247/T3,13,B3264, emm77/ST399/T28, and emm28/ST52/T28), and all were identified in the retrospective study. Overall, the 673 isolates represented 25 emm types. All LR isolates were clustered into two emm types: emm6 (six emm6 subtypes) and emm75. All the 156 emm6 isolates had LR, harbored the Ser79/Ala mutation in the parC gene product, and had the same sequence type (ST), ST382. Most (21/33) of the emm75 isolates had LR, showed the Ser79/Phe plus Asp91/Asn double mutation in the parC gene product, and were ST150. The Asp91/Asn mutation by itself did not confer resistance to FQs.

Patients with chronic obstructive pulmonary disease are generally subjected to multiple regimens of antimicrobial treatment. The development of high-level levofloxacin resistance (i.e., a minimum inhibitory concentration 18 mg/mL) in 8 patients whose previous pneumococcal isolates showed susceptibility is described. Molecular methods were used to characterize the strains and to study the sequential changes in fluoroquinolone targets.The prevalence of fluoroquinolone-resistant Streptococcus pneumoniae remains low in most parts of the world, but it seems clear that, as the use of fluoroquinolones increases, the possibility that resistant isolates will appear will also increase. The tetrameric enzymes DNA gyrase (encoded by the gyrA and gyrB genes) and DNA topoisomerase IV (encoded by the parC and parE genes) are intracellular fluoroquinolone targets. Most levofloxacin-resistant clinical isolates possess single mutations in a discrete region of the genes encoding the ParC and GyrA subunits of topoisomerase IV and DNA gyrase, termed the quinolone resistance-determining region (QRDR). Although there are many reports concerning the prevalence of fluoroquinolone resistance in S. pneumoniae, few reports describe the emergence of this resistance during treatment.S. pneumoniae is a frequent cause of acute bacterial exacerbation of chronic obstructive pulmonary disease (COPD). Patients with COPD are subjected to frequent courses of antimicrobial treatment because of acute bacterial exacerbations. Because previous antimicrobial use has been directly associated with the development of antimicrobial resistance in S. pneumoniae [1], it is not surprising that drug-resistant pneumococci are more prevalent in patients with COPD than they are in the general adult population [2]. This finding prompted us to conduct a surveillance study to analyze the changes in the antimicrobial susceptibility patterns of pneumococcal strains causing repetitive episodes of infection, focusing on fluoroquinolone resistance. The present study describes the development of levofloxacin resistance during treatment, the sequential genetic changes observed in the DNA gyrase and topoisomerase IV of successive isolates, and the persistence of colonization with the same strain over time in patients with COPD receiving fluoroquinolone therapy.From January 1999 through November 2004, we searched for patients who had at least 2 S. pneumoniae isolates that were obtained during episodes of acute exacerbation of COPD. Only patients whose isolates were of the same serotype and genotype and for whom the first isolates were levofloxacin susceptible and the subsequent isolates were levofloxacin resistant were included in the study. The design of the study was prospective and descriptive, because we did not influence treatment or the number of samples requested from the patients included in the study. Some patients had more samples than others, depending on the number of exacerbations of their respiratory process and on the criteria of the pulmonologist or general pract...