Invasive isolates of staphylococci and enterococci were collected from 15 tertiary care centres in five Colombian cities from 2001 to 2002. A total of 597 isolates were available for analysis. Identification was confirmed by both automated methods and multiplex PCR assays in a central laboratory. Staphylococcus aureus and coagulase-negative staphylococci (CoNS) corresponded to 49.6% and 29.6% of isolates, respectively, and 20.8% were identified as enterococci. MICs of ampicillin, ciprofloxacin, chloramphenicol, erythromycin, gentamicin, linezolid, oxacillin, rifampicin, teicoplanin, tetracycline, trimethoprim/sulfamethoxazole (SXT) and vancomycin were determined using an agar dilution method as appropriate. Screening for vancomycin-resistant S. aureus was also carried out on brain-heart infusion agar plates supplemented with vancomycin. The presence of mecA and van genes was investigated in methicillin-resistant staphylococci and glycopeptide-resistant enterococci (GRE), respectively. All staphylococci were susceptible to vancomycin, teicoplanin and linezolid. No VISA isolates were found. In S. aureus and CoNS, the lowest rates of resistance were found for SXT (7.4%) and chloramphenicol (10.7%), respectively. Resistance to oxacillin in S. aureus and CoNS was 52% and 73%, respectively. The mecA gene was detected in 97.5% of methicillin-resistant S. aureus isolates. In enterococci, resistance to glycopeptides was 9.7%: vanA (58.3%) and vanB (41.7%) genes were found. Pulsed-field gel electrophoresis indicated that the GRE isolates were closely related. Rates of resistance to ampicillin, ciprofloxacin, chloramphenicol, rifampicin and high levels of gentamicin and streptomycin were 9.7%, 27.4%, 8.9%, 43%, 17% and 28.2%, respectively. All enterococci were susceptible to linezolid.

The period following heart failure hospitalization (HFH) is a vulnerable time with high rates of death or recurrent HFH.OBJECTIVE To evaluate clinical characteristics, outcomes, and treatment response to vericiguat according to prespecified index event subgroups and time from index HFH in the Vericiguat Global Study in Subjects With Heart Failure With Reduced Ejection Fraction (VICTORIA) trial. DESIGN, SETTING, AND PARTICIPANTSAnalysis of an international, randomized, placebo-controlled trial. All VICTORIA patients had recent (<6 months) worsening HF (ejection fraction <45%). Index event subgroups were less than 3 months after HFH (n = 3378), 3 to 6 months after HFH (n = 871), and those requiring outpatient intravenous diuretic therapy only for worsening HF (without HFH) in the previous 3 months (n = 801). Data were analyzed between May 2, 2020, and May 9, 2020.INTERVENTION Vericiguat titrated to 10 mg daily vs placebo. MAIN OUTCOMES AND MEASURESThe primary outcome was time to a composite of HFH or cardiovascular death; secondary outcomes were time to HFH, cardiovascular death, a composite of all-cause mortality or HFH, all-cause death, and total HFH. RESULTS Among 5050 patients in the VICTORIA trial, mean age was 67 years, 24% were women, 64% were White, 22% were Asian, and 5% were Black. Baseline characteristics were balanced between treatment arms within each subgroup. Over a median follow-up of 10.8 months, the primary event rates were 40.9, 29.6, and 23.4 events per 100 patient-years in the HFH at less than 3 months, HFH 3 to 6 months, and outpatient worsening subgroups, respectively. Compared with the outpatient worsening subgroup, the multivariable-adjusted relative risk of the primary outcome was higher in HFH less than 3 months (adjusted hazard ratio, 1.48; 95% CI, 1.27-1.73), with a time-dependent gradient of risk demonstrating that patients closest to their index HFH had the highest risk. Vericiguat was associated with reduced risk of the primary outcome overall and in all subgroups, without evidence of treatment heterogeneity. Similar results were evident for all-cause death and HFH. Addtionally, a continuous association between time from HFH and vericiguat treatment showed a trend toward greater benefit with longer duration since HFH. Safety events (symptomatic hypotension and syncope) were infrequent in all subgroups, with no difference between treatment arms.CONCLUSIONS AND RELEVANCE Among patients with worsening chronic HF, those in closest proximity to their index HFH had the highest risk of cardiovascular death or HFH, irrespective of age or clinical risk factors. The benefit of vericiguat did not differ significantly across the spectrum of risk in worsening HF.

Increasing resistance of Streptococcus pneumoniae to macrolides represents a challenge for clinicians. New ketolides have an enhanced activity against macrolide-resistant strains. Four hundred and seventy-four strains of S. pneumoniae were collected during the 2000-2001 season in Quebec through a surveillance network. Macrolide resistance was 20.2%, and significantly higher in non-invasive strains versus invasive ones (22.4% versus 14.8%), and in children (30%) versus adults (14.8%). For susceptible strains, MIC(90)s of ABT-773 and telithromycin were 0.008 and 0.015 mg/L. Among the 96 macrolide-resistant strains, 56 (58%) were erm(B), 35 (37%) carried the mef(A) gene, four were carrying both genes and one none. ABT-773 and telithromycin were very active against all these resistant strains irrespective of the resistance mechanism, with MIC(90)s of 0.25 and 0.5 mg/L, respectively.

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Chaining in enterococci revisited: correlation between chain length and gelatinase phenotype, and gelE and fsrB genes among clinical isolates of Enterococcus faecalis Enterococci, like streptococci, are typically described as showing chaining in Gramstains of clinical samples. The degree of chaining seems to vary amongst enterococcal clinical isolates; however, there are no recent studies validating chaining by enterococci since they were classified out of the genus Streptococcus nor any studies of the mechanism of cellular chain length. A marked increase in chaining seen in an Enterococcus faecalis OG1RF mutant (TX5128) has been explained by the lack of the GelE protease (gelatinase) suggesting the possibility that chaining among clinical isolates (one-third of which are gelatinase non-producers) might be associated with the absence of GelE (Singh et al., 2005; Waters et al., 2003). GelE is an enterococcal zinc-metalloprotease (Bleiweis & Zimmerman, 1964) that is capable of degrading a broad spectrum of substrates, including insoluble collagen fragments (Makinen & Makinen, 1994) and polymerized fibrin (Waters et al., 2003). Synthesis of GelE in E. faecalis is regulated by the fsr locus (Qin et al., 2001), a quorum-sensing system that positively regulates expression of gelE. The fsr locus and gelatinase production have been shown to contribute to the virulence of E. faecalis OG1RF in several models, including mouse peritonitis, Caenorhabditis elegans and biofilm formation (