María Nieves Larrosa

National survey of Escherichia coli causing extraintestinal infections reveals the spread of drug-resistant clonal groups O25b:H4-B2-ST131, O15:H1-D-ST393 and CGA-D-ST69 with high virulence gene content in Spain

OBJECTIVES To evaluate the current prevalence of the three clonal groups O25b:H4-B2-ST131, O15:H1-D-ST393 and CGA-D-ST69 (where ST stands for sequence type) among Escherichia coli isolates causing extraintestinal infections in Spain and to characterize their virulence background, 500 consecutive non-duplicate E. coli isolates causing extraintestinal infections were analysed. METHODS The 500 isolates were collected during February 2009 from five hospitals in different Spanish regions. Phylogenetic groups, STs, serotypes, virulence genes, PFGE profiles, antimicrobial resistance and extended-spectrum β-lactamase (ESBL) enzymes were determined. RESULTS The three clonal groups accounted for 19% of the 500 isolates. Furthermore, they accounted for 37% of the isolates exhibiting trimethoprim/sulfamethoxazole plus ciprofloxacin resistance, 34% of aminoglycoside-resistant isolates and 30% of multidrug-resistant isolates. Clonal group ST131 was the most prevalent, and accounted for 12% of isolates overall and for 23% of multidrug-resistant isolates. The ST131 isolates exhibited a significantly higher virulence score (mean of virulence genes 8.1) compared with the ST393 (6.0) and ST69 (5.4) isolates. The prevalence of ESBL-producing isolates was 7%. Six (10%) of the 59 ST131 isolates were positive for CTX-M-15 and one (6%) of the 16 ST393 isolates was positive for CTX-M-14, whereas none of the 22 ST69 isolates produced ESBL enzymes. CONCLUSIONS The three clonal groups investigated accounted for 30% of the multidrug-resistant isolates, which gives evidence of an important clonal component in the emergence of resistances among extraintestinal pathogenic E. coli. Notably, a single high virulence clonal group (O25b:H4-B2-ST131) causes approximately 1 in every 10 extraintestinal infections in Spain, representing an important public health threat. A new variant of the ST131 clonal group, which is non-ESBL-producing but trimethoprim/sulfamethoxazole resistant and with high virulence content, is reported.

Impact of the emergence of non-vaccine pneumococcal serotypes on the clinical presentation and outcome of adults with invasive pneumococcal pneumonia

The introduction of the 7-valent pneumococcal conjugate vaccine in children has led to a change in the pattern of pneumococcal serotypes causing pneumococcal disease. The aim of this study was to compare the clinical presentation and outcome of invasive pneumococcal pneumonia (IPP) in adults between the pre and post-vaccine era. We have conducted an observational study of all adults hospitalized with IPP, from 1996 to 2001 (pre-vaccine period), and from 2005 to 2009 (post-vaccine period). Incidence, serotype distribution and clinical data were compared between both periods. A total of 653 episodes of IPP were diagnosed. The overall incidence of IPP increased from 14.2 to 17.9 cases per 100 000 population-year (p 0.003). In the post-vaccine period IPP caused by vaccine serotypes decreased (-36%; 95% CI, -52 to -15) while IPP caused by non-vaccine serotypes increased (71%; 95% CI, 41-106). IPP in the post-vaccine period was associated with higher rates of septic shock (19.1% vs. 31.1%, p <0.001). Among patients aged 50-65 years there was a trend towards a greater proportion of case-fatalities (11.6-23.5%, p 0.087). Independent risk factors for septic shock were IPP caused by serotype 3 (OR 2.38; 95% CI, 1.16-4.87) and serotype 19A (OR 6.47, 95% CI, 1.55-27). Serotype 1 was associated with a lower risk of death (OR 0.1; 95% CI, 0.01-0.78). In conclusion, the incidence of IPP in the post-vaccine period has increased in our setting, it is caused mainly by non-vaccine serotypes and it is associated with higher rates of septic shock.

Risk factors for respiratory failure in pneumococcal pneumonia. The importance of pneumococcal serotypes

Pneumococcal serotypes are one of the main determinants of pneumococcal disease severity; however, data about their implication in respiratory failure are scarce. We conducted an observational study of adults hospitalised with invasive pneumococcal pneumonia to describe the host- and pathogen-related factors associated with respiratory failure. Of 1258 adults with invasive pneumococcal disease, 615 (48.9%) had respiratory failure at presentation. Patients with respiratory failure were older (62.1 years versus 55.4 years, p<0.001) and had a greater proportion of comorbid conditions. They also had a greater proportion of septic shock (41.7% versus 6.1%, p<0.001), required admission to the intensive care unit more often (38.4% versus 4.2%, p<0.001) and had a higher mortality (25.5% versus 3.5%, p<0.001). After adjustment, independent risk factors for respiratory failure were: age >50 years (OR 1.63, 95% CI 1.15–2.3), chronic lung disease (OR 1.54, 95% CI 1.1–2.15), chronic heart disease (OR 1.49, 95% CI 1.01–2.22) and infection caused by serotypes 3 (OR 1.97, 95% CI 1.23–3.16), 19A (OR 2.34, 95% CI 1.14–4.42) and 19F (OR 3.55, 95% CI 1.22–10.28). In conclusion, respiratory failure is a frequent complication of pneumococcal pneumonia and causes high morbidity and mortality. Pneumococcal serotypes 3, 19A and 19F are the main risk factors for this complication. Respiratory failure in invasive pneumonia is determined by older age, comorbidities and serotypes 3, 19A and 19F http://ow.ly/qHN6D

Detection of three stable genetic clones of CTX-M-15-producing Klebsiella pneumoniae in the Barcelona metropolitan area, Spain

1. Jacoby GA, Gacharna N, Black TA et al. Temporal appearance of plasmid-mediated quinolone resistance genes. Antimicrob Agents Chemother 2009; 53: 1665–6. 2. Robicsek A, Jacoby GA, Hooper DC. The worldwide emergence of plasmid-mediated quinolone resistance. Lancet Infect Dis 2006; 6: 629–40. 3. Torpdahl M, Hammerum AM, Zachariasen C et al. Detection of qnr genes in Salmonella isolated from humans in Denmark. J Antimicrob Chemother 2009; 63: 406–8. 4. Fang H, Huang H, Shi Y et al. Prevalence of qnr determinants among extended-spectrum b-lactamase-positive Enterobacteriaceae clinical isolates in southern Stockholm, Sweden. Int J Antimicrob Agents 2009; 34: 268–70. 5. Pallecchi L, Riccobono E, Mantella A et al. High prevalence of qnr genes in commensal enterobacteria from healthy children in Peru and Bolivia. Antimicrob Agents Chemother 2009; 53: 2632–5. 6. Osterblad M, Hakanen A, Manninen R et al. A between-species comparison of antimicrobial resistance in enterobacteria in fecal flora. Antimicrob Agents Chemother 2000; 44: 1479–84. 7. Osterblad M, Pensala O, Peterzens M et al. Antimicrobial susceptibility of Enterobacteriaceae isolated from vegetables. J Antimicrob Chemother 1999; 43: 503–9. 8. Robicsek A, Strahilevitz J, Sahm DF et al. qnr prevalence in ceftazidime-resistant Enterobacteriaceae isolates from the United States. Antimicrob Agents Chemother 2006; 50: 2872–4. 9. qnr Numbering and Sequence. http://www.lahey.org/qnrStudies (27 July 2009, date last accessed.) 10. Kehrenberg C, Friedrichs S, De Jong A et al. Novel variant of the qnrB gene, qnrB12, in Citrobacter werkmanii. Antimicrob Agents Chemother 2008; 52: 1206–7.

Potential Use of Fosfomycin-Tromethamine for Treatment of Recurrent Campylobacter Species Enteritis

ABSTRACT We report 2 cases of recurrent Campylobacter coli enteritis caused by macrolide- and fluoroquinolone-resistant strains in 2 patients with hypogammaglobulinemia, successfully treated with a prolonged course of fosfomycin-tromethamine with no side effects. Fosfomycin-tromethamine may be a feasible alternative therapy for recurrent enteritis caused by Campylobacter species resistant to first-line drugs.

Early oral switch to linezolid for low-risk patients with Staphylococcus aureus bloodstream infections: a propensity-matched cohort study

Background Oral switch to linezolid is a promising alternative to standard parenteral therapy (SPT) in Staphylococcus aureus bacteremia (SAB). Methods We conducted a prospective cohort study of all adult cases of SAB between 2013 and 2017 in a Spanish University Hospital. We compared the efficacy, safety, and length of hospital stay of patients receiving SPT and those where SPT was switched to oral linezolid from day 3 to 9 of treatment until completion. We excluded complicated SAB and osteoarticular infections. A k-nearest neighbor algorithm was used for propensity score matching with a 2:1 ratio. Results After propensity score matching we included 45 patients of the linezolid group and 90 patients of the SPT group. Leading SAB-sources were catheter-related (49.6%), unknown origin (20.0%), and skin and soft tissue (17.0%). Patients in the linezolid group had less chronic renal disease (4.4% vs 22.2%). We observed no difference in 90-day relapse between the linezolid group and the SPT group (2.2% vs 4.4% respectively; P=0.87). No statistically significant difference was observed in 30-day all-cause mortality between the linezolid group and the SPT group (2.2% vs 13.3%; P=0.08). The median length of hospital stay after onset was 8 days in the linezolid group and 19 days in the SPT group (P<0.01). No drug-related events leading to discontinuation were noted in the linezolid group. Conclusions Treatment of SAB in selected low-risk patients with an oral switch to linezolid from day 3 to 9 of treatment until completion yielded similar clinical outcomes as SPT, allowing earlier discharge from the hospital.

In Vivo Reversion to the Wild-Type beta-Lactam Resistance Phenotype Mediated by a Plasmid Carrying ampR and qnrA1 in Enterobacter cloacae

ABSTRACT Resistance to β-lactams and quinolones in two isogenic Enterobacter cloacae isolates was studied. One was susceptible to cefoxitin and amoxicillin-clavulanate. The other one showed its natural β-lactam resistance pattern. Both isolates had a nonfunctional AmpR regulator. However, within the second one, the presence of a plasmid carrying ampR and qnrA1 allowed reversion to the wild-type β-lactam resistance phenotype and decreased susceptibility to fluoroquinolones.