Multiple system organ response induced by hyperoxia in a clinically relevant animal model of sepsis.

Oxygen therapy is currently used as a supportive treatment in septic patients to improve tissue oxygenation. However, oxygen can exert deleterious effects on the inflammatory response triggered by infection. We postulated that the use of high oxygen concentrations may be partially responsible for the worsening of sepsis-induced multiple system organ dysfunction in an experimental clinically relevant model of sepsis. We used Sprague-Dawley rats. Sepsis was induced by cecal ligation and puncture. Sham-septic controls (n = 16) and septic animals (n = 32) were randomly assigned to four groups and placed in a sealed Plexiglas cage continuously flushed for 24 h with medical air (group 1), 40% oxygen (group 2), 60% oxygen (group 3), or 100% oxygen (group 4). We examined the effects of these oxygen concentrations on the spread of infection in blood, urine, peritoneal fluid, bronchoalveolar lavage, and meninges; serum levels of inflammatory biomarkers and reactive oxygen species production; and hematological parameters in all experimental groups. In cecal ligation and puncture animals, the use of higher oxygen concentrations was associated with a greater number of infected biological samples (P < 0.0001), higher serum levels of interleukin-6 (P < 0.0001), interleukin-10 (P = 0.033), and tumor necrosis factor-α (P = 0.034), a marked decrease in platelet counts (P < 0.001), and a marked elevation of reactive oxygen species serum levels (P = 0.0006) after 24 h of oxygen exposure. Oxygen therapy greatly influences the progression and clinical manifestation of multiple system organ dysfunction in experimental sepsis. If these results are extrapolated to humans, they suggest that oxygen therapy should be carefully managed in septic patients to minimize its deleterious effects.

Antimicrobial resistance and molecular epidemiology of Panton-Valentine leukocidin-positive community-associated methicillin-resistant Staphylococcus aureus from Gran Canaria (Canary Islands, Spain).

Among 3967 Staphylococcus aureus recovered from a Gran Canaria hospital (2003-2010), 28 strains were Panton-Valentine leukocidin-positive community-associated methicillin-resistant Staphylococcus aureus and were included in this study. Most isolates (89.3%) caused skin and skin-structure infections. Isolates belonging to clonal complex (CC)8 (ST8 and ST931; USA300) prevailed (82.1%). Among these, 5 (21.7%) were resistant to at least 3 antimicrobial classes.

Fenotipos y mecanismos de resistencia a macrólidos y lincosamidas en aislados de Streptococcus agalactiae con significación clínica en un período de ocho años (2002-2010) / Phenotypes and mechanisms of resistance to macrolides and lincosamides in Streptococcus agalactiae isolates with clinical significance in an eight-year period (2002-2010)

Introducción. Streptococcus agalactiae es el agente etiológico más prevalente de enfermedad invasiva en el recién nacido (sepsis, neumonía y meningitis), además de tener un papel importante en fiebres puerperales, infecciones del tracto urinario e infecciones postquirúrgicas. El objetivo de nuestro trabajo fue conocer la evolución de la resistencia a macrólidos y lincosamidas. Métodos. El fenotipo de resistencia se estableció mediante aproximación de discos (eritromicina-clindamicina): M (bomba de expulsión) o MLSB (metilasa). Los mecanismos genéticos de resistencia se establecieron mediante PCR para los genes ermB, ermA, ermTR, mefA/E. El tipado molecular se realizó por macrorrestricción de ADN cromosómico y electroforesis en campo pulsado. Resultados. Durante 8 años se aislaron 300 cepas de S. agalactiae, de las que 78 (26%) cepas fueron resistentes a eritromicina y 70 (23%) cepas fueron resistentes a lincosamidas. El 21% presentaron fenotipo MLSB constitutivo (todas portadoras del gen ermB, excepto una) y CMI90 para eritromicina ≥ 256 mg/L. El 2.3% presentaron fenotipo MLSB inducible (todas portadoras del gen ermTR) con CMI90 = 6 mg/L y el 2,7% fenotipo M (todas portadoras de los genes mefA/E) con CMI90 = 6 mg/L. El estudio de identidad clonal reveló dos clones predominantes que incluían el 56,6% de las cepas estudiadas. El 90,5% de las cepas del clon A portaban el gen ermB. Conclusiones. El estado de resistencia en nuestra área geográfica se encuentra en el límite superior del detectado en el resto del país, pero no se ha observado incremento a lo largo del periodo estudiado(AU)

Introduction. Streptococcus agalactiae is the most prevalent agent of invasive disease in the newborn (sepsis, pneumonia, and meningitis), as well as an important cause of puerperal fever, urinary tract infection and surgical site infection. The aim of our study was to know the evolution of macrolide and lincosamide resistance in this microorganism. Methods. Resistance phenotypes were established according to the erythromycin-clindamycin induction test: M (efflux pump) or MLSB (methylase). Genetic mechanisms were detected by PCR for the following genes: ermB, ermA, ermTR, and mefA/E. Molecular typing was based on chromosomal DNA macrorestriction and detection of fragments using pulsed-field gel electrophoresis. Results. During 8 years, 300 isolates of S. agalactiae were recovered. Seventy-eight (26%) were resistant to macrolides, and seventy (23%) were resistant to lincosamides. Constitutive MLSB was observed in 21% of the isolates (all but one carrying the ermB gene), with a erythromycin MIC90 ≥ 256 mg/L. Inducible MLSB was observed in 2.3% of the isolates (all carrying the ermTR gene), with a MIC90 of 6 mg/L. M phenotype was observed in 2.7% of the isolates (all carrying the mefA/E gene), with a MIC90 of 6 mg/L. Molecular typing revealed the presence of two major clones (A and B) comprising 56.6% of the isolates. Most of the isolates (90.5%) belonging to clon A carried the ermB gene. Conclusions. Macrolide resistance in our area is similar to that observed in the rest of Spain, but there has been no increase in the incidence rate along the study period(AU)