Coinfección por Mycobacterium africanum y Mycobacterium avium en una paciente con SIDA / Mycobacterium africanum and Mycobacterium avium co-infection in an AIDS patient

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[Role of double strand DNA break repair for quinolone sensitivity in Escherichia coli: therapeutic implications]. / El papel de la reparación de roturas de doble cadena de ADN en Escherichia coli en la sensibilidad a quinolonas: implicaciones terapéuticas.

INTRODUCTION: Quinolones are one of the types of antibiotics with higher resistance rates in the last years. At molecular level, quinolones block type II topoisomerases producing double strand breaks (DSBs). These DSBs could play a double role, as inductors of the quinolone bactericidal effects but also as mediators of the resistance and tolerance mechanisms. MATERIAL AND METHODS: In this work we have studied the molecular pathways responsible for DSBs repair in the quinolone susceptibility: the stalled replication fork reversal (recombination-dependent) (RFR), the SOS response induction, the translesional DNA synthesis (TLS) and the nucleotide excision repair mechanisms (NER). For this reason, at the European University in Madrid, we analysed the minimal inhibitory concentration (MIC) to three different quinolones in Escherichia coli mutant strains coming from different type culture collections. RESULTS: recA, recBC, priA and lexA mutants showed a significant reduction on the MIC values for all quinolones tested. No significant changes were observed on mutant strains for TLS and NER. DISCUSSION: These data indicate that in the presence of quinolones, RFR mechanisms and the SOS response could be involved in the quinolone susceptibility.

El papel de la reparación de roturas de doble cadena de ADN en Escherichia coli en la sensibilidad a quinolonas: implicaciones terapéuticas / Role of double strand DNA break repair for quinolone sensitivity in Escherichia coli: therapeutic implications

Introducción. Las quinolonas son uno de los tipos de antibióticos cuyas tasas de resistencia se han visto incrementadas en los últimos años. A nivel molecular, bloquean a las topoisomerasas tipo II generando cortes de doble cadena (double strand breaks, DSBs) en el ADN. Se ha propuesto que estos DSBs podrían tener un doble papel, como mediadores de su efecto bactericida y también como responsables de desencadenar los mecanismos de resistencia y tolerancia a las quinolonas. Material y métodos. En el presente trabajo hemos estudiado la implicación de los mecanismos de reparación de DSBs en la sensibilidad a las quinolonas: reanudación de horquillas de replicación paradas dependiente de recombinación (RFR), inducción de la respuesta SOS, reparación por síntesis translesional (TLS) y escisión de nucleótidos (NER). Para ello, en los laboratorios de la Universidad Europea de Madrid, se han analizado las concentraciones mínimas inhibitorias (CMIs) de tres quinolonas diferentes en mutantes procedentes de varias colecciones de cultivos tipo de Escherichia coli. Resultados. Mutantes en recA, recBC, priA y lexA mostraron una disminución significativa de la CMI a todas las quinolonas. No se observaron cambios significativos en estirpes mutantes en los mecanismos de reparación por TLS y NER. Discusión. Estos datos indican que, en presencia de quinolonas, los mecanismos de RFR y la inducción de la respuesta SOS estarían implicados en la aparición de mecanismos de sensibilidad a quinolonas (AU)

Introduction. Quinolones are one of the types of antibiotics with higher resistance rates in the last years. At molecular level, quinolones block type II topoisomerases producing double strand breaks (DSBs). These DSBs could play a double role, as inductors of the quinolone bactericidal effects but also as mediators of the resistance and tolerance mechanisms. Material and methods. In this work we have studied the molecular pathways responsible for DSBs repair in the quinolone susceptibility: the stalled replication fork reversal (recombination-dependent) (RFR), the SOS response induction, the translesional DNA synthesis (TLS) and the nucleotide excision repair mechanisms (NER). For this reason, at the European University in Madrid, we analysed the minimal inhibitory concentration (MIC) to three different quinolones in Escherichia coli mutant strains coming from different type culture collections. Results. recA, recBC, priA and lexA mutants showed a significant reduction on the MIC values for all quinolones tested. No significant changes were observed on mutant strains for TLS and NER. Discussion. These data indicate that in the presence of quinolones, RFR mechanisms and the SOS response could be involved in the quinolone susceptibility (AU)

Long-term use of selective decontamination of the digestive tract does not increase antibiotic resistance: a 5-year prospective cohort study.

PURPOSE: Despite the evidence, the use of selective decontamination of the digestive tract (SDD) remains controversial, largely because of concerns that it may promote the emergence of antibiotic-resistant strains. The purpose of this study was to evaluate the long-term incidence of carriage of antibiotic-resistant bacteria (ARB), its clinical impact on developing infections and to explore risk factors of acquiring resistance. METHODS: This study was conducted in one 18-bed medical-surgical intensive care unit (ICU). All consecutive patients admitted to the ICU who were expected to require tracheal intubation for longer than 48 h were given a 4-day course of intravenous cefotaxime, and enteral polymyxin E, tobramycin, amphotericin B in an oropharyngeal paste and digestive solution. Oropharyngeal and rectal swabs were obtained on admission and once a week. Diagnostic samples were obtained on clinical indication. RESULTS: During 5 years 1,588 patients were included in the study. The incidence density of ARB was stable: 18.91 carriers per 1,000 patient-days. The incidence of resistant Enterobacteriaceae was stable; the resistance of Pseudomonas aeruginosa to tobramycin, amikacin and ciprofloxacin was strongly reduced; there was an increase of P. aeruginosa resistant to ceftazidime and imipenem, associated with the increase in imipenem consumption; the incidence of other nonfermenter bacilli and oxacillin-resistant Staphylococcus aureus was close to zero. Ninety-seven patients developed 101 infections caused by ARB: 23 pneumonias, 20 bloodstream infections and 58 urinary tract infections. Abdominal surgery was the only risk factor associated with ARB acquisition [risk ratio 1.56 (1.10-2.19)]. CONCLUSIONS: Long-term use of SDD is not associated with an increase in acquisition of resistant flora.

Vancomycin MICs did not creep in Staphylococcus aureus isolates from 2002 to 2006 in a setting with low vancomycin usage.

OBJECTIVES: The aim of this study was to evaluate MIC trends for clinical isolates of Staphylococcus aureus to vancomycin over a 5 year period (2002-06) in a hospital in Spain. METHODS: All clinical isolates of S. aureus (one per patient) from clinical samples of patients at Hospital Universitario de Getafe from January 2002 to December 2006 were used. MICs of vancomycin were determined by the CLSI broth microdilution procedure. For analysis of MIC trends over the 5 years, we grouped the isolates into those with MIC < or =1 mg/L [2428 methicillin-susceptible S. aureus (MSSA) and 518 methicillin-resistant S. aureus (MRSA)] and those with MIC > or =2 mg/L (MIC = 2 mg/L: 141 MSSA and 47 MRSA; MIC = 4 mg/L: 5 MSSA and 1 MRSA). MICs for the different groups in the different years were compared with the linear-trend chi(2) test. RESULTS: A total of 3141 strains of S. aureus collected over the 5 year period was included in this analysis. Of these, 2574 (82%) strains were MSSA and 566 (18%) strains were MRSA. One of the 566 MRSA strains (0.18%) and 5 of the 2574 MSSA strains (0.19%) were vancomycin-intermediate (not significant). The rest were susceptible. The overall percentage of MRSA isolates with a vancomycin MIC of > or =2 mg/L was much higher than that of MSSA during the 5 year period [8.5% (48/566) versus 5.7% (146/2574); P = 0.012]. No statistically significant change in the percentage of isolates with a vancomycin MIC of > or =2 mg/L was observed over the years for MRSA (chi(2) = 0.01; P = 0.91) or MSSA (chi(2) = 0.08; P = 0.78). Annual consumption of parenteral vancomycin in our hospital in daily defined doses/100 stays was: 2002 (1.91), 2003 (1.63), 2004 (1.74), 2005 (2.06) and 2006 (1.64). CONCLUSIONS: In a setting of low consumption of vancomycin and with a large collection of S. aureus clinical isolates, we have demonstrated the stability of vancomycin MICs over time.