Survival of hematological patients after discharge from the intensive care unit: a prospective observational study.

INTRODUCTION: Although the survival rates of hematological patients admitted to the ICU are improving, little is known about the long-term outcome. Our objective was to identify factors related to long-term outcome in hematological patients after ICU discharge. METHODS: A prospective, observational study was carried out in seven centers in Spain. From an initial sample of 161 hematological patients admitted to one of the participating ICUs during the study period, 62 were discharged alive and followed for a median time of 23 (1 to 54) months. Univariate and multivariate analysis were performed to identify the factors related to long term-survival. Finally, variables that influence the continuation of the scheduled therapy for the hematological disease were studied. RESULTS: Mortality after ICU discharge was 61%, with a median survival of 18 (1 to 54) months. In the multivariate analysis, an Eastern Cooperative Oncology Group score (ECOG) >2 at ICU discharge (Hazard ratio 11.15 (4.626 to 26.872)), relapse of the hematological disease (Hazard ratio 9.738 (3.804 to 24.93)) and discontinuation of the planned treatment for the hematological disease (Hazard ratio 4.349 (1.286 to 14.705)) were independently related to mortality. Absence of stem cell transplantation, high ECOG and high Acute Physiology and Chronic Health Evaluation II (APACHE II) scores decreased the probability of receiving the planned therapy for the hematological malignancy. CONCLUSIONS: Both ICU care and post-ICU management determine the long-term outcome of hematological patients who are discharged alive from the ICU.

Diseminación nosocomial de Staphylococcus hominis resistente al linezolid en dos hospitales de Mallorca / Nosocomial spread of linezolid-resistant Staphylococcus hominis intwohospitals in Majorca

Introducción A partir del 2008 se detectaron varios aislados de Staphylococcus hominis (S. hominis) multirresistentes, incluyendo resistencia al linezolid y a la teicoplanina, en pacientes ingresados en dos hospitales de Mallorca. Por ello, se inició un estudio para determinar la epidemiología molecular y el mecanismo de resistencia al linezolid. Métodos El estudio de epidemiología molecular se realizó mediante electroforesis en campo pulsado (ECP), tras digestión con ApaI. Se efectuó amplificación de un fragmento de los genes ARNr 23S (con secuenciación posterior) y cfr. Resultados Desde marzo de 2008 hasta febrero de 2009 se detectaron 15 aislados de S. hominis resistentes al linezolid y a la teicoplanina, procedentes de 14 pacientes. Todos ellos excepto uno habían ingresado en las Unidades de Cuidados Intensivos de alguno de los dos hospitales. La mayoría de los aislados (9) se obtuvieron en hemocultivos. Gran parte de los pacientes infectados (12 de los 15 episodios infecciosos, el 80,0%) recibieron pautas de linezolid antes de la detección del aislado resistente. La ECP reveló la presencia de un único clon entre los aislados de S. hominis resistentes al linezolid. Se detectó la mutación G2576T en todas las cepas resistentes, mientras que la PCR del gen cfr fue negativa en las mismas. Todos los aislados fueron también resistentes a la penicilina, oxacilina, trimetoprim-sulfametoxazol, ciprofloxacino, levofloxacino y tobramicina; y sensibles a la eritromicina, tetraciclina, gentamicina y daptomicina. La CMI a la vancomicina fue de 4μg/ml en todos ellos. Conclusiones La detección de cepas de estafilococos resistentes al linezolid resalta la necesidad de racionalizar el uso del linezolid y mantener un control activo de dicha resistencia con objeto de preservar la utilidad clínica de este antimicrobiano (AU)

Objective: Since March 2008, several linezolid and teicoplanin-resistant Staphylococcus hominis (S. hominis)isolates have been recovered from patients admitted to the two major hospitals on the island of Majorca, Spain. For this reason, a study was conducted to determine the molecular epidemiology of these isolates and the mechanism of linezolid resistance. Methods: The molecular epidemiology study was performed by pulsed-field gel electrophoresis (PFGE)analysis, after digestion with ApaI. Linezolid resistance mechanisms were evaluated by PCR amplification of a fragment of the domain V of the 23S rRNA gene (followed by sequencing) and cfr gene. Results: From March 2008 to February 2009, 15 linezolid and teicoplan in-resistant S. hominis isolates were recovered from 14 patients. All of them, except one, were hospitalised in the intensive care units of either of the two institutions. Isolates were obtained mainly from blood cultures (9). The majority of infected patients (12 of 15 infectious episodes, 80.0%) had received courses of linezolid prior to detection of the resistant isolate. PFGE analysis revealed the presence of a unique clone among linezolid resistant S. hominisisolates. The G2576T mutation was detected in all the linezolid resistant strains. None of the resistant isolates showed a positive PCR for the cfr gene. All of the isolates were also resistant to penicillin, oxacillin, trimethoprim-sulfamethoxazole, ciprofloxacin, levofloxacin, and tobramicin; whereas all of them were susceptible to erythromycin, tetracycline, gentamicin, and daptomycin. The MIC of vancomycin was4 g/ml for all the strains. Conclusions: The detection of linezolid resistant Staphylococci highlights the need to rationalise the use of linezolid, and maintain an active surveillance of its resistance to preserve the clinical usefulness of this antimicrobial (AU)

[Nosocomial spread of linezolid-resistant Staphylococcus hominis in two hospitals in Majorca]. / Diseminación nosocomial de Staphylococcus hominis resistente al linezolid en dos hospitales de Mallorca.

OBJECTIVE: Since March 2008, several linezolid and teicoplanin-resistant Staphylococcus hominis (S. hominis) isolates have been recovered from patients admitted to the two major hospitals on the island of Majorca, Spain. For this reason, a study was conducted to determine the molecular epidemiology of these isolates and the mechanism of linezolid resistance. METHODS: The molecular epidemiology study was performed by pulsed-field gel electrophoresis (PFGE) analysis, after digestion with ApaI. Linezolid resistance mechanisms were evaluated by PCR amplification of a fragment of the domain V of the 23S rRNA gene (followed by sequencing) and cfr gene. RESULTS: From March 2008 to February 2009, 15 linezolid and teicoplanin-resistant S. hominis isolates were recovered from 14 patients. All of them, except one, were hospitalised in the intensive care units of either of the two institutions. Isolates were obtained mainly from blood cultures (9). The majority of infected patients (12 of 15 infectious episodes, 80.0%) had received courses of linezolid prior to detection of the resistant isolate. PFGE analysis revealed the presence of a unique clone among linezolid resistant S. hominis isolates. The G2576T mutation was detected in all the linezolid resistant strains. None of the resistant isolates showed a positive PCR for the cfr gene. All of the isolates were also resistant to penicillin, oxacillin, trimethoprim-sulfamethoxazole, ciprofloxacin, levofloxacin, and tobramicin; whereas all of them were susceptible to erythromycin, tetracycline, gentamicin, and daptomycin. The MIC of vancomycin was 4µg/ml for all the strains. CONCLUSIONS: The detection of linezolid resistant Staphylococci highlights the need to rationalise the use of linezolid, and maintain an active surveillance of its resistance to preserve the clinical usefulness of this antimicrobial.

Characterization of a large outbreak by CTX-M-1-producing Klebsiella pneumoniae and mechanisms leading to in vivo carbapenem resistance development.

All extended-spectrum beta-lactamase (ESBL)-producing Enterobacteriaceae isolates from patients admitted to and adult intensive care unit were prospectively documented from 2002 to 2005, when a large outbreak (51 patients affected) of multiresistant ESBL-producing Klebsiella pneumoniae infection was detected. The involvement of a single K. pneumoniae clone was demonstrated by pulsed-field gel electrophoresis. In addition to the ESBL-mediated resistance, the epidemic strain uniformly showed cross-resistance to ciprofloxacin, gentamicin, tobramycin, trimethoprim-sulfamethoxazole, and tetracycline, whereas resistance to the beta-lactam-beta-lactamase inhibitor combinations was variable. The ESBL involved was CTX-M-1, as demonstrated by isoelectric focusing, PCR amplification, and sequencing. CTX-M-1 as well as the aminoglycoside resistance determinants were encoded in a 50-kb plasmid that could be transferred to Escherichia coli only by transformation. In two of the infected patients, carbapenem resistance development (MICs of 8 to 12, 16, and >32 microg/ml for imipenem, meropenem, and ertapenem, respectively) was documented, both in clinical samples and in intestinal colonization studies. The analysis of the outer membrane proteins of the carbapenem-susceptible and -resistant isolates revealed that the former expressed only one of the two major porins, OmpK36, whereas the latter did not express either of them. In one of the cases, the lack of expression of OmpK36 was demonstrated to be mediated by the interruption of the coding sequence by the insertion sequence IS26. This is the first report of a large outbreak of CTX-M-1-producing Enterobacteriaceae and, curiously, the first documented description in the literature of CTX-M-1 in K. pneumoniae, despite the fact that this enzyme has been found in multiple species. Furthermore, we document and characterize for the first time carbapenem resistance development in CTX-M-1-producing Enterobacteriaceae.

Regional variability in population acute myocardial infarction cumulative incidence and mortality rates in Spain 1997 and 1998.

BACKGROUND: Myocardial infarction (MI) incidence and mortality display a high geographic variation. AIMS: The objective of the present study was to analyze MI mortality, cumulative incidence rate variability in seven regions of Spain from 1997 to 1998. METHODS AND RESULTS: Standardized methods were used to identify, find, register, and classify MI cases that were classified as definite, possible, insufficient-data MI, and non-MI. The total population of the seven monitored regions was 7,364,682 inhabitants. Of the 11,256 cases fulfilling eligibility criteria to investigate, 10,660 were selected to calculate MI rates: 6554 (61.5%) non-fatal definite MI, 1179 (11.1%) fatal definite MI, 1859 (17.4%) fatal possible MI, 1068 (10.0%) fatal cases with insufficient data. The IBERICA 25-74 years age-standardized cumulative incidence rates for men and women, were 207 (range: 175-252) and 45 (range: 36-65) per 100,000, respectively. The age-standardized mortality rates for men and women, were 73 (range: 62-94) and 20 (range: 13-29) per 100,000, respectively. Age-standardized case-fatality was 31.4 and 24.2% in men aged 25-74 and 35-64 years, respectively, and 32.7 and 27.0%, respectively, in women. CONCLUSIONS: MI cumulative incidence and mortality rates are low compared with other industrialized countries but, vary considerably among regions in a Mediterranean country like Spain.