Community-acquired pneumonia during the first post-pandemic influenza season: a prospective, multicentre cohort study.

OBJECTIVES: To determine the aetiology, clinical features and prognosis of CAP during the first post-pandemic influenza season. We also assessed the factors associated with severe disease and tested the ability of a scoring system for identifying influenza A (H1N1)pdm09-related pneumonia. METHODS: Prospective cohort study carried out at 10 tertiary hospitals of Spain. All adults hospitalised with CAP from December 01, 2010 to March 31, 2011 were analysed. RESULTS: A total of 747 adults with CAP required hospitalisation. The aetiology was determined in 315 (42.2%) patients, in whom 154 (21.9%) were due to bacteria, 125 (16.7%) were due to viruses and 36 (4.8%) were mixed (due to viruses and bacteria). The most frequently isolated bacteria were Streptococccus pneumoniae. Among patients with viral pneumonia, the most common organism identified were influenza A (H1N1)pdm09. Independent factors associated with severe disease were impaired consciousness, septic shock, tachypnea, hyponatremia, hypoxemia, influenza B, and influenza A (H1N1)pdm09. The scoring system evaluated did not differentiate reliably between patients with influenza A (H1N1)pdm09-related pneumonia and those with other aetiologies. CONCLUSIONS: The frequency of bacterial and viral pneumonia during the first post-pandemic influenza season was similar. The main identified virus was influenza A (H1N1)pdm09, which was associated with severe disease. Although certain presenting clinical features may allow recognition of influenza A (H1N1)pdm09-related pneumonia, it is difficult to express them in a reliable scoring system.

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.