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Received 25 August 2004; returned 20 October 2004; revised 22 November 2004; accepted 23 November 2004Objectives: The antifungal drug susceptibilities of 351 isolates of Candida species, obtained throughactive laboratory-based surveillance in the period January 2002–December 2003, were determined(Candida albicans 51%, Candida parapsilosis 23%, Candida tropicalis 10%, Candida glabrata 9%,Candida krusei 4%).Methods: The MICs of amphotericin B, flucytosine, fluconazole, itraconazole, voriconazole andcaspofungin were established by means of the broth microdilution reference procedure of theEuropean Committee on Antibiotic Susceptibility Testing.Results and conclusions: Amphotericin B and flucytosine were active in vitro against all strains. A totalof 24 isolates (6.8%) showed decreased susceptibility to fluconazole (MIC>_ 16mg/L) and 43 (12.3%)showed decreased susceptibility to itraconazole (MIC>_ 0.25mg/L). Voriconazole and caspofungin wereactive in vitro against the majority of isolates, even those that were resistant to fluconazole.Keywords: fluconazole resistance, caspofungin, voriconazole, EUCAST

We performed a prospective study of Staphylococcus aureus nasal carriage in patients on chronic haemodialysis to determine the role of cutaneous colonization in the aetiology of recurrent nasal colonization. From February 2000 to September 2001, 71 patients on chronic haemodialysis in the dialysis unit at a university hospital were screened monthly for S. aureus nasal carriage. Carriers received nasal mupirocin for five days and were tested for nasal and cutaneous carriage two days later and monthly thereafter. Using genotyping results, recurrence was defined as relapse if pretreatment and subsequent nasal isolates were clonally identical; if the isolates were different, it was considered recolonization. Thirty-nine patients (55%) were nasal carriers: 11 initially and 28 during follow-up. Among the mupirocin-treated patients, the eradication of S. aureus nasal carriage rate was 88.5%. Nasal recurrence was documented in 17 patients (43.5%), and S. aureus nasal strains were available for molecular typing in 14 patients with a total of 23 recurrence episodes. On the basis of pulsed-field gel electrophoresis analysis, 16 (70%) recurrence episodes were considered relapses and seven were considered (30%) recolonizations. Among the episodes of relapse, prior cutaneous colonization was detected in only three cases. In haemodialysis patients, the majority of nasal carriage recurrences after mupirocin therapy were due to relapses. Cutaneous colonization does not appear to be relevant in the development of these relapses.

The aim of this prospective study was to assess the relative epidemiological role of digestive tract colonization by Acinetobacter baumannii , in comparison with other body site colonizations, in patients admitted to intensive care units (ICUs). From January to May 1995, axillary, pharyngeal and rectal swabs were taken together within the first 48 h of admission, and then weekly during ICU stay. Seventy-three patients were included, 48 of them (66%) had axillary, pharyngeal, or rectal colonization with A. baumannii , nine (19%) of these 48 during the first 48 h and the remaining 28 (77%) during the first week. Twenty-one (29%) had clinical samples positive for A. baumannii and axillary, pharyngeal, or rectal colonization. In 15 of these 21 (71%), colonization on body sites occurred prior to isolation from clinical samples (mean seven days, range 1–20). Throughout admission, rates of detection of A. baumannii were 75% (3648) for axillary or pharyngeal swabs and 77% (3748) for rectal swabs. Combination of two body site swabs yielded culture positive rates of 90% (4348) for axillary-pharyngeal or axillary-rectal sites, and 96% (4648) for pharyngeal-rectal. Two epidemic clones were defined by antibiotype and pulsed-field gel electrophoresis (PFGE) of Sma I DNA digests in 43 isolates from 11 patients. We conclude that body sites of patients were a major reservoir for A. baumannii infections in the outbreak. This finding casts doubt on the value of selective decontamination of the digestive tract as an additional infection control measure in this kind of outbreak. The weekly performance of pharyngeal and rectal swabs appears to detect A. baumannii colonization early among ICU patients and enables barrier methods to be applied rapidly.

In the course of an outbreak of extended-spectrum beta-lactamase-producing Klebsiella pneumoniae (ESBL-KP) in an intensive care unit (ICU), we conducted active surveillance to determine the risk factors for ESBL-KP faecal colonization of patients. We used weekly rectal samples during a four-month period. ESBL-KP was found in the faeces of 72 of 188 (38%) patients, and 42 (58%) of them were colonized within the first week of admission to the ICU. The probability of remaining free of faecal colonization was less than 20% at 30 days of ICU admission. The risk factors associated with ESBL-KP faecal colonization were clinical severity score at admission (P = 0.004), arterial catheterization (P = 0.002), total parenteral nutrition (P = 0.04), urinary catheterization (P = 0.01), mechanical ventilation (P0.001), and previous antibiotic therapy (P = 0.04). A logistic regression analysis identified duration of urinary catheterization (OR:3.5; 95% CI 1.2-10.3) and mechanical ventilation (OR:4.6; 95% CI 1.1-19.3) as independent risk factors for ESBL-KP faecal colonization. Our results suggest that in an ESBL-KP prevalent environment, manipulations that facilitate cross-infection are the most relevant in the acquisition of the micro-organism and risk increases throughout hospitalization.

These guidelines are an update of recommendations for the diagnosis of invasive fungal infections by the Spanish Society of Clinical Microbiology and Infectious Diseases (SEIMC) published in 2004 (Enferm Infecc Microbiol Clin. 2004, 22:32-9). In this updated version of the guidelines, a comprehensive review of the most recent diagnostic innovations and levels of evidence to recommend those diagnostic procedures are included. We first analyse conventional diagnostic methods, microscopic examination and culture, underlining their limitations which have led to the development of alternative methods, such as fungal antigen and DNA quantification. Those alternative methods of diagnosis are analysed by fungal infection. We also briefly review the methods for molecular identification of fungal species and recommendations for carrying out susceptibility tests for antifungal drugs, including reference procedures, commercial techniques and their indications.

We read with interest the recently published article from Alonso-Echanove et al. ([1][1]) on the proficiency of Spanish clinical laboratories in detecting vancomycin-resistant enterococci (VRE). In their conclusions, they found an overall acceptable proficiency in the detection of such strains by 22

Background: In this study we describe the clinical and molecular characteristics of an outbreak due to carbapenem-resistant Klebsiella pneumoniae (CR-KP) producing CTX-M-15 and OXA-48 carbapenemase. Isogenic strains, carbapenem-susceptible K. pneumoniae (CS-KP) producing CTX-M-15, were also involved in the outbreak. Results: From October 2010 to December 2012 a total of 62 CR-KP and 23 CS-KP were isolated from clinical samples of 42 patients (22 had resistant isolates, 14 had susceptible isolates, and 6 had both CR and CS isolates). All patients had underlying diseases and 17 of them (14 patients with CR-KP and 3 with CS-KP) had received carbapenems previously. The range of carbapenem MICs for total isolates were: imipenem: 2 to >32 mu g/ml vs. 32 mu g/ml vs. 32 mu g/ml vs.

Fecal colonization with multiresistant Acinetobacter baumannii was evaluated in 189 consecutive patients in intensive care units (ICUs) during two different 2-month periods (October-November 1993 and May-June 1994). Rectal swabs were obtained weekly from admission to discharge from the ICU. Overall, 77 patients (41%) had multiresistant A. baumannii fecal colonization ; colonization was detected in 55 (71%) of the patients within the first week of their ICU stay. Clinical infections due to multiresistant A. baumannii occurred more frequently in patients with fecal colonization than in those without fecal colonization (26% vs. 5%, respectively ; P

We performed an evaluation of early cytomegalovirus antigen detection (Shell-vial method) for rapid diagnosis of cytomegalovirus infection in patients at risk. A comparative, parallel, prospective study against conventional cell culture in 913 clinical specimens was carried out. Shell-vial technique detected an early cytomegalovirus antigen in culture using an indirect immunofluorescent method with monoclonal antibodies. Cytomegalovirus was detected in 210 specimens (23.0%). In 24 instances (11.4%), cytomegalovirus was only detected by culture, in contrast with 54 specimens (25.7%) that were only positive in Shell-vial (p less than 0.001; McNemar test). Mean detection time for cell culture was 9.2 days, and 16-24 h for the Shell-vial technique. This is a rapid, sensitive, specific and simple to perform method for diagnosis of cytomegalovirus infection. Nevertheless, the predictivity of cytomegalovirus disease was not improved by this technique.

Beginning in 1992, a sustained outbreak of multiresistant Acinetobacter baumannii infections was noted in our 1,000-bed hospital in Barcelona, Spain, resulting in considerable overuse of imipenem, to which the organisms were uniformly susceptible. In January 1997, carbapenem-resistant (CR) A. baumannii strains emerged and rapidly disseminated in the intensive care units (ICUs), prompting us to conduct a prospective investigation. It was an 18-month longitudinal intervention study aimed at the identification of the clinical and microbiological epidemiology of the outbreak and its response to a multicomponent infection control strategy. From January 1997 to June 1998, clinical samples from 153 (8%) of 1,836 consecutive ICU patients were found to contain CR A. baumannii . Isolates were verified to be A. baumannii by restriction analysis of the 16S-23S ribosomal genes and the intergenic spacer region. Molecular typing by repetitive extragenic palindromic sequence-based PCR and pulsed-field gel electrophoresis showed that the emergence of carbapenem resistance was not by the selection of resistant mutants but was by the introduction of two new epidemic clones that were different from those responsible for the endemic. Multivariate regression analysis selected those patients with previous carriage of CR A. baumannii (relative risk [RR], 35.3; 95% confidence interval [CI], 7.2 to 173.1), those patients who had previously received therapy with carbapenems (RR, 4.6; 95% CI, 1.3 to 15.6), or those who were admitted into a ward with a high density of patients infected with CR A. baumannii (RR, 1.7; 95% CI, 1.2 to 2.5) to be at a significantly greater risk for the development of clinical colonization or infection with CR A. baumannii strains. In accordance, a combined infection control strategy was designed and implemented, including the sequential closure of all ICUs for decontamination, strict compliance with cross-transmission prevention protocols, and a program that restricted the use of carbapenem. Subsequently, a sharp reduction in the incidence rates of infection or colonization with A. baumannii , whether resistant or susceptible to carbapenems, was shown, although an alarming dominance of the carbapenem-resistant clones was shown at the end of the study.

The effect of a selective decontamination of the digestive tract (SDD) regimen including polymyxin and tobramycin on several body site reservoirs was compared between a test group and a control group in intensive care unit (ICU) patients with faecal multi-resistant Acinetobacter baumannii colonization. SDD significantly reduced faecal and pharyngeal carriage when compared with the control group at the end of ICU stay (48% versus 91%, P = 0.001, and 38.5% versus 78%, P = 0.01, respectively), but failed to reduce axillary colonization (75% versus 78%, P = 0.6). In addition, the isolation of A. baumannii from new clinical samples was lower in patients with SDD (45.5% versus 81%, P = 0.05). No resistance to polymyxin was observed. We conclude that the digestive tract reservoir of A. baumannii in ICU patients may be decreased by a SDD regimen.

Introduction Candidemia in critically ill patients is usually a severe and life-threatening condition with a high crude mortality. Very few studies have focused on the impact of candidemia on ICU patient outcome and attributable mortality still remains controversial. This study was carried out to determine the attributable mortality of ICU-acquired candidemia in critically ill patients using propensity score matching analysis. Methods A prospective observational study was conducted of all consecutive non-neutropenic adult patients admitted for at least seven days to 36 ICUs in Spain, France, and Argentina between April 2006 and June 2007. The probability of developing candidemia was estimated using a multivariate logistic regression model. Each patient with ICU-acquired candidemia was matched with two control patients with the nearest available Mahalanobis metric matching within the calipers defined by the propensity score. Standardized differences tests (SDT) for each variable before and after matching were calculated. Attributable mortality was determined by a modified Poisson regression model adjusted by those variables that still presented certain misalignments defined as a SDT > 10%. Results Thirty-eight candidemias were diagnosed in 1,107 patients (34.3 episodes/1,000 ICU patients). Patients with and without candidemia had an ICU crude mortality of 52.6% versus 20.6% (P < 0.001) and a crude hospital mortality of 55.3% versus 29.6% (P = 0.01), respectively. In the propensity matched analysis, the corresponding figures were 51.4% versus 37.1% (P = 0.222) and 54.3% versus 50% (P = 0.680). After controlling residual confusion by the Poisson regression model, the relative risk (RR) of ICU- and hospital-attributable mortality from candidemia was RR 1.298 (95% confidence interval (CI) 0.88 to 1.98) and RR 1.096 (95% CI 0.68 to 1.69), respectively. Conclusions ICU-acquired candidemia in critically ill patients is not associated with an increase in either ICU or hospital mortality.