Biomedical subjects

Yehuda Carmeli

Publications and source records attributed to Yehuda Carmeli.

At least 19 recordsLinked to original sources

PubMed2006

Enterococcal bacteraemia: epidemiological, microbiological, clinical and prognostic characteristics, and the impact of high level gentamicin resistance.

Enterococci are increasingly common nosocomial pathogens that can cause serious infections and often acquire antibiotic resistance. This study focused on the epidemiological, microbiological and clinical characteristics of enterococcal bacteraemia with special attention to the impact of high level gentamicin resistance (HLGR) on prognosis. 117 cases of enterococcal bacteraemia constituted 8% of all bacteraemic episodes during the y 2002. The most common source of infection was the urinary tract, more than half of the episodes were polymicrobial and the vast majority of cases was healthcare-associated. 50 of 117 isolates (43%) were resistant to gentamicin. Infection-related mortality (22 of 117, 19%) was associated with 2 independent variables in multivariate analysis: severity-of-illness score (OR=39.6, p<0.00001) and HLGR (OR=6.4, p=0.006). It was concluded that HLGR adversely affects the outcome of bacteraemic enterococcal infection.

Adult↗

PubMed2006

Genotypic and phenotypic analysis of Clostridium difficile correlated with previous antibiotic exposure.

To analyze Clostridium difficile susceptibility results and genotypes in relation to antibiotic exposures that precipitated C. difficile-associated diarrhea (CDAD), we examined 83 nosocomial C. difficile isolates recovered at a tertiary care center in Boston, Massachusetts. MICs were determined by E-test methodology using modified Brucella agar. Isolates were genotyped by pulsed-field gel electrophoresis and restriction enzyme analysis. Antibiotic susceptibilities were: ciprofloxacin (0%), clindamycin (59%), trovafloxacin (63%), ceftriaxone (73%), piperacillin/tazobactam (100%), metronidazole (100%), and vancomycin (100%). The two most common strain groups, isolated from a total of 33 patients, were much more likely to be resistant to clindamycin, erythromycin, and trovafloxacin than other strain groups [79% (26 of 33) versus 2% (1 of 50), respectively]. Clindamycin exposure was strongly associated with CDAD caused by isolates that exhibited multiple resistance to clindamycin, erythromycin, and trovafloxacin (prevalence odds ratio, 4.2; 95% confidence interval, 1.1-16.8), whereas other antimicrobials did not yield significant associations. Resistance of specific C. difficile strains to clindamycin and other antimicrobial agents may contribute to their hospital dissemination and explain, in part, the propensity of clindamycin to trigger nosocomial outbreaks.

Adult↗

PubMed2006

Efficacy of antibodies against the N-terminal of Pseudomonas aeruginosa flagellin for treating infections in a murine burn wound model.

BACKGROUND: In an era of increasing drug resistance, immunotherapy is a desirable treatment against Pseudomonas aeruginosa infections. The flagellum, which is an important pseudomonal virulence factor, was targeted for immunotherapy. The aim of the study was to evaluate the efficacy of polyclonal immunotherapy targeted against the N-terminal of flagellin (anti-N'-fla-b) for treating severe P. aeruginosa infection in a murine burn wound model. METHODS: Groups of 12 mice were infected (subeschar) with P. aeruginosa strain PA01, and were treated either with systemic anti-N'-fla-b immunoglobulin G (IgG), nonspecific IgG, or imipenem. The control groups included mice with burn alone, mice with untreated infected burn, and mice without burn infected with P. aeruginosa. Three separate regimens were examined: prophylaxis (preinfection), therapeutic (postinfection), and combined. The efficacy of anti-N'-fla-b was evaluated by monitoring the mortality and morbidity (relative weight loss) during a period of 2 weeks. RESULTS: Anti-N'-fla-b IgG immunotherapy significantly decreased the mortality rate of infected burned mice followed by severe P. aeruginosa infection. The mortality rate in the anti-N'-fla-b-treated groups ranged from 0 to 17 percent compared with 58 to 83 percent in nontreated groups infected with 2 to 5 x 10(6) colony-forming units of P. aeruginosa (p < 0.05). The mortality rate in the anti-N'-fla-b-treated groups was similar to that of groups treated with imipenem. The three tested regimens yielded similar results. Morbidity paralleled survival results. Histopathologic examination revealed an earlier reepithelialization of the infected wound in the anti-N'-fla-b-treated mice compared with untreated mice. CONCLUSION: Immunotherapy with anti-N'-fla-b IgG, given either as prophylaxis or therapeutically, effectively reduced mortality and morbidity and improved wound healing in a severely P. aeruginosa-infected murine burn model.

Animals↗

PubMed2006

The establishment of a Pseudomonas aeruginosa-infected burn-wound sepsis model and the effect of imipenem treatment.

INTRODUCTION: We present a standardized Pseudomonas aeruginosa (PA) infected burn-wound model in mice for evaluating new antimicrobials and therapy strategies for PA infections and demonstrate the effect of the antibiotic imipenem in this model. METHODS: A 6%-8% total body surface area, full-thickness, scald-burn wound was induced in anesthetized mice. Two study groups (PA-infected burn) were compared with 1 treatment group (systemic imipenem) and 3 control groups (noninfected burn, infected nonburned, and burn with distant infection). Seven-day mortality, quantitative culture from eschars and from spleens, weight loss, and time to healing were compared. RESULTS: The 25%-100% mortality rate in the nontreated PA-infected burn group was directly related to the infecting inoculum. Imipenem treatment reduced the mortality rate to 0-17%. No control animal died. Systemic bacterial dissemination at 48 hours was significantly higher in the study group. Morbidity paralleled survival results. Wound healing was quicker in the imipenem-treated group and control groups compared with the infected nontreated group. CONCLUSIONS: The mice model is a useful tool for evaluating new antibacterial agents and strategies for treating PA-infected burn injuries. Imipenem was found to be efficacious in the treatment of severe PA sepsis.

Animals↗

PubMed2006

Differential effects of levofloxacin and ciprofloxacin on the risk for isolation of quinolone-resistant Pseudomonas aeruginosa.

Due to the greater in vitro activity of ciprofloxacin than that of levofloxacin against Pseudomonas aeruginosa, the likelihood of isolating a clinical strain of quinolone-resistant (QR) P. aeruginosa might be greater after exposure to levofloxacin than ciprofloxacin. We examined the risk of isolating QR P. aeruginosa in association with prior levofloxacin or ciprofloxacin exposure. A case-case-control study was conducted. Two groups of cases, one with nosocomial QR P. aeruginosa infections and one with nosocomial quinolone-susceptible (QS) P. aeruginosa infections, were compared to a control group of hospitalized patients without P. aeruginosa infections. Bivariable and multivariable analyses were used to determine risk factors for isolation of QR P. aeruginosa and QS P. aeruginosa. One hundred seventeen QR P. aeruginosa and 255 QS P. aeruginosa cases were identified, and 739 controls were selected. Exposures to ciprofloxacin were similar among all three groups (8% for controls, 9.4% for QR P. aeruginosa cases, and 7.5% for QS P. aeruginosa cases; P >/= 0.6). Levofloxacin use was more frequent in the QR P. aeruginosa cases than in the controls (35.9% and 22.1%, respectively; odds ratio [OR] = 2.0; 95% confidence interval [CI] = 1.3 to 3.0) and less frequent in QS P. aeruginosa cases (14.1% of QS P. aeruginosa cases; OR = 0.6; 95% CI = 0.4 to 0.9). In multivariable analysis, levofloxacin, but not ciprofloxacin, was a significant risk factor for isolation of QR P. aeruginosa (OR for levofloxacin = 1.7 [95% CI = 1.0 to 2.9]; OR for ciprofloxacin = 1.2 [95% CI = 0.6 to 2.5]). Levofloxacin was associated with a reduced risk of isolation of QS P. aeruginosa (OR = 0.6; 95% CI = 0.4 to 0.9), whereas ciprofloxacin had no significant effect (OR = 1.0; 95% CI = 0.6 to 1.8). In conclusion, the use of levofloxacin, but not ciprofloxacin, was associated with isolation of QR P. aeruginosa.

Aged↗

PubMed2006

Endocarditis caused by extended-spectrum-beta-lactamase-producing Klebsiella pneumoniae: emergence of resistance to ciprofloxacin and piperacillin-tazobactam during treatment despite initial susceptibility.

Three episodes of bacteremia occurred in the course of prosthetic valve endocarditis caused by an extended-spectrum-beta-lactamase (ESBL)-producing Klebsiella pneumoniae strain. The second isolate developed resistance to ciprofloxacin and the third isolate to piperacillin-tazobactam (PIP-TZ) following sequential therapy with each agent. The first isolate was resistant to PIP-TZ only at high inocula, the second isolate acquired increased transcription of the acrA gene, and the third isolate became resistant to PIP-TZ due to loss of beta-lactamase inhibition by TZ. We question if and how PIP-TZ susceptibility should be reported for ESBL-producing Enterobacteriaceae.

Ciprofloxacin↗

PubMed2006

Plasmid-mediated imipenem-hydrolyzing enzyme KPC-2 among multiple carbapenem-resistant Escherichia coli clones in Israel.

Carbapenem resistance in Escherichia coli is rare. We report four genetically unrelated carbapenem-resistant E. coli isolates cultured from four patients hospitalized in Tel Aviv Medical Center. PCR, sequencing, and Southern blot analysis identified KPC-2 as the imipenem-hydrolyzing enzyme in all four strains, carried on different plasmids with a possible common origin. This is the first discovery of KPC-2 in E. coli and the first report of this enzyme originating outside the United States.

Carbapenems↗

PubMed2006

Multidrug-resistant Pseudomonas aeruginosa: risk factors and clinical impact.

Pseudomonas aeruginosa, a leading nosocomial pathogen, may become multidrug resistant (MDR). Its rate of occurrence, the individual risk factors among affected patients, and the clinical impact of infection are undetermined. We conducted an epidemiologic evaluation and molecular typing using pulsed-field gel electrophoresis (PFGE) of 36 isolates for 82 patients with MDR P. aeruginosa and 82 controls matched by ward, length of hospital stay, and calendar time. A matched case-control study identified individual risk factors for having MDR P. aeruginosa, and a retrospective matched-cohort study examined clinical outcomes of such infections. The 36 isolates belonged to 12 PFGE clones. Two clones dominated, with one originating in an intensive care unit (ICU). Cases and controls had similar demographic characteristics and numbers of comorbid conditions. A multivariate model identified ICU stay, being bedridden, having high invasive devices scores, and being treated with broad-spectrum cephalosporins and with aminoglycosides as significant risk factors for isolating MDR P. aeruginosa. Having a malignant disease was a protective factor (odds ratio [OR] = 0.2; P = 0.03). MDR P. aeruginosa was associated with severe outcomes compared to controls, including increased mortality (OR = 4.4; P = 0.04), hospital stay (hazard ratio, 2; P = 0.001), and requirement for procedures (OR = 5.4; P = 0.001). The survivors functioned more poorly at discharge than the controls, and more of the survivors were discharged to rehabilitation centers or chronic care facilities. The epidemiology of MDR P. aeruginosa is complex. Critically ill patients that require intensive care and are treated with multiple antibiotic agents are at high risk. MDR P. aeruginosa infections are associated with severe adverse clinical outcomes.

Aged↗

PubMed2006

Clinical and economic impact of bacteremia with extended- spectrum-beta-lactamase-producing Enterobacteriaceae.

We studied outcomes of extended-spectrum beta-lactamase (ESBL) production in Enterobacteriaceae bacteremia. Inpatients with bacteremia caused by ESBL-producing Escherichia coli, Klebsiella spp., or Proteus spp. (cases) were compared with patients with bacteremia caused by non-ESBL producers (controls). Outcomes included mortality, mortality due to infection, length of stay (LOS), delay in appropriate therapy (DAT), discharge to a chronic care facility, and hospital cost. Ninety-nine cases and 99 controls were enrolled. Thirty-five percent of cases died, versus 18% of controls (odds ratio [OR], 2.5; 95% confidence interval [CI], 1.3 to 4.7; P=0.01). Thirty percent of cases died due to infection, versus 16% of controls (OR, 2.3; 95% CI, 1.1 to 4.5; P=0.03). The median LOS after bacteremia for cases was 11 days (interquartile range, 5 to 21), versus 5 days for controls (interquartile range, 3 to 9) (P<0.001). DAT occurred in 66% of cases, versus 7% of controls (OR, 25.1; 95% CI, 10.5 to 60.2; P<0.001). Cases were more likely than controls to be discharged to chronic care (52% versus 21%; OR, 4.0; 95% CI, 1.9 to 8.3; P<0.001). The average hospital cost for cases was 65,509 Israeli shekels, versus 23,538 shekels for controls (P<0.001). After adjusting for differences between groups by using multivariable analysis, ESBL production remained a significant predictor of mortality (OR, 3.6; 95% CI, 1.4 to 9.5; P=0.008), increased LOS (1.56-fold; P=0.001), DAT (OR, 25.1; 95% CI, 10.5 to 60.2; P<0.001), and increased cost (1.57-fold; P=0.003). The mean increase in equivalent cost attributable to ESBL production was $9,620. ESBL production was associated with severe adverse outcomes, including higher overall and infection-related mortality, increased LOS, DAT, discharge to chronic care, and higher costs.

Adult↗

PubMed2006

Predictors of mortality in patients with bloodstream infection due to ceftazidime-resistant Klebsiella pneumoniae.

Bloodstream infection (BSI) due to multidrug-resistant Klebsiella is associated with high rates of morbidity and mortality. The aim of this study was to identify predictors of in-hospital mortality among patients with BSI due to ceftazidime-resistant (CAZ-R) Klebsiella pneumoniae at a tertiary care medical center. Patients with CAZ-R K. pneumoniae BSI were identified by our microbiology laboratory between January 1995 and June 2003. Clinical data were collected retrospectively. Logistic regression was used to identify independent predictors of all causes of in-hospital mortality. Of 779 patients with K. pneumoniae BSI, 60 (7.7%) had BSI due to CAZ-R K. pneumoniae; 43 (72%) of these were nosocomial infections. Pulsed-field gel electrophoresis identified a single predominant strain in 17 (28%) patients. The in-hospital mortality rate was 43% (n = 26). Among patients with CAZ-R K. pneumoniae BSI, those who died were similar to survivors with respect to demographic, clinical, and antimicrobial susceptibility characteristics. Only 43 (72%) patients received effective therapy within 5 days of BSI. In bivariable analysis, delay in initiation of effective therapy for >72 h after diagnosis of BSI was associated with death (P = 0.03). Strain genotype was not predictive of outcome. In multivariable analysis, delay in initiation of effective therapy for >72 h after diagnosis of BSI was an independent predictor of death (odds ratio, 3.32; 95% confidence interval, 1.07 to 10.3). Thus, among patients with BSI due to CAZ-R K. pneumoniae, a delay in the initiation of effective therapy of greater than 72 h after BSI was associated with a >3-fold increase in mortality risk.

Adolescent↗

PubMed2006

Utility of the VITEK 2 Advanced Expert System for identification of extended-spectrum beta-lactamase production in Enterobacter spp.

Forty clinical isolates of Enterobacter spp. were identified as extended-spectrum beta-lactamase (ESBL) producers by disk diffusion. The VITEK 2 Advanced Expert System (AES) identified the ESBL phenotype in only 25 isolates (62.5%), and erroneously reported cephalosporin susceptibility in 11 isolates (28%). Refinements in the AES are required in order to improve ESBL detection in Enterobacter.

Enterobacter↗

PubMed2006

Antimicrobial resistance and patient outcomes: the hazards of adjustment.

Outcomes studies of infections with resistant bacteria often do not account appropriately for intermediate variables--events in the causal pathway between the exposure and the outcome--when controlling for confounders. We discuss how failure to distinguish between confounders and intermediate variables can bias the analysis, and we address methods of approaching this issue.

Bacterial Infections↗

PubMed2005

Mechanisms by which antibiotics promote dissemination of resistant pneumococci in human populations.

Mechanisms by which antimicrobials contribute to dissemination of pneumococcal resistance are incompletely characterized. A serial cross-sectional study of nasopharyngeal pneumococcal carriage in healthy, home-living children <or=6 years of age was conducted in four rural communities-two in Utah (1998-2003) and two in Idaho (2002-2003). Prevalence odds ratios for carriage of resistant pneumococci (OR(res)) and of susceptible pneumococci (OR(sus)) were estimated. Dynamic transmission models were developed to facilitate a mechanistic interpretation of OR(res) and OR(sus) and to compare the population impact of distinct antimicrobial classes. A total of 5,667 cultures were obtained; 25% of the cultures were positive, and 29% of isolates exhibited reduced susceptibility to penicillin. The adjusted OR(res) for recent individual and sibling cephalosporin use was 2.2 (95% confidence interval: 1.4, 3.4) and 1.8 (95% confidence interval: 1.0, 3.3), respectively. Neither individual nor sibling penicillin use was associated with increased OR(res). Rather, recent use of penicillins was associated with decreased carriage of susceptible pneumococci (OR(sus) = 0.2, 95% confidence interval: 0.1, 0.3). In simulations, both types of effects promoted dissemination of resistant pneumococci at the population level. Findings show that oral cephalosporins enhance the risk of acquiring resistant pneumococci. Penicillins accelerate clearance of susceptible strains. The effect of penicillins in increasing resistance is shared equally by treated and untreated members of the population.

Anti-Bacterial Agents↗

PubMed2005

The impact of methicillin resistance in Staphylococcus aureus bacteremia on patient outcomes: mortality, length of stay, and hospital charges.

OBJECTIVE: To evaluate the impact of methicillin resistance in Staphylococcus aureus on mortality, length of hospitalization, and hospital charges. DESIGN: A cohort study of patients admitted to the hospital between July 1, 1997, and June 1, 2000, who had clinically significant S. aureus bloodstream infections. SETTING: A 630-bed, urban, tertiary-care teaching hospital in Boston, Massachusetts. PATIENTS: Three hundred forty-eight patients with S. aureus bacteremia were studied; 96 patients had methicillin-resistant S. aureus (MRSA). Patients with methicillin-susceptible S. aureus (MSSA) and MRSA were similar regarding gender, percentage of nosocomial acquisition, length of hospitalization, ICU admission, and surgery before S. aureus bacteremia. They differed regarding age, comorbidities, and illness severity score. RESULTS: Similar numbers of MRSA and MSSA patients died (22.9% vs 19.8%; P = .53). Both the median length of hospitalization after S. aureus bacteremia for patients who survived and the median hospital charges after S. aureus bacteremia were significantly increased in MRSA patients (7 vs 9 days, P = .045; 19,212 dollars vs 26,424 dollars, P = .008). After multivariable analysis, compared with MSSA bacteremia, MRSA bacteremia remained associated with increased length of hospitalization (1.29 fold; P = .016) and hospital charges (1.36 fold; P = .017). MRSA bacteremia had a median attributable length of stay of 2 days and a median attributable hospital charge of 6916 dollars. CONCLUSION: Methicillin resistance in S. aureus bacteremia is associated with significant increases in length of hospitalization and hospital charges.

Aged↗

PubMed2005

Impact of severity of illness bias and control group misclassification bias in case-control studies of antimicrobial-resistant organisms.

BACKGROUND: Case-control studies often analyze risk factors for antibiotic resistance. Recently published articles have illustrated that randomly selected control-patients may be preferable to those with the susceptible phenotype of the organism. A possible methodologic problem with randomly selected control-patients is potential bias due to control group misclassification. This occurs if some control-patients did not have clinical cultures performed and thus might have been unidentified case-patients. If this bias exists, these studies might be expected to report lower odds ratios (ORs) because control-patients would be more like case-patients. OBJECTIVE: To analyze potential biases that might arise due to control group misclassification and potentially larger selection biases that may be introduced if control-patients are required to have at least one clinical culture. PATIENTS: One hundred twenty case-patients, 770 control-patients in group 1, and 510 control-patients in group 2. METHODS: Two case-control studies. Case-patients had clinical cultures positive for imipenem-resistant Pseudomonas aeruginosa. The first group of control-patients were random. The second group of control-patients were identical to those in group 1 except being required to have at least one clinical culture. RESULTS: Univariate analyses showed higher ORs for case-patients versus control-patients in group 1 (imipenem [OR, 12.5], piperacillin-tazobactam [OR, 3.7], and vancomycin [OR, 4.7]) as compared with case-patients versus control-patients in group 2 (imipenem [OR, 8.0], piperacillin-tazobactam [OR, 2.5], and vancomycin [OR, 3.0]). CONCLUSION: Requiring control-patients to have at least one clinical culture introduces a selection bias likely because it eliminates patients with less severe illness.

Anti-Bacterial Agents↗

PubMed2005

The case-case-control study design: addressing the limitations of risk factor studies for antimicrobial resistance.

OBJECTIVE: There are significant limitations of the standard case-control study design for identifying risk factors for resistant organisms. The objective of this study was to develop a study design to overcome these limitations. DESIGN: Theoretical analysis of different types of study designs that can be used in risk factor studies for resistant organisms. RESULTS: We developed the case-case-control study design, which uses two separate case-control analyses within a single study. The first analysis compares patients infected with resistant bacteria (resistant cases) with control-patients without infection caused by the target organism, who are therefore representative of the source population; and the second analysis compares patients infected with the susceptible phenotype of the target organism (susceptible cases) with the same control-patients without infection caused by the target organism. These two analyses provide risk models for (1) isolation of the resistant phenotype of the target organism as compared with the source population and (2) isolation of the susceptible phenotype of the organism as compared with the source population. When these two risk models are compared and contrasted, risk factors specifically associated with isolation of the resistant phenotype can be identified. CONCLUSIONS: The case-case-control study design is an effective method for identifying risk factors for antimicrobial-resistant pathogens. Although the case-case-control study design has limitations, it is, in our opinion, more informative and less flawed than the standard case-control study design.

Anti-Bacterial Agents↗

PubMed2005

Update on Pseudomonas aeruginosa and Acinetobacter baumannii infections in the healthcare setting.

PURPOSE OF REVIEW: Infections with Pseudomonas aeruginosa and Acinetobacter baumannii are of great concern for hospitalized patients, especially with multidrug-resistant strains. This review focuses on recent data that may help us to understand the emergence, spread, and persistence of antibiotic resistance, and summarizes the optional treatment feasible for these resistant bacteria. RECENT FINDINGS: Multidrug-resistant P. aeruginosa and A. baumannii are increasingly causing nosocomial infections; multidrug-resistant clones are spreading into new geographic areas, and susceptible strains are acquiring resistance genes. New extended-spectrum beta-lactamases and carbapenemases are emerging, leading to pan-resistant strains. Current studies focus on the effect of antibiotics on gene expression in P. aeruginosa biofilms and their contribution to resistance to therapy. Treatment options for multidrug-resistant P. aeruginosa and A. baumannii infections are limited in most cases to carbapenems. Sulbactam is a treatment option for pan-resistant A. baumannii, and or renewed use of an old drug, colistin, is being entertained for pan-resistant A. baumannii and P. aeruginosa. Immunotherapy is a promising new modality being explored. Prevention of emergence of resistance through combination therapy and pharmacokinetic strategies are studied. SUMMARY: The emergence and spread of multidrug-resistant P. aeruginosa and A. baumannii and their genetic potential to carry and transfer diverse antibiotic resistance determinants pose a major threat in hospitals. The complex interplay of clonal spread, persistence, transfer of resistance elements, and cell-cell interaction contribute to the difficulty in treating infections caused by these multidrug-resistant strains. In the absence of new antibiotic agents, new modalities of treatment should be developed.

Acinetobacter Infections↗

PubMed2005

Prior antimicrobial therapy and risk for hospital-acquired Candida glabrata and Candida krusei fungemia: a case-case-control study.

The incidence of infections caused by Candida glabrata and Candida krusei, which are generally more resistant to fluconazole than Candida albicans, is increasing in hospitalized patients. However, the extent to which prior exposure to specific antimicrobial agents increases the risk of subsequent C. glabrata or C. krusei candidemia has not been closely studied. A retrospective case-case-control study was performed at a university hospital. From 1998 to 2003, 60 patients were identified with hospital-acquired non-C. albicans candidemia (C. glabrata or C. krusei; case group 1). For comparison, 68 patients with C. albicans candidemia (case group 2) and a common control group of 121 patients without candidemia were studied. Models were adjusted for demographic and clinical risk factors, and the risk for candidemia associated with exposure to specific antimicrobial agents was assessed. After adjusting for both nonantimicrobial risk factors and receipt of other antimicrobial agents, piperacillin-tazobactam (odds ratio [OR], 4.15; 95% confidence interval [CI], 1.04 to 16.50) and vancomycin (OR, 6.48; CI, 2.20 to 19.13) were significant risk factors for C. glabrata or C. krusei candidemia. For C. albicans candidemia, no specific antibiotics remained a significant risk after adjusted analysis. Prior fluconazole use was not significantly associated with either C. albicans or non-C. albicans (C. glabrata or C. krusei) candidemia. In this single-center study, exposure to antibacterial agents, specifically vancomycin or piperacillin-tazobactam, but not fluconazole, was associated with subsequent hospital-acquired C. glabrata or C. krusei candidemia. Further studies are needed to prospectively analyze specific antimicrobial risks for nosocomial candidemia across multiple hospital centers.

Anti-Infective Agents↗