Bloodstream infections caused by extended-spectrum--lactamase (ESBL)-producing Klebsiella pneumoniae isolates are a major concern for clinicians, since they markedly increase the rates of treatment failure and death. One hundred forty-seven patients with K. pneumoniae bloodstream infections were identified over a 5-year period (January 1999 to December 2003). The production of ESBLs in bloodstream isolates was evaluated by molecular methods. A retrospective case-case-control study was conducted to identify risk factors for the isolation of ESBLproducing K. pneumoniae or non-ESBL-producing K. pneumoniae isolates in blood cultures. Forty-eight cases infected with ESBL-producing K. pneumoniae isolates and 99 cases infected with non-ESBL-producing K. pneumoniae isolates were compared to controls. Risk factors for isolation of ESBL-producing K. pneumoniae isolates were exposure to antibiotic therapy (odds ratio [OR], 11.81; 95% confidence interval [CI], 2.72 to 51.08), age (OR, 1.14; 95% CI, 1.08 to 1.21), and length of hospitalization (OR, 1.10; 95% CI, 1.04 to 1.16). Independent determinants for isolation of non-ESBL-producing K. pneumoniae were previous urinary tract infection (OR, 8.50; 95% CI, 3.69 to 19.54) and length of hospitalization (OR, 1.07; 95% CI, 1.04 to 1.10). When the initial response was assessed at 72 h after antimicrobial therapy, the treatment failure rate for the ESBL-producing K. pneumoniae-infected group was almost twice as high as that of the non-ESBL-producing K. pneumoniae-infected group (31% versus 17%; OR, 2.19; 95% CI, 0.98 to 4.89). The 21-day mortality rate for all patients was 37% (54 of 147); it was 52% (25 of 48) for patients with ESBL-producing K. pneumoniae bloodstream infections and 29% (29 of 99) for patients with non-ESBLproducing K. pneumoniae bloodstream infections (OR, 2.62; 95% CI, 1.28 to 5.35). In summary, this investigation identifies epidemiological characteristics that distinguish ESBL-producing K. pneumoniae infections from non-ESBL-producing K. pneumoniae ESBL bloodstream infections.
Extended-spectrum--lactamase (ESBL)-producing strains of Escherichia coli are a significant cause of bloodstream infections (BSI) in hospitalized and nonhospitalized patients. We previously showed that delaying effective antimicrobial therapy in BSI caused by ESBL producers significantly increases mortality. The aim of this retrospective 7-year analysis was to identify risk factors for inadequate initial antimicrobial therapy (IIAT) (i.e., empirical treatment based on a drug to which the isolate had displayed in vitro resistance) for inpatients with BSI caused by ESBL-producing E. coli. CI, 1.11 to 6.29; P ؍ 0.02). IIAT was the strongest risk factor for 21-day mortality and significantly increased the length of hospitalization after BSI onset. Our results underscore the need for a systematic approach to the management of patients with serious infections by ESBL-producing E. coli. Such an approach should be based on sound, updated knowledge of local infectious-disease epidemiology, detailed analysis of the patient's history with emphasis on recent contact with the health care system, and aggressive attempts to identify the infectious focus that has given rise to the BSI.Extended-spectrum -lactamases (ESBLs) are a heterogeneous group of plasmid-mediated bacterial enzymes that confer significant resistance to oxyimino cephalosporin and monobactam antimicrobials (8,28,30). Throughout the world, increasing attention is being focused on the growing involvement of ESBL-producing strains of Escherichia coli in serious infections of hospitalized and nonhospitalized patients (3, 26, 28-30, 34, 35, 39, 45). This trend is due largely to the emergence of CTX-M type ESBLs, a rapidly expanding group of enzymes that are being encountered with increasing frequency, especially in E. coli (24,25,35,36,48). They are encoded by transferable plasmid genes captured from the chromosomes of Kluyvera spp. (6, 36). Acquisition of any ESBL determinant reduces the number of antimicrobial agents to which the microorganism is susceptible (18,25,38). This problem is compounded by the fact that ESBL producers often carry other antimicrobial resistance genes, which are located near the bla gene on the mobile DNA elements that are involved in their dissemination. In these cases, there is a substantial risk that the infecting pathogen will be resistant to the empirically prescribed antimicrobial treatment.In a previous study we found that failure to provide adequate antimicrobial therapy in the initial stages of bloodstream infections (BSI) caused by ESBL-producing Enterobacteriaceae was associated with a strong increase in the risk of 21-day mortality (45). These findings are consistent with those of other investigators (1,18,19,35,39,40). However, much less is known about the specific factors that increase the likelihood of ineffective empirical treatment in these cases (18). Identification of risk factors that are predictive of resistance to empirically prescribed antimicrobials should facilitate attempts to define more-effective managemen...
Staphylococci are an increasing cause of bloodstream infections. Rapid reliable identification of these organisms is essential for accurate diagnosis and prompt effective treatment. We evaluated the ability of the VITEK 2 system (bioMérieux, Inc, Hazelwood, Mo.) to identify these organisms rapidly and accurately. A total of 405 clinically relevant nonduplicate staphylococcal isolates (Staphylococcus aureus, n ؍ 130; coagulasenegative staphylococci, n ؍ 275) collected from blood cultures were tested. VITEK 2 results were considered correct when they were identical to those furnished by the comparison method based on the ID 32 STAPH system (bioMérieux, Marcy l'Etoile, France) plus supplementary manual testing. When discrepancies occurred, isolate identity was verified by molecular typing. The VITEK 2 correctly identified 387 (95.6%) isolates at the species level: 379 (including all but one [99.2%] of 130 S. aureus isolates and 249 of 275 [90.5%] coagulase-negative isolates) were identified by the automated reading; for the other eight, supplemental tests suggested by the manufacturer had to be used. Only one strain (0.2%) was misidentified (Staphylococcus hominis as Staphylococcus epidermidis), and four (1%), all S. epidermidis, were not identified. For the remaining 13 strains (including 10 S. hominis), the VITEK 2 system was unable to discriminate among two species, and no supplemental tests were suggested for conclusive identification. Over 90% of results were obtained within 4 h. These results suggest that the VITEK 2 system can provide rapid, accurate, and reliable species-level identification of staphylococci responsible for bloodstream infections, although there is room for improvement in the identification of certain coagulase-negative species, especially S. hominis.Bloodstream infections are a major cause of morbidity and mortality. The frequency, etiology, and epidemiology of these infections have changed over the years. Staphylococcus aureus is now recognized as an important cause of both hospital and community-acquired bloodstream infections (1,3,8,9,27,30). During the last 2 decades, the increased use of invasive procedures and broad-spectrum antibiotics, together with the growing number of immunocompromised and/or seriously ill patients, has led to the emergence of coagulase-negative staphylococci, particularly Staphylococcus epidermidis, and these organisms plays a prominent role in nosocomial bloodstream infections (1,2,3,8,9,17,18,29). Rapid and reliable species identification of these organisms is essential for accurate diagnosis and prompt effective treatment of these infections (6,7,10,16). Several manual and commercial identification methods have been developed and are now routinely used (4,5,15,23,24,25,26,31). The fully automated VITEK 2 system (bioMérieux, Inc, Hazelwood, Mo.) can provide identification results for gram-positive cocci in a few hours thanks to the improved sensitivity of its fluorescence-based technology, and this feature represents a major improvement over earlier versi...
To evaluate the changing characteristics of HIV-associated bacteremia in the highly active antiretroviral therapy (HAART) era, we conducted a prospective case control study, comparing two periods of time, before (period A) and after (period B) the introduction of HAART. In total, 174 patients with bacteremia and 348 controls were studied. By comparing incidence in periods A and B, a statistically significant reduction of bacteremia, from 11.8 to 6.3/100 person-years (PY), was observed (p = .0001). Incidence of hospital-acquired bacteremia decreased from 5.8 episodes/100 PY in period A to 2.4/100 PY in period B (p = .0005). A similar trend was also observed for community-acquired episodes of bacteremia, with a value close to statistical significance. Logistic regression analysis indicated that intravenous drug abuse, central venous catheter (CVC) use, high value on APACHE III score, and neutropenia were independent risk factors for bacteremia in both the study periods. Interestingly, comparing the prevalence of bacteremia risk factors in the two study periods, we observed a significant reduction in the use of CVC (p = .04, period A versus period B) and in neutropenia (p = .04). The crude mortality rate was 31% in period A and 23% in period B (p = not significant [ns]). Logistic regression analysis indicated that an high value of Acute Physiology and Chronic Health Evaluation III (APACHE III) score (p < .001) predicted an increased risk of death. Analysis of prognostic factors of bacteremia did not significantly differ in both the study periods. We conclude that HAART has determined a significant reduction of the incidence and a modification of the characteristics of bacteremia. This reduced incidence may produce a substantial impact on future morbidity and health care costs of patients with HIV.
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