Bloodstream infections (BSI) caused by extended-spectrum ␤-lactamase (ESBL)-producing organisms markedly increase the rates of treatment failure and death. We conducted a retrospective cohort analysis to identify risk factors for mortality in adult in-patients with BSI caused by ESBL-producing Enterobacteriaceae (ESBL-BSI). Particular attention was focused on defining the impact on the mortality of inadequate initial antimicrobial therapy (defined as the initiation of treatment with active antimicrobial agents >72 h after collection of the first positive blood culture). A total of 186 patients with ESBL-BSI caused by Escherichia coli (n ‫؍‬ 104), Klebsiella pneumoniae (n ‫؍‬ 58), or Proteus mirabilis (n ‫؍‬ 24) were identified by our microbiology laboratory from 1 January 1999 through 31 December 2004. The overall 21-day mortality rate was 38.2% (71 of 186). In multivariate analysis, significant predictors of mortality were inadequate initial antimicrobial therapy (odds ratio [OR] ‫؍‬ 6.28; 95% confidence interval [CI] ‫؍‬ 3.18 to 12.42; P < 0.001) and unidentified primary infection site (OR ‫؍‬ 2.69; 95% CI ‫؍‬ 1.38 to 5.27; P ‫؍‬ 0.004). The inadequately treated patients (89 of 186 [47.8%]) had a threefold increase in mortality compared to the adequately treated group (59.5% versus 18.5%; OR ‫؍‬ 2.38; 95% CI ‫؍‬ 1.76 to 3.22; P < 0.001). The regimens most commonly classified as inadequate were based on oxyimino cephalosporin or fluoroquinolone therapy. Prompt initiation of effective antimicrobial treatment is essential in patients with ESBL-BSI, and empirical decisions must be based on a sound knowledge of the local distribution of pathogens and their susceptibility patterns.Bloodstream infections (BSI) caused by organisms that produce extended-spectrum ␤-lactamase (ESBLs) are associated with increased rates of treatment failure and death (1, 14, 15, 19, 22, 25, 28, 30-33, 38, 39, 41, 43, 46, 47, 50, 51). ESBLs are plasmid-mediated beta-lactamases that confer resistance to oxyimino cephalosporins and monobactams (7,33). In most cases, they are the result of mutations involving the classical TEM-1/TEM-2 and SHV-1 type ␤-lactamase genes, although exceptions to this rule (e.g., CTX-M ␤-lactamases) are becoming more and more common (13,27,33,39).Patients at high risk for infection by ESBL-producing organisms are often seriously ill, with histories of lengthy hospital stays and prolonged exposure to invasive medical devices and/or procedures (3,5,13,15,25,35,41,43,49). Prior exposure to antimicrobial therapy is also a well-recognized risk factor for acquisition of an ESBL-producing organism (25,35,43,47).The presence of an ESBL determinant significantly reduces the number of antimicrobial agents to which the infecting organism is susceptible (9). In addition, because of their nosocomial origin and the frequent links between ESBL genes and other resistance genes on the mobile DNA elements that are involved in their dissemination, ESBL producers often present complex multidrug-resistant phenotypes (7,27,33,42).Inade...

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.

No abstract

No abstract

Background: Diagnosis of HIV infection is recently occurring with increasing frequency in middleaged and in older individuals. As HAART became available, a minimal beneficial effect on immunological outcome in older in respect of younger subjects has been reported. In fact, both the intensity and the rapidity of the immunological response appeared to be reduced in elderly subjects. On the contrary, only few reports have indicated a similar immunological outcome both in older and younger HIV-positive subjects. Interestingly, older age did not seem to significantly affect the long-term virological outcome of HAART treated subjects.