Recently, an extended-spectrum beta-lactamase (PER-1) was found to be disseminated among Acinetobacter spp. and Pseudomonasaeruginosa isolates in Turkey. A population-based cohort study was conducted to elucidate predictive mortality factors in patients with nosocomial infections caused by Acinetobacter spp. and P. aeruginosa, with particular reference to PER-1-type extended-spectrum beta-lactamase (ESBL) production. The study group comprised 16 and 21 non-survivors and 82 and 126 survivors in cohorts infected with Acinetobacter and P. aeruginosa, respectively. In the Acinetobacter-infected cohort, nosocomial pneumonia, hypotension and infection with a PER-positive isolate were independent predictors of mortality. In the P. aeruginosa-infected cohort, impaired consciousness, a PER-positive isolate, male sex and (with a negative relative risk) urinary tract infection were independent predictors of death. This study demonstrated the relationship of PER-1-type ESBL-producing Acinetobacter spp. and P. aeruginosa with poor clinical outcome.

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Two Salmonella enterica serovar Typhimurium strains from different clonal origins, both producing an extended-spectrum β-lactamase (TEM-52), were isolated from a patient. This enzyme was encoded on a single plasmid and was found at very low levels in one strain, while being encoded on multiple plasmids and in multiple different Eco RI fragments in the other strain.

Background: There are few studies about hospital-acquired pneumonia (HAP) developing in non-intensive care units (non-ICUs). Objectives: The aim of this study was to determine the incidence rate of non-ICU HAP, the risk factors associated with mortality and the survival rates of HAP patients at 6 weeks and 1 year. Patients and Methods: Between March 2005 and February 2006, 154 adult patients (97 males) with HAP were prospectively evaluated. Immunocompromised patients who were developing pneumonia were excluded from the study. The HAP incidence was calculated and survival was noted at 6 weeks and 1 year later. Kaplan-Meier methods were used for survival analysis; Cox regression was used to identify the risk factors associated with HAP-induced mortality. Results: During the study, and not counting those in the ICU, 45,679 adult patients were hospitalized. Of these, 154 patients developed HAP (incidence 3.3 cases/1,000 patients). The mean age of those developing HAP was 64.53 ± 14.92 years (range 15–98). Survival rates at the 3rd, 7th, 14th, 42nd and 365th day were 91, 89, 69, 49 and 29%, respectively. Independent risk factors associated with 6-week mortality were: age [relative risk (RR) 1.026; 95% confidence interval (CI) 1.008–1.045], chronic renal failure (RR 1.8; 95% CI 1.087–3.086), aspiration risk (RR 2.86; 95% CI 1.249–6.564), steroid use (RR 2.35; 95% CI 1.306–4.257), and multilobar infiltration (RR 2.1; 95% CI 1.102–4.113). Conclusion: HAP – even if it develops in non-ICU environments – is hard to treat and has a higher mortality rate.