Colonization of patients and contamination of the patients' environment by MRSA under conditions of single-room isolation.

Meticillin-resistant Staphylococcus aureus (MRSA) are endemic in hospitals worldwide and present a major concern in hospital hygiene. The aim of the present study was to investigate the relationship between patients' MRSA colonization of the body and the frequency of environmental contamination. Twenty-five MRSA-positive hospitalized surgical patients and their environment in isolation rooms were screened on four occasions over a 14-day period. Out of 1099 samples from patients, 330 (30.0%) were MRSA-positive. The median number of MRSA-positive body sites per screening decreased significantly from the 1st (3, range 1-9) to the 14th (2, range 0-9, p=0.011) day of isolation. Contamination was found in 45% of the 100 environmental sampling dates and MRSA was detected in a low proportion of the 1000 environmental surface samples: 105/1000 (10.5%). The number of positive results for each sampling date decreased from the 1st (median 1, range 0-8) to the 14th (median 0, range 0-3, p=0.21) day of isolation. The results show a very strong correlation between the number of MRSA-positive body sites of individual patients and the MRSA contamination of the patient's hospital room (r=0.700, p<0.001). Pulsed-field gel electrophoresis (PFGE) analysis demonstrated a 98% agreement between patient and environmental samples. MRSA colonization of the groin area correlates most strongly with colonization of the body and environment. Seventy-five of 240 (31%) samples taken in rooms of patients with colonization of the groin were MRSA-positive, whereas only 27 of 760 (3.6%) samples taken in rooms of patients without colonization of the groin produced positive results (odds ratio 12.3; 95% confidence interval, 7.7-20). It is concluded that MRSA patients without colonization of the groin have a relatively low risk of environmental spread of MRSA and thus a reduced risk of transmission.

High and low response in relation to nitric oxide formation but not to lipid peroxidation in patients with sepsis.

OBJECTIVES: Nitric oxide overproduction in sepsis syndrome was suspected to be responsible for hemodynamic derangement and, by induction of lipid peroxidation, for tissue damage. Therefore, nitric oxide formation and lipid peroxidation were quantified in septic patients (SP) vs. patients with localized infection (IF) or without inflammation (C). Nitric oxide formation in sepsis was additionally compared with data for clinical status. DESIGN: Prospective study with consecutive sampling of patients. SETTING: A university hospital intensive care unit and research laboratories. PATIENTS: SP, 24 patients; IP, 7; and C, 13. INTERVENTIONS: Plasma measurement of nitrate, lipid peroxides (primary endpoints), and N-hydroxy-L-arginine (secondary end point) MEASUREMENTS AND MAIN RESULTS: For nitrate, there was a sequence of C < IP = SP. Among SP, one group with significantly higher nitrate (high-responders for nitric oxide; SP-HR) vs. IP and C and a second group (low-responders; SP-LR) with increased concentration only vs. C could be identified. For SP-HR vs. IP, a strong time kinetics in nitric oxide formation was obvious, indicated by significant nitrate increase already 1 day before sepsis started, tripling up to the peak concentration, and then a lowering but still increased value on the first day after sepsis. N-hydroxy-L-arginine was significantly increased in SP-HR vs. C. For lipid peroxides, the concentrations were comparable in SP and IP, but both significantly increased vs. C. Clustering and coincident kinetics of lipid peroxidation related to nitric oxide were not obvious. Furthermore, there was no strong correlation of clinical data and nitric oxide clustering in sepsis. CONCLUSIONS: High- and low-responders for nitric oxide were identified among septic patients. This finding was not associated with significant differences in lipid peroxidation or clinical data.