Implementation of isolation precautions: role of a targeted information flyer.

Isolation precautions are advocated in most countries for patients harbouring multi-drug-resistant organisms. We evaluated the impact of a targeted information flyer on the implementation of isolation precautions for patients with methicillin-resistant Staphylococcus aureus (MRSA). A flyer providing a quick reference to the steps to be implemented following detection of MRSA was sent systematically by the microbiologists with all results displaying MRSA. Infection control staff compared isolation precautions in two three-month periods: the first (control) period before implementation of the flyer and the second (intervention) period after implementation of the flyer. Compared with the control period, compliance with isolation precautions increased significantly in the intervention period. In intensive care units, there was a sign posted on the door for 31 of 38 (82%) patients in the control period, and 33 out of 34 (97%) in the intervention period (P=0.06). Use of gowns increased from 82% to 100% (P=0.01), use of dedicated materials increased from 84% to 100% (P=0.03), availability of alcohol hand rub increased from 82% to 94% (P=0.10), and the proportion of MRSA patients in private rooms increased from 71% to 91% of the cases (P=0.07). In conclusion, compliance with isolation precautions increased after attaching a flyer to all MRSA-positive bacteriological results.

[Evolution of susceptibility of aerobic gram-negative aerobic bacilli to quinolones and fluoroquinolones in a university hospital (1992-2000)]. / Evolution de la sensibilité aux quinolones et aux fluoroquinolones des bacilles à Gram négatif aérobies isolés dans un hôpital universitaire (1992-2000).

Susceptibility to quinolones of aerobic gram-negative bacilli was assessed in a 2000-bed university hospital from 1992 to 2000. There was a significant downward trend in the rate of susceptibility to nalidixic acid (Nal) for Enterobacteriaceae as a whole from 1992 to 2000 (86% vs 82%), and E. coli (92% vs 84%), and an upward trend for K. pneumoniae (74% vs 82%), the latter being related to the control of the spread of epidemic ESBL producing strains. The overall susceptibility of Enterobacteriaceae to ciprofloxacin (Cip) paralleled the susceptibility to Nal: decreased susceptibility for Enterobacteriaceae as a whole (96% vs 89%) and E. coli (99% vs 91%). A clear decrease in the level of susceptibility to Cip occurred during the study period among the Nal-resistant strains as demonstrated by the decrease in the median zone diameter (D) observed among the Nal-resistant strains of E. coli (26 mm in 1992 vs 19 mm in 1998-2000). The zone diameter distribution pattern changed from an unimodal distribution in 1992 to a trimodal distribution in 2000 secondary to the occurrence of a population of resistant strains (D = 13 mm) and of a highly resistant population (D = 6 mm). Finally, the susceptibility to Cip of P. aeruginosa strains remained stable around 62% throughout the study period.

Trends in quinolone susceptibility of Enterobacteriaceae among inpatients of a large university hospital: 1992-98.

OBJECTIVES: To assess trends in quinolone susceptibility of Enterobacteriaceae isolated in a large university hospital. METHODS: Between 1992 and 1998, bacterial isolates were collected each year during a 3-month period to evaluate annual changes in susceptibility. In addition, the activities of fluoroquinolones (pefloxacin, norfloxacin, ofloxacin, ciprofloxacin) against nalidixic acid-resistant strains were determined by disk diffusion and MIC methodologies during the first and last year of the study. RESULTS: The susceptibility of Enterobacteriaceae to nalidixic acid was unchanged between 1992 and 1998 (86% versus 85%). However, at the species level, the susceptibility rates to nalidixic acid decreased for Escherichia coli from 92% to 89%, and for Enterobacter cloacae from 87% to 82%. In contrast, there was a 10% increase in the nalidixic acid susceptibility rates for Klebsiella pneumoniae (74% versus 83%), which was thought to be due to the control of the spread of epidemic extended-spectrum beta-lactamase (ESBL)-producing strains. The overall susceptibility of the Enterobacteriaceae to the fluoroquinolones remained high during the study period, greater than 90% in the case of ciprofloxacin. However, nalidixic acid-resistant Escherichia coli showed decreased susceptibility to ciprofloxacin between 1992 and 1998, as reflected by a decrease in median zone diameter (26 mm to 19 mm), an increase in MIC(50) (0.25 mg/L to 1 mg/L) and a shift in MIC distribution (unimodal in 1992 to bimodal in 1998). This has resulted in the reduced susceptibility of Escherichia coli to fluoroquinolones between 1992 and 1998 (pefloxacin, 95-90%; ciprofloxacin, 99-95%). CONCLUSIONS: The susceptibility of Escherichia coli to quinolones has decreased, and the level of susceptibility of the resistant strains has increased over the 7-year study period.

Anticancer drugs induce necrosis of human endothelial cells involving both oncosis and apoptosis.

The endothelium is the first physiological barrier between blood and tissues and can be injured by physical or chemical stress, particularly by the drugs used in cancer therapy. We found that four anticancer agents: etoposide, doxorubicin, bleomycin and paclitaxel induced apoptosis in human umbilical vein endothelial cells (HUVECs) (as judged by DNA fragmentation) with a time- and concentration-dependent decrease in bcl-2 protein but without the involvement of p53. As revealed by immunoblotting, bax protein was expressed in HUVECs treated with 1 mg/ml etoposide whereas bcl-2 protein disappeared. Oncosis occurred parallel to apoptosis with the release of lactate dehydrogenase into the supernatant, and, for doxorubicin and etoposide with the inversion of the distribution of angiotensin I-converting enzyme between supernatant and cells. Among the four tested anticancer drugs, only doxorubicin induced an oxidative stress, with significative malondialdehyde production. Thus, human endothelial cells in confluent cultures seem to be in an equilibrium of resistance to apoptosis related to bcl-2 expression; this equilibrium can be disrupted by a chemical stress, such as the antiproliferative drugs known as pro-apoptotic for tumour cells. For doxorubicin and bleomycin, this cellular toxicity can be related to their unwanted effects in human cancer therapy. Low doses of doxorubicin, paclitaxel or etoposide, however, could induce apoptosis of endothelial cells of new vessels surrounding the tumour, thus leading to specific vessel regression with minimal toxic effects for the endothelium of the other vessels. These findings provide evidence of relationships between endothelial toxicity of anticancer drugs and the key role of bcl-2 for resistance of endothelium cells toward apoptosis; moreover lack of p53 and bax in quiescent cells contributes to resistance of endothelial cells to DNA-damaging agents.