Objective To evaluate the efficacy and safety of intravenous fluconazole for the prevention of intra-abdominal Candida infections in high-risk surgical patients. Design Randomized, prospective, double-blind, placebo-controlled study. Setting Two university-affiliated hospitals in Switzerland. Patients Forty-nine surgical patients with recurrent gastrointestinal perforations or anastomotic leakages. Interventions Prophylaxis with intravenous fluconazole (400 mg per day) or placebo continued until resolution of the underlying surgical condition. Measurements and Main Results Patients were evaluated daily, and specimens for culture were obtained three times per week during prophylaxis. The primary study end points were the frequency of and the time to intra-abdominal Candida infections. Secondary end points were the frequency of candidiasis (intraabdominal and extra-abdominal) and the emergence or persistence of Candida colonization. Among patients who were not colonized at study entry, Candida was isolated from surveillance cultures during prophylaxis in 15% of the patients in the fluconazole group and in 62% of the patients in the placebo group (relative risk, 0.25; 95% confidence interval, 0.07 to 0.96; p = .04). Candida peritonitis occurred in one of 23 patients (4%) who received fluconazole and in seven of 20 patients (35%) who received placebo (relative risk, 0.12; 95% confidence interval, 0.02 to 0.93; p = .02). In addition, one catheter-related Candida albicans sepsis occurred in a fluconazole-treated patient. Thus, overall, candidiasis developed in two fluconazole patients and seven placebo patients (relative risk, 0.25; 95% confidence interval, 0.06 to 1.06; p = .06). C. albicans accounted for 87% of the Candida species isolated before or during prophylaxis, and all C. albicans strains were susceptible to fluconazole. Fluconazole was well tolerated, and adverse events occurred at similar frequencies in both treatment groups. Conclusions Fluconazole prophylaxis prevents colonization and invasive intra-abdominal Candida infections in high-risk surgical patients. (Crit Care Med 1999; 27:1066-1072)
Abstract Infection control in hospitals is not mandatory in Switzerland as in the United States. There are more than 300 acute-care hospitals in Switzerland. Hospitals are reimbursed by patient-days rather than diagnosis-related group. However, all five Swiss university hospitals have developed an infection control program. The major criteria for setting up and running these programs are reviewed; data are based on a questionnaire and personal interviewing of each institution. Most of the major criteria exist in all five institutions. Resources allocated to infection control differ markedly. The number of infection control nurses per 250 beds varies between 0.2 and 0.75 for the five hospitals; the activity of those in charge of infection control differs between hospitals. A comparison is made between the Swiss and U.S. programs with regard to some aspects of healthcare and infection control.
Months from HA measurement P=0.0052 Hyaluronic Acid as a Prognostic Marker of Hepatic Encephalopathy and Liver-related Death in HIV/Viral Hepatitis Coinfected Patients L Peters1, A Mocroft2, V Soriano3, J Rockstroh4, B Ledergerber5, A Karlsson6, B Knysz7, C Pradier8, K Zilmer9, JD Lundgren1, 10, for the EuroSIDA study group. 1Copenhagen HIV Programme, University of Copenhagen, Denmark, 2University College Medical School, Royal Free Campus, London, UK, 3Hospital Carlos III, Madrid, Spain, 4University of Bonn, Germany, 5University Hospital Zurich, Switzerland, 6Venhalsan, Sodersjukhuset, Stockholm, Sweden, 5Department of Infectious Diseases, Wroclaw Medical University, Wroclaw, Poland 8CHU Nice Hopital de l Archet 1, Nice, France, 9West-Tallin Central Hospital, Tallinn, Estonia, 10Centre for Viral Disease/KMA, Rigshospitalet, Copenhagen, Denmark
Background. In 1998, a study in the intensive care unit (ICU) of our institution suggested possible transmission of Pseudomonas aeruginosa from faucet to patient and from patient to patient. Infection-control measures were implemented to reduce the degree of P. aeruginosa colonization in faucets, to reduce the use of faucet water in certain patient care procedures, and to reduce the rate of transmission from patient to patient. Objective. To evaluate the effect of the control measures instituted in 1999 to prevent P. aeruginosa infection and colonization in ICU patients. Design. Prospective, molecular, epidemiological investigation. Setting. A 870-bed, university-affiliated, tertiary care teaching hospital. Methods. The investigation was performed in a manner identical to the 1998 investigation. ICU patients with a clinical specimen positive for P. aeruginosa were identified prospectively. Swab specimens from the inner part of the ICU faucets were obtained for the culture on 9 occasions between September 1997 and December 2000. All patients and environmental isolates were typed by pulsed-field gel electrophoresis (PFGE). Results. Compared with the 1998 study, in 2000 we found that the annual incidence of ICU patients colonized or infected with P. aeruginosa had decreased by half (26.6 patients per 1,000 admissions in 2000 vs 59.0 patients per 1,000 admissions in 1998), although the populations of patients were comparable. This decrease was the result of the decreased incidence of cases in which an isolate had a PFGE pattern identical to that of an isolate from a faucet (7.0 cases per 1,000 admissions in 2000, vs 23.6 per 1,000 admissions in 1998) or from another patient (6.5 cases per 1,000 admissions in 2000 vs 16.5 cases per 1,000 admissions in 1998), whereas the incidence of cases in which the isolate had a unique PFGE pattern remained nearly unchanged (13.1 cases per 1,000 admissions in 2000 vs 15.6 cases per 1,000 admissions in 1998). Conclusions. These results suggest that infection control measures were effective in decreasing the rate of P. aeruginosa colonization and infection in ICU patients, confirming that P. aeruginosa strains were of exogenous origin in a substantial proportion of patients during the preintervention period.
Even with a good surveillance program, nosocomial infections may be not recognized because of several reasons: absence of symptoms or prolonged incubation period (eg, viral bloodborne infections, tuberculosis); problems with the microbiological diagnosis, because adequate specimens may be difficult to obtain or special methods should be used (eg, fungal infections, virus, new agents); shorter hospital stays (eg, surgical-site infections); difficulty in distinguishing between nosocomial and community-acquired infections (eg, influenza); and failure to detect clinically relevant colonization (eg, multiresistant microorganisms). Because of the important potential consequences of occult nosocomial infections, specific surveillance programs should be designed to address these problems.
ABSTRACT Staphylococcus aureus harbors redundant adhesins mediating tissue colonization and infection. To evaluate their intrinsic role outside of the staphylococcal background, a system was designed to express them in Lactococcus lactis subsp. cremoris 1363. This bacterium is devoid of virulence factors and has a known genetic background. A new Escherichia coli-L. lactis shuttle and expression vector was constructed for this purpose. First, the high-copy-number lactococcal plasmid pIL253 was equipped with the oriCol E1 origin, generating pOri253 that could replicate in E. coli . Second, the lactococcal promoters P23 or P59 were inserted at one end of the pOri253 multicloning site. Gene expression was assessed by a luciferase reporter system. The plasmid carrying P23 (named pOri23) expressed luciferase constitutively at a level 10,000 times greater than did the P59 -containing plasmid. Transcription was absent in E. coli . The staphylococcal clumping factor A ( clfA ) gene was cloned into pOri23 and used as a model system. Lactococci carrying pOri23- clfA produced an unaltered and functional 130-kDa ClfA protein attached to their cell walls. This was indicated both by the presence of the protein in Western blots of solubilized cell walls and by the ability of ClfA-positive lactococci to clump in the presence of plasma. ClfA-positive lactococci had clumping titers (titer of 4,112) similar to those of S. aureus Newman in soluble fibrinogen and bound equally well to solid-phase fibrinogen. These experiments provide a new way to study individual staphylococcal pathogenic factors and might complement both classical knockout mutagenesis and modern in vivo expression technology and signature tag mutagenesis.