No abstract available.
Staphylococcus aureus* ; Staphylococcus*

BACKGROUNDS : Infections due to vancomycin-resistant enterococci (VRE) have been reported with increasing frequency in many parts of the world. However, VRE infection is still very rare in Korea. To assess the potential risk of VRE infection in a hospital where such infection is rarely reported, we screened hospitalized patients for fecal colonization with VRE and performed a clinical and epidemiological investigation of VRE colonization. MATERIALS AND METHODS: We screened 405 stool specimens from in- and outpatients for the presence of enterococci using EnterococcoselTM agar (BBLR, USA). Dark-brown or black colonies were tested for enterococci and speciated, followed by confirmation for vancomycin resistance using brain-heart infusion agar containing vancomycin (6microgram/mL). Antimicrobial susceptibilities were determined by agar dilution, disk diffusion, and Vitek GPS-IZ. We also performed pulsed-field gel electrophoresis (PFGE) after SmaI digestion of DNA and polymerase chain reaction for detection of vanA, B and C. To define risk factors for colonization, we reviewed the medical records of patients colonized with VRE or vancomycin- susceptible enterococci (VSE). RESULTS: Twelve (4.1%) of 295 hospitalized patients were colonized with VRE. Six were identified as Enterococcus(E) faecium, 2 each as E. faecalis and E. gallinarum, and 1 each as E. casseliflavus and E. avium. In contrast, only one(0.9%) VRB (E. casseliflavus) was isolated from outpatients. Patients in the intensive careunit (5.4%) and patients whose stool specimens were submitted for Clostridium difficile toxin assay (6.8%) were colonized at higher rate than other inpatients (2.5%), but not at a statistically significant level. Three strains had high-level resistance to van comycin(minimum inhibitory concentration, MIC>256microgram/mL), and the others had low-level resistance (MIC8-16microgram/mL) by agar dilution. But disk diffusion method and Vitek system had problems in detecting some strains with low-level resistance. PFGE patterns of VRE were diverse, suggesting that VRE have been introduced from multiple sources. The vans gene was detected in 3 isolates and vanC gene was found in 9 isolates. Compared with the patients with VSE colonization, patients with VRE had a significantly longer hospital stay, had more frequent invasive procedures or therapeutic interventions such as ventilator, total parenteral nutrition and hemodialysis, showed renal insufficiency more frequently, and were more likely to have received ciprofloxacin or clindamycin therapy. CONCLUSIONS: Although the incidence of VRE infection remains low in Korea, the findings from this study indicate that VRE are not uncommon intestinal colonizers among hospitalized patients. Strict infection control measures including screening for VRE, especially those from patients at risk, close surveillance, judicious use of antibiotics and patient isolation must be implemented to prevent infection and transmission of VRE.
Agar ; Anti-Bacterial Agents ; Ciprofloxacin ; Clindamycin ; Clostridium difficile ; Colon* ; Diffusion ; Digestion ; DNA ; Electrophoresis, Gel, Pulsed-Field ; Humans ; Incidence ; Infection Control ; Inpatients ; Korea ; Length of Stay ; Mass Screening ; Medical Records ; Outpatients ; Parenteral Nutrition, Total ; Patient Isolation ; Polymerase Chain Reaction ; Renal Dialysis ; Renal Insufficiency ; Risk Factors ; Vancomycin ; Vancomycin Resistance ; Ventilators, Mechanical

BACKGROUNDS : Infections due to vancomycin-resistant enterococci (VRE) have been reported with increasing frequency in many parts of the world. However, VRE infection is still very rare in Korea. To assess the potential risk of VRE infection in a hospital where such infection is rarely reported, we screened hospitalized patients for fecal colonization with VRE and performed a clinical and epidemiological investigation of VRE colonization. MATERIALS AND METHODS: We screened 405 stool specimens from in- and outpatients for the presence of enterococci using EnterococcoselTM agar (BBLR, USA). Dark-brown or black colonies were tested for enterococci and speciated, followed by confirmation for vancomycin resistance using brain-heart infusion agar containing vancomycin (6microgram/mL). Antimicrobial susceptibilities were determined by agar dilution, disk diffusion, and Vitek GPS-IZ. We also performed pulsed-field gel electrophoresis (PFGE) after SmaI digestion of DNA and polymerase chain reaction for detection of vanA, B and C. To define risk factors for colonization, we reviewed the medical records of patients colonized with VRE or vancomycin- susceptible enterococci (VSE). RESULTS: Twelve (4.1%) of 295 hospitalized patients were colonized with VRE. Six were identified as Enterococcus(E) faecium, 2 each as E. faecalis and E. gallinarum, and 1 each as E. casseliflavus and E. avium. In contrast, only one(0.9%) VRB (E. casseliflavus) was isolated from outpatients. Patients in the intensive careunit (5.4%) and patients whose stool specimens were submitted for Clostridium difficile toxin assay (6.8%) were colonized at higher rate than other inpatients (2.5%), but not at a statistically significant level. Three strains had high-level resistance to van comycin(minimum inhibitory concentration, MIC>256microgram/mL), and the others had low-level resistance (MIC8-16microgram/mL) by agar dilution. But disk diffusion method and Vitek system had problems in detecting some strains with low-level resistance. PFGE patterns of VRE were diverse, suggesting that VRE have been introduced from multiple sources. The vans gene was detected in 3 isolates and vanC gene was found in 9 isolates. Compared with the patients with VSE colonization, patients with VRE had a significantly longer hospital stay, had more frequent invasive procedures or therapeutic interventions such as ventilator, total parenteral nutrition and hemodialysis, showed renal insufficiency more frequently, and were more likely to have received ciprofloxacin or clindamycin therapy. CONCLUSIONS: Although the incidence of VRE infection remains low in Korea, the findings from this study indicate that VRE are not uncommon intestinal colonizers among hospitalized patients. Strict infection control measures including screening for VRE, especially those from patients at risk, close surveillance, judicious use of antibiotics and patient isolation must be implemented to prevent infection and transmission of VRE.
Agar ; Anti-Bacterial Agents ; Ciprofloxacin ; Clindamycin ; Clostridium difficile ; Colon* ; Diffusion ; Digestion ; DNA ; Electrophoresis, Gel, Pulsed-Field ; Humans ; Incidence ; Infection Control ; Inpatients ; Korea ; Length of Stay ; Mass Screening ; Medical Records ; Outpatients ; Parenteral Nutrition, Total ; Patient Isolation ; Polymerase Chain Reaction ; Renal Dialysis ; Renal Insufficiency ; Risk Factors ; Vancomycin ; Vancomycin Resistance ; Ventilators, Mechanical

No Abstract available
Cross Infection*

No abstract available.
Mass Screening*

No abstract available.
Mass Screening*

No abstract available.
Penicillin Resistance* ; Penicillins* ; Streptococcus pneumoniae* ; Streptococcus*

No abstract available.
Enterococcus*

No abstract available.
Enterococcus*

BACKGROUNDS : Extended spectrum beta-lactamases (ESBL) are plasmid-mediated enzymes that confer broad-spectrum resistance to aztreonam, most penicillins, and cephalosporins including ceftazidime, cefotaxime and ceftriaxone. But with most routine susceptibility tests, ESBL-producing strains may not appear to be resistant, which makes it difficult to predict the effectiveness of the beta-lactam agents. In this study, we performed several test procedures to detect ESBL in blood isolates of Klebsiella pneumoniae and examined the risk factors for bacteremia due to ESBL-producing K. pneumoniae. MATERIALS AND METHODS: Of 87 blood culture Isolates of K. pneumoniae during the first 7 month of 1996, 39 showed reduced susceptibilities to at least one of the 4 antibiotics, aztreonam, cefotaxime, ceftazidime and ceftriaxone. Twenty-three of the 39 isolates were assailable for screening for ESBL. Antibiotic resistance was tested by the agar dilution method and beta-lactamase assay using nitrocefin disks. Effect of beta-lactamase inhibition was examined by the doubledisk synergy test using aztreonam, cefotakime, ceftazldime, and ticarc illin/clavulanate disks and by ESBL Etest involving ceftazidime and cert tazidime/clavulanate. Ability to transfer the beta-lactam resistance was tested by conjugation. We also reviewed the medical records of the patients with K. pneumoniae. (21 with and 41 without ESBL) bacteremia to ananlyze their clinical characteristics. RESULTS: Of 23 strains tested, reduced susceptibilities to cefotaxime, aztreon am and ceftazidime were shown in 23, 18, and 18 strains, respectively. All strains were positive for beta-lactamase and its activity was trasfered to E. coli in all strains. Activities of beta-lactamases were shown to be inhibited by clavulanate in 21 strains by the double-disk method, but in only 15 strains by the ESBL Etest. Nineteen of 21 bacteremia were nosocomially acquired. ESBL-producing strains were associated with length of hospitalization, stay in intensive care unit, use of invasive procedures and administration of antibiotics Including penicillins and third-generation cephalosporins. CONCLUSIONS: Although an increasing incidence of and outbreaks by ESBL-producing strains are reported, detection of ESBLs has proved to be difficult. Using several testing methods such as double-disk synergy test, ESBL Etest and conjugation, we estimated that 40.9% of blood isolates of K. pneumoniae produce ESBL. We should pursue for more sensitive and reliable screening methods for the detection of ESBL.
Agar ; Anti-Bacterial Agents ; Aztreonam ; Bacteremia ; beta-Lactam Resistance ; beta-Lactamases* ; Cefotaxime ; Ceftazidime ; Ceftriaxone ; Cephalosporins ; Clavulanic Acid ; Disease Outbreaks ; Drug Resistance, Microbial ; Hospitalization ; Humans ; Incidence ; Intensive Care Units ; Klebsiella pneumoniae* ; Klebsiella* ; Mass Screening ; Medical Records ; Penicillins ; Pneumonia ; Risk Factors