Epidemiology and clinical features of bloodstream infections caused by AmpC-type-beta-lactamase-producing Klebsiella pneumoniae.

Cases of bacteremia caused by AmpC-type-beta-lactamase-producing Klebsiella pneumoniae isolates were retrospectively studied to determine the epidemiologic features and clinical outcomes of bloodstream infections. Among 389 blood isolates recovered from 1998 to 2002, 65 isolates (16.7%) were found to be extended-spectrum beta-lactamase (ESBL) or AmpC beta-lactamase producers.

High prevalence of extended-spectrum beta-lactamase-producing strains among blood isolates of Enterobacter spp. collected in a tertiary hospital during an 8-year period and their antimicrobial susceptibility patterns.

Of 72 blood isolates of Enterobacter spp. collected over an 8-year period, 50% (36 of 72) were derepressed or partially derepressed AmpC mutants. The extended-spectrum beta-lactamase (ESBL) production rate was 43% (31 of 72 isolates), and 67.

Epidemiology of Salmonella enterica serotype typhi infections in Korea for recent 9 years: trends of antimicrobial resistance.

The aim of this study is to characterize the epidemiological features of typhoid fever, categorized as class 1 notifiable disease in Korea and to analyze the recent change of antimicrobial resistance of Salmonella enterica serotype Typhi isolated nationwide. We retrospectively analyzed the 1,692 culture-proven cases from 1992 to 2000, using the data of the Korean National Institute of Health. The overall incidence of culture-proven typhoid fever was 0.

Salmonella enterica serovar typhi strains isolated in Korea containing a multidrug resistance class 1 integron.

Six strains of Salmonella enterica serovar Typhi which were resistant to ampicillin, chloramphenicol, trimethoprim-sulfamethoxazole, streptomycin, tetracycline, and gentamicin were isolated in Korea. This multidrug resistance was transferred by a conjugative plasmid of about 50 kb. The plasmid harbored a class 1 integron, which included six resistance genes, aacA4b, catB8, aadA1, dfrA1, aac(6')-IIa, and the novel blaP2, in that order.