Naslov
Extended-Spectrum beta-Lactamases in Clinical Isolates of Klebsiella pneumoniae from Zagreb

Autori
Bedenić, Branka ; Žagar, Živojin ; Fridrih, Sandra

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
7^th International Congress for Infectious Diseases. Book of Abstracts / - Hong Kong, 1996, 179-179

Skup
7^th International Congress for Infectious Diseases

Mjesto i datum
Hong Kong, Kina, 10.06.1996. - 13.06.1996

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
extended-spectrum beta-lactamases; Klebsiella pneumoniae; microbial resistance

Sažetak
The aim of the study was to determine the frequency and distribution of extended-spectrum beta-lactamases in the clinical isolates of Klebsiella pneumoniae from the hospitals in Zagreb. The susceptibility to antibiotics of 41 multiresistant clinical isolates of Klebsiella pneumoniae was tested by broth microdilution method. MIC90 of amoxycillin and nalidixic acid was >1024, of cefuroxime 512 mg/L, of ceftazidime 256 mg/L, of amoxycillin/clavulanic acid, aztreonam and gentamicin 128 mg/L, rifampicin 32 mg/L, of cefotaxime andceftriaxone 16 mg/L, of cefetamet and cefpirome 8 mg/L, of cefotetan 4 mg/L and imipenem 0.5 mg/L. The strongest animicrobial activity was observed with imipenem. 53.6% of the strains were resistant to ceftazidime, 46.3% to aztreonam and 39% to cefotaxime. Resistance due to extended-spectrum beta-lactamases was transferred to a suitable E. coli recipient by transconjugation. Strains resistant to ceftazidime and cefotaxime were mated in order to determine the transferability of their resistance characters. 15 of 22 (68%) ceftazidime resistant strains and 5 of 16 (22%) cefotaxime resistant strains transferred their resistance to E. coli recipient. The frequency of transfer ranged from 10-3 to 10-6 per donor cell. The transconjugants had the same pattern of resistance as their respective donors. Non transferable resistance in 32% of ceftazidime and 78% of cefotaxime resistant strains was probably caused either by hyperproduction of chromosomally mediated class I beta-lactamases or decreased expression of outer membrane proteins (porins) resulting in decreased penetration of the antibiotic into the bacterial cell.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti

POVEZANOST RADA