RESISTANCE TO EXTENDED-SPECTRUM CEPHALOSPORINS, CAUSED BY PER-1 BETA-LACTAMASE, IN SALMONELLA-TYPHIMURIUM FROM ISTANBUL, TURKEY

Citation
H. Vahaboglu et al., RESISTANCE TO EXTENDED-SPECTRUM CEPHALOSPORINS, CAUSED BY PER-1 BETA-LACTAMASE, IN SALMONELLA-TYPHIMURIUM FROM ISTANBUL, TURKEY, Journal of Medical Microbiology, 43(4), 1995, pp. 294-299
Citations number
17
Categorie Soggetti
Microbiology
ISSN journal
00222615
Volume
43
Issue
4
Year of publication
1995
Pages
294 - 299
Database
ISI
SICI code
0022-2615(1995)43:4<294:RTECCB>2.0.ZU;2-K
Abstract
Two Salmonella typhimurium isolates were studied, one as a representat ive from a series of neonatal meningitis cases treated at an Istanbul teaching hospital, the other from a gastro-enteritis case seen at a di fferent Istanbul hospital. Both isolates were resistant to extended-sp ectrum cephalosporins, as well as penicillins, aminoglycosides and chl oramphenicol. Cephalosporin resistance depended on production of PER-1 beta-lactamase, which is an extended-spectrum class A enzyme that is only distantly related to TEM and SHV enzymes, and which was previousl y known only from Pseudomonas aeruginosa isolates. The PER-1 gene was carried by an 81-MDa plasmid, which also determined resistance to amin oglycosides and chloramphenicol. Although it was not self-transmissibl e to Escherichia coli, this element did transfer if mobilised with pla smid pUZ8. The two S. typhimurium isolates gave indistinguishable DNA restriction patterns and, in addition to their 81-MDa plasmid, also co ntained 52- and 2.8-MDa plasmids, the last of these encoded TEM-1 enzy me. The two isolates were identical in serotype, antibiogram and plasm id-profile but nevertheless differed in phage type, and, therefore, re presented distinct strains. The emergence of cefotaxime and ceftriaxon e resistance in salmonellae is disturbing, since these agents are pref erred therapy for neonatal meningitis caused by members of the genus.