Tatjana Tot1, Sara Kibel2, Sanda Sardelić3, Khalil Nemer4, Ana Benčić5, Jasmina Vraneš6, Marija Krilanović7, Marko Jelić8, Marko Tripković9, Marina Bubonja-Šonje10, Branka Bedenić11. 1. MD, General Hospital Karlovac, Andrije Štampar Street 3, 47000, Karlovac, Croatia. 2. MD, University of Osijek School of Medicine, Josip Huttler street 4, 31000, Osijek, Croatia. 3. MD, PhD, University Hospital Centre Split, Spinčić street, 21000 Split, Croatia. 4. MD, Public Health Institute of Sisak Moslavina County, Kralj Tomislav street 1, 44000 Sisak, Croatia. 5. MD, University Hospital Centre Sestre Milosrdnice, Vinogradska 29, 10000 Zagreb, Croatia. 6. MD, PhD, Prof., School of Medicine, University of Zagreb, Šalata 3, 10000 Zagreb, Andrija Štampar Teaching Public Health Institute, Mirogojska 16, 10000 Zagreb, Croatia. 7. MD, Public Health Institute of Dubrovnik-Neretva County, dr. Ante Šercer street 4a, 20000, Dubrovnik, Croatia. 8. PhD, University Hospital for Infectious Diseases, Mirogojska 8, 10000 Zagreb, Croatia. 9. MD, University Hospital Center Zagreb, Kišpatićeva 12, 10000 Zagreb, Croatia. 10. MD, PhD, Prof., University Hospital Center Rijeka, School of Medicine University of Rijeka, Braće Branchetta 20/1, 51000, Rijeka, Croatia. 11. MD, PhD, Prof., University of Zagreb School of Medicine, Clinical Department for Clinical and Molecular Microbiology, University Hospital Center Zagreb, Kišpatić Street 12, Zagreb, Croatia.
Abstract
INTRODUCTION: Recently, a marked increase in the rate of colistin resistant Klebsiella pneumoniae was observed in Croatian hospitals and the outpatient setting. This prompted us to analyze the molecular epidemiology of these isolates and the mechanisms of spread. METHODS: In total 46 colistin-resistant K. pneumoniae isolates from five hospitals and the community were analyzed. The presence of genes encoding broad and extended-spectrum β-lactamases, plasmid-mediated AmpC β-lactamases and carbapenemases was determined by PCR. Plasmids were characterized by PCR based replicon typing. Isolates were genotyped by pulsed-field gel electrophoresis. Virulence traits such as hemolysins, hyperviscosity and resistance to serum bactericidal activity were determined by phenotypic methods. RESULTS: High resistance rates were observed for cefuroxime, ceftazidime, cefotaxime, ceftriaxone and ertapenem, ciprofloxacin and gentamicin. The majority of OXA-48 producing isolates were resistant to ertapenem but susceptible to imipenem and meropenem. Nine strains transferred ertapenem resistance to E. coli recipient strain. Thirty-nine strains were phenotypically positive for ESBLs and harbored group 1 of CTX-M β-lactamases. OXA-48 was detected in 39 isolates, KPC-2 in four and NDM-1 in one isolate. The isolates belonged to six PFGE clusters. All isolates were found to be resistant to serum bactericidal activity and all except four strains positive for KPC, produced β-hemolysins. String test indicating hypermucosity was positive in only one KPC producing organism. CONCLUSIONS: The study demonstrated the ability of K. pneumoniae to accumulate different resistance and virulence determinants. We reported dissemination of colistin resistant K. pneumoniae in five hospitals, located in different geographic regions of Croatia and in the outpatients setting. mcr genes responsible for transferable colistin resistance were not found, indicating that resistance was probably due to chromosomal mutations. GERMS.
INTRODUCTION: Recently, a marked increase in the rate of colistin resistant Klebsiella pneumoniae was observed in Croatian hospitals and the outpatient setting. This prompted us to analyze the molecular epidemiology of these isolates and the mechanisms of spread. METHODS: In total 46 colistin-resistant K. pneumoniae isolates from five hospitals and the community were analyzed. The presence of genes encoding broad and extended-spectrum β-lactamases, plasmid-mediated AmpC β-lactamases and carbapenemases was determined by PCR. Plasmids were characterized by PCR based replicon typing. Isolates were genotyped by pulsed-field gel electrophoresis. Virulence traits such as hemolysins, hyperviscosity and resistance to serum bactericidal activity were determined by phenotypic methods. RESULTS: High resistance rates were observed for cefuroxime, ceftazidime, cefotaxime, ceftriaxone and ertapenem, ciprofloxacin and gentamicin. The majority of OXA-48 producing isolates were resistant to ertapenem but susceptible to imipenem and meropenem. Nine strains transferred ertapenem resistance to E. coli recipient strain. Thirty-nine strains were phenotypically positive for ESBLs and harbored group 1 of CTX-M β-lactamases. OXA-48 was detected in 39 isolates, KPC-2 in four and NDM-1 in one isolate. The isolates belonged to six PFGE clusters. All isolates were found to be resistant to serum bactericidal activity and all except four strains positive for KPC, produced β-hemolysins. String test indicating hypermucosity was positive in only one KPC producing organism. CONCLUSIONS: The study demonstrated the ability of K. pneumoniae to accumulate different resistance and virulence determinants. We reported dissemination of colistin resistant K. pneumoniae in five hospitals, located in different geographic regions of Croatia and in the outpatients setting. mcr genes responsible for transferable colistin resistance were not found, indicating that resistance was probably due to chromosomal mutations. GERMS.
Authors: C Mammina; C Bonura; F Di Bernardo; A Aleo; T Fasciana; C Sodano; M A Saporito; M S Verde; R Tetamo; D M Palma Journal: Euro Surveill Date: 2012-08-16
Authors: N Woodford; M E Ward; M E Kaufmann; J Turton; E J Fagan; D James; A P Johnson; R Pike; M Warner; T Cheasty; A Pearson; S Harry; J B Leach; A Loughrey; J A Lowes; R E Warren; D M Livermore Journal: J Antimicrob Chemother Date: 2004-09-03 Impact factor: 5.790