JAC Advance Access originally published online on July 30, 2006
Journal of Antimicrobial Chemotherapy 2006 58(4):857-860; doi:10.1093/jac/dkl308
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In vivo selection of OmpK35-deficient mutant after cefuroxime therapy for primary liver abscess caused by Klebsiella pneumoniae
1 Division of Infectious Diseases, Department of Internal Medicine, Kaohsiung Medical Center, Chang Gung Memorial Hospital, Chang Gung University College of Medicine 123 Ta-Pei Road, Niao-Sung, Kaohsiung 833, Taiwan 2 Department of Clinical Pathology, Lin-Kou Medical Center, Chang Gung Memorial Hospital 5 Fu-Hsin Street, Kweishan, Taoyuan 333, Taiwan 3 Department of Medical Biotechnology and Laboratory Science, College of Medicine, Chang Gung University 259 Wenhua 1st Road, Kweishan, Taoyuan 333, Taiwan 4 Department of Applied Microbiology, National Chiayi University 300 University Road, Chiayi 600, Taiwan
Received 18 November 2005; returned 5 April 2006; revised 8 May 2006; accepted 5 July 2006
*Corresponding author. Tel: +886-3-3281200 ext. 8363; Fax: +886-3-3971827; E-mail: sulh{at}adm.cgmh.org.tw
Objectives: The aim of the study was to characterize the genetic basis of ß-lactam resistance developed in clinical isolates of Klebsiella pneumoniae after exposure to cefuroxime.
Methods: Clinical features of two episodes of liver abscess caused by K. pneumoniae in a diabetic patient were reported. Four isolates (KP1/KP2 and KP3/KP4) of K. pneumoniae were recovered from cultures of blood/pus in the first and second episodes, respectively. Laboratory investigation of the K. pneumoniae isolates included genotyping by PFGE, resistance gene analysis by PCR amplification and DNA sequencing, and outer membrane protein analysis by SDS–PAGE.
Results: KP3 and KP4 were recovered after a 21 day cefuroxime therapy and demonstrated identical genotypes to that of KP1 and KP2. However, compared with KP1 and KP2, emerging resistance to piperacillin, cefalotin, cefuroxime and cefoxitin was observed. The other antibiotics tested, except ampicillin, retained the same effectiveness against the four isolates, although increases (4- to 8-fold) in the MICs of cefotaxime, ceftriaxone, ceftazidime, cefepime, flomoxef and aztreonam were observed in KP3 and KP4. None of the isolates produced extended-spectrum ß-lactamases or plasmid-mediated AmpC ß-lactamases. Deficiency in the expression of an outer membrane protein (OmpK35) was observed in the cefuroxime-resistant isolates, KP3 and KP4.
Conclusions: The increased resistance to cephalosporins in these clinical isolates of K. pneumoniae after exposure to cefuroxime might be related to the loss of OmpK35.
Keywords: outer membrane protein deficiency , ß-lactam resistance , cephalosporins , OMPs
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