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Background  The emergence of carbapenem-resistant  Klebsiella pneumoniae  (CRKP) poses a looming threat to human health. Although there are numerous studies regarding porin alteration in association with the production of ESBLs and/or AmpC β-lactamase, a systematic study on the treatment-emergence of porins alteration in antibiotic resistance does not yet exist. The aim of this study was to investigate the underlying mechanism of resistance of  K. pneumoniae  during carbapenem treatment.    Results  Here, we report three strains (FK-2624, FK-2723 and FK-2820) isolated from one patient before and after imipenem treatment during hospitalization. Antibiotic susceptibility testing indicated that that the first isolate, FK-2624, was susceptible to almost all tested antimicrobials, being resistant only to fosfomycin. The subsequent isolates FK-2723 and FK-2820 were multidrug resistant (MDR). After imipenem therapy, FK-2820 was found to be carbapenem-resistant. PCR and Genome Sequencing analysis indicated that  oqxA,  and  fosA5 , were identified in all three strains. In addition, FK-2624 also harbored  bla  SHV  -  187  and  bla  TEM-116 . The  bla  SHV  -  187  and  bla  TEM-116  genes were not detected in FK-2723 and FK-2820.  bla  DHA  -1 ,  qnrB4 ,  aac (6′)-IIc, and bla  SHV  -  12 ,  EreA2, CatA2, SulI, and tetD , were identified in both FK-2723 and FK-2820. Moreover, the genes  bla  DHA -1,  qnrB4 ,  aac (6′)-IIc  were co-harbored on a plasmid. Of the virulence factors found in this study,  ybtA, ICEKp6, mrkD, entB, iroN, rmpA2–6, wzi16  and capsular serotype K57 were found in the three isolates. The results of pairwise comparisons, multi-locus sequencing typing (MLST) and pulsed-field gel electrophoresis (PFGE) revealed high homology among the isolates. Sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) results showed that isolate FK-2820 lacked OmpK36, with genome sequence data validating that there was a premature stop codon in the  ompK36  gene and real-time RT-PCR suggesting high turnover of the  ompK36  non-sense transcript in FK-2820, with the steady-state mRNA level 0.007 relative to the initial isolate.    Conclusion  This study in China highlight that the alteration of outer membrane porins due to the 14-day use of imipenem play a potential role in leading to clinical presentation of carbapenem-resistance. This is the first description of increased resistance developing from a carbapenem-susceptible  K. pneumoniae  with imipenem treatment driven by outer membrane remodeling.

bmc microbiology

First description of antimicrobial resistance in carbapenem-susceptible Klebsiella pneumoniae after imipenem treatment, driven by outer membrane remodeling