Background Carbapenem-resistant Klebsiella pneumoniae (CRKP) have been a clinically significant pathogen worldwide, but related reports about their virulence features in hospital-acquired infections (HAI) are pretty lacking.
Methods CRKP causing HAI were continuously collected in 2018 from a hospital in central China. Isolates identification and antimicrobial susceptibility test were done using VITEK-2 compact system or MALDI-TOF MS. String test, multilocus sequence typing, carbapenemase genes, virulence genes and capsular antigen genes detection were conducted to understand their phenotype and genetic background. As well as case datas were collected and compared to assess their virulence characteristics.
Results A total of 62 isolates of CRKP from 62 patients with HAI were collected. 41 carbapenemase genestic-confirmed hypervirulent Klebsiella pneumoniae (CR-hvKP) and 21 carbapenem resistant non-hypervirulent Klebsiella pneumoniae (CR-NhvKP) were screened out. Most CRKP causing HAI were ST11 KPC-2 producing strains and maily causing pneumonia. Only for blaKPC-2 there was a significant difference between CR-hvKP and CR-NhvKP (p<0.001). No significant difference of the two group strains in resistance against amikacin, trimethoprim-sulfamethoxazoleare, cefepime, ceftazidime, imipenem, piperacillin-tazobactam, colistin and tigecycline were found except levofloxacin (p<0.001), and all strains showed sensitive to tigecycline and colistin. In the CR-hvKP group, IucA (64.5%) were the most commonly detected virulence gene, followed by iroN (48.4%), prmpA2 (30.6%) and prmpA (4.8%), only 1 (2.4%) capsular serotype positive strain and 2 (4.9%) hypermucoviscosity phenotype strains were detected, while no hypermucoviscosity phenotype or capsular antigen gene positive strain was detected in the CR-NhvKP group. And there was no significant difference between the two groups in age, types of infection, departmental distribution, survival time or the final outcome of infection.
Conclusion ST11 KPC-2-producing Klebsiella pneumoniae are most prevalent CRKP in HAI. Virulence gene espacially iucA has a high proportion and worth paying attention to. Hypermucoviscous phenotype and virulence-associated capsular serotype in CRKP both have a low prevalence. CRKP harboring virulence genes have a higher expression of KPC-2 and less sensitive to levofloxacin than those harboring no virulence gene, and there is no significant difference for virulence manifestations between the two groups.