, Volume 38, Issue 6, pp 459–464 | Cite as

Clinical and microbiological characteristics of Klebsiella pneumoniae isolates causing community-acquired urinary tract infections

  • W.-H. Lin
  • M.-C. Wang
  • C.-C. Tseng
  • W.-C. Ko
  • A.-B. Wu
  • P.-X. Zheng
  • J.-J. WuEmail author
Clinical and Epidemiological Study



Klebsiella pneumoniae is the second most common species causing urinary tract infections (UTI). However, the host factors and virulence genes of K. pneumoniae related to UTI are poorly understood. The aim of this study was to analyze the capsular phenotype and virulence genes of K. pneumoniae isolates and host factors potentially relevant to community-acquired UTI.


Fifty-four K. pneumoniae isolates from patients with community-acquired UTI, 76 isolates from healthy adults, and 29 from patients with community-acquired pneumonia were compared. The virulence genes (rmpA, magA, uge, and wabG) and serotype (K1, K2, K5, K20, K54, or K57) were characterized by polymerase chain reaction (PCR). The modified string test was used to determine the hypermucoviscosity.


Diabetes mellitus was the most frequent underlying disease among UTI patients (53.7%, 29/54). No predominant K serotype was found in UTI strains. The hypermucoviscosity phenotype and rmpA gene were more often found in UTI isolates than in those from healthy adults (27.8 vs. 2.6%, P < 0.01; 29.6 vs. 11.8%, P < 0.01, respectively), whereas no significant difference in the frequency of magA, uge, wabG, or serotype genes was found. The prevalence of rmpA was significantly lower in isolates from patients with immunosuppression, chronic renal insufficiency, and urinary tract obstruction. Multivariate analysis showed that immunosuppression was negatively associated with the prevalence of rmpA.


Hypermucoviscosity was highly correlated with the presence of the rmpA gene in UTI strains, and rmpA may have a role in community-acquired UTI, especially in hosts without immunosuppression.


Urinary tract infection Hypermucoviscosity Klebsiella pneumoniae Virulence factor 



We are very grateful to Robert M. Jonas for his helpful comments on the manuscript. This work was supported in part by grants NSC97-2311-B-006-004-MY3 and NSC96-2320-B-006-008 from the National Science Council and by grant NCKUH-9804021 from the National Cheng-Kung University Hospital, Taiwan.

Conflict of interest



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Copyright information

© Urban & Vogel 2010

Authors and Affiliations

  • W.-H. Lin
    • 1
    • 2
  • M.-C. Wang
    • 2
  • C.-C. Tseng
    • 2
  • W.-C. Ko
    • 2
  • A.-B. Wu
    • 2
  • P.-X. Zheng
    • 3
  • J.-J. Wu
    • 1
    • 3
    Email author
  1. 1.Institute of Clinical MedicineNational Cheng-Kung University Hospital, National Cheng Kung University College of MedicineTainanTaiwan
  2. 2.Department of Internal MedicineNational Cheng-Kung University Hospital, National Cheng Kung University College of MedicineTainanTaiwan
  3. 3.Department of Medical Laboratory Science and BiotechnologyNational Cheng-Kung University College of MedicineTainanTaiwan

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