Abstract
The Gram-negative opportunistic pathogen Klebsiella pneumoniae is responsible for causing a spectrum of nosocomial and community-acquired infections. Globally, K. pneumoniae is a frequently encountered hospital-acquired opportunistic pathogen that typically infects patients with indwelling medical devices. Biofilm formation on these devices is important in the pathogenesis of these bacteria, and in K. pneumoniae, type 3 fimbriae have been identified as appendages mediating the formation of biofilms on biotic and abiotic surfaces. The factors influencing the regulation of type 3 fimbrial gene expression are largely unknown but recent investigations have indicated that gene expression is regulated, at least in part, by the intracellular levels of cyclic di-GMP. In this review, we have highlighted the recent studies that have worked to elucidate the mechanism by which type 3 fimbrial expression is controlled and the studies that have established the importance of type 3 fimbriae for biofilm formation and nosocomial infection by K. pneumoniae.
Financial & competing interests disclosure
Part of the work described in this review was supported by NIH grant RO1AI1050011 The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.