Virulence Factors in Hypervirulent Klebsiella pneumoniae

Abstract

Hypervirulent Klebsiella pneumoniae (hvKP) has spread globally since first described in the Asian Pacific Rim. It is an invasive variant that differs from the classical K. pneumoniae (cKP), with hypermucoviscosity and hypervirulence, causing community-acquired infections, including pyogenic liver abscess, pneumonia, meningitis, and endophthalmitis. It utilizes a battery of virulence factors for survival and pathogenesis, such as capsule, siderophores, lipopolysaccharide, fimbriae, outer membrane proteins, and type 6 secretion system, of which the former two are dominant. This review summarizes these hvKP-associated virulence factors in order to understand its molecular pathogenesis and shed light on new strategies to improve the prevention, diagnosis, and treatment of hvKP-causing infection.

Keywords: Klebsiella pneumoniae; capsule; hypermucoviscous; hypervirulence; siderophores; virulence factors.

FIGURE 1

(A) Genes are known to influence capsule biosynthesis, including genes at cps locus and regulators affecting the cps expression directly or indirectly. The corresponding promoters that some regulators act on refer to studies of Walker and Miller (2020). Hypercapsule is sufficient but not necessary for hypermucoviscous phenotype, demonstrating that hypermucoviscous phenotype is not solely due to excessive capsule expression. (B) The siderophore systems enterobactin (ent), yersiniabactin (ybt), salmochelin (iro) and aerobactin (iuc) are present. Take enterobactin as an example to show the process of iron acquisition, which FepA is the transporter specific to enterobactin.