Conserved FimK Truncation Coincides with Increased Expression of Type 3 Fimbriae and Cultured Bladder Epithelial Cell Association in Klebsiella quasipneumoniae.

Klebsiella spp. commonly cause both uncomplicated urinary tract infection (UTI) and recurrent UTI (rUTI). Klebsiella quasipneumoniae, a relatively newly defined species of Klebsiella, has been shown to be metabolically distinct from Klebsiella pneumoniae, but its type 1 and type 3 fimbriae have not been studied. K. pneumoniae uses both type 1 and type 3 fimbriae to attach to host epithelial cells. The type 1 fimbrial operon is well conserved between Escherichia coli and K. pneumoniae apart from <i>fimK</i>, which is unique to Klebsiella spp. FimK contains an N-terminal DNA binding domain and a C-terminal phosphodiesterase (PDE) domain that has been hypothesized to cross-regulate type 3 fimbriae expression via modulation of cellular levels of cyclic di-GMP. Here, we find that a conserved premature stop codon in <i>K. quasipneumoniae fimK</i> results in truncation of the C-terminal PDE domain and that <i>K quasipneumoniae</i> strain KqPF9 cultured bladder epithelial cell association and invasion are dependent on type 3 but not type 1 fimbriae. Further, we show that basal expression of both type 1 and type 3 fimbrial operons as well as cultured bladder epithelial cell association is elevated in KqPF9 relative to uropathogenic K. pneumoniae TOP52. Finally, we show that complementation of KqPF9<i>ΔfimK</i> with the TOP52 <i>fimK</i> allele reduced type 3 fimbrial expression and cultured bladder epithelial cell attachment. Taken together these data suggest that the C-terminal PDE of FimK can modulate type 3 fimbrial expression in K. pneumoniae and its absence in <i>K. quasipneumoniae</i> may lead to a loss of type 3 fimbrial cross-regulation. <b>IMPORTANCE</b> <i>K. quasipneumoniae</i> is often indicated as the cause of opportunistic infections, including urinary tract infection, which affects &gt;50% of women worldwide. However, the virulence factors of <i>K. quasipneumoniae</i> remain uninvestigated. Prior to this work, <i>K. quasipneumoniae</i> and K. pneumoniae had only been distinguished phenotypically by metabolic differences. This work contributes to the understanding of <i>K. quasipneumoniae</i> by evaluating the contribution of type 1 and type 3 fimbriae, which are critical colonization factors encoded by all Klebsiella spp., to <i>K. quasipneumoniae</i> bladder epithelial cell attachment <i>in vitro.</i> We observe clear differences in bladder epithelial cell attachment and regulation of type 3 fimbriae between uropathogenic K. pneumoniae and <i>K. quasipneumoniae</i> that coincide with a structural difference in the fimbrial regulatory gene <i>fimK</i>.