Abstract
Stenotrophomonas maltophilia is an emerging multidrug-resistant, Gram-negative opportunistic pathogen. It causes many healthcare-associated infections such as sepsis, endocarditis, meningitis, and catheter-related urinary tract infections. It also affects individuals with cystic fibrosis, exacerbating their lung condition. S. maltophilia often causes pathogenesis through the formation of biofilms. However, the molecular mechanisms S. maltophilia uses to carry out these pathogenic steps are unclear. The SMF-1 chaperone/usher pilus has been thought to mediate S. maltophilia attachment. To confirm this role, we created an isogenic deletion of the smf-1 pilin gene and observed a defect in biofilm compared to wild type. We also discovered an additional chaperone/usher pilus gene cluster: cbl. Mutation of cbl also affects biofilm levels. Intriguingly, through transmission electron microscopy studies, we found suggestive evidence that the mutation of one pilus (e.g. smf) is not phenotypically compensated by another (e.g. cbl). Additionally, infection of Galleria mellonella larvae revealed increased virulence of an smf-1 deletion mutant and an smf-1 cbl double deletion mutant. Together, these studies show that pili have an important role in switching between acute and chronic infections in conducting S. maltophilia virulence. Understanding their activity may help identify therapeutic targets for this pathogen.