Connections between <i>Klebsiella pneumoniae</i> bloodstream dynamics and serotype-independent capsule properties

<i>Klebsiella pneumoniae</i> bacteremia is a significant public health burden with a 26% mortality rate, which increases when the infecting isolate is multidrug resistant. An important virulence factor of <i>K. pneumoniae</i> is its capsule, the protective polysaccharide coat that surrounds the outer membrane and is made up of individual capsular polysaccharide (CPS) chains. The capsule can differ in composition, abundance, surface attachment, and length of the individual CPS chains. Long, uniform CPS chains are associated with a high level of mucoidy. Typically, mucoidy is produced by the hypervirulent <i>K. pneumoniae</i> (hvKp) pathotype, which is associated with invasive community-acquired infections. In contrast, the classical <i>K. pneumoniae</i> (cKp) pathotype tends to be less mucoid or non-mucoid and is associated with nosocomial infections and multidrug resistance. There are over 80 serotypes of <i>K. pneumoniae</i> capsule. Capsule swap experiments have begun to reveal the effect of serotype on virulence and immune interactions. Clinically, the K2 capsule serotype is a common serotype associated with neonatal bloodstream infections. Both cKp and hvKp can produce K2 capsule, but how K2-encoding cKp and hvKp strains differ in a bloodstream infection remains unknown. To fill this gap in knowledge, we characterized the surface properties of K2 serotype cKp and hvKp bloodstream infection isolates then tested the fitness of these strains in bloodstream infection-related <i>in vitro</i> and <i>in vivo</i> assays. Understanding how K2 cKp and hvKp strains differ in pathogenic potential provides further insights into how <i>K. pneumoniae</i> capsule properties influence bloodstream infection pathogenesis.