Pathogenesis of Kingella kingae Disease

The pathogenesis of Kingella kingae disease begins with colonization of the oropharynx, a process facilitated by type IV pili and a non-pilus trimeric autotransporter adhesin called Knh, factors that mediate adherence to respiratory epithelial cells. A potent RTX cytotoxin with broad cellular specificity may play a role in disrupting the epithelial barrier and facilitating invasion of the bloodstream, possibly in concert with a viral coinfection. Once in the bloodstream, the organism can disseminate to sites of invasive disease, primarily the joints, bones, and endocardium. Survival in the bloodstream and dissemination are likely aided by expression of a capsular polysaccharide and an exopolysaccharide galactan. The evidence for antigenic diversity of K. kingae surface exposed protein epitopes and the observation that type IV pili are selected against during invasive disease suggest that immune system pressure plays an important role in K. kingae pathogenicity.