Kingella kingae is increasingly recognized as a leading cause of osteomyelitis, septic arthritis, and bacteremia among children between 6 months and four years of age. K. kingae has also been identified as an important cause of endocarditis among young children. K. kingae is commonly found in the oropharynx and can transition from a state of commensalism to invasive disease through the help of various colonization and virulence factors. The main factors are type IV pili, an adhesin called Knh, an RTX family pore forming toxin called RtxA, a polysaccharide capsule, and a galactan exopolysaccharide. Type IV pili and Knh facilitate bacterial adherence to the epithelium. The RtxA toxin is capable of lysing host cells. The surface polysaccharides aid in evasion of the immune system. Endocarditis is a severe clinical manifestation of K. kingae with a mortality rate of 16%. In this study we examined a collection of 12 isolates from patients with endocarditis to characterize their virulence determinants. We found that capsule was expressed in all strains, and the type a capsule predominates in the K. kingae endocarditis isolates. Twitching motility and adherence are type IV pili mediated phenotypes. Our results demonstrated that half of the strains show defects in twitching motility. Adherence to epithelial cells was variable, but most isolates demonstrated high levels of adherence. Lastly, we found that the pamC1 allele, which encodes a type 1 galactan exopolysaccharide structure, is the dominant form in K. kingae endocarditis strains. Our results serve as a starting point for understanding how these endocarditis strains differ phenotypically from other K. kingae strains, and in the long-term will help us find novel ways to treat or prevent infective endocarditis caused by K. kingae.