It is best known as a cause of septic arthritis, osteomyelitis, spondylodiscitis, bacteraemia, and endocarditis, and less frequently lower respiratory tract infections and meningitis.

When it causes disease, the clinical presentation is often subtle and preceded by a recent history of stomatitis or upper respiratory infection.

Kingella kingae is thought to begin infection by colonizing the pharynx, crossing the epithelium by using an RTX toxin, and entering the circulation and reaching deeper tissues, such as bones and joints.

Kingella kingae expresses type IV pili, which allow for enhanced adhesion to respiratory epithelial and synovial cells and thus increased likelihood of colonization.

PilS and PilR, regulatory transcription factors best known from the Pseudomonas aeruginosa pilus system, also may regulate pilA expression.

It generally targets the lumbar region of the spinal cord, and the only true way of diagnosing it is through biopsy or needle aspiration, as blood plate growth gives many false negatives.

Diagnostic tools include low-grade fever, elevated inflammatory markers (ESR and CRP), but white blood cell counts are generally unreliable since they vary among infected patients.

As an oropharyngeal colonizer, K. kingae is transmitted by respiratory secretions, saliva, and potentially oral contact with contaminated objects.

The infection can occur in the respiratory or urinary tracts, as it is a part of the normal flora in those two areas, and will develop into sepsis or septic arthritis.