Disseminated gonococcal infection (DGI) occurs when Neisseria gonorrhoeae, a gram-negative diplococcus, invades the bloodstream from a primary mucosal infection site (cervix, urethra, pharynx, or rectum) and spreads to distant sites. DGI complicates approximately 0.5-3% of untreated gonococcal infections. N. gonorrhoeae has evolved sophisticated immune evasion mechanisms that facilitate dissemination: (1) pili undergo phase and antigenic variation, constantly changing their surface proteins to evade antibody recognition; (2) Opa (opacity-associated) proteins mediate attachment to host cells and can be turned on/off through slipped-strand mispairing, altering immune recognition; (3) lipooligosaccharide (LOS) is sialylated with host sialic acid, camouflaging the bacterium from complement-mediated killing; (4) IgA1 protease cleaves secretory IgA, disabling mucosal immunity. DGI classically manifests in two overlapping clinical phases: 1. Bacteremic/triad phase (60-70% of DGI): migratory polyarthralgia (multiple joint pains that migrate from joint to joint over hours to days), tenosynovitis (tendon sheath inflammation — especially dorsum of hands, wrists, ankles), and dermatitis (characteristic papular, pustular, or hemorrhagic lesions on an erythematous base, typically on distal extremities — often painless, scattered, few in number). Blood cultures are positive in ~30-50% during this...