Gonococci are classified as either serum-sensitive or serum-resistant based upon their sensitivity to killing by complement activation serum-resistant strains have the potential to cause disseminated infection. Neisseria gonorrhoeae induces localized infection at the anatomic site of inoculation, typically urethra, cervix, pharynx, or anus in adults and the eye conjunctiva or the pharynx of newborns, but dissemination can occur. Ruffling then allows gonococci to enter host cells in large vacuoles called macropinosomes and subsequently multiply within infected cells. This causes extensive rearrangement of the host cell actin, resulting in large projections called ruffles. This communication is initiated by the binding of pili to the CR3. Invasion of cervical epithelium involves bacterial cells interacting with host cell complement receptors type 3 (CR3). LOS attaches to sperm cells and likely leads to transmission from males to uninfected sexual partners.

Other surface proteins involved in cellular attachment include Opa, opacity-associated proteins, and LOS, lipooligosaccharide. Pili also provide motility and protection. Their ability to lengthen and retract allows the bacteria to attach from a distance and move closer to the epithelial cells, promoting cellular invasion. Hair-like appendages, pili cover the bacterial surface. gonorrhoeae utilize pili to initiate adhesion to epithelial cells. Gonorrhea has multiple surface proteins that facilitate adhesion.

gonorrhoeae infection starts with the adhesion of gonococci to epithelial cells, followed by local cellular invasion.

Untreatable gonorrhea symptoms