Neisseria gonorrhoeae is a Gram-negative diploccus responsible for gonorrhoea. Humans are their only natural host. Infection is mediated by pili attachment to host urogenital mucosal epithelial cells, from which they migrate into the sub-epithelium and interact with neutrophils, macrophages, and other phagocytic cells, providing them a protected intracellular environment. Unlike N. meningitidis, N. gonorrhoeae does not produce a polysaccharide capsule. Instead of a distinct bacterial toxin, pathogenesis is largely a result of a strong inflammatory response. Efficient horizontal genetic exchange through DNA tranformation is an important aspect of Neisseria epidemiology and has been shown to involve PilE, the major pilus subunit, and pilC, the minor pilus-associated protein. N. gonorrhoeae can spontaneously halt PilE and pilus formation through irreversible deletion of the pilE locus. Genetic change driving antigenic variation is mediated by both RecA-independent illegitimate recombination, which tends to reversibly turn genes on and off, and RecA dependent recombination, which implies physical exchange of chromosomal and extra-chromosomal DNA.