Neisseria gonorrhoeae physiology and pathogenesis

Abstract

Neisseria gonorrhoeae is an obligate human pathogen that is the cause of the sexually transmitted disease gonorrhoea. Recently, there has been a surge in gonorrhoea cases that has been exacerbated by the rapid rise in gonococcal multidrug resistance to all useful antimicrobials resulting in this organism becoming a significant public health burden. Therefore, there is a clear and present need to understand the organism's biology through its physiology and pathogenesis to help develop new intervention strategies. The gonococcus initially colonises and adheres to host mucosal surfaces utilising a type IV pilus that helps with microcolony formation. Other adhesion strategies include the porin, PorB, and the phase variable outer membrane protein Opa. The gonococcus is able to subvert complement mediated killing and opsonisation by sialylation of its lipooligosaccharide and deploys a series of anti-phagocytic mechanisms. N. gonorrhoeae is a fastidious organism that is able to grow on a limited number of primary carbon sources such as glucose and lactate. The utilization of lactate by the gonococcus has been implicated in a number of pathogenicity mechanisms. The bacterium lives mainly in microaerobic environments and can grow both aerobically and anaerobically with the aid of nitrite. The gonococcus does not produce siderophores for scavenging iron but can utilize some produced by other bacteria, and it is able to successful chelate iron from host haem, transferrin and lactoferrin. The gonococcus is an incredibly versatile human pathogen; in the following chapter, we detail the intricate mechanisms used by the bacterium to invade and survive within the host.

Keywords: Colonization; Gonorrhoea; Neisseria; Pathogenesis; Physiology.