Pathogenesis and immunology of experimental gonococcal infection: role of iron in virulence.
Addition of iron componds to inocula of the relatively avirulent T3 or T4 colony types of gonococci increased their lethality for chicken embryos after intravenous inoculation but had little or no effect on the highly virulent T1 or T2 types. The toxicity of nonviable inocula, killed cells or sonicates, was not significantly affected by ecogenous iron. Addition of the iron-binding protein conalbumin reduced or delayed the lethal effect of T1, but not T3, gonococci although growth of both colony types in the allantoic cavity of the embryo was inhibited by this protwin. This effect can be attributed specifically to deprivation of iron since the iron-complexed form of conalbumin had no apparent influence on growth or virulence. The results indicate that the ability to acquire iron in vivo is a significant factor in gonococcal virulence. The virulent colony types appear to have enhanced ability to compete with the host for iron and this may be related to the presence of pili, other surface components, or the synthesis of iron-chelating compounds.
D000818:Animals; D002642:Chick Embryo; D006069:Gonorrhea / Q000209:etiology / Q000276:immunology*; D007501:Iron / Q000494:pharmacology / Q000502:physiology*; D009344:Neisseria gonorrhoeae / Q000472:pathogenicity*; D014774:Virulence / Q000187:drug effects
D007501:Iron