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Neisseria gonorrhoeaeNeisseria gonorrhoeae Neisseria gonorrhoeae Neisseria gonorrhoeae Neisseria gonorrhoeae Neisseria gonorrhoeaeNeisseria gonorrhoeae
? Clinical Manifestations
Symptomatic or asymptomatic localized infections include urethritis, cervicitis, proctitis, pharyngitis, and conjunctivitis. Disseminated infections occur either by extension to adjacent organs (pelvic inflammatory disease, epididymitis) or by bacteremic spread (skin lesions, tenosynovitis, septic arthritis, endocarditis, and meningitis).
? Structure
Cells are Gram-negative cocci, usually seen in pairs with the adjacent sides flattened.
? Classification and Antigenic Types
N gonorrhoeae strains have been typed on the basis of their growth requirements (auxotyping) or by antigenic differences in the porin protein (serotyping). More recently, restriction fragment length polymorphisms in genes encoding ribosomal RNA (ribotyping) and the separation of large DNA fragments by pulsed- field gel electrophoresis have been used to type isolates.
? Pathogenesis
Gonorrhea is usually acquired by sexual contact. Gonococci adhere to columnar epithelial cells, penetrate them, and multiply on the basement membrane. Adherence is facilitated through pili and opa proteins. Gonococcal lipopolysaccharide stimulates the production of tumor necrosis factor, which causes cell damage. Gonococci may disseminate via the bloodstream. Strains that cause disseminated infections are usually resistant to serum and complement.
? Host Defenses
Infection stimulates inflammation and local immunity; however, it is not known whether the secretory immune response is protective. Serum antibodies also appear. Individuals with genetic defects in late-Copyright © 1996
The University of Texas Medical Branch at Galveston