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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).
Cells are Gram-negative cocci, usually seen in pairs with the adjacent sides flattened.
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.
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.
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-acting complement components are at increased risk for disseminated infections. Protection, if it exists, may be strain specific.
Gonorrhea is a sexually transmitted disease of worldwide importance. The highest attack rate in both men and women occurs between 15 and 29 years of age. Host-related factors such as the number of sexual partners, contraceptive practices, sexual preference, and population mobility contribute to the incidence of gonorrhea.
Gonorrhea cannot be diagnosed solely on clinical grounds. For men, a Gram-stained smear of urethral exudate showing intracellular Gram-negative diplococci is diagnostic. For women, and for men when a direct smear is not definitive, culturing on selective medium is often required. N gonorrhoeae must be differentiated from other Neisseria species. Where appropriate, isolates should be examined for antibiotic resistance. A non-amplified DNA probe test is commercially available. This test does not require viable organisms and is useful where maintenance of viability during specimen transport is a problem; however, it is not as sensitive as culture. Serologic tests are not recommended for uncomplicated infections.
Recommended treatment for uncomplicated infections is a third-generation cephalosporin or a fluoroquinolone plus an antibiotic (e.g., doxycycline) effective against possible coinfection with Chlamydia trachomatis . Sex partner(s) should be referred and treated. No effective vaccine yet exists. Condoms are effective in preventing gonorrhea.
Infection with N meningitidis has two presentations, meningococcemia, characterized by skin lesions, and acute bacterial meningitis. Fulminant disease (with or without meningitis) is characterized by multisystem involvement and high mortality.
Cell morphology is identical to that of N gonorrhoeae. The antiphagocytic polysaccharide capsule is a prominent feature.
N meningitidis is grouped, on the basis of capsular polysaccharides, into 12 serogroups, some of which are subdivided according to the presence of outer membrane protein and lipopolysaccharide antigens.
Infection is by aspiration of infective particles, which attach to epithelial cells of the nasopharyngeal and oropharyngeal mucosa, cross the mucosal barrier, and enter the bloodstream. If not cleared blood-borne bacteria may enter the central nervous system and cause meningitis.
Meningococci establish systemic infections only in individuals who lack serum bacterial antibodies directed against the capsular or noncapsular antigens of the invading strain, or in patients deficient in the late-acting complement components.
Asymptomatic carriage of meningococci in the nasopharynx provides a reservoir for infection but also enhances host immunity. Attack rates peak in infants 3 months to 1 year old. Meningococcal meningitis occurs both sporadically (mainly groups B and C meningococci) and in epidemics (mainly group A meningococci), with the highest incidence during late winter and early spring.
Symptoms are suggestive; diagnosis is confirmed by identifying N meningitidis in specimens of blood, cerebrospinal fluid, and nasopharyngeal secretions collected before antibiotic administration.
Penicillin is the drug of choice. Household contacts require chemoprophylaxis with rifampin. Groups A, C, AC, and ACYW135 capsular polysaccharide vaccines are available. In children under 1 year old, antibody levels decline rapidly after immunization. Routine vaccination is not recommended.
Moraxella is an oxidase-positive bacterium, sometimes mistaken for Neisseria, that may be isolated from eye infections and respiratory tract infections. M catarrhalis causes lower respiratory infection in adults with chronic lung disease and is a common cause of otitis media, sinusitis, and conjunctivitis in children. Kingella and Eikenella species are short bacilli or coccoid bacteria that act as opportunistic pathogens. They are sometimes secondary invaders of damaged tissues.
