Abstract
The skin and mucous membranes are the principal barriers to invasion of the body by microorganisms. Besides functioning as a mechanical barrier, the mucosae are endowed with an array of still poorly characterized specific and nonspecific host defense capabilities. These include the production of mucus, secretory immunoglobulin (IgA), lysozyme, lactoferrin, and alpha-antitrypsin, in conjunction with a low-grade exudation of leukocytes.1 In addition, the mucosal surfaces of the upper respiratory, gastrointestinal, and lower vaginal and urinary tracts support a large number of “nonpathogenic” microorganisms that comprise the so-called “normal flora.” This commensal flora plays an important and complex role in protecting the host from microbial invasion. Mechanisms for this protection likely include the following: (1) competition for the same nutrients (interference); (2) competition for the same receptors on host cells (tropism); (3) production of bacteriocins, that is, bacterial products that are toxic to other organisms, usually of the same species; and (4) stimulation of crossprotective immune factors such as the “natural antibodies.”1The “normal” flora is inconstant and may be altered by dietary factors, debilitation, hormonal events (such as menstruation, pregnancy, and possibly use of oral contraceptives), personal hygiene, medications, intercurrent infection, and probably many others. Antibiotic therapy and menstruation can have a profound effect on the composition of this group of microorganisms.2 Disturbance of the delicate host-commensal relationship may cause a clinically significant infection due to these “nonpathogens.” This may occur in response to the aforementioned factors (eg, pregnancy predisposing to vaginal candidiasis) or because of disruption of the anatomic barrier (eg, local mucosal infection at a site of trauma, or injury from cytotoxic drugs) or in association with exogenous infection (eg, rhinoviral infection leading to secondary bacterial otitis media). Invasion by “normal flora” may result in serious systemic illness. A clear example of the latter is the development of infective endocarditis caused by viridans streptococci following a dental procedure.
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