The pathogenesis of AOM is multifactorial. Viral respiratory tract infection precedes AOM in 41% of children (8,15). The most common viruses were respiratory syncytial virus, influenza A and B, and adenoviruses. Viruses might facilitate bacterial infection due to their ability to increase nasopharyngeal colonization by potential bacterial pathogens, alter host defenses, and impair cellular and humoral immunity, through production of inflammation that obstructs the Eustachian tube which can lead to introduction of nasopharyngeal flora to the middle ear (16). These virus-induced effects may be partially responsible for the high rate of unresponsiveness of AOM to antimicrobials and probably contribute to the frequency of relapse, recurrence, or chronicity (8,15).

The horizontally placed Eustachian tube, which opens at a lower level in the infant's nasopharynx than in that of the child or adult, may allow easy access to infection through regurgitated milk or vomitus. The infant has a poorly developed immunity to upper respiratory infections of viral origin or bacterial sequela.

Obstruction of the tube can result in the formation of negative pressure in the middle ear and subsequent formation of a transudate in that space. This space can become contaminated with bacteria through reflux of mucus from the nasopharynx, causing middle-ear infection. This mode of infection can explain the route by which aerobic and anaerobic bacteria, which are part of the oral flora, gain access to the middle ear.

The anaerobic organisms that were recovered from the middle ear of infected children are part of the normal oropharyngeal flora. The isolation of anaerobes, all known pathogens of the upper and lower respiratory tracts, suggests a primary or ancillary role for these bacteria in the etiology of AOM.

Some anaerobic (Prevotella and Peptostreptococcus spp.) and aerobic (alpha- and gamma-hemolytic streptococci) bacteria that are part of the normal oropharyngeal flora can possess in vitro interference capability against oropharyngeal pathogens. These interfering organisms were found in greater numbers in the oropharynx and adenoids of children who are not otitis media prone, compared with otitis media-prone individuals (17,18). The utilization of antimicrobials that spare the normal flora can assist in preserving the interfering flora and reduce colonization by potential pathogens. Two recent study compared the effect of antimicrobials used to treat AOM in children on the nasopharyngeal flora (19,20). Both of these studies compared treatment with amoxicillin-clavulanate in one study to a second generation cephalosporin (cefprozil) (19), and the other to an extended-spectrum third generation cephalosporin (cefdinir) (20). Amoxicillin-clavulanate has a broad spectrum of antimicrobial efficacy-including activity against potentially interfering organisms, while the cephalosporins are less inhibitory of these organisms. The oropharyngeal flora at the end of treatment of AOM with amoxicillin-clavulanate therapy was more depleted of organisms with protective potential than the oral flora following cefprozil or cefdinir therapies (19,20). The patients in one of the studies were followed for three months and these changes were still apparent (20). Recolonization with pathogens occurred more rapidly in those treated with amoxicillin-clavulanate even after three months.

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