Eustachian tube dysfunction is the most important factor in the pathogenesis of middle ear infections. The most commonly cited problem is an abnormal palatal-muscle, eustachian-tube vector, which commonly occurs in young children. With adolescent growth, descent of the soft-palate-muscle sling relative to the eustachian tube orifice improves the eustachian tube opening. However, poor tubal function may persist with mucosal disease (allergic, inflammatory, immunologic impairment, or immotile cilia), extrinsic compression (enlarged adenoid or nasopharyngeal tumor), or palatal muscle dysfunction (cleft palate and other craniofacial anomalies). Persistent eustachian-tube dysfunction induces a relative negative pressure in the middle-ear space. The lack of aeration and the accumulation of effusions provide an environment conducive to the development of OME or AOM.

Bacteriologic studies identify Streptococcus pneumoniae and Hemophilus influenzae most frequently as the pathogenic organisms in AOM. Group A beta-

hemolytic streptococcus, Staphylococcus aureus, and Branhamella catarrhalis are less frequent causes of AOM. Gram-negative enteric bacilli are isolated on occasion in infants up to 6 weeks of age with AOM.

When AOM continues beyond 2 weeks as a result of inadequate antimicrobial therapy, progressive thickening of the mucosa lining the middle ear obstructs free drainage of purulent secretions, thereby permitting bone destruction and extension of infection. This process may eventuate in mastoiditis and possibly other local or intracranial extensions of suppuration.

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