Pathogenesis

The infrequent occurrence of AST has been attributed to several factors: its high concentration of iodine, rich supply of blood and lymphatics, and its unique anatomical isolation. Because the thyroid is encapsulated and without direct communication with neighboring structures, it may also be resistant to infection by direct extension from contiguous organs (86). A testimony of the gland's resistance to infection is the rare occurrence of post-surgical thyroid infection (98).

Various routes of infection have been suggested: hematogenous (91,92), direct spread from a adjacent site (93), a thyroglossal cyst or fistula (94), or a perforated esophagus (99). A predisposing factor to infection is the presence of previous diseased areas of the thyroid, such as goiter or adenomata, which are especially prevalent in females (92,99). A preceeding infection has been observed occasionally in other sites in the body. In recent series of AST, about one quarter of the patients were immunocompromised; half of these had AIDS (88).

The anaerobes recovered from inflamed thyroid are part of oral flora (4), and may, therefore, reach the gland in the same fashion as the aerobic pathogens. The recovery of these organisms as the only isolate of inflamed gland suggests that anaerobic bacteria may play an important role in the pathogenesis of AST, and they indicate the need for clinical awareness of these anaerobic bacteria as potential causes of this disease.

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