Diphtheria, in its local manifestations, is essentially a capillary toxic process inducing necrosis of the affected tissue. This necrosis does not ordinarily lead to deep ulceration; the resulting inflammatory reaction induces the exudation of considerable fibrin, which, with the necrotic tissue and inflammatory cellular elements, forms a covering of varying thickness firmly attached to the affected surface. When this membrane is removed, a defect, the diphtheritic ulcer, is produced; the necrobiotic process is so superficial that the ulcer is usually shallow and involves only the mucosal surface. If the membrane is removed, the ulcer is rapidly covered by a new pseudomembrane composed largely of fibrin and erythrocytes; rarely, usually in mixed infections, is there deep-seated necrosis and ulceration, with subsequent scar formation. In general, the mucosal defect is covered by epithelium regenerated from the adjacent intact areas during the healing process.1
In the trachea, owing to the presence of
BULLOWA JGM, JACOBI M. ULCERATIVE LARYNGITIS DUE TO CORYNEBACTERIUM ULCERANS. Am J Dis Child. 1931;41(1):120–125. doi:10.1001/archpedi.1931.01940070127016
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