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  Pathogenesis

Pathogenesis:

C. diphtheria is existed as normal flora in the respiratory tract, wounds and in convalescent carriers. It spreads from one person to other by droplets, grows on mucous membranes or in skin abrasions. Toxigenic strains generate toxin that is liberated into the surrounding and absorbed. Toxin has 2 portions; the portion B transports A into the cell. Portion A inactivates EF2 complex and protein synthesis in the cell is closed. Diphtheria is an acute communicable disease manifested by both local infection of the upper respiratory tract and the systemic effect of toxin. There are 2 stages of diphtheria, the initial local presentation as a harsh pharyngitis. During this time a hard membrane over the air passage is made and causes suffocation. Later in the systemic stage the circulating exotoxin affects the tissues of the host which are most notable in the heart and peripheral nerves.

Pathology:

The toxin is absorbed in the mucous membrane leading to the demolition of epithelium and the initiation of inflammatory reaction. Necrotic epithelium turns into embedded in fibrin and red and white cells. A grayish ‘pseudo-membrane’ is formed generally over tonsils, pharynx or larynx. Any tear in the membrane will cause bleeding.

The bacilli continuously produce toxin within the membrane. The toxin causes harm, necrosis in the heart muscle, liver, kidneys and adrenals, at times accompanied by hemorrhage. The toxin also generates nerve damage resultant in paralysis of the soft palate, eye muscles and muscles of extremities [i.e., in hands and legs].

 

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