Clinical Manifestations and Pathology

Even virulent diphtheria begins quietly, after a brief incubation period. Its victims rarely suffer the high fever, vomiting, or myalgias common in acute viral illnesses, and the sore throat is much less pronounced than it is in streptococcal pharyngitis. As the organism multiplies and invades pharyngeal tissues, however, the area around the neck can swell dramatically, and internally the passage of air becomes difficult. The "bullneck" appearance of a diphtheria sufferer differs from the streptococcus victim because there is little enlargement of the regional lymphatic nodes. If the victim can open his or her mouth, an observer usually will see a membrane 1 to 3 millimeters thick, its rough edge curling away from the tonsils, palate, uvula, or pharynx. Depending upon the amount of destruction of local blood vessels, this "shield" can range in color from a more benign-appearing yellowish white, to green or even black. An exudate that remains white, whether or not it looks like a membrane, is usually not due to diphtheria.

The German pathologist Edwin Klebs first identified the C. diphtheriae in 1883 by peeling off this membrane and culturing the bleeding surface underneath. The following year Friedrich Loffler developed an enriched medium on which to grow the delicate bacillus, which could be rapidly overgrown by other organisms cultured from the mouth and pharynx. Both noted the absence of other affected organs at autopsy of diphtheria victims. The bacillus is not distributed through the body, but the toxin alone seems to have the lethal effects described above. Most perplexing is the peripheral nervous system involvement, contributing to a characteristic progression of paralysis in diphtheria victims: first the palate, then the eyes, then the heart, pharynx, and larynx (with respiratory muscles), and finally the limbs. In virulent diphtheria, patients appear quite toxic, and, although the fever is not usually high, the pulse is elevated.

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