Classic diphtheria characteristically involves membranous inﬂammation of the upper respiratory tract, with involvement of other tissues, especially the myocardium and peripheral nerves. The organism itself is rarely invasive, but a potent exotoxin produced by some strains (toxigenic strains) causes tissue damage through local and systemic actions. There is also a cutaneous form of diphtheria, which is typically less severe. The detection of either C. diphtheriae or C. ulcerans is notifiable to the medical officer of health, and the isolates should be referred to ESR for toxin detection. Transmission is by respiratory tract droplets, or by direct contact with skin lesions or contaminated articles. Humans are the only known host for diphtheria, and the disease is spread by close personal contact with a case or carrier. The disease remains communicable for up to four weeks after infection, but carriers of C. diphtheriae may continue to shed the organism and be a source of infection for much longer.
Diphtheria has a gradual onset after an incubation period of two to five days. Symptoms and signs may be mild at first, but progress over one to two days with the development of a mildly painful tonsillitis or pharyngitis with an associated greyish membrane. Diphtheria should be suspected particularly if the membrane extends to the uvula and soft palate. The nasopharynx may also be obstructed by a greyish membrane, which leaves a bleeding area if disturbed. The breath of a patient with diphtheria has a characteristic mousy smell.
The major complication of diphtheria is respiratory obstruction, although the majority of deaths are due to the effects of diphtheria toxin on various organs. Of particular importance are the effects of the toxin on the myocardium (leading to myocarditis and heart failure), peripheral nerves (resulting in demyelination and paralysis), and the kidneys (resulting in tubular necrosis). The neuropathy begins two to eight weeks after disease onset, while the myocarditis can be early or late.