Diphtheria is a paradigm of the toxigenic infectious diseases. In 1883, Klebs demonstrated that Corynebacterium diphtheriae was the agent of diphtheria. One year later, Loeffler found that the organism could only be cultured from the nasopharyngeal cavity, and postulated that the damage to internal organs resulted from a soluble toxin. By 1888, Roux and Yersin showed that animals injected with sterile filtrates of C diphtheriae developed organ pathology indistinguishable from that of human diphtheria; this demonstrated that a potent exotoxin was the major virulence factor.
Diphtheria is most commonly an infection of the upper respiratory tract and causes fever, sore throat, and malaise. A thick, gray-green fibrin membrane, the pseudomembrane, often forms over the site(s) of infection as a result of the combined effects of bacterial growth, toxin production, necrosis of underlying tissue, and the host immune response. Recognition that the systemic organ damage was due to the action of diphtheria toxin led to the development of both an effective antitoxin-based therapy for acute infection and a highly successful toxoid vaccine.
Although toxoid immunization has made diphtheria a rare disease in those regions where public health standards mandate vaccination, outbreaks of diphtheria still occur in nonimmunized and immunocompromised groups. In marked contrast, widespread outbreaks of diphtheria reaching epidemic proportions have been observed in those regions where active immunization programs have been halted.
Copyright © 1996, The University of Texas Medical Branch at Galveston.