Clinical Information

Diphtheria is an acute, contagious, febrile illness caused by the bacterium Corynebacterium diphtheriae. The disease is classically characterized by a combination of localized inflammation in the upper respiratory tract with the formation of a diphtheric pseudomembrane over the oropharynx, including the tonsils, pharynx, larynx, and posterior nasal passages. C diphtheriae produces a potent diphtheria exotoxin that is absorbed systemically and can lead to cardiac failure and paralysis of the diaphragm.

Tetanus results from contamination of wounds or lacerations with Clostridium tetani spores from the environment. The spores germinate to actively replicating bacterial cells localized within the wound and produce the heat-labile toxin tetanospasmin. Tetanospasmin attaches to peripheral nerve endings and travels to the central nervous system where it blocks inhibitory impulses to motor neurons and leads to severe, spastic muscle contractions, a classic characteristic of tetanus.

Both diseases are preventable by vaccination with diphtheria toxoid, which stimulates antidiphtheria toxoid antibodies, and tetanus toxoid (formaldehyde-treated tetanospasmin), which stimulates development of antitetanus toxoid antibodies. In the United States, these toxoids are administered to children as part of the combined diphtheria, tetanus, and acellular pertussis (TDaP) vaccine.

Two to 3 weeks following vaccination, a patient's immunological response may be assessed by measuring the antidiphtheria toxoid IgG antibody and total antitetanus toxoid IgG antibody levels in serum. An absence of either antibody formation postvaccination may relate to immune deficiency disorders, either congenital or acquired, or iatrogenic due to immunosuppressive drugs.