Diphtheria is a severe infectious disorder caused by toxigenic Corynebacterium diphtheriae.

Bacterial exotoxin plays the principal role in the pathogenesis of disease, blocking intracellular protein synthesis in tissues and organs.

Diphtheria is manifested by characteristic fibrinous inflammation with growing vascular permeability. It results in the formation of tight “pseudomembranes” covering the tonsils, pharynx, or larynx. Proteinaceous pseudomembranes contain fibrin that is firmly attached to innermost tissues.


Diphtheria is an anthroponotic disease. Patients with diphtheria and carriers are the main sources of infection. The disease is communicated by the airborne route.

Exotoxin traverses the mucous membranes and causes the destruction of epithelium with inflammatory response and microcirculatory and coagulation disorders. The expanding necrotic pseudomembranes impede normal airflow. Any attempt to remove the pseudomembrane results in bleeding. Pseudomembrane respiratory obstruction (or diphtheritic croup) can cause patient suffocation. The regional neck lymph nodes enlarge and neck swelling progresses resulting in total neck edema (“bull neck”).

Toxin absorption leads to distant toxic action with tissue damage, parenchymatous degeneration, fatty infiltration and necrosis in myocardium, liver, kidneys, and adrenals, sometimes accompanied by hemorrhages. The toxin also produces nerve damage often followed by paralysis of the soft palate, eye muscles, or limbs.

In dental practice the most common is the local form of diphtheria where pseudomembranes cover patient’s tonsils.

Toxic and hypertoxic clinical forms are characterized with burst progression of the disease resulting in toxic shock that may cause patient death in two-three days.

▶Laboratory diagnosis of diphtheria depends on rapid determination of diphtherial exotoxin and isolation of toxigenic bacteria.

The presence of exotoxin in clinical specimen (primarily, in tonsillar pseudomembranes) is detected by enzyme-linked immunosorbent assay (ELISA test) or by immunoprecipitation. The toxigenicity of С. diphtheriae culture can be shown also by incorporation of bacteria into cell culture monolayers. Toxin diffuses into cells monolayer and causes cell destruction. Finally, PCR is used as the most sensitive, rapid and specific method for determination of gene encoding diphtheria toxin.

▶The treatment of diphtheria basically rests on the early administration of specific antitoxic antibodies that block toxin action.

▶Specific prophylaxis is afforded by active immunization. Usually combined DPT (or diphtheria-pertussis-tetanus) vaccine or combined tetanus-diphtheria toxoids are used. All the children must gain the repetitive course of diphtheria toxoid immunizations followed by several boosters in every 10 years.