Diphtheria

Diphtheria is an acute respiratory infection caused by C. diphtheriae transmitted by airborne droplets; exotoxin is the main pathogenic factor. Features are pharyngeal/laryngeal/nasal mucosal congestion/swelling with gray-white pseudomembrane and systemic toxemia; severe cases develop toxic myocarditis and peripheral nerve palsy.

Common Symptoms

Tonsillar congestion; gray membrane on tonsils; restlessness; nasal obstruction; cyanosis; nausea

Causes and Pathogenesis

(1) Etiology: C. diphtheriae is a Gram-positive rod 2-3 × 0.5-1 µm, arranged in V/X/Y forms, with swollen ends and metachromatic granules (Neisser: yellow-brown cells, blue-black granules; Albert: green cells, blue-black granules; Ponder: pale blue cells, dark blue granules). It grows well on potassium tellurite (black colonies), classified as mitis/intermedius/gravis; all types produce the same toxin. Virulence requires infection by a β-phage carrying the tox gene; non-toxigenic strains can be converted by phage and reverted by anti-phage serum. The lethal dose is 130 ng/kg. Exotoxin is heat-labile (inactivated at 75°C), highly antigenic; 0.3-0.5% formalin for 1 month yields toxoid. It is environmentally resistant (days on toys/clothes) but killed by 0.1% mercuric chloride/5% phenol in 1 min or 58°C/10 min. (2) Pathogenesis: Weakly invasive, it multiplies in superficial epithelium without bacteremia; local mucosal damage (measles, scarlet fever, pertussis, URI) enhances invasion. Toxin consists of A and B subunits linked by disulfide bonds; B binds the pro-HB-EGF receptor and translocates A into the cytoplasm; A ADP-ribosylates and inactivates elongation factor-2 (EF-2), stopping peptide-chain elongation and killing cells. Local necrosis, vascular dilation, fibrin exudate, and leukocytes form the pseudomembrane (gray-white, yellow with secondary infection, black if hemorrhagic); laryngeal/tracheal pseudomembranes detach and cause asphyxiation. Toxin absorption is greatest from pharynx, then tonsil/larynx/trachea; once intracellular it cannot be neutralized by antitoxin—hence early high-dose antitoxin. Systemic effects: early cardiac dilation, fatty change, focal hyalinization, necrosis, conduction bundle involvement; peripheral nerves (especially IX, X cranial) with myelin degeneration, usually reversible; renal tubular cloudy swelling, adrenal congestion/hemorrhage, hepatic fatty change and central necrosis.

Treatment

Drug therapy, symptomatic treatment, supportive therapy

Preventive Measures

1. Control sources: isolate/treat patients until symptoms resolve and two nasopharyngeal cultures are negative (minimum 2 weeks). Culture contacts, observe 7 days; unimmunized toddlers receive toxoid + antitoxin. Morning checks in nurseries; treat carriers with penicillin 5-7 days. Contacts: (1) culture+toxin positive → treat as case, isolate, penicillin, antitoxin if symptomatic; (2) culture positive, toxin positive → case; (3) both negative → discharge; (4) culture negative, toxin positive → vaccinate. 2. Active immunization: DPT or purified diphtheria toxoid. Passive: antitoxin 1000-20000 U IM (adults) / 1000 U (children), lasts 2-3 weeks; protective level 10 U/L; Schick/ELISA measures immunity; incidence correlates inversely with population immunity (85-95% in some Chinese areas).

Department to Visit

It is recommended to visit the Infectious Diseases department; an appointment can be booked on this platform before the visit.

Warm reminder: The above information is for health science reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek medical attention at a regular hospital promptly.