Define Diphtheria. Describe its clinical features, complications, management and types.

Definition

Diphtheria is an acute infection caused by toxigenic Corynebacterium diphtheriae, whose exotoxin causes local pseudomembrane formation and distant toxic effects (heart, nerves). It spreads by respiratory droplets.

Clinical Features

• Sore throat and low-grade fever with a greyish, adherent pseudomembrane over the tonsils/pharynx that bleeds on attempted removal.
• 'Bull neck' — marked cervical lymphadenopathy with soft-tissue oedema.
• Extension into the larynx → airway obstruction (a medical emergency).

Complications

• Toxic myocarditis (a leading cause of death).
• Neuropathy — palatal palsy (nasal speech, regurgitation) and later peripheral neuritis.
• Airway obstruction.

Management & Prevention

• Diphtheria antitoxin — give early (neutralises unbound toxin; do not wait for culture).
• Antibiotics — penicillin or erythromycin (eradicate the organism, stop toxin production).
• Airway management, cardiac monitoring, isolation and bed rest; treat contacts.
• Prevention — DPT vaccination (and boosters).

Clinical Types

• Pharyngo-tonsillar (commonest) — pseudomembrane + bull neck.
• Laryngeal — hoarseness, stridor, airway obstruction.
• Nasal — serosanguineous discharge; cutaneous diphtheria (skin).

A Note on WHY the Antitoxin Cannot Wait

• The rule that determines survival in diphtheria is understanding why the antitoxin must be given immediately — on clinical suspicion, before any culture result — and why a day's delay may make it useless.
• The organism itself remains confined to the throat: it does not invade.
• What kills is its exotoxin, which is absorbed into the bloodstream and travels to the heart and nerves.
• And here is the crucial point: antitoxin can only neutralise toxin that is still free in the circulation.
• Once the toxin has bound to the myocardium or to the nerve tissue, it is irreversibly fixed — and no amount of antitoxin can remove it or undo the damage.
• So every hour that passes, more toxin becomes irrevocably bound, and the eventual severity of the myocarditis (which causes heart failure, arrhythmia and sudden death, typically in the second week) and the neuritis (palatal palsy, then a descending paralysis) is progressively determined.
• Hence: give the antitoxin AT once on clinical suspicion — do not wait for the culture.
• The clinical picture is characteristic: a toxic-looking child with a low-grade fever, a grey adherent membrane over the tonsils and pharynx that bleeds when removed, and gross cervical lymphadenopathy giving a 'bull neck'.