Clinical Scenario:
A 7-year-old boy with incomplete immunization presents with fever, sore throat and progressive dysphagia. Examination shows a thick, firmly adherent grayish-white membrane over the tonsils and pharynx with marked cervical lymphadenopathy. Diphtheria antitoxin and erythromycin are started on clinical suspicion.
On the 9th day of illness, he develops increasing fatigue and tachycardia. His pulse is irregular, blood pressure is 88/54 mmHg, and ECG shows frequent ventricular ectopic beats with ST-T wave abnormalities. Troponin-I is markedly elevated.
Which of the following best explains this complication?
A. Direct bacterial invasion of myocardium
B. Immune-complex deposition in myocardium
C. Myocardial injury from circulating diphtheria toxin
D. Secondary bacterial myocarditis
E. Viral coinfection of myocardium
Correct answer & Explanation
Correct Answer: C. Myocardial injury from circulating diphtheria toxin
Explanation: Diphtheria Complication
This child has typical diphtheria, characterized by fever, sore throat, dysphagia, cervical lymphadenopathy, and a thick, firmly adherent grayish-white pseudomembrane over the tonsils and pharynx. The pseudomembrane is a particularly important clinical clue because it results from local tissue necrosis associated with toxin-producing Corynebacterium diphtheriae.
The development of tachycardia, hypotension, ventricular ectopic beats, ST-T abnormalities, and markedly elevated troponin-I during the second week of illness strongly indicates diphtheritic myocarditis.
The key mechanism is systemic absorption and circulation of diphtheria toxin.
Diphtheria toxin is produced by toxigenic strains of C. diphtheriae. Once absorbed into the circulation, the toxin can affect organs distant from the original pharyngeal infection, particularly the myocardium and peripheral nervous system. CDC specifically states that diphtheria toxin can cause myocardial damage and that myocarditis is a major complication of respiratory diphtheria.
At the cellular level, diphtheria toxin inhibits protein synthesis by inactivating elongation factor-2 (EF-2). This causes cellular injury and death. In the heart, toxin-mediated myocardial injury can produce myocarditis, conduction abnormalities, ventricular arrhythmias, myocardial dysfunction, and cardiogenic shock.
The ECG abnormalities and elevated troponin in this child therefore represent toxin-mediated myocardial injury rather than direct invasion of the myocardium by the bacteria.
Why does myocarditis occur around the second week?
Diphtheritic myocarditis typically develops during the second to third week of illness, although the timing can vary. This delayed systemic complication is an important examination clue.
The CDC describes myocarditis as a major complication of respiratory diphtheria and emphasizes that serious complications are primarily related to the effects of diphtheria toxin.
Why the other options are incorrect
A. Direct bacterial invasion of myocardium — Incorrect
The major systemic complications of diphtheria are toxin-mediated. C. diphtheriae primarily colonizes the respiratory mucosa; myocardial injury is not caused by direct bacterial invasion of cardiac tissue.
B. Immune-complex deposition in myocardium — Incorrect
Diphtheritic myocarditis is not primarily an immune-complex-mediated disease. The characteristic myocardial injury results from the systemic effects of diphtheria toxin.
D. Secondary bacterial myocarditis — Incorrect
There is no need to invoke a second bacterial infection. The combination of respiratory diphtheria followed by cardiac abnormalities during the subsequent days is classic for diphtheria toxin–mediated myocarditis.
E. Viral coinfection of myocardium — Incorrect
Viral myocarditis can certainly cause elevated troponin, ECG abnormalities, arrhythmias, and myocardial dysfunction, but it does not explain the characteristic temporal relationship to severe respiratory diphtheria as well as toxin-mediated myocardial injury does.
Clinical Pearl
In a child with respiratory diphtheria, the appearance of:
Tachycardia + arrhythmia/ECG abnormalities + hypotension + elevated cardiac biomarkers
should immediately raise concern for diphtheritic myocarditis.
The important mechanism to remember is:
Toxigenic C. diphtheriae → diphtheria toxin → systemic absorption → inhibition of cellular protein synthesis → myocardial injury → myocarditis/arrhythmias/cardiac dysfunction
Diphtheria antitoxin is given urgently because it can neutralize circulating toxin, but it cannot reverse toxin that has already become fixed to tissues. This is why treatment should begin on clinical suspicion rather than waiting for laboratory confirmation.
You can also practice another MCQ on Congestive Cardiac Failure.
References
- Centers for Disease Control and Prevention. Clinical guidance for diphtheria. CDC; 2026. [Read the clinical guidance]
- Centers for Disease Control and Prevention. Clinical features of diphtheria. CDC; 2026. [Read the clinical features]
