European Journal of Cardiovascular Medicine

Leptospirosis and scrub typhus are significant public health concerns in tropical countries, often presenting as undifferentiated febrile illnesses. These zoonotic infections, although epidemiologically distinct, share overlapping clinical features and geographic distribution, particularly in South and Southeast Asia. While both conditions are known to cause multisystem involvement, cardiac complications remain relatively uncommon and are frequently underdiagnosed, especially in children.

Leptospirosis, caused by pathogenic spirochetes of the genus Leptospira, is typically acquired through exposure to contaminated water and can manifest along a broad clinical spectrum—from a mild febrile illness to severe multi-organ dysfunction involving the renal, hepatic, pulmonary, and cardiovascular systems (1,2). Cardiac involvement in leptospirosis may include electrocardiographic abnormalities such as atrioventricular conduction delays, nonspecific ST-T changes, and sinus bradycardia, often without overt myocarditis (3,4). In rare instances, severe sinus bradycardia has been documented, potentially requiring intervention (5).

Scrub typhus, caused by Orientia tsutsugamushi and transmitted via chigger mite bites, is another leading cause of acute febrile illness in endemic areas. While it primarily targets the vascular endothelium and reticuloendothelial system, it can also lead to cardiovascular involvement, including myocarditis, pericardial effusion, and rhythm disturbances. Though rare, persistent sinus node dysfunction and sick sinus syndrome requiring pacing have been reported following scrub typhus infection (6,7).

This report describes the case of an adolescent female who developed recurrent symptomatic bradycardia following two separate episodes of tropical infections—first leptospirosis, followed by scrub typhus. The case highlights an unusual clinical course marked by persistent sinus bradycardia, syncopal events, and recovery without structural cardiac disease. It underscores the need for greater awareness of potential cardiac sequelae in pediatric tropical infections and emphasizes the importance of close ECG monitoring during and after the acute illness, as early recognition and appropriate management can significantly improve patient outcomes.

A 13-year-old female with no prior comorbidities presented to the emergency department with a one-month history of insidious-onset abdominal pain localised to the periumbilical region. The pain was dull, non-radiating, continuous, and aggravated in the early morning, with partial relief after food intake. Associated symptoms included dysuria, white vaginal discharge, decreased appetite, and reduced oral intake. Two days prior to admission, she developed a high-grade fever (101–102°F) with chills and rigours, followed by dizziness and a syncopal episode. There were no complaints of vomiting, diarrhoea, rash, respiratory symptoms, or bleeding manifestations.

At presentation, the child was conscious but hypotensive (BP 86/48 mmHg), bradycardic (HR 53/min), and had cold peripheries. Clinical examination revealed a soft abdomen with mild right hypochondrial tenderness but no guarding or organomegaly. Cardiovascular and respiratory system examinations were unremarkable except for bradycardia. An initial ECG showed sinus bradycardia. A screening 2D echocardiogram revealed structurally normal heart anatomy with mild physiological pulmonary regurgitation. Laboratory evaluation showed normal renal and hepatic function, with negative blood and urine cultures. Dengue, malaria, and typhoid serologies were negative. Leptospira IgM was positive, confirming the diagnosis of leptospirosis with decompensated shock. She was managed with inotropes and intravenous fluids and initiated on doxycycline, leading to clinical improvement. She was discharged after stabilization and advised to close outpatient follow-up.

In the subsequent weeks, the child developed persistent bradycardia along with left-sided chest pain, recurrent headaches, and intermittent episodes of syncope. She was followed up in the pediatric cardiology clinic. Serial ECGs revealed sinus bradycardia with no evidence of heart block. Given the suspicion of intermittent complete heart block or junctional escape rhythm, 24-hour Holter monitoring was conducted, which did not demonstrate any significant arrhythmias, pauses, or conduction abnormalities. A repeat echocardiogram remained normal. Given her ongoing symptoms, she was empirically started on oral prednisolone and orciprenaline, with close monitoring.

Approximately six weeks after the initial episode, the child presented again with a fever for three days, associated with vomiting (non-projectile, non-bilious), unilateral (left-sided) headache, and a 30-minute episode of loss of consciousness. There were no seizure-like features, no urinary or faecal incontinence, and no post-ictal confusion. On detailed history, it was revealed that the child had missed orciprenaline doses for two days prior to this episode due to poor oral intake during febrile illness. On examination, she was conscious and alert (GCS 15/15) with stable perfusion, although bradycardia persisted. Systemic examination remained within normal limits. Repeat ECG showed sinus bradycardia without conduction block