Guillain-Barré syndrome following dengue infection in a child in Lebanon: a case report and review of the literature

Abstract

Dengue virus infection is increasingly recognized as a cause of neurological complications, including post-infectious immune-mediated neuropathies such as Guillain–Barré syndrome (GBS). We report a rare pediatric case from Lebanon with anti-GD1a positivity, highlighting the evolving epidemiology of dengue and the importance of recognizing neurological complications in emerging transmission settings. A previously healthy 3-year-old girl residing in Ghana presented with progressive bilateral lower extremity pain and refusal to bear weight approximately two weeks after returning from a one-week trip to Iraq and nine weeks after returning to Lebanon from Ghana. Neurological examination revealed evolving reflex changes from hyperreflexia to areflexia with preserved sensation. Cerebrospinal fluid demonstrated albuminocytologic dissociation, while spinal magnetic resonance imaging showed cauda equina nerve-root enhancement. Electrophysiological studies supported a demyelinating polyneuropathy. Dengue serology supported recent primary infection (initial IgM positivity with negative IgG, with subsequent IgG seroconversion), and antiganglioside testing revealed anti-GD1a positivity. The patient was treated with intravenous immunoglobulin (2 g/kg over 2 days), resulting in rapid clinical improvement and near-complete recovery within two weeks. This case highlights dengue as a potential trigger of GBS in young children through autoimmune mechanisms involving antiganglioside antibodies. It underscores the expanding range of dengue infection to previously non-endemic countries like Lebanon, potentially driven by climate change, expanding vector distribution, and increasing international travel. This raises the importance of considering dengue in the differential diagnosis of acute neuropathies in emerging regions such as the Middle East, particularly in the context of increasing global travel and climate change-induced vector expansion.