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Background <p>Guillain–Barré syndrome (GBS) is an acute immune‑mediated polyradiculoneuropathy and remains a leading cause of acquired neuromuscular paralysis. In children, it typically follows infection, but association with malaria is rare.</p> Case presentation <p>We report a four‑year‑old Lebanese girl living in Nigeria, who developed progressive weakness, dysphagia, inspiratory stridor, and gait ataxia 2&#xa0;weeks after treatment for <i>Plasmodium falciparum</i> malaria. Neurological examination revealed lower‑extremity weakness with areflexia, bulbar involvement causing stridor, unilateral facial weakness, and gait ataxia (Hughes score 4). Cerebrospinal fluid analysis showed albumin‑cytologic dissociation, and nerve conduction studies demonstrated acute inflammatory demyelinating polyradiculoneuropathy. Given the rapid progression and severity, therapeutic plasma exchange (PE) was administered (five exchanges over 10&#xa0;days) along with supportive care. Strength improved steadily, and at 1&#xa0;month she was able to walk and run independently (Hughes score 0).</p> Conclusions <p>This case expands the limited pediatric literature on malaria-associated GBS and highlights the importance of recognizing evolving bulbar and neurological symptoms after <i>Plasmodium falciparum</i> infection. Early supportive care and immunotherapy may contribute to favorable neurological recovery.</p>

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Guillain–Barré syndrome following Plasmodium falciparum malaria in a child: a case report

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月8日

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  • Simone Khalifeh,
  • Fatima Hussein,
  • Raja Sawaya,
  • Adam Najm,
  • Christine Saliba,
  • Ali Ismail

摘要

Background

Guillain–Barré syndrome (GBS) is an acute immune‑mediated polyradiculoneuropathy and remains a leading cause of acquired neuromuscular paralysis. In children, it typically follows infection, but association with malaria is rare.

Case presentation

We report a four‑year‑old Lebanese girl living in Nigeria, who developed progressive weakness, dysphagia, inspiratory stridor, and gait ataxia 2 weeks after treatment for Plasmodium falciparum malaria. Neurological examination revealed lower‑extremity weakness with areflexia, bulbar involvement causing stridor, unilateral facial weakness, and gait ataxia (Hughes score 4). Cerebrospinal fluid analysis showed albumin‑cytologic dissociation, and nerve conduction studies demonstrated acute inflammatory demyelinating polyradiculoneuropathy. Given the rapid progression and severity, therapeutic plasma exchange (PE) was administered (five exchanges over 10 days) along with supportive care. Strength improved steadily, and at 1 month she was able to walk and run independently (Hughes score 0).

Conclusions

This case expands the limited pediatric literature on malaria-associated GBS and highlights the importance of recognizing evolving bulbar and neurological symptoms after Plasmodium falciparum infection. Early supportive care and immunotherapy may contribute to favorable neurological recovery.