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

Abstract

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.

Supplementary Information

The online version contains supplementary material available at https://doi.org/10.1186/s12936-026-06024-6.

Background

Guillain–Barré syndrome encompasses a spectrum of post‑infectious autoimmune neuropathies characterized by rapidly progressive, symmetrical weakness, areflexia, and variable sensory or cranial nerve involvement [1, 2]. Molecular mimicry between microbial antigens and peripheral nerve gangliosides is thought to trigger antibodies that damage myelin or axons [2]. Campylobacter jejuni, cytomegalovirus, and influenza are well‑recognized antecedent infections [2]. Malaria‑associated GBS is rare and has been described mainly as isolated case reports and small case series [3].

According to the European Academy of Neurology/Peripheral Nerve Society, GBS diagnosis consists of required clinical features, supportive clinical features and supportive laboratory features. The following are the required features: progressive weakness of arms and legs, absent or decreased tendon reflexes in affected limbs and progressive worsening for no more than 4 weeks [1]. Features that support GBS diagnosis are relative symmetry, relatively mild/absent sensory symptoms and signs, cranial nerve involvement (especially bilateral facial palsy), autonomic dysfunction, respiratory insufficiency (due to muscle weakness), pain (muscular/radicular in back or limb) and recent (< 6 weeks) history of infection (or recent surgery) [1]. As for supportive laboratory features, they include CSF findings, presence of specific antibodies in blood and electrodiagnosis. Although with GBS there is increased CSF protein, normal CSF protein does not totally rule out GBS diagnosis. CSF White cells are usually < 5 × 10⁶/L. Blood Anti- GQ1b antibodies are found in Miller Fisher syndrome. Electrodiagnosis, namely nerve conduction studies (NCS), show evidence of polyneuropathy. NCS may be normal during first days of disease [1].

Pediatric cases may present atypically, including stridor and swallowing difficulty from cranial nerve involvement [4]. Ataxia may occur in GBS overlap or variant syndromes (e.g., anti‑GQ1b‑associated phenotypes) [5]. Early recognition and immunotherapy—intravenous immunoglobulin or PE—can improve outcomes [1]. We describe a child who developed demyelinating GBS after Plasmodium falciparum malaria and recovered after PE and supportive care.

Case presentation

A previously healthy four‑year‑old Lebanese girl living in Nigeria developed high‑grade fever (reported maximum 40°C) thirteen days before presenting to the Emergency Department at the American University of Beirut Medical Center. In Nigeria, she had fever without chills, night sweats, headache, fatigue, myalgia, vomiting, abdominal pain, or diarrhea. Peripheral blood thin and thick smears performed at a medical center in Nigeria demonstrated malaria parasites, with ring forms morphologically consistent with Plasmodium falciparum identified on thin film. The laboratory report noted low parasitic density. Initial laboratory studies (Supplementary Table S1) revealed neutrophil‑predominant leukocytosis without anemia or thrombocytopenia. She received oral artemether–lumefantrine for three days (six-dose regimen) with fever resolution.

On illness day 9, she developed lower‑extremity weakness and unsteady gait without trauma and was hospitalized in Nigeria. On illness day 11, repeat peripheral blood smears again demonstrated P. falciparum ring forms on thin film and malaria parasites on thick film. Repeat laboratory values (Supplementary Table S1) showed improvement and included normal creatine phosphokinase and rheumatoid factor. During that admission, she received intravenous artesunate for three days and two doses of intravenous ceftriaxone.

Between illness days 12 and 13, neurological symptoms progressed to gait ataxia with dysphonia and dysphagia to fluids. On illness day 14, she presented to our institution with headache, irritability, and photophobia. She also had slurred speech and inspiratory stridor requiring high‑flow nasal cannula (no assisted ventilation) and was functionally bedridden, with a Hughes score of 4 [6]. She was afebrile and had no seizures, loss of consciousness, respiratory symptoms other than stridor, gastrointestinal symptoms, or urinary symptoms. Vaccinations and neurodevelopment were reported as normal, with no sick contacts and no animal exposure. The chronological progression of the patient’s illness, investigations, treatment, and recovery is summarized in Fig. 1.

Fig. 1.

Clinical timeline of illness, investigations, and management

On neurological examination, she was alert (Glasgow Coma Scale score of 15) but agitated and uncooperative. Cranial nerve assessment demonstrated right-sided facial weakness characterized by lagophthalmos, along with left mouth corner deviation, consistent with asymmetric facial nerve involvement. Bulbar dysfunction was evident, with dysphonia, dysphagia to liquids, and inspiratory stridor. There was no documented ophthalmoplegia or visual disturbance.

Motor examination, assessed using the Medical Research Council (MRC) muscle strength scale, revealed preserved upper-extremity strength (5/5) and significant lower-extremity weakness, graded at approximately 2/5 proximally (hip flexion) and 3/5 distally (knee extension and ankle dorsiflexion). The patient was unable to bear weight.

Deep tendon reflexes were absent at the knees bilaterally, consistent with a peripheral neuropathic process. Upper-extremity reflexes could not be reliably assessed because of poor cooperation.

Plantar responses were initially reported as upgoing bilaterally. However, in the context of acute areflexic weakness and subsequently confirmed demyelinating polyneuropathy, this finding was interpreted cautiously and may have reflected variability during pediatric examination in an irritable child. Importantly, plantar responses later became downgoing during hospitalization (Table 1).

Table 1.

Laboratory and investigational findings at presentation to the American University of Beirut Medical Center

Category	Parameters
Complete blood count	WBC 13,000 cells/mm3; Hemoglobin 13.2 g/dL; Hematocrit 38%; MCV 70.5 fL; RDW 15.0%; Neutrophils 66%; Lymphocytes 26%; Platelets 776,000 cells/mm3
Basic metabolic panel	Glucose 85 mg/dL; BUN 17 mg/dL; Creatinine 0.36 mg/dL; Sodium 140 mmol/L; Potassium 4.4 mmol/L; Chloride 103 mmol/L; Carbon dioxide 20 mmol/L; Anion gap 17 mmol/L; Magnesium 2.2 mg/dL; Calcium 10.8 mg/dL; Inorganic phosphate 5.6 mg/dL
Liver function tests	Total bilirubin 0.4 mg/dL; Direct bilirubin 0.1 mg/dL; AST 32 IU/L; ALT 17 IU/L; Alkaline phosphatase 200 U/L; GGT 21 IU/L
Inflammatory, immunologic, and other studies	CRP 1.7 mg/L; CPK 70 IU/L; Whole‑blood G6PD 8.0 U/g Hb (normal); serum anti-ganglioside antibodies (GD1a, GD1b, GM1, GT1a, GQ1b): negative; anti-MAG antibody: negative; Quantitative immunoglobulins: IgG 12.25 g/L; IgA 0.97 g/L; IgM 1.20 g/L (normal)
Cerebrospinal fluid	RBC: none; total nucleated cells 7; differential reported as lymphocyte‑predominant; glucose 54 mg/dL; protein 3.66 g/L (elevated; ref 0.1–0.5 g/L); meningitis PCR panel negative; Gram stain negative; cytology negative; culture no growth; malaria PCR negative; 16S DNA sequencing negative

Differential diagnosis at this stage included GBS, cerebral malaria, post‑malarial neurological syndrome, under‑treated malaria, stroke, and encephalitis.

She was supported with high‑flow nasal cannula and received intravenous artesunate at 0, 12, and 24 h (3 mg per dose as documented). Cerebrospinal fluid studies demonstrated albumin‑cytological dissociation. Nerve conduction studies were performed in the posterior tibial and sural nerves bilaterally and the right median and ulnar nerves. Motor studies of both posterior tibial nerves demonstrated preserved distal compound muscle action potentials with > 50% proximal amplitude drop at the popliteal fossa relative to ankle stimulation, with slowed conduction velocities. Posterior tibial F‑wave responses were absent bilaterally; sural sensory responses were normal bilaterally. Right median motor responses showed a ~ 50% proximal drop with reduced conduction velocity; right ulnar motor responses showed a ~ 35% proximal drop with no evidence of conduction block at the olecranon fossa. Sensory responses of the right median and ulnar nerves were absent. Needle EMG of the tibialis anterior muscles bilaterally showed normal motor unit morphology without spontaneous activity and markedly reduced recruitment. Electrophysiological features supporting demyelination included significant proximal-to-distal CMAP amplitude reduction, slowed conduction velocities, absent F-wave responses, and relative preservation of sural sensory responses (sural-sparing pattern) (Table 2). Overall, these findings are consistent with a demyelinating polyneuropathy, specifically acute inflammatory demyelinating polyradiculoneuropathy (AIDP), based on established electrophysiological features described in current GBS guidelines and literature [1]. In view of the bilateral symmetric lower-extremity weakness, absent deep tendon reflexes in both knees and progressive worsening over less than 4 weeks, the clinical presentation of the patient had all the required features for GBS diagnosis as stated by the European Academy of Neurology/Peripheral Nerve Society. Furthermore, the electrophysiological finding of AIDP, in conjunction with cerebrospinal fluid profile, supported the diagnosis of GBS.

Table 2.

Summary of nerve conduction study findings

Nerve	Side	Distal CMAP amplitude (mV)	Proximal CMAP amplitude (mV)	Conduction velocity (m/s)	Key finding
Posterior tibial	Left	7.6	2.9	31	> 50% Proximal drop, slowed CV
Posterior tibial	Right	5.8	2.6	34	> 50% Proximal drop, slowed CV
Sural	Left	12 µV	–	47	Preserved sensory response
Sural	Right	13 µV	–	43	Preserved sensory response
Median (motor)	Right	7.4	3.9	25	~ 50% Proximal drop, slowed CV
Ulnar (motor)	Right	3.3	2.2	30	~ 35% Proximal drop
Median (sensory)	Right	Absent	–	–	Absent SNAP
Ulnar (sensory)	Right	Absent	–	–	Absent SNAP
Posterior tibial F-wave	Left	Absent	–	–	Absent F-wave
Posterior tibial F-wave	Right	Absent	–	–	Absent F-wave

There was no evidence of malarial retinopathy on ophthalmological examination. Brain and spine MRI demonstrated enhancement consistent with GBS involvement: with bilateral enhancement of the trigeminal and the acoustic‑facial nerves (Fig. 2) and leptomeningeal enhancement along the conus medullaris and cauda equina nerve roots (Fig. 3).

Fig. 2.

Brain MRI: a T1 with contrast showing bilaterally enhancing trigeminal nerves (blue circles). b T1 with contrast showing bilaterally enhancing acoustic-facial nerves (blue arrows)

Fig. 3.

Spine MRI: Sagittal images showing leptomeningeal enhancement of the conus medullaris and cauda equina nerve roots on post‑contrast imaging

A femoral venous catheter was inserted for initiation of therapeutic PE. The patient received five exchange sessions during the admission. During hospitalization, intermittent hypertension was treated with amlodipine 2.5 mg once daily. She received saline nebulization and chest physiotherapy for noisy breathing/stridor, remained euglycemic on maintenance intravenous fluids, and tolerated a soft diet. Gabapentin (5 mg/kg twice daily) was administered for neuropathic pain.

High‑flow oxygen was weaned to room air. Facial weakness improved gradually and lower‑extremity coordination improved. By hospital day 9, mouth deviation, dysphonia, and ptosis had resolved, though stridor persisted with crying. Plantar responses became downgoing. At discharge (11‑day admission), she could take a few assisted steps; upper‑extremity strength was near‑normal (4/5) while proximal lower‑extremity strength remained reduced (hip flexion ~ 2/5; knee extension and dorsiflexion ~ 3/5). She continued outpatient physiotherapy after discharge. At telehealth follow‑up one week later, she was observed walking independently and running more than 10 m (Hughes score 0) [6].

Discussion

This case highlights a rare pediatric presentation of GBS following Plasmodium falciparum malaria, characterized by prominent bulbar symptoms, inspiratory stridor, ataxia, cranial nerve involvement, and supportive neuroimaging findings. Malaria‑associated GBS remains uncommon in the literature; both Plasmodium falciparum and P. vivax infections have been described as antecedents in published cases [3]. In children and adolescents, published reports remain sparse, with documented recoveries after supportive care alone or after immunotherapy such as PE [7–9].

Bulbar symptoms and stridor. Bulbar involvement is uncommon in pediatric GBS but can manifest as dysphagia, hoarseness, and inspiratory stridor due to cranial nerve paresis. Pediatric presentations with stridor have been described and may be misdiagnosed as upper airway disease, delaying recognition of neuromuscular weakness [4]. In our patient, inspiratory stridor and dysphagia were prominent early features; early supportive respiratory care and definitive immunotherapy were therefore prioritized.

Ataxia and GBS variants/overlap. Ataxia may suggest a GBS variant or overlap syndrome (for example, anti‑GQ1b‑associated phenotypes). Such overlap presentations broaden the clinical spectrum and reinforce immune‑mediated pathophysiology [5]. In our patient, anti‑ganglioside antibodies (including anti‑GQ1b) were tested and were negative, and neurophysiology supported acute inflammatory demyelinating polyneuropathy. The electrophysiological findings in our patient are consistent with demyelinating GBS patterns described in current guidelines, including conduction slowing, F-wave absence, and relative sural-sparing, further supporting the diagnosis of AIDP.

Context within known GBS triggers. Guillain, Barré, and Strohl first described the syndrome in 1916 [10]. In contemporary series, approximately two‑thirds of cases follow an antecedent infection; Campylobacter jejuni is a common trigger, and other reported infectious associations include Haemophilus influenzae and hepatitis E virus [2, 11, 12]. Outbreak and post‑infectious associations have also been described with arboviruses such as Zika and Chikungunya [13, 14]. Neurological adverse event reports after COVID‑19 vaccination have been analyzed in large surveillance datasets [15]. These diverse triggers support an immune‑mediated mechanism, and the very small number of malaria‑associated cases suggests either rarity or under‑recognition in endemic settings [3].

Reappearance of Plasmodium falciparum on peripheral blood smear. 8 days after end of oral treatment with the six-dose regimen of artemether–lumefantrine. The possible reasons could be treatment failure, and less likely reinfection. Artemether–lumefantrine, an expensive drug, is recommended by the World Health Organization for the treatment of uncomplicated malaria. This oral preparation was initially designed for use against chloroquine-resistant Falciparum malaria [16]. Treatment failure of the combination artemether–lumefantrine, has been reported in the literature [17, 18]. Subtherapeutic blood levels of lumefantrine were detected in treatment failure cases, probably related to the highly lipophilic nature of this drug and its variable absorption [18]. Also different sets of parasite populations have been suggested to have caused the recurrent episodes [17]. Partial artemisinin resistance due to polymorphism of the parasite’s Pfk13 gene leads to delayed clearance of the parasite and delayed response to therapy [19]. Reinfection is another possibility; however the patient did not have recurrence of fever after the end of her oral therapy.

Choice of therapy: plasma exchange versus intravenous immunoglobulin. Therapeutic PE was among the earliest validated immunotherapies for GBS [20, 21]. High‑dose intravenous immunoglobulin subsequently emerged as an effective alternative [22, 23], and contemporary guidelines recommend either IVIG or PE when initiated early in the disease course, based on severity and feasibility [24]. In the broader evidence base, comparative syntheses suggest similar overall efficacy of IVIG and PE, while acknowledging differences in logistics, cost, and adverse event profiles [25, 26]. Pediatric data include retrospective and randomized studies suggesting that PE can be effective and may reduce certain resource endpoints in selected severe pediatric cases [27–29]. Cost analyses further highlight that PE may be a cost‑efficient alternative in some settings [30]. In our patient—given rapid progression with bulbar involvement—PE was selected and was followed by rapid functional recovery.

Prognosis and outcomes. Children with GBS generally recover well compared with adults, though respiratory or bulbar involvement and autonomic instability may indicate higher risk and warrant close monitoring [6, 31]. Functional disability can be tracked using tools such as the Hughes Functional Grading Scale [6], which has been widely used in GBS clinical studies. Prognostic indicators and pediatric outcome models have also been evaluated in cohort studies [32]. Our patient’s early bulbar symptoms raised concern for deterioration, but timely immunotherapy and supportive care were associated with full functional recovery by early follow‑up.

Limitations

This report has several limitations. First, as a single case report, causal association between Plasmodium falciparum malaria and GBS cannot be definitively established. Second, although malaria diagnosis was supported by repeated positive thick and thin peripheral blood smears performed in an endemic region, original microscopy images were unavailable because the slides had been discarded prior to retrospective retrieval. Third, the initial extensor plantar responses were atypical for classic GBS and were interpreted cautiously in the context of a young, irritable child with limited cooperation during neurological examination. Nevertheless, the overall clinical presentation, cerebrospinal fluid findings, neurophysiological studies, MRI findings, and subsequent clinical course remained most consistent with AIDP.

Conclusions

This report expands the limited literature on malaria-associated GBS in children by describing a severe demyelinating presentation following Plasmodium falciparum infection, characterized by bulbar dysfunction, inspiratory stridor, ataxia, cranial nerve involvement, and supportive MRI findings. The case highlights the importance of considering GBS in children presenting with evolving neurological symptoms after malaria, particularly when atypical bulbar manifestations are present. Early recognition, supportive care, and timely immunotherapy may contribute to favorable neurological recovery.

Maximizing the prevention of malaria infection, including the administration of malaria vaccine in endemic areas, is highly needed.

List of abbreviations

AIDP

Acute inflammatory demyelinating polyradiculoneuropathy

AUBMC

American University of Beirut Medical Center

CPK

Creatine phosphokinase

CRP

C‑reactive protein

CSF

Cerebrospinal fluid

ED

Emergency department

GBS

Guillain–Barré syndrome

GCS

Glasgow Coma Scale

G6PD

Glucose‑6‑phosphate dehydrogenase

HFNC

High‑flow nasal cannula

IV

Intravenous

IVIG

Intravenous immunoglobulin

MRI

Magnetic resonance imaging

NCS

Nerve conduction study

PE

Plasma exchange

Author contributions

AI was the treating clinician and conceived the manuscript. CS assisted in the literature review and drafting. AN reviewed the case, retrieved imaging, and assisted in the literature review. RS is the neurophysiologist who performed and reported the nerve conduction studies and electromyography. FH assisted in literature review and drafting. SK supervised the team, unified the sections, and finalized the manuscript. All authors read and approved the final manuscript.

Funding

The authors received no specific funding for this work.

Availability of data and materials

All data generated or analyzed during this study are included in this published article and its supplementary material.

Declarations

Competing interests

SK, FH, RS, AN, CS, and AI declare that they have no competing interests.

Ethics approval and consent to participate

This case report was prepared in accordance with the Declaration of Helsinki. Written informed consent to participate was obtained from the patient’s parents/legal guardians. Ethical approval was not required for publication of a single de‑identified case report in accordance with local institutional policy (committee name/reference number: not applicable/available upon request).

Consent for publication

Written informed consent for publication of this case report and any accompanying images was obtained from the patient’s parents/legal guardians. A copy of the written consent is available for review by the Editor upon request.