Clinical recovery of severe infantile Angiostrongylus cantonensis meningoencephalomyelitis treated with pulse methylprednisolone: A case report and review of literature

Abstract

BACKGROUND

Angiostrongylus cantonensis (A. cantonensis) is the leading cause of eosinophilic meningitis worldwide. Although infection is often self-limiting in adults, infants may develop severe meningoencephalomyelitis, associated with high morbidity and mortality. The optimal corticosteroid regimen for infants with severe disease and extensive central nervous system involvement remains unclear, and standard-dose corticosteroid therapy may be ineffective in acute fulminant cases.

CASE SUMMARY

A 10-month-old female infant was admitted with fever and vomiting, followed by rapid progression to deep coma, generalized seizures, flaccid quadriplegia, respiratory failure requiring mechanical ventilation, and neurogenic shock necessitating vasopressor support. Eosinophilic meningomyelitis was confirmed by marked eosinophilia in the cerebrospinal fluid (CSF) (42%). The CSF analysis with polymerase chain reaction was positive for A. cantonensis (Ct value 30.41; approximately 1.55 × 10⁵ copies). Magnetic resonance imaging revealed diffuse bilateral cerebral lesions with longitudinal cervical myelitis (C3 to C6). The patient was treated with high-dose methylprednisolone (30 mg/kg/day for 5 days), combined with albendazole (15 mg/kg/day for 21 days), which resulted in substantial neurological improvement. The patient was weaned off mechanical ventilation on day 16 and discharged on day 49 with mild residual weakness in the lower extremities. At five months post-discharge, the neurodevelopmental assessment was largely age-appropriate, with marked resolution of the motor and cognitive functions.

CONCLUSION

Pulse methylprednisolone is more effective than standard-dose corticosteroids for treating severe infantile A. cantonensis meningoencephalomyelitis with extensive, life-threatening neurological involvement.

Key Words: Angiostrongylus cantonensis; Eosinophilic meningoencephalomyelitis; Infant; Albendazole; Pulse methylprednisolone; Case report

Core Tip: Angiostrongylus cantonensis meningoencephalomyelitis in infants is rare and often fatal. We report a case of a 10-month-old infant with deep coma, flaccid quadriplegia, and neurogenic shock who achieved near-complete neurological recovery. Early administration of pulse methylprednisolone (30 mg/kg/day for 5 days) combined with albendazole was associated with a favorable outcome. This case supports the early use of high-dose pulse corticosteroid therapy to attenuate inflammatory neurological injury and improve the prognosis in critically ill infants with severe eosinophilic meningoencephalomyelitis.

INTRODUCTION

Angiostrongylus cantonensis (A. cantonensis) (rat lungworm) is a food-borne zoonotic nematode that is the leading cause of eosinophilic meningitis worldwide[1]. Once largely confined to Southeast Asia and the Pacific Islands, its range has expanded, likely influenced by global trade and climate change[2]. Humans are accidental hosts that are typically infected through the ingestion of raw or undercooked intermediate hosts (e.g., snails and slugs) or paratenic hosts carrying third-stage larvae[1]. In adults, the disease classically presents with severe headache, meningeal signs, and paresthesia[3,4]. In infants, manifestations are often non-specific (e.g., fever, vomiting, somnolence, irritability), mimicking viral or bacterial meningoencephalitis and delaying diagnosis[5]. Symptomatic infection in children < 2 years of age is uncommon and is thought to result from the accidental ingestion of infected mollusks or contaminated vectors[6]. Although most pediatric cases, especially in older children, are mild and respond to standard therapy, a subset, predominantly infants, develops fulminant meningoencephalomyelitis with diffuse central nervous system (CNS) inflammation[7]. Notably, neurological sequelae have been reported despite standard albendazole-corticosteroid regimens, suggesting that conventional approaches may be inadequate for the most severe presentations[8]. Therefore, we report a case of a 10-month-old infant with coma, quadriplegia, respiratory failure, shock, and extensive magnetic resonance imaging (MRI) abnormalities who achieved substantial neurological recovery after high-dose pulse methylprednisolone plus albendazole treatment.

CASE PRESENTATION

Chief complaints

A 10-month-old female infant residing in the Mekong Delta region of Vietnam was admitted in May 2025 with the chief complaints of high-grade fever, persistent vomiting, and irritability.

History of present illness

Onset phase (days 1-2): The patient developed persistent high-grade fever, recurrent vomiting, anorexia, acute diarrhea (four to five episodes per day), scattered urticarial rash, irritability, and crying. The patient was initially managed at a provincial hospital in the Mekong Delta, where a preliminary diagnosis of suspected purulent meningitis was made, and intravenous cefotaxime therapy was initiated. Initial blood investigations showed leukocytosis (23.77 × 10⁹/L), with a predominant increase in eosinophilia (2.61 × 10⁹/L) and an elevated C-reactive protein (CRP) level (35 mg/L). Lumbar puncture revealed cerebrospinal fluid (CSF) pleocytosis (89 cells/μL) with lymphocytic predominance and a positive Pandy reaction.

Progressive phase (days 3-6): Despite 48 hours of empirical antibiotic therapy, the patient’s clinical status deteriorated, with persistent fever, increasing lethargy, and emerging lower limb weakness, prompting the patient’s transfer to a tertiary referral center. On admission, she was lethargic, with a bulging anterior fontanel and an ongoing urticarial rash. Neurological examination revealed mild paraparesis, with lower extremity muscle strength graded at 3/5-4/5, while upper extremity strength remained intact (5/5).

Critical phase (days 7-9): Within 48 hours of admission, neurological deficits progressed with ascending weakness involving the upper limbs (muscle tone 4/5) and further deterioration of lower limb tone (3/5). The following day, the patient developed generalized tonic-clonic seizures that rapidly progressed to deep coma, respiratory failure, and quadriplegia. Emergency endotracheal intubation was performed, and the patient was transferred to the pediatric intensive care unit (PICU) for advanced interventions.

History of past illness

The patient was born at full term via spontaneous vaginal delivery without perinatal complications. Immunization was performed according to the National Immunization Schedule. There was no history of hospitalization, allergy, or chronic illness.

Personal and family history

At 10 months of age, the patient’s anthropometric measurements were within the normal range. She weighed 7.5 kg and was 70 cm tall. According to the World Health Organization growth standards, her weight corresponded to the 15^th percentile and her length to the 30^th percentile for age and sex, indicating appropriate growth. Epidemiological investigation revealed that the child frequently played with soil near a fish pond adjacent to her home and had a habit of putting soil-contaminated toys into her mouth. This behavior suggests a potential oral transmission route via accidental ingestion of third-stage larvae from an intermediate host (snail or paratenic host). The family reported no history of consuming raw or undercooked snails. No family members exhibited similar symptoms, and there was no known family history of immunodeficiency or neurological diseases.

Physical examination

On admission, her vital signs revealed a temperature (40 °C), tachycardia (175 beats/minute), hypotension (70/30 mmHg), and prolonged capillary refill (3 seconds). The patient presented a mild atypical urticarial-like rash scattered over the trunk and limbs. Neurological examination revealed a deep coma without response to painful stimuli, mild bulging of the anterior fontanelle, and flaccid quadriplegia (muscle strength of 0/5 in all extremities). The pupils were bilaterally equal (2 mm) with preserved light reflexes. Urinary retention and mild generalized edema were present, but the previously noted urticarial rash resolved.

Laboratory examinations

The serial laboratory results are summarized in Table 1. Peripheral blood analysis showed leukocytosis (21.87 × 10⁹/L) with marked eosinophilia (3.2 × 10⁹/L), microcytic hypochromic anemia [hemoglobin level 9.6 g/dL, mean corpuscular volume (MCV) 62.5 fL], and electrolyte disturbances, including progressive severe hyponatremia (125 mmol/L) and hypokalemia (2.2 mmol/L), and increased CRP (65 mg/L). Kidney and liver function tests and serum lactate and procalcitonin levels were within reference ranges. CSF analysis revealed a progressive increase in eosinophilic leukocytes, elevated protein concentrations, and low CSF glucose levels. Real-time polymerase chain reaction (PCR) of the CSF was positive for A. cantonensis (Ct = 30.41; approximately 1.55 × 10⁵ copies) (Table 1). Detection was performed using a TaqMan probe-based real-time PCR assay with previously published species-specific primers and probes. Amplification was conducted with TaqMan Universal Master Mix II (Thermo Fisher Scientific, Waltham, MA, United States) on an Applied Biosystems 7500 Real-Time PCR System (Applied Biosystems, Foster City, CA, United States). Further serological evaluation performed three weeks after disease onset demonstrated negative enzyme-linked immunosorbent assay (ELISA) results for anti-A. cantonensis immunoglobulin M (IgM) and immunoglobulin G (IgG) antibodies. Testing was conducted using the NEWLIFE ELISA kit (United States) and the Institut Virion/Serion GmbH Immunomat SERION system (Wuerzburg, Germany). Simultaneously, comprehensive microbiological and immunological investigations found no evidence of other etiologies, including bacterial, viral, mycobacterial, or other parasites.

Table 1 Clinical and laboratory characteristics from disease onset to discharge.

Phases	Clinical status	Laboratory findings	Imaging	Interventions
At provincial hospital (day 1)	Continuous high fever, severe vomiting, anorexia, excessive crying, acute diarrhea (4-5/day), scattered urticarial rash	Blood: WBC 23.77 (× 109/L); Eos 2.61 (× 109/L); CRP 35 mg/L; CSF: 89 cells/μL (lymphocytic predominance), Pandy (+)	Not performed	Cefotaxime
At emergency department admission (day 3)	Persistent fever, lethargy, bulging fontanelle, urticarial rash, paraparesis (muscle tones of lower limbs 3/5 and upper limbs 5/5)	Blood: WBC 17 (× 109/L); Eosin 2.54 (× 109/L); CRP 65 mg/L; Na+ 130 mmol/L; routine cultures of blood and CSF: Negative; repeated CSF: 142 cells/μL; Eos 32.4%; protein 0.47 g/L	Brain CT-scan: No evidence of acute hemorrhage, mass effect, or significant ventriculomegaly	Cefotaxime + vancomycin
On PICU admission (day 6)	High fever 40 °C, coma, respiratory failure, shock status (HR 175 bpm; BP 70/30 mmHg), flaccid quadriplegia, muscle tones 0/5, urinary retention, mild edema	WBC 21.87 (× 109/L), eosin 3.2 (× 109/L) Na+ 125 mmol/L, K+ 2.2 mmol/L; PCR-CSF: Positive for A. cantonensis; (Ct 30.41; approximately 1.55 × 105 copies); repeated CSF: 266 cells/μL; Eos 22%; protein 2.3 g/L	Brain MRI: Diffuse; white/gray matter; lesions, ventricular; dilation; spine MRI: Signal; abnormalities C3-C6, lumbosacral meningeal; enhancement	Mechanical ventilation; fluid resuscitation and vasopressor use; cerebral anti-edema with 3% NaCl; methylprednisolone (30 mg/kg/day); albendazole (15 mg/kg/day)
At PICU discharge (day 28)	Afebrile, alert, communicative, respiratory and urinary continence improvement, muscle tones: Upper limbs 2/5, and lower limbs 3/5; hospital acquired pneumonia	WBC improved; immunology: Oligoclonal band (+) type 2; PCR of blood and sputum samples revealed; Acinetobacter and Pseudomonas spp.; CSF: 125 cells/μL		Extubation, intensive physical therapy, tapered oral prednisolone, and intravenous antibiotics for hospital acquired pneumonia
At hospital discharge (day 49)	Fully alert, independent feeding	Normalized full blood counts and CSF findings	Brain MRI: Thin right subdural hygroma, ventriculomegaly	Discharged, continue home physical therapy

HR: Heart rate; BP: Blood pressure; WBC: White blood cell; G/L: Giga per liter (× 10⁹/L); Eos: Eosinophils; CRP: C-reactive protein; CSF: Cerebrospinal fluid; CT: Computed tomography; MRI: Magnetic resonance imaging; EEG: Electroencephalogram; PCR: Polymerase chain reaction.

Imaging examinations

Brain MRI, performed using a 3.0 Tesla SIGNA Architect system (GE HealthCare), revealed widespread bilateral hyperintense lesions affecting both the gray and white matter of the frontal, parietal, and occipital lobes, accompanied by ventricular dilatation (Figure 1A). No evidence of acute hemorrhage, a mass effect, or significant ventriculomegaly was observed. Spinal MRI demonstrated an abnormal hyperintense signal on T2-weighted imaging in the cervical cord (C3-C6), with symmetrical involvement of the anterior horns, correlating with the patient’s clinical presentation of flaccid quadriplegia and respiratory failure due to motor-neuron involvement (Figure 1B and C). Meningeal thickening and enhancement were observed in the lumbosacral region of the spine.

Figure 1 Initial neuroimaging findings. A: Axial T2-weighted brain magnetic resonance imaging showing diffuse bilateral hyperintense lesions involving the gray and white matter of the frontal, parietal, and occipital lobes with associated ventricular dilatation. No acute hemorrhage, mass effect, or significant ventriculomegaly was detected; B: Sagittal T2-weighted cervical spine magnetic resonance imaging (MRI) revealing longitudinal hyperintense signal from C3 to C6 with mild cord expansion consistent with inflammatory edema; C: Axial T2-weighted cervical spine MRI demonstrating symmetric anterior horn hyperintensity, correlating with flaccid quadriplegia and respiratory failure. The orange arrows indicate the lesion locations in the brain and cervical spine.

MULTIDISCIPLINARY EXPERT CONSULTATION

Consultations with pediatric infectious diseases, neurology, and PICU specialists confirmed the diagnosis and guided management, with a consensus to initiate high-dose corticosteroids and delay antihelminthic therapy to reduce the risk of a Herxheimer-like inflammatory reaction.

FINAL DIAGNOSIS

The patient, with no prior medical history, was diagnosed with severe meningoencephalomyelitis caused by A. cantonensis, complicated by neurogenic shock and acute respiratory failure, requiring mechanical ventilation.

TREATMENT

The patient received comprehensive supportive management, including invasive mechanical ventilation, osmotic therapy for cerebral edema with 3% hypertonic saline, vasopressor support with norepinephrine, and empirical broad-spectrum intravenous antibiotics (meropenem and vancomycin). High-dose intravenous methylprednisolone (30 mg/kg/day) was administered for five consecutive days to attenuate the inflammatory response and limit CNS injury. Notably, albendazole (15 mg/kg/day) was introduced on the third day of corticosteroid therapy to minimize the risk of a pseudo-Herxheimer inflammatory reaction associated with larval death. After completing pulse therapy, the patient was switched to oral prednisolone at an initial dose of 2 mg/kg/day with gradual tapering over 5 weeks, while albendazole was continued to complete a 21-day course.

OUTCOME AND FOLLOW-UP

Treatment response and clinical course

After five days of high-dose methylprednisolone therapy, the patient demonstrated marked clinical improvement, including defervescence and partial recovery of consciousness, as evidenced by eye opening in response to painful stimuli. Residual neurological deficits persisted, including quadriplegia (muscle tone 2/5) and urinary retention. Laboratory evaluation revealed ongoing peripheral eosinophilia (3.24 × 10⁹ cells/L), while repeat CSF analysis showed a reduced cell count (170 cells/μL) with 28.4% eosinophils. By day 12, the patient regained consciousness and was able to interact appropriately. Respiratory function improved sufficiently to allow weaning from mechanical ventilation by day 16. Gradual motor improvement was observed (upper limbs 2/5, lower limbs 3/5), accompanied by a further reduction in CSF cellularity (125 cells/μL). Intensive physiotherapy was initiated.

Follow-up investigations

Immunological tests were negative for anti-neuromyelitis optica (aquaporin-4) and anti–myelin oligodendrocyte glycoprotein antibodies. Oligoclonal bands were positive (type 2), with elevated CSF IgG (25.14 mg/dL) relative to serum IgG (387.8 mg/dL), consistent with intrathecal immunoglobulin synthesis. Electroencephalography revealed predominant theta activity, which was more pronounced in the left hemisphere, without epileptiform discharges. During recovery, the patient developed recurrent fever with elevated levels of inflammatory markers (CRP, 55 mg/L; procalcitonin, 3 ng/mL). In addition, further PCR tests of blood and sputum samples revealed Acinetobacter baumannii and Pseudomonas aeruginosa, which were consistent with the diagnosis of hospital-acquired pneumonia, managed with appropriate intravenous antibiotics.

Discharge status

The patient was discharged on day 49 with a stable clinical status after 7 weeks of hospitalization. The patient was able to eat independently after the treatment. Motor function markedly improved, with muscle tone of 5/5 in the upper limbs and 3/5 in the lower limbs. Pre-discharge magnetic resonance imaging revealed residual findings, including a thin right subdural hygroma and persistent ventriculomegaly (Figure 2). CSF analysis demonstrated a marked reduction in inflammatory activity (56 cells/μL), and hematological parameters returned to normal. Home-based physical therapy was recommended at the time of discharge from the hospital.

Figure 2 Pre-discharge and follow-up magnetic resonance imaging findings. Pre-discharge brain magnetic resonance imaging demonstrating a thin right-sided subdural hygroma along the cerebral convexity and persistent ventriculomegaly as residual treatment-related sequelae. The orange arrows indicate the lesion locations in the brain.

Follow-up visits

At five months post-discharge, the patient’s neurodevelopment was age-appropriate, with normal muscle tone. Motor skills include standing with support, cruising along furniture, pushing a walker over extended distances, and standing independently. Language development comprises approximately five two-syllable words and several single words with good receptive language. The head circumference measured 44 cm, slightly below the average population but above the 3^rd percentile. Follow-up brain MRI demonstrated a marked reduction in the lateral ventricular diameter (8 mm compared with 12 mm at admission), complete resolution of the subdural hygroma, and normal brain parenchyma (Figure 3A). Cervical spinal cord imaging (C3-C6) revealed normal signal intensity without evidence of cord atrophy (Figure 3B).

Figure 3 Follow-up magnetic resonance imaging findings. A: Brain magnetic resonance imaging (MRI) at 17 months of age showing marked reduction in lateral ventricular size (8 mm vs 12 mm at admission), complete resolution of the subdural hygroma, and normal brain parenchyma with preserved cortical sulci. Ventricular enlargement is indicated by an asterisk; B: Cervical spine MRI demonstrating normal spinal cord signal from C3 to C6 without evidence of cord atrophy. The orange arrows indicate the lesion locations in the brain and cervical spine.

DISCUSSION

We report a rare case of fulminant A. cantonensis meningoencephalomyelitis in a 10-month-old infant who presented with deep coma, flaccid quadriplegia, and neurogenic shock, representing the extreme end of the disease spectrum. In contrast to the typically self-limited course observed in adults, fulminant neuroangiostrongyliasis in infants is associated with high mortality and a substantial risk of long-term neurological sequelae in survivors. Nevertheless, the present case demonstrated near-complete functional recovery following combined pulse methylprednisolone and albendazole therapy. This case study highlights the potential benefits of early high-dose corticosteroid therapy in preventing irreversible neuronal damage in critically ill infants.

Infants aged less than 2 years have disproportionately higher rates of severe disease and mortality than older children and adults[9,10]. This vulnerability is multifactorial. Infants may carry a higher larval burden, with CSF larvae detected in up to 73% of cases (vs 18%-42% in older children), predisposing them to more diffuse neural injury[9]. Neurological damage is compounded by mechanical injury from larval migration and granulomatous inflammation around degenerating larvae, which may promote thrombo-occlusive vasculopathy[3,11]. Moreover, an immature Th2-skewed immune response with exaggerated eosinophil activation and degranulation can release neurotoxic mediators that affect Purkinje cells and motor neurons (the Gordon phenomenon)[12-16]. Developmental immaturity of the blood-brain barrier, synaptogenesis, and ongoing myelination may further heighten susceptibility to inflammatory injury[17-21]. Diagnosis is frequently delayed because non-specific symptoms (e.g., fever, lethargy, vomiting, and irritability) mimic common viral or bacterial meningoencephalitis, limiting early targeted therapy[5].

A literature review (1997-2024) identified 17 reported cases of A. cantonensis meningoencephalomyelitis in children aged < 24 months (Supplementary Table 1). Patient outcomes varied greatly; 3 of 17 patients (17.6%) died, typically in association with coma, quadriplegia, respiratory failure, and multiorgan involvement; 3 of 17 (17.6%) survived with permanent neurological sequelae; and 11 of 17 (64.7%) achieved complete recovery without residual deficits. Favorable outcomes were attributed to early recognition and timely initiation of corticosteroid therapy. Nonetheless, the patient in our case study exhibited greater severity, comparable to fatal or severely disabled cases, as characterized by deep coma, complete quadriplegia, ventilator-dependent respiratory failure, and neurogenic shock.

The rationale for administering high-dose methylprednisolone (30 mg/kg/day for five days) was based on several considerations. First, from a pathophysiological perspective, neurological injury in A. cantonensis infection is primarily mediated by an intense host inflammatory response to the larvae and their degradation products rather than by direct parasitic damage, rendering anti-inflammatory therapy a critical component of management[14,22]. Corticosteroids suppress inflammation, reduce cerebral edema, lower intracranial pressure, and protect neurons from inflammation-induced injury[23,24]. In cases of diffuse CNS involvement, such as the present case, standard-dose corticosteroid therapy (1-2 mg/kg/day) may be insufficient to adequately control acute inflammatory responses. Second, regarding disease severity, our patient fulfilled all criteria for life-threatening disease: Deep coma, complete quadriplegia, respiratory failure requiring mechanical ventilation, neurogenic shock requiring vasopressors, and diffuse cerebral and spinal cord lesions on MRI. Current guidelines provide general recommendations but lack specific dosing for life-threatening pediatric conditions[25]. Third, there is supporting literature regarding this approach. Our literature review identified three pediatric cases utilizing pulse methylprednisolone (10-30 mg/kg/day) for A. cantonensis meningoencephalomyelitis (Supplementary Table 2). All three patients presented with severe neurological compromise and achieved good-to-complete recovery[7,26,27]. Fourth, based on experience with other neurological conditions, pulse corticosteroid therapy has been successfully employed in various pediatric CNS inflammatory disorders, including autoimmune encephalitis, transverse myelitis, and acute disseminated encephalomyelitis, typically using methylprednisolone at 20-30 mg/kg/day for 3-5 days[28].

The case reported by Abe et al[26] from Hawaii represents the only published report describing the prolonged administration of high-dose methylprednisolone (30 mg/kg/day for 16 days) in an infant with severe disease. Both the Hawaiian case and our patient involved infants of comparable age presenting with fulminant neurological involvement, including quadriplegia, respiratory failure requiring mechanical ventilation, and extensive cervical spinal cord involvement (C3-C6/C7 vertebrae). In both cases, treatment consisted of high-dose methylprednisolone combined with albendazole. Notable differences between the two cases were related to the timing and duration of corticosteroid therapy. In the Hawaii case, the initial misdiagnosis of Guillain-Barré syndrome resulted in the administration of intravenous immunoglobulin and delayed initiation of corticosteroids until day 16 of the illness, necessitating prolonged high-dose therapy. In contrast, corticosteroids were initiated earlier in our patient (day 6) and were administered as a 5-day pulse regimen. Correspondingly, neurological recovery in our patient was more rapid and complete, with earlier discharge and age-appropriate psychomotor development documented at 17 months of follow-up, whereas residual neurological deficits persisted for a longer duration in the Hawaiian case[26]. These results indicate that early initiation of pulse methylprednisolone at 30 mg/kg/day for 5 days may yield better outcomes in patients with severe disease. The outcome observed in this patient may be attributable to an earlier diagnosis and early initiation of targeted interventions. Thus, this prevented a prolonged period of non-specific initial treatment and reduced the duration of mechanical ventilation.

Antihelmintic therapy remains controversial because rapid larval death may trigger a pseudo-Herxheimer-type inflammatory reaction via antigen release[29]. However, guidelines and small trials support combined albendazole-corticosteroid regimens, which may shorten symptom duration, particularly headaches[25,30]. In this case, albendazole (15 mg/kg/day) was initiated on day 3 of pulse corticosteroid therapy to ensure adequate anti-inflammatory coverage before antihelminthic-induced antigen release, thereby minimizing the risk of clinical deterioration.

The definitive diagnosis of A. cantonensis has historically depended on larval identification in the CSF; however, the yield is low even in severe disease[14]. Serological assays (ELISA IgG/IgM) have variable performance and are constrained by delayed seroconversion, with antibodies typically appearing 10-30 days after infection, potentially later in infants due to immunological immaturity[31]. Notably, IgM/IgG ELISA remained negative at week 3, whereas the CSF PCR was positive early. Recent data further support molecular approaches; a 2025 pediatric series from Guangdong reported 100% CSF detection by metagenomic next-generation sequencing, including seronegative cases[32]. Collectively, these findings underscore the importance of molecular diagnostics, particularly targeted real-time PCR, for early and accurate diagnosis[33].

In children with life-threatening A. cantonensis meningoencephalomyelitis presenting with severe encephalopathy, quadriplegia, or diffuse CNS involvement on neuroimaging, pulse methylprednisolone may be considered when standard-dose corticosteroids fail to adequately control inflammation. Early CSF PCR testing should be prioritized to facilitate timely diagnosis, particularly in young infants in whom serologic testing may be delayed or falsely negative[25]. A recent Vietnamese encephalitis study reported a high proportion of abnormal CSF findings with unidentified etiologies, highlighting the potential underdiagnosis of CNS infections due to limitations in advanced molecular diagnostics, including multiplex PCR, GeneXpert Ultra, and metagenomic next-generation sequencing[34]. As demonstrated in the present case, eosinophilic meningoencephalomyelitis remains rare, frequently overlooked in clinical practice, and associated with substantial neurological sequelae. At our pediatric hospital, CNS infections caused by Japanese encephalitis virus, herpes simplex virus, dengue virus, and enteroviruses have been associated with high mortality and severe neurological outcomes among survivors[35,36].

This report offers detailed clinical, laboratory, and neuroimaging characterization of a rare, life-threatening infantile neuroangiostrongyliasis, with a diagnosis confirmed by real-time PCR. We further documented pulse methylprednisolone use in a critically ill infant with extensive CNS involvement and sustained neurological recovery after 5 months of follow-up. The limitations include the single-case study design, which precludes causal attribution and does not exclude spontaneous improvement, given the heterogeneous course of A. cantonensis infection. Prospective controlled studies are needed to define the optimal corticosteroid dosage and duration in patients with severe infantile disease.

CONCLUSION

This study highlights a rare and life-threatening presentation of A. cantonensis meningoencephalomyelitis in an infant. The favorable outcome suggests that early initiation of pulse methylprednisolone therapy at a dosage of 30 mg/kg/day for 5 consecutive days, in combination with albendazole, may be an effective therapeutic strategy in severe, life-threatening infantile cases. This regimen may help mitigate inflammatory neurological injury and improve prognosis when promptly managed in critically ill patients.

ACKNOWLEDGEMENTS

The authors are sincerely grateful to the patient and his family for their cooperation and for providing consent for the publication of this case. We would like to acknowledge the dedicated efforts of the emergency, infectious diseases intensive care unit, and neurology teams involved in the management of this patient. We are grateful to the patients, research staffs, and nurses for their support in this study.