Case
A 1-year-old Brazilian girl from Amazonas developed a pruritic rash, fever, nausea, and vomiting over approximately 18 days. Despite evaluation at several healthcare facilities, her illness progressed.
On admission to a tropical and infectious diseases referral hospital in Manaus, her temperature was 39.1 °C. She was irritable and drowsy, with persistent vomiting and asthenia.
The immediate concern was meningitis or encephalitis.
Clinical Reasoning Pause 1
What is the initial clinical syndrome?
This is a subacute febrile meningoencephalitic illness in a young child.
At presentation, the differential diagnosis remains broad and includes:
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bacterial meningitis,
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viral meningitis or encephalitis,
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tuberculous or fungal meningitis,
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parasitic infection,
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inflammatory disease,
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and toxic or metabolic encephalopathy.
The patient’s age makes the assessment more difficult. A 1-year-old child cannot reliably describe headache, neck stiffness, photophobia, or paresthesias. Irritability, vomiting, drowsiness, and behavioral change may be the principal manifestations of meningeal inflammation.
Key reasoning point: In a young child, meningitis may present through changes in behavior and consciousness rather than the classic symptoms described by adults.
The first diagnostic clue
The peripheral leukocyte count was 21,630 cells/mm³, with eosinophils accounting for 15% of circulating leukocytes.
Cerebrospinal fluid examination demonstrated pleocytosis, with eosinophils reported to comprise 31% of the leukocyte count. Cranial computed tomography and magnetic resonance imaging showed no significant abnormalities.
The eosinophils fundamentally changed the diagnostic problem.
Clinical Reasoning Pause 2
What does eosinophilia in the cerebrospinal fluid mean?
Eosinophilic meningitis is generally defined by:
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at least 10 eosinophils/µL in the cerebrospinal fluid, or
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eosinophils comprising more than 10% of the total cerebrospinal fluid leukocyte count.
This patient met the reported criteria for eosinophilic meningitis.
The finding does not establish a specific cause, but it substantially narrows the differential diagnosis. Important infectious causes include Angiostrongylus cantonensis, Gnathostoma species, Baylisascaris procyonis, Toxocara species, neurocysticercosis, and selected fungal infections. Noninfectious causes include medications, malignancy, hypereosinophilic syndromes, and inflammatory disorders.
Typical bacterial and viral infections become less likely when eosinophils represent such a substantial proportion of the cerebrospinal fluid leukocytes.
Key reasoning point: Eosinophilic meningitis is a syndrome, not a final diagnosis. Once recognized, it should trigger a focused etiologic investigation.
The initial investigation
Polymerase chain reaction assays for herpes simplex virus types 1 and 2, cytomegalovirus, Epstein–Barr virus, and varicella-zoster virus were nonreactive. Testing for toxoplasmosis and rubella was also nonreactive.
Cerebrospinal fluid culture showed no microbial growth. Rapid tests for HIV and syphilis were nonreactive. Several stool examinations using direct, Lutz, Ritchie, Willis, and Kato–Katz methods were negative.
The patient received dexamethasone, ceftriaxone, ondansetron, analgesia, and supportive care. Her fever and vomiting resolved, and her drowsiness and level of consciousness improved.
After clinical stabilization, her family requested discharge for social reasons. They were instructed to return for reassessment and repeat cerebrospinal fluid examination.
Clinical Reasoning Pause 3
Do negative stool examinations exclude a parasitic infection?
No.
Humans are accidental dead-end hosts of A. cantonensis. After infective third-stage larvae are ingested, they migrate to the central nervous system but generally do not mature into reproductive adult worms in humans.
Consequently, larvae or eggs are not expected to be identified routinely in human stool.
The negative stool examinations therefore did not exclude neuroangiostrongyliasis.
Key reasoning point: A negative test is reassuring only when the suspected disease is biologically capable of producing a positive result with that test.
Clinical recurrence
The child returned as scheduled with recurrent fever reaching 38.7 °C, dysentery, and altered consciousness.
Repeat cerebrospinal fluid was xanthochromic and turbid. It contained 453 cells/mm³, with glucose of 7 mg/dL, protein of 184.9 mg/dL, lactate of 499.3 mg/dL, and persistent eosinophilia.
The recurrence demonstrated that the underlying inflammatory process had not resolved. The combination of a subacute meningoencephalitic illness, peripheral eosinophilia, cerebrospinal fluid eosinophilia, negative routine microbiologic studies, and unrevealing neuroimaging increasingly favored a parasitic cause.
The diagnostic turning point
At this stage, A. cantonensis infection was specifically considered.
Serologic testing by enzyme-linked immunosorbent assay and Western blot was positive for antibodies against A. cantonensis. In the clinical context, these findings supported the diagnosis of eosinophilic meningitis caused by A. cantonensis.
According to the authors, this represents the first confirmed human infection reported in the State of Amazonas.
Clinical Reasoning Pause 4
Does the absence of travel argue against the diagnosis?
Not necessarily.
The child had no reported history of travel to a recognized endemic area. However, A. cantonensis had previously been identified in giant African snails, Achatina fulica, in Manaus and Maués.
The parasite was therefore already present in an appropriate intermediate host within Amazonas.
The absence of travel did not exclude angiostrongyliasis. Instead, it supported the possibility that the infection had been acquired locally.
Key reasoning point: Geographic epidemiology is not static. Once an intermediate host carrying a pathogen becomes established locally, traditional assumptions about endemic boundaries must be reconsidered.
Understanding the life cycle
The life cycle explains both the route of infection and the diagnostic limitations.
Rats are the definitive hosts of A. cantonensis. Snails and slugs serve as intermediate hosts. Humans may become infected by ingesting raw or undercooked mollusks, paratenic hosts, or vegetables contaminated by infected mollusks or their secretions.
After ingestion, third-stage larvae migrate to the central nervous system. In humans, they generally fail to reach reproductive maturity. The clinical illness results largely from the inflammatory response to migrating and degenerating larvae.
A specific exposure was not identified in this child. This does not exclude the infection, particularly in a 1-year-old who may have unrecognized environmental exposure.
Management and outcome
The patient was treated with corticosteroid therapy, albendazole, analgesia, and supportive care.
Corticosteroid therapy is directed at the host inflammatory response, which contributes substantially to the neurologic manifestations of neuroangiostrongyliasis. When albendazole is administered, concomitant corticosteroid treatment may help control inflammation associated with larval injury or death.
After more than 30 days of hospitalization, the child improved and was discharged without recognized neurological sequelae. Laboratory confirmation of A. cantonensis infection became available approximately one month after her final discharge.
Because this is a single case, the favorable outcome cannot establish the comparative effectiveness of the treatment regimen.
Reconstructing the diagnostic pathway
Initial presentation
Pruritic rash and prolonged fever
Progression to vomiting, irritability, drowsiness, and asthenia
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Initial syndrome
Subacute meningitis or meningoencephalitis
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Pivotal laboratory finding
Peripheral eosinophilia
Cerebrospinal fluid pleocytosis with marked eosinophilia
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Focused differential diagnosis
Parasitic infection becomes a leading consideration
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Initial investigation
Negative viral studies
Negative cerebrospinal fluid culture
Negative HIV and syphilis testing
Normal cranial CT and MRI
Negative stool examinations
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Clinical recurrence
Recurrent fever and altered consciousness
Xanthochromic, turbid cerebrospinal fluid
Marked hypoglycorrhachia, elevated protein and persistent pleocytosis
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Targeted investigation
Positive enzyme-linked immunosorbent assay and Western blot for A. cantonensis
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Epidemiologic integration
No travel to a recognized endemic area
Previous identification of A. cantonensis in giant African snails in Amazonas
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Final diagnosis
Locally acquired eosinophilic meningitis caused by Angiostrongylus cantonensis
Why this case matters
This case demonstrates how a single laboratory feature can redirect an otherwise broad evaluation of meningitis.
The presenting symptoms were nonspecific. Neuroimaging was normal. Routine microbiologic studies were unrevealing. No definite exposure was identified, and the patient had not traveled to a traditionally recognized endemic area.
The eosinophils provided the organizing clue.
The case also has epidemiologic importance. Previous identification of A. cantonensis in local snails suggested that the parasite was already present in the environment. Confirmation of human infection therefore raises concern for locally acquired transmission and supports increased clinical and public health awareness.
Clinical Pearls
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Eosinophils in cerebrospinal fluid should not be dismissed.
Their presence meaningfully narrows the differential diagnosis of meningitis. -
Eosinophilic meningitis is a syndrome rather than an etiologic diagnosis.
Parasitic, fungal, inflammatory, medication-related, and malignant causes should be considered. -
A negative stool examination does not exclude neuroangiostrongyliasis.
Humans are dead-end hosts in whom A. cantonensis generally does not complete its reproductive cycle. -
Normal neuroimaging does not exclude meningitis.
The diagnosis rests primarily on the clinical presentation and cerebrospinal fluid findings. -
Absence of travel does not exclude an emerging infection.
Identification of infected intermediate hosts may indicate previously unrecognized local transmission. -
The patient’s age influences the presentation.
Infants and young children may manifest meningitis through irritability, vomiting, lethargy, or altered behavior rather than typical adult symptoms. -
Temporary improvement does not establish etiologic resolution.
Corticosteroids may suppress inflammation even when the underlying cause has not yet been identified.
Pitfalls to Avoid
Pitfall 1: Anchoring on routine bacterial or viral meningitis
Empirical treatment may be appropriate initially, but marked cerebrospinal fluid eosinophilia should prompt reconsideration of the differential diagnosis.
Pitfall 2: Treating eosinophilic meningitis as the final diagnosis
The eosinophilic pattern identifies the syndrome. Additional investigation is required to determine its cause.
Pitfall 3: Using negative stool testing to exclude A. cantonensis
The parasite usually does not mature and reproduce in humans. Stool testing therefore has limited value for excluding neuroangiostrongyliasis.
Pitfall 4: Excluding infection because there is no travel history
Local establishment of infected intermediate hosts may precede recognition of human disease.
Pitfall 5: Being reassured by normal cranial imaging
Computed tomography and magnetic resonance imaging may be normal despite clinically important meningeal inflammation.
Pitfall 6: Assuming improvement proves eradication of the disease
The initial improvement may have reflected control of inflammation rather than definitive treatment of the underlying infection.
CARE-Style Timeline
| Time | Clinical event |
|---|---|
| Approximately 18 days before admission | Pruritic rash followed by persistent fever, nausea, and vomiting |
| Day 0 | Referral to a tropical and infectious diseases hospital in Manaus |
| Day 1 | Blood and cerebrospinal fluid collected; peripheral eosinophilia and cerebrospinal fluid pleocytosis identified |
| Day 3 | Eosinophilic meningitis recognized; dexamethasone, ceftriaxone, and supportive treatment administered |
| Day 19 | Clinical improvement followed by discharge at the family’s request, with planned reassessment |
| Day 24 | Return with recurrent fever, dysentery, and altered consciousness |
| Day 26 | Repeat lumbar puncture shows xanthochromic, turbid cerebrospinal fluid, marked hypoglycorrhachia, elevated protein, and persistent pleocytosis |
| Subsequent hospitalization | Corticosteroid therapy, albendazole, analgesia, and supportive care administered |
| Day 35 | Discharged after clinical improvement without recognized neurological sequelae |
| Day 62 | Enzyme-linked immunosorbent assay and Western blot confirm antibodies against A. cantonensis |
Test Your Clinical Reasoning
Question 1
Which finding most directly changes this patient’s initial differential diagnosis from routine meningitis to eosinophilic meningitis?
A. Fever of 39.1 °C
B. Persistent vomiting
C. Normal cranial magnetic resonance imaging
D. Eosinophils comprising 31% of cerebrospinal fluid leukocytes
E. Peripheral leukocyte count of 21,630 cells/mm³
Answer: D. Eosinophils comprising 31% of cerebrospinal fluid leukocytes
Explanation: Eosinophils comprising more than 10% of the cerebrospinal fluid leukocyte count meet a commonly used definition of eosinophilic meningitis. Fever, vomiting, leukocytosis, and normal imaging are nonspecific and do not independently identify the eosinophilic syndrome.
Question 2
Which organism is most strongly associated with eosinophilic meningitis acquired through ingestion of larvae carried by snails or slugs?
A. Taenia saginata
B. Angiostrongylus cantonensis
C. Enterobius vermicularis
D. Giardia duodenalis
E. Ascaris lumbricoides
Answer: B. Angiostrongylus cantonensis
Explanation: Rats are the definitive hosts of A. cantonensis, while snails and slugs serve as intermediate hosts. Humans accidentally acquire infection by ingesting infective third-stage larvae in mollusks, paratenic hosts, or contaminated produce.
Question 3
Why did the negative stool examinations not exclude A. cantonensis infection?
A. Stool examinations become positive only after corticosteroid treatment
B. The parasite is detectable only during febrile episodes
C. Humans are dead-end hosts in whom the parasite generally does not complete its reproductive cycle
D. Albendazole prevents microscopic identification of the parasite
E. Stool testing is reliable only in adult patients
Answer: C. Humans are dead-end hosts in whom the parasite generally does not complete its reproductive cycle
Explanation: After infective larvae are ingested, they migrate to the central nervous system but usually do not mature into reproductive adult worms in humans. Stool examinations are therefore not expected to demonstrate larvae or eggs and cannot reliably exclude neuroangiostrongyliasis.
Question 4
How should the absence of travel be interpreted when A. cantonensis has already been identified in local intermediate hosts?
A. It excludes angiostrongyliasis
B. It proves that the serologic results are false-positive
C. It supports the possibility of locally acquired transmission
D. It indicates congenital infection
E. It makes environmental exposure impossible
Answer: C. It supports the possibility of locally acquired transmission
Explanation: Identification of A. cantonensis in giant African snails in Amazonas demonstrates that an appropriate intermediate host carrying the parasite was already present locally. In that setting, the absence of travel supports possible autochthonous transmission rather than excluding the diagnosis.
Question 5
What is the principal rationale for corticosteroid treatment in neuroangiostrongyliasis?
A. To eradicate adult worms in the intestine
B. To prevent viral coinfection
C. To suppress the inflammatory response to migrating or degenerating larvae
D. To increase antibody production
E. To prevent eosinophils from entering the peripheral blood
Answer: C. To suppress the inflammatory response to migrating or degenerating larvae
Explanation: Much of the neurologic illness results from the host’s eosinophilic inflammatory response to larvae within the central nervous system. Corticosteroids reduce this inflammation and are particularly important when anthelmintic therapy is used.
Clinical Take-Home Message
When a patient with meningitis has eosinophils in the blood or cerebrospinal fluid, the differential diagnosis must be redirected toward parasitic and other causes of eosinophilic meningitis. In this child, marked cerebrospinal fluid eosinophilia, negative routine infectious studies, recurrence after initial improvement, targeted positive serology, and evidence that infected intermediate hosts were already present locally led to the diagnosis of Angiostrongylus cantonensis infection.
Negative stool testing and the absence of travel do not exclude neuroangiostrongyliasis. Understanding the parasite’s life cycle and the changing geographic distribution of its hosts is essential to recognizing emerging local transmission.
Source
Maciel M, Araújo J, Silva D, Fasogbon I, Monteiro W, Araújo G, Barrionuevo M, Yakubu M. First report of eosinophilic meningitis caused by Angiostrongylus cantonensis in the State of Amazonas, Brazil: a case report. Journal of Medical Case Reports. 2026. https://doi.org/10.1186/s13256-026-06503-z.
Journal of Medical Case Reports is the world’s first international, PubMed-listed, medical journal devoted to publishing case reports from all medical disciplines and will consider any original case report that expands the field of general medical knowledge, and original research relating to case reports. The journal is open access, and strongly endorses the CARE guidelines for case reports, requiring authors to submit populated CARE checklists with submissions to improve transparency in reporting.