Neurocysticercosis: A Pressing Public Health Concern in India During the 2025 Monsoon
Neurocysticercosis (NCC), a parasitic infection of the central nervous system caused by the larval stage (cysticercus cellulosae) of the pork tapeworm Taenia solium, has emerged as a pressing public health concern in India during the 2025 monsoon season.
Recent reports, particularly from major cities such as Mumbai, highlight a disturbing rise in cases. The surge is attributed to monsoon-related flooding, sewage contamination, and compromised sanitation, which facilitate the fecal oral transmission of tapeworm eggs. Even individuals who do not consume pork remain at risk due to contaminated water and food.
Epidemiology and Global Context
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NCC is the most common parasitic infection of the human nervous system and is a leading cause of acquired epilepsy worldwide.
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The World Health Organization (WHO) recognizes NCC as one of the leading causes of preventable epilepsy, especially in low- and middle-income countries.
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Globally, an estimated 2.5–8 million people are affected, with India, Latin America, sub-Saharan Africa, Southeast Asia, and China being endemic regions.
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In endemic areas, 30–50% of late-onset epilepsy cases are attributed to NCC
Etiology and Life Cycle
Life Cycle Steps:
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Eggs/proglottids are excreted in human feces.
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Pigs ingest eggs → oncospheres hatch → penetrate intestinal wall → travel via blood → form cysticerci in muscles.
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Humans ingest undercooked pork containing cysticerci → develop taeniasis (intestinal infection).
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Humans ingest eggs directly (via fecal–oral route, contaminated food/water, or autoinfection) → larvae migrate to tissues including brain, muscles, and eyes → cysticercosis.
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When cysticerci lodge in the CNS → neurocysticercosis.
Pathophysiology
When T. solium eggs are ingested, the oncospheres invade the intestinal wall, enter the bloodstream, and reach the CNS. The larvae form cysts that pass through four pathological stages:
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Vesicular stage: Viable cyst, minimal inflammation.
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Colloidal vesicular stage: Cyst degeneration, intense inflammation, brain edema.
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Granular-nodular stage: Further degeneration, reduced inflammation.
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Calcified stage: Inactive lesion, potential source of recurrent seizures.
CNS Locations
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Parenchymal: Within brain tissue; most common; often presents with seizures.
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Ventricular: Inside brain ventricles; may cause obstructive hydrocephalus.
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Subarachnoid (cisternal): Around brain base; can cause arachnoiditis or meningitis-like symptoms.
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Spinal: Rare; causes focal neurological deficits.
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Ocular: Retina/vitreous; may cause visual loss.
Special Forms:
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Racemose NCC: Grape-like cyst clusters without scolex; highly inflammatory.
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Giant cysts: Large cysts causing mass effect.
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Mobile ventricular cysts: May cause intermittent CSF obstruction (“ball-valve” effect).
Clinical Manifestations
Symptoms depend on cyst number, location, and stage:
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Common:
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Seizures (70–90% in endemic areas)
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Headache, vomiting, papilledema (raised intracranial pressure)
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Focal neurological deficits
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Less common:
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Cognitive decline
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Psychiatric disturbances (depression, psychosis)
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Vision problems (ocular NCC)
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Stroke-like symptoms (due to vasculitis)
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Diagnosis
WHO Diagnostic Criteria
Definitive NCC if:
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Histological demonstration of parasite.
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Visualization of scolex on neuroimaging.
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Positive EITB serology + highly suggestive imaging.
Probable NCC if:
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Compatible imaging + epidemiological exposure + supportive tests.
Neuroimaging
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CT scan: Best for detecting calcified lesions.
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MRI: Superior for viable cysts, ventricular/subarachnoid lesions.
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Pathognomonic sign: “Scolex” appearing as a hyperdense dot (“hole-with-dot” sign).
Serological Tests
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Enzyme-linked immunoelectrotransfer blot (EITB): High specificity.
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ELISA (enzyme-linked immunoassay): More widely available but less specific.
CSF Analysis
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Lymphocytic pleocytosis, elevated protein, normal/low glucose in some cases.
Differential Diagnosis
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Tuberculoma
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Brain abscess
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Metastatic tumors
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Gliomas
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Toxoplasmosis (especially in HIV-positive patients)
Treatment
Treatment is stage-, location-, and symptom-dependent.
Antiparasitic drugs:
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Albendazole: 15 mg/kg/day (max 800 mg) × 7–14 days.
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Praziquantel: 50–100 mg/kg/day × 15–21 days.
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Combination therapy for multiple lesions.
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Administer with corticosteroids to reduce inflammation.
Anti-inflammatory drugs:
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Dexamethasone or prednisone for edema control.
Antiepileptic drugs (AEDs):
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Required for seizure control; often continued for 6–12 months post-resolution.
Surgical interventions:
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Endoscopic removal for ventricular cysts.
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Ventriculoperitoneal shunt for hydrocephalus.
Contraindications to antiparasitic therapy:
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Untreated raised intracranial pressure.
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Ocular cysticercosis (risk of vision loss).
Prognosis
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Early treatment → good outcomes.
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Parenchymal lesions often resolve completely.
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Calcified lesions can cause chronic epilepsy.
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Ventricular/subarachnoid NCC has higher morbidity/mortality.
Prevention
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Improved sanitation and sewage systems.
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Thorough cooking of pork.
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Routine handwashing and food hygiene.
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Veterinary measures: treat pigs, prevent free roaming.
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Identify and treat human tapeworm carriers.
Socioeconomic Impact
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Causes significant productivity loss due to epilepsy-related disability.
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Increases healthcare costs in rural, endemic regions.
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Impacts education and employment in affected individuals.
Recent Research and Advances
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Development of pig vaccines to interrupt transmission.
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Use of molecular diagnostics for greater accuracy.
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Public health control programs in Peru and Mexico have significantly reduced prevalence through integrated approaches.
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Studies on optimal combination therapy for better lesion resolution.
Public Health Perspective
NCC control requires a One Health approach integrating human medicine, veterinary control, and environmental sanitation. Community education, routine deworming programs, and pig management are essential for sustainable prevention.
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