Cysticercosis

Cysticercosis is caused by the cestode Taenia solium, whose larval stage preferentially invades subcutaneous tissue, brain, muscle, and the eye ^[2]. Neurocysticercosis is specifically defined as infection of the central nervous system and meninges by the larval stage of T. solium and is recognized as the most common helminthic infection of the CNS worldwide ^[1].

NCC exhibits considerable clinical pleomorphism because larvae may lodge in the brain parenchyma, subarachnoid space, ventricular system, or spinal cord, each producing distinct pathological changes ^[1]. Seizures and epilepsy are the most frequent manifestations, although patients may also present with headache, focal neurological deficits, intracranial hypertension, or cognitive decline ^[1]. Updated diagnostic criteria organize findings into absolute criteria (histological confirmation, subretinal cysts, scolex visualization), neuroimaging criteria of varying weight, and clinical or exposure criteria, with definitive diagnosis requiring neuroimaging supported by exposure history or serology ^[3].

NCC is endemic throughout most of the developing world where pigs are raised and consumed, and it has been identified as one of the few diseases targeted for eradication ^[2]. The disease also appears in developed countries through immigration and travel, making it a matter of global concern ^[2]. Country-level data from Madagascar illustrate the burden: human cysticercosis seroprevalence has been estimated at 7–21%, and NCC accounts for more than half of pediatric epilepsy cases in that setting ^[4]. In Madagascar, porcine cysticercosis has been documented since 1901, and human taeniasis together with bovine cysticercosis represents a substantial additional burden ^[4].

Human cysticercosis results from ingestion of T. solium eggs shed by human tapeworm carriers (taeniasis), completing a cycle that also involves pigs as intermediate hosts ^[1]. The eggs contaminate the environment, and humans become accidental intermediate hosts when they ingest them, allowing larvae to disseminate to neural and other tissues ^[1].

Prevention requires interventions that interrupt each step of the T. solium life cycle, including identification and treatment of human tapeworm carriers, control of porcine cysticercosis, and reduction of environmental egg contamination ^[1][2]. NCC has been selected as one of the few diseases targeted for eradication, and control programs—such as Madagascar's national initiative aiming to reduce seroprevalence—combine mass screening, sanitation improvements, and veterinary measures ^[1][4]. Such integrated approaches address taeniasis in humans, infection in pigs, and environmental exposure simultaneously ^[2].

1. 1Del Brutto OH et al. Human Neurocysticercosis: An Overview. Pathogens. 2022 Oct 20. PMID: 36297269. doi: 10.3390/pathogens11101212.PubMed: https://pubmed.ncbi.nlm.nih.gov/36297269/
2. 2Garcia HH et al. Taenia solium Cysticercosis and Its Impact in Neurological Disease. Clin Microbiol Rev. 2020 Jun 17. PMID: 32461308. doi: 10.1128/CMR.00085-19.PubMed: https://pubmed.ncbi.nlm.nih.gov/32461308/
3. 3Del Brutto OH et al. Revised diagnostic criteria for neurocysticercosis. J Neurol Sci. 2017 Jan 15. PMID: 28017213. doi: 10.1016/j.jns.2016.11.045.PubMed: https://pubmed.ncbi.nlm.nih.gov/28017213/
4. 4Carod JF et al. Cysticercosis in Madagascar. J Infect Dev Ctries. 2020 Sep 30. PMID: 33031077. doi: 10.3855/jidc.13450.PubMed: https://pubmed.ncbi.nlm.nih.gov/33031077/
5. 5Pujari A et al. Cysticercosis in ophthalmology. Surv Ophthalmol. 2022 Mar-Apr. PMID: 34339720. doi: 10.1016/j.survophthal.2021.07.002.PubMed: https://pubmed.ncbi.nlm.nih.gov/34339720/