Human cysticercosis arises when a person ingests eggs of the tapeworm Taenia solium, typically from a carrier, and becomes an intermediate host in whom larval stages develop in tissues [1][2]. Neurocysticercosis is the specific involvement of the central nervous system and meninges by these larvae and is the most frequent helminthic infection of the CNS globally [1][2].
Aperçu de la maladie
ParasitaireCysticercosis is a parasitic infection caused by ingestion of Taenia solium eggs and is the most common helminthic infection of the central nervous system worldwide, representing a leading cause of acquired epilepsy [1][2][3][4]. The disease is endemic in most developing countries where pigs are raised and consumed, though it also appears in developed nations through immigration and travel [3][4]. Control efforts target eradication by interrupting the parasite's life cycle in carriers, pigs, and the environment [1][4].
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Larvae may settle in brain parenchyma, subarachnoid space, ventricular system, or spinal cord, producing diverse pathological changes that explain the disease's clinical variability [1][2]. Seizures or epilepsy are the most common manifestation, while other affected individuals show headache, focal deficits, intracranial hypertension, or cognitive decline [1][2]. Definitive diagnosis relies on neuroimaging interpreted alongside clinical and immunological data, because neither manifestations nor immune tests alone are specific [1][2][5].
Neurocysticercosis is the most common parasitic disease of the CNS and is endemic across most developing regions with pig farming and consumption, while also present in developed countries via migration and travel [3][4]. In Madagascar, human cysticercosis shows an estimated seroprevalence of 7% to 21%, with neurocysticercosis responsible for over half of pediatric epilepsy cases [3]. The country has documented porcine infection since 1901 and reports a substantial burden of taeniasis and bovine cysticercosis [3].
Transmission occurs through ingestion of T. solium eggs from contaminated food or, most often, directly from a Taenia carrier via the fecal-oral route [1][2]. After entering the intestine, eggs develop into oncospheres that cross the wall and lodge in human tissues, especially the nervous system, where cysticerci form [2].
Disease control should aim to eradicate cysticercosis by implementing programs that address every step of the T. solium life cycle, including adult tapeworm carriers, infected pigs, and environmental egg contamination [1]. National strategies such as those in Madagascar have sought to lower seroprevalence through control and elimination programs and public screening campaigns to raise awareness [3][4].
- 1 Del 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 Del Brutto OH et al. Neurocysticercosis. Handb Clin Neurol. 2014. PMID: 24365429. doi: 10.1016/B978-0-7020-4088-7.00097-3. PubMed: https://pubmed.ncbi.nlm.nih.gov/24365429/
- 3 Carod 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/
- 4 Garcia 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/
- 5 Del 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/
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