Parasitic Infections of the Nervous System

Garcı́a, Héctor H.; Nath, Avindra; Brutto, Oscar H. Del

doi:10.1055/s-0039-1693036

Cited by 13 publications

(23 citation statements)

References 77 publications

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“…Neurocysticercosis (NCC), the infection of the human central nervous system by larval cysts of the pork tapeworm Taenia solium, is an important cause of neurologic disease in most of the world. Brain cysts and the associated host inflammatory response lead to seizures, intracranial hypertension, and other neurological symptoms [1,2].…”

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confidence: 99%

Frequency and Determinant Factors for Calcification in Neurocysticercosis

Bustos

Arroyo

Gilman

et al. 2020

Clinical Infectious Diseases

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Background Neurocysticercosis (NCC) is a major cause of acquired epilepsy in most of the world. Larval cysts in the human brain eventually resolve and either disappear or leave a calcified scar that is associated with seizures. This study assessed the proportion of residual calcification in parenchymal NCC, and defined risk factors associated with calcification. Methods Data from 220 patients with parenchymal NCC from three randomized trials of antiparasitic treatment was assessed to determine what proportion of the cysts that resolved six months after antiparasitic treatment ended up in a residual calcification at one year. Also, we evaluated the risk factors associated with residual calcification. A multilevel Poisson regression model was used to estimate the risks of calcification. Results The overall proportion of calcification was 38% (188/497 cysts, from 147 patients). Predictors for calcification at the cyst level were cysts larger than 14 mm (RR 1.34; 95% C.I. 1.02-1.75), and cysts with edema at baseline (RR 1.39; 95% C.I. 1.05-1.85). At the patient level, having had more than 24 months with seizures (RR: 1.25, 95% C.I. 1.08-1.46), mild antibody response (RR: 1.14; 95% C.I. 1.002-1.27), increased dose albendazole regime (RR: 1.26; 95% C.I. 1.14-1.39), lower doses of concomitant dexamethasone (RR: 1.36; 95% C.I. 1.02-1.81), not receiving early antiparasitic re-treatment (RR: 1.45; 1.08-1.93), or complete cure (RR: 1.48; 1.29-1.71). Conclusions/Significance Approximately 38% of parenchymal cysts calcify after antiparasitic treatment. Some factors associated to calcification are modifiable and may be approached to decrease or avoid calcification, potentially decreasing the risk for seizure relapses.

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confidence: 99%

Frequency and Determinant Factors for Calcification in Neurocysticercosis

Bustos

Arroyo

Gilman

et al. 2020

Clinical Infectious Diseases

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“…RNA-seq read data are available for download via the NCBI sequence read archive (BioProject ID: PRJNA716607). Differential expression analysis showed the highest number of differentially expressed transcripts (DETs) 7 dpi when more transcripts were downregulated (6,943) than upregulated (4,128). The number of DETs decreased 14 and 21 dpi, and upregulated transcripts prevailed over downregulated ones (Fig 6B and S1 Table).…”

Section: Infected Spinal Cords Displayed Transcriptional Upregulation...mentioning

confidence: 95%

“…Invasion of the CNS is either a natural part of their somatic migration or represents an unwanted, ectopic localization [1]. The clinical manifestation of helminth neuroinfections ranges from mostly asymptomatic to very severe, leading to sensory or cognitive deficits and seizures or epilepsy [2][3][4]. Many factors, such as parasite burden or localization within the CNS, influence the course and outcome of the neuroinfection [5].…”

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confidence: 99%

Mechanisms of the host immune response and helminth-induced pathology during Trichobilharzia regenti (Schistosomatidae) neuroinvasion in mice

et al. 2022

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Helminth neuroinfections represent serious medical conditions, but the diversity of the host-parasite interplay within the nervous tissue often remains poorly understood, partially due to the lack of laboratory models. Here, we investigated the neuroinvasion of the mouse spinal cord by Trichobilharzia regenti (Schistosomatidae). Active migration of T. regenti schistosomula through the mouse spinal cord induced motor deficits in hindlimbs but did not affect the general locomotion or working memory. Histological examination of the infected spinal cord revealed eosinophilic meningomyelitis with eosinophil-rich infiltrates entrapping the schistosomula. Flow cytometry and transcriptomic analysis of the spinal cord confirmed massive activation of the host immune response. Of note, we recorded striking upregulation of the major histocompatibility complex II pathway and M2-associated markers, such as arginase or chitinase-like 3. Arginase also dominated the proteins found in the microdissected tissue from the close vicinity of the migrating schistosomula, which unselectively fed on the host nervous tissue. Next, we evaluated the pathological sequelae of T. regenti neuroinvasion. While no demyelination or blood-brain barrier alterations were noticed, our transcriptomic data revealed a remarkable disruption of neurophysiological functions not yet recorded in helminth neuroinfections. We also detected DNA fragmentation at the host-schistosomulum interface, but schistosomula antigens did not affect the viability of neurons and glial cells in vitro. Collectively, altered locomotion, significant disruption of neurophysiological functions, and strong M2 polarization were the most prominent features of T. regenti neuroinvasion, making it a promising candidate for further neuroinfection research. Indeed, understanding the diversity of pathogen-related neuroinflammatory processes is a prerequisite for developing better protective measures, treatment strategies, and diagnostic tools.

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“…Signs of systemic schistosomiasis are typically absent. 1,17,54,55 On CT and MRI, cerebral neuroschistosomiasis lesions appear as solitary or multiple subcortical mass lesions surrounded by hypodense or T2-hyperintense edema, with heterogeneous contrast enhancement and irregular borders. A linear enhancement pattern surrounded by multiple enhancing nodules (the arborized pattern) is suggestive but nonspecific for neuroschistosomiasis (FIGURE 6-9).…”

Section: Key Pointsmentioning

confidence: 99%

Parasitic Infections of the Nervous System

Garcı́a¹

2021

CONTINUUM: Lifelong Learning in Neurology

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PURPOSE OF REVIEW: This article reviews how parasites affect the human nervous system, with a focus on four parasitic infections of major public health importance worldwide, two caused by protozoa (malaria and toxoplasmosis) and two by helminths (neurocysticercosis and schistosomiasis).RECENT FINDINGS: Parasitic infections in humans are common, and many can affect the central nervous system where they may survive unnoticed or may cause significant pathology that can even lead to the death of the host. Neuroparasitoses should be considered in the differential diagnosis of neurologic lesions, particularly in individuals from endemic regions or those with a history of travel to endemic regions. SUMMARY: Cerebral malaria is a significant cause of mortality, particularly in African children, in whom infected red blood cells affect the cerebral vessels, causing severe encephalopathy. Neurocysticercosis is the most common cause of acquired epilepsy worldwide and has varied clinical presentations, depending on the number, size, and location of the parasites in the nervous system as well as on the host's inflammatory response. Toxoplasmosis is distributed worldwide, affecting a significant proportion of the population, and may reactivate in patients who are immunosuppressed, causing encephalitis and focal abscesses. Schistosomiasis causes granulomatous lesions in the brain or the spinal cord.

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Parasitic Infections of the Nervous System

Cited by 13 publications

References 77 publications

Frequency and Determinant Factors for Calcification in Neurocysticercosis

Frequency and Determinant Factors for Calcification in Neurocysticercosis

Mechanisms of the host immune response and helminth-induced pathology during Trichobilharzia regenti (Schistosomatidae) neuroinvasion in mice

Parasitic Infections of the Nervous System

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