Parasitic Infections of the Nervous System

Abstract

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.

Figure 6–1

Life cycle of the malaria parasite. Modified from malariasite.com/life-cycle.

Figure 6–2. Pathology of cerebral malaria

A, Macroscopic pathology of cerebral malaria (left) compared to a normal brain (right) B, Close-up view of the brain demonstrating the typical “flea-bitten” appearance resulting from multiple ring hemorrhages in the white matter.

Figure 6–3

Malarial retinopathy in pediatric patients from Malawi showing white-centered hemorrhages (A), vessel color changes (B), and perimacular whitening (C, circle). Reprinted from Taylor TT and Molyneux ME, Ann NY Acad Sci. © 2015 New York Academy of Sciences.

Figure 6–4

Eccentric target sign in neurotoxoplasmosis (axial post contrast T1-weighted MRI, left) and target sign in neurotuberculosis, CT before (center) and after contrast (right). Panel A reprinted from Kumar GG, Mahadevan A, Guruprasad AS, et al. Eccentric target sign in cerebral toxoplasmosis: neuropathological correlate to the imaging feature. J Magn Reson Imaging 2010;31(6):1469–1472. doi:10.1002/jmri.22192 Panels B and C reprinted from Van Dyk A, Neuroradiology. © 1988 Springer-Verlag.

Figure 6–5

Imaging of the patient in Case 6–1. Axial CT shows a large rim enhancing lesion in the right basal ganglia associated with perilesional edema and midline shift (A) with marked improvement seen after 2 weeks of anti-Toxoplasma treatment (B).

Figure 6–6

Types and stages of neurocysticercosis. Top: A. Multiple viable parenchymal cysts (axial MRI); B. Large occipital cyst with contrast enhancement (axial MRI); C. Enhancing lesion with contrast enhancement and edema (sagittal MRI), and D, Multiple parenchymal calcifications (non-contrasted CT). Bottom: E. Cysticercotic encephalitis (axial MRI); F. Cyst in the left lateral ventricle (axial MRI); G. Subarachnoid neurocysticercosis of the Sylvian fissure (axial MRI), and H. Subarachnoid neurocysticercosis in the basal cisterns (axial MRI). Modified from García HH, et al, Current consensus guidelines for treatment of neurocysticercosis. Clin Microbiol Rev. 2002 Oct;15(4):747–56).

Figure 6–7

Imaging of the patient in Case 6–2. A, Coronal T2-weighted MRI shows a cortical cystic lesion with surrounding edema in the left occipital lobe. B, Axial fast imaging employing steady state acquisition (FIESTA) MRIs demonstrate two additional cysts, one near the midline and another near convexity, both with a hyperintense liquid content and a central hypointense scolex.

Figure 6–8

Imaging of the patient in Case 6–3. A, Initial head CT reveals diffuse ventriculomegaly with transependymal edema. Cystic lesions are not clearly defined. B, Axial fast imaging employing steady state acquisition (FIESTA) MRI reveals multiple parasitic lesions in the cysts in the right perimesencephalic cistern and the lower left sylvian fissure.

Figure 6–9

Axial postcontrast T1-weighted MRI shows patchy enhancement in an arborized pattern in cerebral schistosomiasis. Reprinted with permission from Cho T, Continuum (Minneap Minn). © 2018 American Academy of Neurology.

Figure 6–10

Imaging of the patient in Case 6–4. Spinal schistosomiasis. A, Sagittal post-contrast T1-weighted MRI of the spine shows an intramedullary lesion in the lower thoracic spine. B, Pathologic (H&E) specimen from the same lesion shows a granuloma around a Schistosoma egg.