Neurologic Infections in Travelers

Malveeka Sharma, MD, MPH; Joseph R. Zunt, MD, MPH


Semin Neurol. 2019;39(3):399-414. 

In This Article



Schistosomiasis (also known as bilharzia) affects approximately 200 million people worldwide every year. Neuroschistosomiasis is a severe presentation of schistosomiasis. Schistosomiasis is endemic in 78 tropical countries with infection mainly affecting people living in poor, rural areas and approximately 90% of affected people living in Africa.[3] An increase in ecotourism has led to higher rates of infection in tourists. The prevalence of neurologic manifestations is not well defined but is most likely under-recognized.[4]

Life Cycle, Ecology, Species

Schistosomiasis is a helminthic infection caused by a blood-dwelling trematode; of the five schistosomal species, Schistosoma mansoni, S. japonicum, and S. haematobium can produce neuroschistosomiasis.[5]S. japonicum is found mainly in China, the Philippines, and Indonesia. S. mansoni is found in Africa, Southeast Asia, the Middle East, the Caribbean, Brazil, Venezuela, and Suriname, while S. haematobium is found in Africa, the Middle East, and Corsica.[3] Humans are definitive hosts, with freshwater snails serving as intermediate hosts. Humans become infected through contact with the motile tail of the cercaria stage of the trematode which can penetrate the skin. The parasite then migrates into the circulation via the venous system.

Clinical Manifestations and Neurologic Symptoms

Clinical manifestations vary with the invading species. S. mansoni is commonly associated with spinal cord involvement, invading via retrograde flow through the Batson vertebral epidural venous plexus. Clinically, patients commonly present similar to transverse myelitis, with flaccid paraplegia with a dermatomal level present on examination and typically accompanied by sphincter dysfunction. Spinal cord symptoms may develop during the acute infection or within weeks of infection. In addition, a rare postinfectious immune-mediated phenomenon has been described in which there is a hypersensitive reaction to ova in sensitized population when new schistosomal antigens are introduced.[4]

Cerebral manifestations are most commonly associated with S. japonicum, with fewer cases associated with S. haematobium. Cerebral forms can be categorized into acute schistosomal encephalopathy (ASE) and pseudotumoral encephalitic schistosomiasis (PES). ASE occurs about 3 weeks postinfection with presentations ranging from headache to unresponsiveness. Focal neurological deficits and seizures are common, but cranial nerve palsies and meningeal signs are rare. Stroke has also been reported.[6] PES has only been identified with S. japonicum infection, occurs most frequently in endemic populations, and is characterized by slowly expanding tumor-like lesions; neurological deficits vary with lesion location. These lesions are most commonly found in the cerebellum, followed by the frontal and occipital lobes, but dural-based lesions have been reported. PES is typically associated with one to two discrete lesions.[6] Other reported manifestations include acute encephalitis, cerebral vasculitis, and cognitive and memory deficits—which most often present in younger patients.


Diagnosis of neuroschistosomiasis can be difficult, but should be suspected in people presenting with encephalopathy or myelopathy and a history of living or traveling to endemic regions. Nonspecific findings of serum eosinophilia and Schistosoma spp. ova in stool may or may not be present. Patients with neuroschistosomiasis rarely have clinical evidence of systemic infection.[4] Definitive diagnosis is made through identification of an egg in tissue biopsy, which is rarely performed. Cerebrospinal fluid (CSF) analysis can show a lymphocytic pleocytosis, high protein concentration, presence of eosinophils, and an increased immunoglobulin G (IgG) index. The combination of enzyme-linked immunosorbent assay (ELISA) and indirect hemagglutination assays gives high sensitivity and specificity, with seroconversion typically taking 4 to 12 weeks.[6] Computed tomography (CT) and magnetic resonance imaging (MRI) can assist in diagnosis, but abnormalities are not pathognomonic and imaging is often not available in endemic regions.[7]


There is no consensus regarding optimal therapy for neuroschistosomiasis. Praziquantel is the schistosomicidal drug of choice and targets adult female worms. Recommended dose varies from 40 mg/kg per day for 3 days (S. mansoni, S. haematobium) to 60 mg/kg per day for 6 days (S. japonicum).[6] Artemether, an antimalarial drug, kills schistosomula (immature stage) during the first 3 weeks of life and is used as a chemoprophylactic agent.[7] The combination of praziquantel and artemether has a synergistic capacity to kill multiple trematodal stages.[6] Oxamniquine is another schistosomicidal drug effective against S. mansoni.[7] Central nervous system (CNS) manifestation of schistosomiasis should be pretreated with steroids prior to initiation of antiparasitic agents. Surgery is performed when necessary for cases of obstructive hydrocephalus or spinal cord compression.[7] Prevention is based on large-scale treatment of populations at risk, access to safe water, improved sanitation, hygiene education, and snail control. The World Health Organization (WHO) has targeted chemoprophylactic treatment with praziquantel in high-risk populations living in endemic regions.[3]