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

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.

Delayed diagnosis of spinal cord schistosomiasis in a non-endemic country: A tertiary referral centre experience.

BACKGROUND: Neuroschistosomiasis is a severe complication of schistosomiasis, triggered by the local immune reaction to egg deposition, with spinal cord involvement the most well recognised form. Early treatment with praziquantel and high dose steroids leads to a reduction of neurological sequelae. The rarity of this condition in returning travellers to high income countries can result in delayed diagnosis and treatment. We aimed to evaluate the diagnosis and management of neuroschistosomiasis in a UK national referral centre. MATERIALS/METHODS: A retrospective review of confirmed clinical cases of spinal schistosomiasis referred to the Hospital for Tropical Diseases, UK, between January 2016 and January 2020 was undertaken. Electronic referral records were interrogated and patient demographic, clinical, laboratory, and radiological data collected. RESULTS: Four cases of neuroschistosomiasis were identified. The median age at diagnosis was 28 (range 21 to 50) with three male patients. All patients had epidemiological risk factors for schistosomiasis based on travel history and freshwater exposure; two in Uganda (River Nile), one in Malawi and one in Nigeria. All patients presented with features of transverse myelitis including back pain, leg weakness, paraesthesia and urinary dysfunction. The mean time from presentation to health services to definitive treatment was 42.5 days (range 16-74 days). Diagnosis was confirmed with CSF serology for schistosomiasis in all cases. Radiological features on MRI spine included enhancement focused predominantly in the lower thoracic spinal cord in three cases and the conus in one patient. All patients received a minimum of three days of oral praziquantel and high dose steroids. At three-month follow-up, one patient had complete resolution of symptoms and three had residual deficit; one patient was left with urinary and faecal incontinence, another had urinary retention, and the final patient has persistent leg pains and constipation. CONCLUSION: We observed a marked delay in diagnosis of neuroschistosomiasis in a non-endemic country. We advocate undertaking a thorough travel history, early use of imaging and CSF schistosomal serology to ensure early diagnosis of neuroschistosomiasis in patients presenting with consistent symptoms. If schistosomal diagnostics are not immediately available, presumptive treatment under the guidance of a tropical medicine specialist should be considered to minimize the risk of residual disability. We advocate for consensus guidelines to be produced and reporting to be performed in a uniform way for patients with spinal schistosomiasis.

Nitric oxide debilitates the neuropathogenic schistosome Trichobilharzia regenti in mice, partly by inhibiting its vital peptidases.

BACKGROUND: Avian schistosomes, the causative agents of human cercarial dermatitis (or swimmer's itch), die in mammals but the mechanisms responsible for parasite elimination are unknown. Here we examined the role of reactive nitrogen species, nitric oxide (NO) and peroxynitrite, in the immune response of mice experimentally infected with Trichobilharzia regenti, a model species of avian schistosomes remarkable for its neuropathogenicity. METHODS: Inducible NO synthase (iNOS) was localized by immunohistochemistry in the skin and the spinal cord of mice infected by T. regenti. The impact of iNOS inhibition by aminoguanidine on parasite burden and growth was then evaluated in vivo. The vulnerability of T. regenti schistosomula to NO and peroxynitrite was assessed in vitro by viability assays and electron microscopy. Additionally, the effect of NO on the activity of T. regenti peptidases was tested using a fluorogenic substrate. RESULTS: iNOS was detected around the parasites in the epidermis 8 h post-infection and also in the spinal cord 3 days post-infection (dpi). Inhibition of iNOS resulted in slower parasite growth 3 dpi, but the opposite effect was observed 7 dpi. At the latter time point, moderately increased parasite burden was also noticed in the spinal cord. In vitro, NO did not impair the parasites, but inhibited the activity of T. regenti cathepsins B1.1 and B2, the peptidases essential for parasite migration and digestion. Peroxynitrite severely damaged the surface tegument of the parasites and decreased their viability in vitro, but rather did not participate in parasite clearance in vivo. CONCLUSIONS: Reactive nitrogen species, specifically NO, do not directly kill T. regenti in mice. NO promotes the parasite growth soon after penetration (3 dpi), but prevents it later (7 dpi) when also suspends the parasite migration in the CNS. NO-related disruption of the parasite proteolytic machinery is partly responsible for this effect.

Experimental Trypanosoma cruzi Infection Induces Pain in Mice Dependent on Early Spinal Cord Glial Cells and NFκB Activation and Cytokine Production.

The neglected tropical infirmity Chagas disease (CD) presents high mortality. Its etiological agent T. cruzi is transmitted by infected hematophagous insects. Symptoms of the acute phase of the infection include fever, fatigue, body aches, and headache, making diagnosis difficult as they are present in other illnesses as well. Thus, in endemic areas, individuals with undetermined pain may be considered for CD. Although pain is a characteristic symptom of CD, its cellular and molecular mechanisms are unknown except for demonstration of a role for peripheral TNF-α in CD pain. In this study, we evaluate the role of spinal cord glial cells in experimental T. cruzi infection in the context of pain using C57BL/6 mice. Pain, parasitemia, survival, and glial and neuronal function as well as NFκB activation and cytokine/chemokine production were assessed. T. cruzi infection induced chronic mechanical and thermal hyperalgesia. Systemic TNF-α and IL-1ß peaked 14 days postinfection (p.i.). Infected mice presented increased spinal gliosis and NFκB activation compared to uninfected mice at 7 days p.i. Glial and NFκB inhibitors limited T. cruzi-induced pain. Nuclear phosphorylated NFκB was detected surrounded by glia markers, and glial inhibitors reduced its detection. T. cruzi-induced spinal cord production of cytokines/chemokines was also diminished by glial inhibitors. Dorsal root ganglia (DRG) neurons presented increased activity in infected mice, and the production of inflammatory mediators was counteracted by glial/NFκB inhibitors. The present study unveils the contribution of DRG and spinal cord cellular and molecular events leading to pain in T. cruzi infection, contributing to a better understanding of CD pathology.

Infectious Myelitis.

Myelitis refers to inflammation of the spinal cord which can result in a spectrum of neurologic impairment. Infectious pathogens are an important etiologic category, and can result in myelitis through direct pathogenic effect or through immune-mediated parainfection; this review focuses on the former category. The spectrum of clinical manifestations is summarized and a diagnostic workup provided to aid clinicians in developing an approach to patients presenting with symptoms suggestive of infectious myelitis. This is followed by an overview of the important viral, bacterial, parasitic, and fungal causes of infectious myelitis. The typical presentations, diagnostic modalities, and treatment approaches are outlined for key pathogens culprit in infectious myelitis to allow clinicians to promptly recognize and diagnose specific infectious etiologies of myelitis.

Histopathological lesions in reproductive organs, distal spinal cord and peripheral nerves of horses naturally infected with Trypanosoma equiperdum.

BACKGROUND: Dourine, a venereal transmitted trypanosomosis caused by Trypanosoma equiperdum, has different clinical signs related to the reproductive and nervous system. Pathologic tissue changes associated with the disease are poorly described. The present study describes the histopathological lesions in naturally T. equiperdum-infected horses in the chronical stage of dourine. RESULTS: Four chronically dourine diseased horses underwent a post-mortem examination. They were Woo test negative, but CATT/T. evansi positive, had a low packed cell volume (PCV) and exhibited obvious clinical signs of dourine. Post-mortem examination did not reveal gross lesions in the organs assumed to be responsible for the symptomatology. On histopathology, genital organs were affected, with mononuclear cell infiltration and erosions and degeneration of seminiferous tubules and perivascular lymphoplasmacytic cuffing in the uterus. In the nervous system, mononuclear cell infiltration was located in peripheral nerves, ganglia and in the spinal cord, leading to axonal degeneration. Real-time PCR using ITS primer revealed the presence of trypanosomes in these organs and conventional PCRs using maxicircle and RoTat1.2 primers further confirmed the involvement of T. equiperdum since the DNAs from the vagina, testicle, distal spinal cord, sciatic and obturator nerves found to be positive for maxicircle and negative for RoTat 1.2. CONCLUSIONS: The histopathological lesions in the spinal cord and peripheral nerves explain the incoordination of the hind legs in T. equiperdum-infected horses, whilst its presence in the genital tract exemplifies the venereal transmission.

Early complicated schistosomiasis in a returning traveller: Key contribution of new molecular diagnostic methods.

Early schistosomiasis poses a serious diagnostic challenge, because current standard diagnostic techniques based on serology and egg microscopy lack sensitivity at the initial presentation. We report spinal cord neuroschistosomiasis in a traveller developing 6 weeks after exposure. The diagnosis was confirmed by Schistosoma mansoni-targeted real-time PCR in blood and cerebrospinal fluid, before the results of conventional methods became positive. Molecular assays represent a paradigm shift for the difficult diagnosis of early schistosomiasis and related complications.

Clinical characteristics of Spirocerca lupi migration in the spinal cord.

Spirocerca lupi is a nematode infecting dogs mostly in tropical and subtropical areas. Although its typical target is the esophageal wall, aberrant migration is not uncommon, including migration of unknown incidence into the spinal cord. While successful treatment of intraspinal S. lupi (ISSL) infection depends on early diagnosis, tools for definitive ante-mortem diagnosis are unavailable. We therefore aimed at characterizing clinical signs and clinical pathology findings of ISSL in dogs. For that, we analyzed medical records of dogs hospitalized in 2005-2016 presenting with neurological signs consistent with ISSL, which were diagnosed definitively post-mortem. Retrieved information included signalment, medical history, chief complaint, physical and neurological evaluation, neuroanatomical localization at presentation, clinical pathology, imaging findings, treatment, outcome and post-mortem findings. Ten midsize to large breed dogs were included, 7 of which had received prophylactic treatment. In all 10 dogs, onset was acute and neurological deterioration until presentation (2 h-6 d) was fast. Neurological examination localized the lesions within the spinal cord and paresis or paralysis was asymmetric in all dogs. Spinal pain was documented in 9/10 dogs. Cerebrospinal fluid (CSF) analysis was abnormal in all dogs and was characterized by pleocytosis in 8/10, whereas cytology revealed the presence of eosinophils in all dogs. Advanced imaging excluded spinal cord compression in all dogs tested. Post-mortem examination detected spinal cord migration tract in all cases. Nematodes were found in the spinal cord parenchyma (8/10) or adjacent to it (2/10) in all dogs. A larva was found in the subarachnoid space of one dog and an adult nematode in the thoracic intervertebral artery of another. Esophageal nodules were found in 5/10 dogs. These findings suggest that the combination of sudden onset of acute asymmetric paresis accompanied by pain, presence of eosinophils in the CSF and lack of compressive lesion may serve as sufficient evidence for tentative diagnosis of ISSL in endemic areas.

Nematode eggs observed in cytology of cerebrospinal fluid diagnostic for intramedullary Spirocerca lupi spinal cord migration.

Spinal spirocercosis due to aberrant Spirocerca lupi nematode migration is an emerging etiology for acute myelitis in dogs in Israel, causing severe, mostly nonsymmetrical hind limb paresis or paralysis, and sometimes tetraparesis or tetraparalysis. So far, incidental identification of parasites during spinal surgery or at necropsy provides the only definite diagnosis, while antemortem diagnosis of this condition has been uncertain. Specifically, antemortem diagnosis is based on the typical clinical presentation of acute, progressive, asymmetrical hind limb paresis or paralysis, with moderate to severe eosinophilic to mixed cerebrospinal fluid (CSF) pleocytosis and increased CSF protein concentration. Exclusion of other differential diagnoses also requires using spinal cord imaging. In this novel report, we document a case of an intradural spinal spirocercosis in a dog, diagnosed antemortem, by detecting S lupi eggs in the CSF, and subsequent treatment, resulting in the resolution of the clinical signs.

Development of an experimental model of schistosomal myeloradiculopathy.

Schistosomal myeloradiculopathy (SMR) is a severe form of presentation of schistosomiasis in which Schistosoma spp. affect the spinal cord. The aims of the present study were to develop an animal model of SMR caused by S. mansoni, to characterize both sensory and motor abnormalities in the infected animals, and to investigate the relationship of the sensory, motor and histological findings with the progression of the infection over time. Mechanical sensitivity and behavioral tests were performed followed by euthanasia in male Wistar rats divided into six groups of five animals each, on days 5, 10, 20 and 30 after infection of S. mansoni eggs. The controls were subjected to the same procedure but were administered phosphate-buffered saline (PBS). The spinal cord was removed and subjected to histological analysis. S. mansoni eggs were found in the spinal cord of 25% of the infected animals, which belonged to the groups that exhibited more significant reduction of the superficial mechanical sensitivity, thermal sensitivity and muscle strength. This model proved to be satisfactory to assess functional changes in Wistar rats and might be used in studies investigating the pathogenesis of SMR. To our knowledge, this is the first experimental model of SMR.

Chagas disease in a Texan horse with neurologic deficits.

A 10-year-old Quarter Horse gelding presented to the Texas A&M University Veterinary Teaching Hospital with a six month-history of ataxia and lameness in the hind limbs. The horse was treated presumptively for equine protozoal myeloencephalitis (EPM) based on clinical signs but was ultimately euthanized after its condition worsened. Gross lesions were limited to a small area of reddening in the gray matter of the thoracic spinal cord. Histologically, trypanosome amastigotes morphologically similar to Trypanosoma cruzi, the agent of Chagas disease in humans and dogs, were sporadically detected within segments of the thoracic spinal cord surrounded by mild lymphoplasmacytic inflammation. Ancillary testing for Sarcocystis neurona, Neospora spp., Toxoplasma gondii and Leishmania spp. was negative. Conventional and real time polymerase chain reaction (PCR) of affected paraffin embedded spinal cord were positive for T. cruzi, and sequencing of the amplified T. cruzi satellite DNA PCR fragment from the horse was homologous with various clones of T. cruzi in GenBank. While canine Chagas disease cases have been widely reported in southern Texas, this is the first report of clinical T. cruzi infection in an equid with demonstrable amastigotes in the spinal cord. In contrast to previous instances of Chagas disease in the central nervous system (CNS) of dogs and humans, no inflammation or T. cruzi amastigotes were detected in the heart of the horse. Based on clinical signs, there is a potential for misdiagnosis of Chagas disease with other infectious diseases that affect the equine CNS. T. cruzi should be considered as a differential diagnosis in horses with neurologic clinical signs and histologic evidence of meningomyelitis that originate in areas where Chagas disease is present. The prevalence of T. cruzi in horses and the role of equids in the parasite life cycle require further study.

The common neural parasite Pseudoloma neurophilia is associated with altered startle response habituation in adult zebrafish (Danio rerio): Implications for the zebrafish as a model organism.

The zebrafish's potential as a model for human neurobehavioral research appears nearly limitless despite its relatively recent emergence as an experimental organism. Since the zebrafish has only been part of the research community for a handful of decades, pathogens from its commercial origins continue to plague laboratory stocks. One such pathogen is Pseudoloma neurophilia, a common microparasite in zebrafish laboratories world-wide that generally produces subclinical infections. Given its high prevalence, its predilection for the host's brain and spinal cord, and the delicate nature of neurobehavioral research, the behavioral consequences of subclinical P. neurophilia infection must be explored. Fish infected via cohabitation were tested for startle response habituation in parallel with controls in a device that administered ten taps over 10 min along with taps at 18 and 60 min to evaluate habituation extinction. After testing, fish were euthanized and evaluated for infection via histopathology. Infected fish had a significantly smaller reduction in startle velocity during habituation compared to uninfected tankmates and controls. Habituation was eliminated in infected and control fish at 18 min, whereas exposed negative fish retained partial habituation at 18 min. Infection was also associated with enhanced capture evasion: Despite the absence of external symptoms, infected fish tended to be caught later than uninfected fish netted from the same tank. The combination of decreased overall habituation, early extinction of habituation compared to uninfected cohorts, and enhanced netting evasion indicates that P. neurophilia infection is associated with a behavioral phenotype distinct from that of controls and uninfected cohorts. Because of its prevalence in zebrafish facilities, P. neurophilia has the potential to insidiously influence a wide range of neurobehavioral studies if these associations are causative. Rigorous health screening is therefore vital to the improvement of the zebrafish as a translational model for human behavior.

[Application of CT and MRI in the Diagnosis of Paragonimiasis in Brain and Spinal Cord].

Clinical data of 22 cases with paragonimiasis in brain and spinal cord in the Central Hospital of Enshi Tujia and Miao Autonomous Prefecture during 2003 -2012 were retrospectively analyzed. Twenty-two cases aged from 6 to 17 years old, including 15 males and 7 females, were from the countryside, and had a history of eating raw crabs. CT and MRI showed that all the cases had cerebral lesion, 16 cases had unilateral lesion of cerebral hemisphere, and 6 cases had bilateral hemisphere lesions. There were mainly two kinds of imaging changes: (1) the infarct and low- density edema of large area with focal hemorrhage; (2) annular lesions. Among the 6 cases with intracerebral hematoma, 2 patients received surgical removal, and all the patients were treated with praziquantel, 25 mg/kg each time, 3 times per day, 3 d for a course. This regimen was repeated at a 7-day interval. All the patients were cured and discharged from hospital.

Intramedullary spinal cord neurocysticercosis presenting as Brown-Séquard syndrome.

BACKGROUND: Cysticercosis is a parasitic disease caused by the larval stage of Taenia Solium. Involvement of the central nervous system by this tapeworm is endemic in developing countries. However, isolated spinal involvement by Taenia Solium is uncommon and having clinical presentation of Brown-Séquard syndrome is even rarer. CASE PRESENTATION: A 43-year-old male who came to the emergency department with clinical presentation of complete Brown-Séquard syndrome. Computed tomography scan of the brain was normal. Magnetic resonance imaging of the thoracic spine revealed an intramedullary mass of the spinal cord at C-7/T-l level. Patient underwent surgery that revealed a cystic lesion and was resected. Histopathological report confirmed the diagnosis of neurocysticercosis. Postoperatively, oral steroid therapy and a four week course of albendazol were administered. CONCLUSIONS: Intramedullary neurcysticercosis represents a diagnostic challenge and should be considered in intramedullary lesions in settings where Taenia solium is endemic. Clinical, pathophysiological and diagnostic aspects of spinal cord intramedullary neurocysticercosis are discussed.

Myxobolus neurophilus Guilford 1963 (Myxosporea: Myxobolidae): a common parasite infecting yellow perch Perca flavescens (Mitchell, 1814) in Saskatchewan, Canada.

The goal of this study was to identify a myxosporidian parasite infecting the central nervous system of yellow perch Perca flavescens (Mitchell, 1814) observed while investigating a fish kill in Saskatchewan, Canada. Fish were collected from seven different lakes, from two distinct watersheds. Sixty-four per cent (54/86) of yellow perch contained myxozoan pseudocysts located throughout the spinal cord and brain. Myxospores measured 16.5 µm (range 16.2-16.8) long and 8.2 µm (range 7.9-8.4) wide and contained two pyriform, mildly dissymmetrical, polar capsules measuring 7.7 µm (range 7.3-8.1) long and 2.7 µm (range 2.4-3.0) wide. The polar capsules each contained a single polar filament, with 7-9 turns per polar filament coil. Sequencing of the 18S SSU rDNA gene demonstrated >99% similarity to Myxobolus neurophilus. In 60% of infected fish, there was a mild to moderate, non-suppurative myelitis or encephalitis, or both, associated with myxospores. Axonal degeneration was present in rare cases. These findings extend the geographical distribution of M. neurophilus and suggest it may be widespread in yellow perch populations in Saskatchewan.

Retrospective study of central nervous system lesions and association with Parelaphostrongylus species by histology and specific nested polymerase chain reaction in domestic camelids and wild ungulates.

Formalin-fixed, paraffin-embedded tissues from elk (Cervus elaphus), goats, and camelids with case histories and lesions suggestive of Parelaphostrongylus tenuis were examined by histology to characterize lesions that could aid in definitively diagnosing P. tenuis infection. Additionally, sections of paraffin-embedded tissue were used in a nested polymerase chain reaction (nPCR) using Parelaphostrongylus-specific primers to determine how PCR results corresponded with histological findings. Histological changes in brain and spinal cord consisted of linear tracks of hemorrhage; tracks or perivascular accumulations of hemosiderin-laden macrophages; acute foci of axonal degeneration and/or linear glial scars; and perivascular, parenchymal, or meningeal accumulations of eosinophils and/or lymphocytes and plasma cells. Of the 43 samples with histologic lesions consistent with neural larval migrans, 19 were PCR positive; however, only 8 were confirmed Parelaphostrongylus by DNA sequencing. Additionally, 1 goat was identified with a protostrongylid that had a 97% identity to both Parelaphostrongylus odocoilei and a protostrongylid nematode from pampas deer (Ozotoceros bezoarticus celer) from Argentina. None of the histologic lesions individually or in combination correlated statistically to positive molecular tests for the nematode. The results indicate that it is possible to extract Parelaphostrongylus DNA from formalin-fixed, paraffin-embedded tissue, but extended fixation presumably can cause DNA crosslinking. Nested PCR provides another diagnostic tool to identify the cause of neurologic disease in camelids and elk with histologic lesions consistent with neural larval migrans. Furthermore, potential novel protostrongylid DNA was detected from a goat with lesions consistent with P. tenuis infection, suggesting that other neurotropic Parelaphostrongylus species may occur locally.

Cerebral and non-cerebral coenurosis in small ruminants.

Cerebral coenurosis is caused by Coenurus cerebralis, the larval stage of Taenia multiceps. The metacestode causes severe lesions in the brain and spinal cord of the intermediate host, so-called "gid" or "stagger" disease. Whereas, the non-cerebral coenurosis caused by Coenurus gaigeri, the larval stage of Taenia gaigeri, particularly affects goats. The cyst form of the Taenia gaigeri is found in intramuscular and subcutaneous tissues. The difference in the sequence of mitochondrial genes of cox1 and nadI and also other variations reported for clinical, morphological and pathological aspects in coenurosis lead to the hypothesis that there is genetic intraspecific variability within this species, such as in other members of the genus Taenia. Nevertheless, it has been shown that sheep and goats have been infected by both cerebral and non-cerebral coenurosis and it has been suggested that such cerebral and non-cerebral metacestodes may belong to different species of Taenia which are host specific for these hosts.

Acute paraplegia caused by Schistosoma mansoni.

Schistosomiasis affects over 200 million people worldwide. Involvement of the CNS is a rare occurrence. We report 2 young males who presented with rapidly progressing paraparesis associated with urinary incontinence. In both cases, MRI of the spine demonstrated a diffusely enhancing mass at the conus medullaris with extensive spinal cord edema. Laboratory investigations revealed mild peripheral eosinophilia and abnormal, but non-specific, CSF analysis. In one patient, the diagnosis was made based on a rising schistosomal titer with a positive rectal biopsy. In the other patient, spinal cord biopsy revealed a granuloma. Both cases were caused by Schistosoma mansoni and patients were treated with praziquantel and steroid therapy. They both made a remarkable neurological recovery. We emphasize that a high index of suspicion should be raised in the differential diagnosis of transverse myelitis in endemic areas.

Spinal cord schistosomiasis: unexpected postmortem finding.

OBJECTIVES: To report a case of a US resident, originally from Liberia, with chronic hepatitis C infection who developed acute neurologic symptoms of the lower limbs. METHODS: Our case is compared to previously reported similar cases, with emphasis on clinical symptoms, investigations, diagnosis, and prognosis. RESULTS: The patient was transferred to the University of Iowa Hospital and Clinics for further management of severe retroperitoneal bleeding and died 2 days after admission. The diagnosis of schistosomiasis was established on examination of the spinal cord at autopsy, where multiple Schistosoma mansoni eggs were seen in the vasculature of the spinal cord. CONCLUSIONS: The diagnosis of schistosomiasis may go undiagnosed in countries where the disease is not endemic but should be considered when investigating spinal cord disease in patients native to an endemic area or international travelers.