Spinal Schistosomiasis: Differential Diagnosis for Acute
Paraparesis in a US Resident
Tapan N. Joshi, MBBS, MS1; Michael K. Yamazaki, MD2; Holly Zhao, MD, PhD2; Daniel Becker, MD1
1International Center for Spinal Cord Injury, Kennedy Krieger Institute, Johns Hopkins School of Medicine, Baltimore,
Maryland;2Department of Physical Medicine & Rehabilitation, University of California Davis School of Medicine,
Received July 21, 2009; accepted November 12, 2009
Background: Spinal schistosomiasis is a severe presentation of Schistosoma mansoni infection, which is
endemic in South America, the Middle East, and sub-Saharan Africa. With increasing international travel, a
disease can spread from an endemic area to another part of the world easily.
Objective: To present a case of a US resident who developed acute paraparesis due to spinal
schistosomiasis after traveling to sub-Saharan Africa.
Participant: A 45-year-old woman presented with abdominal pain radiating into the bilateral lower
extremities. She was diagnosed with a pelvic mass and underwent an urgent hysterectomy with right
salpingo-oopherectomy. Postoperatively, she developed progressive weakness with worsening pain in her
bilateral lower extremities and neurogenic bladder. Magnetic resonance imaging showed an abnormal T2
hyperintense signal in the entire spinal cord below the T3 level with abnormal contrast enhancement from
T9 through the conus medullaris. Spinal fluid analysis showed lymphocytic pleocytosis and elevated protein.
The patient was diagnosed with transverse myelitis. Subsequently, a detailed history revealed a visit to
Ethiopia 2 years earlier. Tests for S mansoni were positive. After treatment with praziquantel and prednisone,
her neurologic function began to improve.
Conclusions: An increasing incidence of international travel is increasing the likelihood of US physicians’
encountering this treatable condition. Travelers with spinal schistosomiasis may not have symptoms of
systemic infection. Therefore, it is important to include spinal schistosomiasis in the differential diagnosis of
acute inflammatory myelopathy, particularly with a history of travel to endemic areas.
J Spinal Cord Med. June 2010;33(3):256–260
Key Words: Schistosomiasis, spinal; Schistosoma; Schistosoma mansoni; Paraparesis; Myelopathy;
Myeloradiculopathy; Praziquantel; Parasites, helminthic
Schistosomiasis is one of the world’s most widespread
parasitic diseases, and it is caused by the trematode
Schistosoma. It has affected 200 million people world-
wide (1). Schistosoma mansoni, 1 of the 3 main species, is
endemic to South America, the Middle East, and sub-
Saharan Africa (2). S mansoni uses a human as a definitive
host and a freshwater snail (Biomphalaria species) as an
intermediate host. Infection ensues upon direct contact
with fresh water that harbors cercariae, a larval form of
schistosome released from snails. Upon exposure, cer-
cariae penetrate the skin of humans and enter the blood
and lymphatic circulation en route to the lungs. After
several days, cercariae migrate to the portal venous
plexus and sexually mature if they meet the opposite sex.
Then the adult pairs travel to the venous plexus
surrounding the intestines, where they begin egg
production. Eggs pass through the intestinal mucosa
and are shed in the stool. Once excreted, they hatch in
fresh water and release the fresh-living motile form,
miracidia, which, in turn, infect specific freshwater snails.
The life cycle is completed when cercariae are released
from the snails into water (2,3).
Acute schistosomiasis secondary to S mansoni infec-
tion presents with fever, headache, myalgia, diarrhea,
and abdominal pain. Acute respiratory symptoms are
reported in up to 70% of individuals. In the chronic
phase, it commonly involves hepatic and gastrointestinal
Please address correspondence to Tapan N. Joshi, MBBS, MS,
Johns Hopkins School of Medicine, International Center for
Spinal Cord Injury, 707 Broadway, Suite 518, Baltimore, MD
21205; p: 718 724 3277; f: 718 985 5789 (e-mail: joshi@
G2010 by the American Paraplegia Society
256 The Journal of Spinal Cord MedicineVolume 33Number 32010
systems causing diarrhea, constipation, intestinal bleed-
ing, intestinal obstruction, hepatomegaly, or portal
hypertension (2). When S mansoni infects the central
nervous system, it commonly causes spinal cord disease
known as spinal schistosomiasis. The central nervous
system becomes infected either by migration of pairs of
adult worms or by embolization of eggs through
retrograde venous flow into the Batson venous plexus,
a valveless paravertebral venous system from the
mesenteric venous system (4). Clinical presentation of
spinal schistosomiasis ranges from radicular pain to
myelopathy causing flaccid paraplegia, bladder inconti-
nence, and dysesthesia.
In times of increasing international travel, a disease
can spread easily from an endemic area to another part of
the world (2). The H1N1 virus outbreak is a recent
example. We present a case of a US resident who
developed acute paraparesis due to spinal schistosomiasis
secondary to traveling to an endemic area, sub-Saharan
A previously healthy 45-year-old white woman presented
with acute abdominal pain radiating into her bilateral
lower extremities. Workup at that time revealed a 7-cm
pelvic mass, and she underwent an urgent hysterectomy
with right salpingo-oophorectomy. Pathology results
indicated no malignancy. Postoperatively, she developed
progressive bilateral lower extremity weakness, areflexia,
sensory impairment, and bladder incontinence with
worsening pain in the bilateral lower extremities.
Magnetic resonance imaging (MRI) showed an abnormal
T2 hyperintense signal in the entire spinal cord below the
T3 level with abnormal contrast enhancement from T9
through the conus medullaris (Figures 1 and 2). The
brain MRI was normal. Cerebrospinal fluid (CSF) was
remarkable for pleocytosis, with 92% lymphocytes and
an elevated protein level of 240 mg/dL. The CSF glucose
Figure 1. T2-weighted magnetic resonance image of the cervical (A) and thoracic (B) spine demonstrates hyperintense
signal in the lower thoracic spine.
Figure 2. Gadolinium-enhanced sagittal T1-weighted mag-
netic resonance image of the thoracolumbar junction shows
patchy enhancement with scattered focal nodular enhance-
ment of the expanded distal spinal cord and conus.
Differential Diagnosis of Spinal Schistosomiasis257
level was within the normal range at 62 mg/dL. There
were no oligoclonal bands. Exhaustive CSF workup for
viral, bacterial, mycobacterial, and fungal infections was
negative. Laboratory workup for connective tissue
disorder, neuromyelitis optica, and human immunodefi-
ciency virus was negative as well (Table 1). The patient
was diagnosed with transverse myelitis and treated
with a course of methylprednisolone 1 g/d followed
by a 5-day course of intravenous immunoglobulin
Although detailed serology results were inconclusive
for the cause, she progressively worsened to flaccid
paraplegia. Further history taking revealed her visit to
Ethiopia 2 years earlier as a river guide. Examination of
stool and urine for schistosomal ova was negative;
however, the titer for schistosomal immunoglobulin G
antibody was markedly elevated to 3.3 median fluores-
cence intensity (FOCUS Diagnostics, Cypress, CA). Her
serum sample was sent to the Centers for Disease Control
and Prevention (CDC) for a S mansoni antibody Falcon
assay screening and enzyme-linked immunosorbent
assay test. This test is 99% sensitive and specific for S
mansoni infection (5). Test results showed an elevated
titer of 48 units/mL and confirmed the diagnosis of spinal
schistosomiasis secondary to S mansoni infection. She
was treated with praziquantel, an antihelminthic, for 5
days and prednisone for 14 days followed by a 4-week
steroid taper. On neurologic examination at discharge,
she was classified as T10 ASIA impairment scale A. She
was wheelchair dependent for mobility.
She did not receive any rehabilitation intervention for
1 year. Follow-up MRI at 9 months showed an improving
T2 hyperintense signal in the thoracolumbar spinal cord
(Figure 3). Neurologic examination showed improve-
ment to T10 ASIA impairment scale C with a lower
extremity motor score of 8/50, normal deep anal
Table 1. Results of Laboratory Workup
BloodTest Normal Value Test Result
West Nile antibody
CSF TestNormal Value Test Result
West Nile IgG/IgM
Myelin basic protein
HTLV 1 and 2
ANA, antinuclear antibody; Ig, immunoglobulin; TSH, thyroid-stimulating hormone; RPR, rapid plasma reagin; VDRL, Venereal
Disease Research Laboratory; NMO, neuromyelitis optica; HIV ELISA, human immunodeficiency virus enzyme-linked immunosor-
bent assay; CSF, cerebrospinal fluid; WBC, white blood cell count; HSV PCR, herpes simplex virus polymerase chain reaction; EBV,
Epstein-Barr virus; CMV, cytomegalovirus; HTLV, human T-cell lymphotropic virus; and AFB, acid-fast bacillus.
258 The Journal of Spinal Cord Medicine Volume 33Number 32010
sensation, and weak voluntary anal contraction. She was
able to walk with braces and continued to manage her
neurogenic bladder by intermittent catheterization and
bowel by colostomy.
Acute inflammatory myeloradiculopathy, also known as
spinal schistosomiasis, is the most common neurologic
complication secondary to S mansoni infection. It com-
monly affects the conus medullaris and cauda equina.
Radicular symptoms are caused by multiple granulomas
deposited on the spinal roots with congestion and edema.
Myelopathy is secondary to necrosis, vacuolization, and
further atrophy of the spinal cord tissue (3,4). In sub-
Saharan Africa, 1% to 5% of nontraumatic spinal cord
injuries are attributed to spinal schistosomiasis (6). Spinal
schistosomiasis is infrequently reported in the USA, except
in immigrants from endemic areas or in individuals who
were stationed in the endemic area (7–9).
made based on the combination of strong clinical,
(10,11). Our patient presented with radicular pain in the
lower extremities and progressed to paraparesis, hypoto-
nia, areflexia, and neurogenic bladder and bowel. This
combination of symptoms is the most common clinical
presentation of spinal schistosomiasis. The patient also had
a travel history to the endemic area, with exposure to fresh
water. Her CSF showed an increase in protein concentra-
tion. It also revealed a normal glucose level and elevated
mononuclear cells. Other potential differential diagnoses
for myelopathy were ruled out, including infectious,
inflammatory, or connective tissue disorders. The en-
zyme-linked immunosorbent assay test provided by the
CDC is particularly sensitive to S mansoni infection and
showed an elevated titer of 48 units/mL. Spinal MRI is
valuable in the diagnosis of schistosomal myeloradiculo-
pathy. In this case, spinal MRI showed hyperintense areas
on T2-weighted sequences and abnormal contrast en-
hancement in the conus medullaris (12,13). This patient
responded well to praziquantel and steroid therapy.
Schistosomiasis affects approximately 25% of the
population of sub-Saharan Africa and accounts for 93% of
the global case burden (14). This patient most likely
became infected while traveling in Ethiopia (15).
Exposure to schistosome cercariae carried in snails during
swimming or river rafting in the fresh water of the river
increased the risk of infection. Incidence of travel-
associated schistosomiasis is affected by the type of
traveling. Business travelers are less likely to be infected
than tourists (16). Travelers to the endemic area who
develop spinal schistosomiasis present an unusual clinical
scenario. They often do not have clinical evidence of
systemic schistosomiasis(10,16). The low
burden may be responsible for the large number of
negative results of parasitologic examinations. Spinal
cord disease usually occurs within weeks to months after
the infection. In rare cases, it has been reported after a
few years (17), as seen in this case.
Most of the time, the diagnosis of spinal schistoso-
miasis is associated with positive retrospective travel
history to the endemic area (18). A high index of
suspicion is needed to diagnose spinal schistosomiasis
Figure 3. T2-weighted magnetic resonance images of the cervical (A), thoracic (B), and lumbar (C) spine demonstrate a
decrease in hyperintense signal within the lower thoracic spinal cord after 9 months.
Differential Diagnosis of Spinal Schistosomiasis259
in travelers for the following reasons: (a) Patients often do
not have systemic involvement. (b) Routine tests for
detection of ova and parasites in urine and stool are often
negative. (c) Onset of myelopathy may be delayed by
months or even years in some patients. (d) Whereas
histopathologic detection of schistosomal ova and
inflammatory granulomas in the spinal cord provides a
definitive diagnosis, such invasive surgery is not always a
feasible option. (e) Full neurologic recovery is observed in
30% of all patients affected by spinal schistosomiasis (3).
Although uncommon in North America, an increas-
ing incidence of international travel increases the
possibility of an encounter of this treatable condition by
US physicians. Therefore, it is prudent to include
schistosomiasis in the differential diagnosis of acute
inflammatory myelopathy, particularly in patients with
a history of travel to endemic areas, especially in
individuals who were exposed to fresh water. It is also
recommended that these travelers be screened (16,19).
The CDC also urges physicians to become familiar with
the clinical manisfestations, diagnostic criteria, and
appropriate treatment for schistosomiasis (20).
Every year millions of Americans travel internationally for
business and recreational activities. Travel to endemic
areas can expose them to infection by S mansoni. Spinal
schistosomiasis is a serious but curable condition, and it
should be considered in the differential diagnosis of acute
inflammatory myelopathy. Screening of all potentially
exposed travelers should be encouraged.
We thank Mollie Lange and Kaanan Raja for editorial
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260 The Journal of Spinal Cord MedicineVolume 33 Number 32010