In early May 1984, CDC received reports that 15 (83%) of 18 American students participating in a travel/study program in Kenya had acquired Schistosoma mansoni infections. Two of these students developed flaccid paraplegia. Although data are incomplete on all 18 students, no unusual attributes could be identified in these two students that might explain why their infections were associated with severe neurologic disease. General background information and the case histories of these students follow.

All 18 students arrived in Kenya on February 13, 1984. From March 5 to March 25, they shared housing in the Machakos district. To provide a place for bathing, the students dammed a small stream; two of the infected students recalled experiencing an itchy rash shortly after bathing at this site. Subsequently, the group separated, as the students took individual assignments in various regions of the country. Between April 26 and May 12, 14 of the 15 infected individuals became acutely ill with fever, diarrhea, malaise, and weight loss.

Student 1: This 21-year-old white male was in good health and had never traveled outside the United States. He was immunized against tetanus, typhoid, cholera, and yellow fever, and received an injection of immune globulin before arriving in Kenya. While in Kenya, he took weekly chloroquine and Fansidar for malaria prophylaxis. In early April, he complained of fever, abdominal pain, and diarrhea without blood or mucus, all of which resolved without therapy. He became ill again on April 26, with fever, chills, sweats, anorexia, mild nonbloody diarrhea, and abdominal pain. There was no hematuria or cough. He was treated orally with chloroquine for a presumptive diagnosis of malaria. On April 28, he developed severe lumbar back pain without tenderness or radiation and had associated numbness, without weakness, in both feet. On May 1, he had difficulty recognizing the position of his feet and had extreme proximal lower extremity weakness. On May 2, he became ataxic and developed urinary retention. A diagnosis of transverse myelitis secondary to schistosomiasis was made when stool examinations showed ova of S. mansoni. The patient was treated with praziquantel and prednisone. He was transported to the United States on May 5.

On evaluation in the United States, the student had no rash, fever, lymphadenopathy, hepatosplenomegaly, or point tenderness on palpation of the spinal column. Neurologic examination revealed a flaccid paraplegia at and below the level of T-10. There was marked sensory loss, including loss of vibratory sensation. Superficial and deep tendon reflexes could not be elicited.

A white blood cell count revealed moderate eosinophilia. A myelogram showed no obstruction or mass, but a CAT scan showed the lumbar cord to be slightly enlarged, without focal abnormalities. Examination of cerebrospinal fluid (CSF) showed pleocytosis and elevated protein; however, eosinophilic pleocytosis was not present. Fecal examination showed 500 S. mansoni eggs per gram of stool; no other helminthic or protozoal pathogens were observed. Serologic tests for antibody to mycoplasma, Epstein Barr virus (EBV), and other viral agents were negative.

On May 15, the patient was transferred to a spinal cord rehabilitation center. His neurologic condition remains unchanged.

Student 2: A 20-year-old white female was in good health and had not previously traveled overseas. She received similar immunizations as Student 1 and took chloroquine and Fansidar weekly for malaria prophylaxis. On April 29, she developed fever, abdominal pain, and nonbloody diarrhea. A Gram stain of her urine showed gram-positive cocci, and she was treated with ampicillin. She also received metronidazole, although it was unclear whether amoebae were found by stool examination. On May 3, she developed severe back pain without radiation, weakness, or urinary symptoms. From May 7 to May 9, she rapidly lost the ability to ambulate. She complained of difficulty initiating her urine stream. On May 9, after a stool examination showed many ova of S. mansoni, she was diagnosed as having schistosomal transverse myelitis and treated with oxamniquine. She was transported to the United States on May 11.

Evaluation in the United States was unremarkable except for a flaccid paralysis and severely decreased sensation to temperature and touch in the lower extremities. Deep tendon reflexes could not be elicited. The level of the lesion was placed at L1-L2.

There was moderate eosinophilia. CSF examination showed pleocytosis and elevated protein; however, eosinophilic pleocytosis was not present. A myelogram showed no obstruction, but a CAT scan of the spine suggested some swelling of the conus medullaris. Stool examination showed only S. mansoni (1,100 eggs per gram of feces). Serologic tests for antibody to mycoplasma, EBV, and other viral agents were negative.

Because the dose of oxamniquine given in Kenya was considered inadequate, the patient was treated with praziquantel. Large doses of dexamethasone were also given. The patient's motor function and sensation improved by the second treatment day. On May 15, she began moving both extremities against gravity. On June 8, the patient was ambulating with assistance at a spinal rehabilitation center. Reported by J Houpis, MD, Brattleboro, Vermont; J Oexmann, MD, J Martin, MD, G Jacobi, MD, Depts of Neurology and Infectious Diseases, Massachusetts General Hospital, Boston; J Reardon, MD, Assistant Director, Div of Communicable and Venereal Diseases, G Waterman, MD, Acting State Epidemiologist, Massachusetts Dept of Health; Helminthic Diseases Br, Div of Parasitic Diseases, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: Although S. mansoni and S. haematobium are endemic to the Machakos district of Kenya (1), no infections with S. haematobium occurred among any of the 18 students. Schistosomiasis of the central nervous system (CNS) was first recognized in the late 19th century and has been most commonly reported as a cerebral granulomatous disease resulting from ectopically located S. japonicum eggs (2). Schistosomal transverse myelitis is rare and has been observed most frequently in infections with S. mansoni (3). Since S. mansoni transverse myelitis (SMTM) was first reported in 1930, about 32 tissue-proven cases and over 28 presumed cases have been reported. When autopsy or surgical biopsy is not performed, a presumptive diagnosis of SMTM is based on the following considerations: (1) the finding of low thoracic/upper lumbar neurological symptoms; (2) demonstration of exposure to schistosomes through parasitologic or serologic techniques; and (3) the exclusion of other known causes of transverse myelitis (5,6). In contrast to schistosomal transverse myelitis, other causes of transverse myelitis commonly affect the mid-thoracic cord (4). Eosinophilic pleocytosis in the CSF is suggestive of schistosomiasis of the CNS but is often not observed, as in the cases reported here.

Other disorders that have been associated with transverse myelitis include numerous viral, bacterial, and fungal infections (especially with enterovirus, EBV, tuberculosis, syphilis, and coccidioidomycosis), postvaccinal reactions, collagen vascular diseases, toxin exposures, and vascular disease. Conditions that can mimic transverse myelitis include tumor, Guillan-Barre syndrome, and multiple sclerosis (4). All of these, including SMTM, are rare, and the observed attack rate of 13% (2/15) in this group of students is unusual, regardless of etiology.

Schistosomal myelopathy results from the inflammatory reaction accompanying the deposition of eggs in the venules located in and around the spinal cord (2,3). How eggs, which are normally oviposited in the venules of the inferior mesenteric vein of the portal system, reach the spinal vascular system is unknown. Several hypotheses have been proposed (2,3,6).

Praziquantel or oxamniquine are the antischistosomal agents available to treat SMTM. Treatment destroys the adult worms and thereby prevents further oviposition. Praziquantel is effective against all schistosomes; however, oxamniquine is only effective against S. mansoni. The dosage of oxamniquine needed varies according to the geographic location where the infection was acquired (7). Steroids are used to suppress the host response around the ectopic eggs (5,6). Myelography may identify discrete granulomatous masses that may be amenable to surgical removal (8). In 50% of reported cases, there is little or no return of neurologic function (2,3,5,6), and intensive rehabilitative care is indicated. When evaluating persons for infection with schistosomes, interpretation of negative tests may be difficult, since extremely mild infections or ectopic localization of worms may preclude detection of eggs with stool or urine examinations. Because of the potential benefit of the recommended therapy, presumptive treatment of patients with diagnoses of transverse myelitis and histories of water exposure in endemic areas should be initiated while awaiting results of parasitologic or serologic tests.

The severity of illness in this group should reemphasize the need

Disclaimer   All MMWR HTML documents published before January 1993 are electronic conversions from ASCII text into HTML. This conversion may have resulted in character translation or format errors in the HTML version. Users should not rely on this HTML document, but are referred to the original MMWR paper copy for the official text, figures, and tables. An original paper copy of this issue can be obtained from the Superintendent of Documents, U.S. Government Printing Office (GPO), Washington, DC 20402-9371; telephone: (202) 512-1800. Contact GPO for current prices.

Page converted: 08/05/98

HOME  |  ABOUT MMWR  |  MMWR SEARCH  |  DOWNLOADS  |  RSS |  CONTACT POLICY  |  DISCLAIMER  |  ACCESSIBILITY

Morbidity and Mortality Weekly Report Centers for Disease Control and Prevention 1600 Clifton Rd, MailStop E-90, Atlanta, GA 30333, U.S.A Department of Health and Human Services

This page last reviewed 5/2/01