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Spinal-cord involvement in the hepato—splenic form of Schistosoma mansoni infection

Spinal-cord disease is a severe presentation of human Schistosoma mansoni and Se. haematobium infection, Se. mansoni being the most frequently reported cause of schistosoma! myeloradiculopathy (SMR) worldwide. The prevalence of spinal-cord schistosomiasis is unknown but it is now believed that the condition is not as rare as once thought (Suchet et al., 1987; Ferrari et al., 1993; Ferrari, 1999). This disease may occur at any time of the infection after the adult female schistosomes have begun to lay eggs. However, it is much more frequent during the early stages of infection (inapparent acute form), during the slow progression to the chronic forms of human schistosomiasis, or concomitantly with the mild chronic forms [i.e. intestinal or hepatointestinal disease (for Se. mansoni) or urinary schistosomiasis without obstructive uropathy (for Se. haematobium)] than during the severe stages of human schistosomiasis (Scrimgeour and Gajduzek, 1985; Pittella, 1991, 1997; Ferrari, 1999). An extremely rare case of SMR, in which the neurological disease developed concomitantly with the severe, chronic, hepatosplenic form of Se. mansoni infection, is described here. A 13-year-old boy was admitted to the hospital of the Federal University of Minas Gerais (HFUMG), in Belo Horizonte, Brazil, because of spinal-cord disease. He had been in good health until 14 weeks before admission, when he developed persistent lumbar back pain. The day after his back ache began, the boy developed dysuria and severe weakness of the lower limbs. The disease progressed acutely such that by day 7 after the onset of the illness the boy was unable to pass urine or walk. At that time he was examined at another institution but refused to be hospitalized. A long-term urethral catheter was put in place. The symptoms remained unchanged for about 3 months, when progressive improvement started. Two weeks later he was admitted to the HFUMG. The results of a general physical examination were then unremarkable except for hepato-splenomegaly and the indwelling urethral catheter. A neurological examination, however, revealed a slight decrease in strength in the proximal muscles of the lower limbs that did not impair ambulation, a slight sensory loss of no more than L1 level, and hyperactivity of the deep tendon reflex in the left ankle. Except for eosinophilia, the blood counts were normal, as were the values for prothrombin time, partial-thromboplastin time, and blood chemicals. The results of serological tests for hepatitis viruses were negative except for evidence of lgG against hepatitis A virus. Chest X-ray plates were unremarkable. Abdominal ultrasonography showed a major enlargement of the left liver lobe, a slight increase in the right lobe, echogenic thickening of the intrahepatic portal branches extending to the periphery of the organ (i.e. grade-Ill fibrosis), wall thickening and dilatation of the portal vein and of its tributary veins, dilatation of the splenic vein, presence of porto-systemic collaterals, marked enlargement of the spleen, and considerable thickening of the gallbladder wall. Urine culture disclosed Streptococcus sp. and Klebsiella pneumonie. The boy's cerebrospinal fluid (CSF) contained five lymphocytes/ ,ul, 131 mg total protein/ dl, and 49 mg glucose/ dl. An ELISA revealed that the CSF also contained lgG against the soluble egg antigen of Se. mansoni (SEA). Myelography, computed-tomographic-myelography and magnetic-resonance imaging were unrevealing. A rectal biopsy yielded viable eggs of Se. mansoni. Treatment with prednisone (1.5 mg/ kg.day) and praziquantel (60 mg/kg.day for 3 days) was started. The urinary-tract infection was treated with antibiotics. A marked improvement was soon noticed and the patient