Cerebral schistosomiasis--an unusual presentation of an intracranial mass lesion.

Schistosomiasis is an intravascular trematode infection affecting at least 200 million people worldwide1. Trematodes are parasitic worms that are flattened dorsoventrally. Their suckers (trematos, Greek ‘holes’), act as organs of attachment. Schistosome worms are blood flukes with a complex life cycle involving freshwater snails that act as intermediate hosts, and the bloodstream of higher order vertebrates that are the definitive hosts. The three major schistosome species (S. mansoni, S. japonicum and S. haematobium) known to infect humans usually reside in the venous systems of the liver, intestines or urinary bladder. Schistosomal species have different geographical distributions. Schistosoma haematobium is encountered mainly in Africa and the Middle East; S. mansoni is additionally seen in South America and the Caribbean; and S. japonicum is primarily found in the Far East2. The main clinical features are related to the life cycle of the schistosome. Initially, larvae from freshwater penetrate the skin resulting in a cercarial dermatitis or ‘swimmer’s itch’. Subsequently, a systemic hypersensitivity response may occur, known as Katayama fever, in response to the migrating schistosomulae3. Finally, chronic pathology is due to granuloma formation in response to egg deposition4. Involvement of the central nervous system (CNS) is uncommon but can be an important complication. The risk of CNS infection depends on the level of immunity and the magnitude of the schistosomal invasion. Histologically, the changes seen in the CNS correspond to the host’s inflammatory reactions to the ova and range from nothing to florid granulomatous inflammation. There are two theories as to how the eggs reach the CNS. Eggs from the portal system could embolise to the brain along the vertebral venous (Batson) plexus5, via atrial/septal defects or patent foramen ovale, or via pulmonary venous shunts, as a result of hepatic and pulmonary hypertension6. Alternatively, the adult worms could enter the Batson plexus and then migrate upwards to the brain and deposit directly their eggs7. The small size and round shape of S. japonicum ova favor an easier migration to the brain, according to the embolisation hypothesis. Conversely, S. mansoni and haematobium ova are larger, with S. mansoni possessing a prominent lateral spine. These differences may explain the relatively more common presentation of transverse myelitis and other spinal syndromes when neurological complications ensue with these species8. Once in the brain, soluble egg antigens are responsible for provoking a peri-ova granulomatous reaction, comprising lymphocytes, macrophages and eosinophils. Host factors determine the severity of response4. Cerebral Schistosomiasis An Unusual Presentation of an Intracranial Mass Lesion