Research development of the pathogenesis pathways for neuroschistosomiasis

Abstract

Abstract:The infection of the central nervous system (CNS) by schistosome may or may not have clinical manifestations.When symptomatic, neuroschistosomiasis (NS) is one of the most severe presentations of schistosome infection. Among the NS symptoms, cerebral invasion is mostly caused by Schistosoma japonicum (S. japonicum), and the spinal cord symptoms are mainly caused by S. mansoni or S. haematobium. There are 2 main pathways by which schistosomes cause NS: egg embolism and worm migration, via either artery or vein system, especially the valveless perivertebral Batson's plexus. The adult worm migrates anomalously through the above pathways to the CNS where they lay eggs. Due to the differences in species of schistosomes and stages of infection, mechanisms vary greatly. The portal hypertension with hepatosplenic schistosomiasis also plays an important role in the pathogenesis. Here the pathways through which NS occurs in the CNS were reviewed.

Establishment of a cerebral schistosomiasis experimental model in rabbits

“…japonicum appears to induce clinical cerebral schistosomiasis more easily than S. mansoni does. The neurological complications of acute NS include delirium and confusional state, loss of consciousness, headache, seizures, dysphasia, visual field impairment, focal motor deficits (hemiparesis, paraplegia), and cerebellar syndrome [11,12] . Brain edema and multiple focal cerebral lesions in the different lobes or areas may affect different functions.…”

“…After injection of egg suspension, the histological observations showed clearly 3 stages: a necrotic-exudative stage, a productive stage, and a healing-by-fibrosis stage [11,14] .…”

“…The pathogenesis of brain invasion is still unknown, although currently available evidence suggests the direct deposition theory (the adult worm migration) and the indirect deposition theory (the egg embolization). Details on the pathways of NS pathogenesis have been discussed previously [11] . The real damage of NS depends on both the amount of eggs and the immune system of the host.…”

“…In fact, in as early as 1970, Jane JA et al [8] designed their experiments in different conditions, based on the aetiological possibilities of the direct or indirect pathways for NS, but the condition in the experiment was unlikely to occur during the nature course of infection. The involvement of CNS by schistosomes is more frequent in patients without systemic symptoms of infection [11,12] .…”

“…Mostly, it is based on the rabbits' neurological symptoms and the lifespan of eggs' granulomas, according to the 3 stages. Necroticexudative granulomas are characteristics of early stages of infection [11][12][13][14] . Freshly-laid eggs are immature and the leukotactic responses to immature eggs are initially slight.…”