Abstract
Neurocysticercosis, caused by infestation of the nervous system by the larval form of Taenia solium, continues to baffle the neurologist, because of varied clinical manifestations. A large body of the literature related to this disease is clinically oriented, enough attention has not been given to parasite related factors modulating the host response. Using immunohistochemical techniques, three features related to the biology of the Cysticercus cellulosa e were studied. Firstly, to the question as to which part of the worm is recognised by the host immune system, the surface glycoprotein is found to be immunolabelled by the CSF from patients of neurocysticercosis. This surface protein is depleted following specific antihelmenthic therapy, thus accounting for a fall in anticysticercal antibosy level in the CSF. Secondly, the cysticercal cyst, by immunochemical and histochemical methods, is found to have "ACTH like" molecule in the body wall and has neurotransmitter and mitochondrial metabolic pathways similar to the host, facilitating the immune evasion and successful parasitisation. Finally, Cysticercus cellulosae is found to contain a "peptide" opening the blood brain barrier at the arteriolar level when injected into mice intravenously. Similar phenomenon may be functional in the patients as well, resulting in cerebral oedema, especially following praziquintel therapy.