Human
neurocysticercosis results from infestation of the central nervous system with the metacestode form (tissue
cyst) of Taenia solium.
Cysticercosis is being increasingly recognized as a cause of
neurologic symptoms in residents and emigrants from developing countries. Taeniid parasites have developed elaborate mechanisms to persist in the tissues of their intermediate hosts. The invasive larvae, termed oncospheres, are susceptible to antibody and
complement. However, by the time that the host has generated an antibody response, the parasites have begun to transform to the more resistant metacestode form. The metacestodes also have means of evading
complement-mediated destruction, including
paramyosin, which inhibits C1q;
taeniaestatin, which inhibits both classical and alternate pathways (likely by inhibiting
factor D and C3
esterase); and sulfated
polysaccharides, which activate
complement away from the parasite. Similarly, antibody does not seem to be able to kill the mature metacestode. The parasites may even stimulate the host to produce antibody, which could be bound via
Fc receptors, and used as a source of
protein. Finally,
taeniaestatin and other parasite molecules may interfere with lymphocyte proliferation and macrophage function, thus paralyzing the cellular immune response. Because the symptoms of
neurocysticercosis are typically associated with a brisk inflammatory response, we hypothesize that disease is primarily the result of injured or dying parasites. This hypothesis raises important questions in assessing the role of
chemotherapy in the management of
neurocysticercosis as well as in evaluation of clinical trials, most of which have been uncontrolled.