Cysticercosis

Human cysticercosis occurs when T solium eggs are ingested via faecal-oral transmission from a tapeworm host. The human then becomes an accidental intermediate host, with development of cysticerci within organs.

Cysticerci may be found in almost any tissue: frequently reported locations are skin, skeletal muscle, heart, eye, and most importantly, the CNS (NCC).

Symptomatology of NCC is largely dependent on the presence of pericystic inflammation, the absence of which will usually manifest as asymptomatic disease. Host inflammatory response to cysticerci depends on the parasite's ability to evade host immunity; therefore, inflammation is restricted to currently degenerating cysts whose ability to evade host defenses is faltering. Lack of inflammation occurs with both healthy cysticerci and those that have involuted, termed active and inactive disease, respectively. Upon involution, cysts undergo granulomatous change and exhibit calcification. Cysts in various stages of viability can be seen simultaneously in one host.

In patients with advanced HIV disease and compromised cell-mediated immunity, NCC may is exist without significant host response and is likely to be asymptomatic. For this reason, in symptomatic patients with CD4 counts under 200 cells/mm³ alternative diagnoses should be considered more likely.