ABSTRACT
Early stages of a primary infection with E. granulosus are characterized by the substantial activation of a cell-mediated type immune reaction against the parasite. The release of oncospheres promotes an increase in leukocytosis, primarily by eosinophils, lymphocytes and macrophages. Host complement pathways contribute to the host inflammatory response and are activated by both living organisms as well as by material derived from dead parasites. Intense, dense granulomas form around the cyst and are responsible for much of the tissue destruction and subsequent clinical pathology associated with the disease.
