Cystic echinococcosis (CE) is a cosmopolitan zoonosis caused by the larval stage of the cestode parasite Echinococcus granulosus sensu lato (s.l.). Primary CE occurs in intermediate hosts (ungulates, accidentally humans) after ingestion of oncosphere-containing eggs, which develop into metacestodes (hydatid cysts) mainly in the host liver and lungs. Secondary CE occurs after spillage of protoscoleces from a fertile cyst within an infected intermediate host, since protoscoleces' developmental plasticity allows them to become new cysts within intermediate hosts or adult worms if ingested by definitive hosts (usually dogs). 1 Human studies on CE susceptibility/resistance are scarce, 2-4 although immune responses and host immunogenetics were suggested to determine the infection outcome. 5,6 Accordingly, studies performed in individuals seropositive for CE, but ultrasound normal, reported a unique antibody profile potentially associated with host resistance. 7 Additionally, mouse strains showing differences in susceptibility to secondary CE exhibited distinct parasite-specific immune responses. 8-10
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