Histogenesis in the metacestode of Echinococcus vogeli and mechanism of pathogenesis in polycystic hydatid disease.

Histogenesis of the metacestode of Echinococcus vogeli was traced mainly in rodents inoculated intraperitoneally with finely minced infective vesicles. The fragments aggregated in the peritoneal cavity and coalesced, forming structures (plaques) from which primary vesicles arose. From primordia in their germinal tissue, exogenous vesicles developed, enlarged, and migrated outward to the surface of the laminated membrane, where they remained attached and proliferated. Each unit of vesicles so formed retained discrete identity and, within 6-8 mo, acquired an adventitia; thereafter, exogenous multiplication ceased and endogenous proliferation supervened. Large numbers of daughter cysts arose in the germinal tissue lining chambers within the units; endogenous proliferation also finally ceased, and the daughter cysts produced brood capsules containing protoscoleces. Primordia of exogenous vesicles were not observed in the walls of daughter cysts. Production of protoscoleces involved 3 processes: they developed in typical brood capsules, singly in minute brood capsules, or directly from germinal tissue. Exogenous proliferation is not characteristic in the natural intermediate host of E. vogeli, the paca. Evidently in primates, the initial proliferation in the liver is followed by extension of the metacestode into the peritoneal cavity and eventual invasion of abdominal and thoracic organs. Exogenous proliferation by a process unique to E. vogeli accounts for the clinical course of polycystic hydatid disease.