Hydatid disease: biology, pathology, imaging and classification

Abstract

Rupture and the sequellae of rupture are more important than the mass effect of hydatid cysts, except in the brain where the mass effect by itself has severe consequences. The biology of hydatid disease, including the complex interaction between primary and secondary hosts, is reviewed. The hydatid cyst always starts as a fluid-filled, cyst-like structure (Type I) which may proceed to a Type II lesion if daughter cysts and/or matrix develop. In some instances the Type II lesion becomes hypermature and due to starvation dies to become a mummified, inert calcified Type III lesion. Type I and II lesions may undergo three types of rupture: contained, communicating and direct. Contained rupture is clinically silent, but communicating rupture may cause biliary obstruction and evacuation or infection of the cyst. Direct rupture has the greatest clinical consequences which include anaphylaxis, dissemination of hydatid disease (secondary hydatosis) within the host, and bacterial infection of the pericyst cavity. The clinical implications of the hydatid disease at different stages are discussed. A plea is made for the development of an international medical hydatid registry employing uniform nomenclature and consistent reporting in order to allow more rational comparisons of different types of management.