DESPITE the number of experimental and clinical studies directed toward an understanding of acute cholecystitis, there are many problems concerned with its etiology that remain unresolved. The experimental approaches to the production of acute cholecystitis are numerous and vary according to the concept of disease. Initially investigators emphasized the role of infection and stasis, although clinical observations indicated that the morphologic change in the gall-bladder wall was not characteristic of the change provoked by bacterial infection and that stasis in the absence of obstruction produced no harm. Cultures of the gall-bladder contents as well as of the wall showed a relatively low incidence of positive results in early phases of acute cholecystitis.1 The infrequency of the disease in children, its common association with stone, the infrequency of its association with suppurative disease involving the portal system, its relation to habitus, to obesity, to sex—these and many other clinical observations