Sprague-Dawley rats were infected by intraperitoneal injection with either the cysticerci of Taenia crassiceps or the tetrathyridia of Mesocestoides corti. Both species of metacestodes reproduce asexually in the peritoneal cavity. The effect of T. crassiceps upon the rats was to cause chronic inflammation of the peritoneum, fibrous adhesions between the visceral organs and hyperplasia of the gut mesenteries which became extended into a large sac-like structure. Dead parasites surrounded by white calcareous material were found free in the peritoneum and attached to the inner body wall and viscera. The histopathology of the hyperplastic mesenteries and fibrous membrane is described. The tetrathyridia of M. corti were found free in the peritoneal cavity as well as in the liver (mainly the left liver-lobe), gut mesenteries and in an outgrowth of the connective tissue associated with the pancreas. The connective tissue outgrowth comprised 2 layers; an inner reticular layer and a thickened marginal layer. Metacestodes were found in collagen-fibrin capsules within the connective tissue. A layer of mucopolysaccharide material was interposed between the parasite and the capsule wall. A possible method by which the parasites gain entry into the connective tissue is described. The connective tissues of rats harbouring either M. corti or T. crassiceps had increased numbers of mast cells compared to connective tissues from control rats. Younger mast cells containing biogenic amines predominated in infected tissues whereas older heparin-containing cells dominated control tissues.

The distribution, fixation properties, and protease phenotypes of mast cells populating lesions caused by the metacestode stage of the cestode Mesocestoides corti in the rat were characterized. Intraperitoneal infection with M. corti induced severe granulomatous types of reactions around the pancreas and further lesions in the liver. These sites were infiltrated with mast cells which contained either rat mast cell protease I or II derived respectively from connective tissue (CTMC) or mucosal mast cells (MMC). A proportion of cells in pancreatic granulomas had staining and fixation properties identical to those of intestinal mucosal mast cells; others were typical connective tissue mast cells. Subcutaneous inoculation of parasites was associated with nodular dermal reactions, and all of the infiltrating mast cells had the fixation and staining properties of CTMC and contained RMCPI uniquely. Increased numbers of RMCPII-containing mast cells were present in the intestines of rats infected intraperitoneally. Significant quantities of RMCPII were present in homogenates of pancreatic granulomas and in livers of rats harbouring intraperitoneal infections but none was detected in skin. These findings suggest that mast cells of different phenotypes are selectively recruited to some, but not all, lesions.

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Laboratory rats were infected by intra-peritoneal injection with the metacestodes of Taenia crassiceps. A soluble extract was prepared from the metacestodes removed from the peritoneal cavity of the rats. Doublediffusion, immuno-electrophoresis and fluorescent labelled antibody staining techniques were used. The extract tested against rabbit anti-normal rat serum was found to contain an antigen common to both the host and the parasite.