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Experiments were performed on five batches of WiStar inbred rats with Walker-256 carcinosarcoma receiving sole treatment photodynamic therapy (PDT), irradiated endotoxin (R-LPS), native-endotoxin (N-LPS) or associated therapy (PDT+ R-LPS) and the control batch (saline) consisted of animals with untreated Walker-256 tumours.The results were as follows: the sole treatment (PDT, R-LPS, N-LPS) gave survival rates between 56.3 and 60.7% and cure rates ranging from 32.1 to 37.5%. The "combined" therapy in multiple doses increased significantly (88.6%) the survival rate of tumour bearing rats as well as the highest incidence of complete tumour regression (7 1 .4%). Cell mediated immunity test values in batch-N exposed to multiple doses of PDT+R-LPS showed higher values as compared to the values noticed in batches I-ill and the control batch-V.Summing up, this work demonstrates that "combined" photodynamic and immunotherapy with irradiated endotoxin stimulates cell-mediated antitumoral activity, induces changes in the tumoral incidence in Walker-256 carcmosarcoma in the rat model.

Enterohemorrhagic Escherichiu coli strains have been associated with hemorrhagic colitis and hemolytic uremic syndrome as well as with sporadic cases of gastrointestinal illness in the United States, Canada, England, and Japan.' By contrast to the situation regarding enteropathogenic and enterohemorrhagic E. coli strains in human and animal models? relatively little information is available on infection with enterohemorrhagic E. coli 0157 : H7 in humans and animals with diabetes mellitus.In this study we investigated the colonizing ability as well as the association of E. coli 0157 : H7 with epithelial cells of the intestinal tract in alloxan-induced diabetes mellitus in young rats and controls.Diabetic and nondiabetic rats infected with E. coli 0157 : H7 were evaluated using three experimental parameters: (1) colonization of the intestinal tract; (2) location of bacteria on enterocyte cells by two methods: (a) plate count of bacteria localized on epithelial cells and (b) association of (3H) thymidine-labeled bacteria on enterocyte cells; and (3) histopathologic observations.The severity of experimental bacterial infection in these experiments with E. coli 0157 : H7 in young rats with diabetes mellitus was characterized by: (1) higher susceptibility to oral infection with E. coli 0157 : H7 in diabetic than in nondiabetic rats; (2) E. coli-colonizing values in the range of lo6-lo7 CFUlg of feces; (3) maximum colonization values in the distal ileum, cecum, and proximal colon; (4) colonization values 100-1,OOO times lower in the controls than in the test lot; (5) association of ()H)-TdR-E. coli 0157 : H7 cells with enterocyte and colonocyte cells in 27.2% of diabetic rats by contrast with only 8.34% of control rats; and (6) the finding that the main histopathologic changes, namely, enterohemorrhagic colitis (FIG. 1) and corticotubular necrosis in kidneys (FIG. 2), were presumably induced by Shiga-like toxins.In the pathogenic factors specific to enterohemorrhagic E. coli 0157 : H7 strains (verocytotoxins, Shiga-like toxins, and plasmid 60 M D~) , ' V~.~ we emphasized the 310 DIMA et al.: SUSCEPTIBILITY TO ENTEROHEMORRHAGIC E. COLI 311 FIGURE 1. Proximal colon. Note the ulcerations of the colonic mucosa and the cell exfoliations in the lumen and leukocytes. Hematoxylin-eosin stain; magnification x 194. 312 ANNALS NEW YORK ACADEMY OF SCIENCES FIGURE 2. Kidneys with severe glomerular lesions. Note the disaggregation of some portions and granular content in the capsular cavity and the severe tubular ulcerative lesions and desquamations. Hematoxylin-eosin stain; magnification x 388.metabolic and immunologic status of animals with diabetes mellit~s,~ which is responsible for the severe evolution of bacterial infection with E. coli 0157 : H7.Summing up, these results demonstrate that young diabetic rats were more susceptible to enterohemorrhagic E. coli 0157 : H7 than were normal rats.