Although an infection with Entamoeba histolytica is most commonly asymptomatic, the potential for invasive, metastatic disease, coupled with its high prevalence, makes amoebiasis a major health problem throughout much of the world. Most amoebiasis-related mortality stems from extra-intestinal infection. In these cases, trophozoites penetrate the epithelial layer and lamina propria of the bowel mucosa, enter the bloodstream, and then disseminate to almost any organ or tissue, most commonly the liver.The mechanisms that allow tissue penetration are not well understood. Ultrastructural and histopathological studies (reviewed in reference 1) have shown that, during invasion of the bowel wall, trophozoites are seen at the margin of ulcerative lesions adjacent to healthy tissue. Degeneration of epithelial cells adjacent to invading trophozoites and dissolution of the basement membrane of the mucosa have been observed (2-4). These findings suggest that histolytic and proteolytic factors may be elaborated to facilitate mucosal damage and invasion.Two general types of histolytic factors have been proposed: cytotoxic factors which may directly damage cells, such as a secreted "amoebapore" ion channel (5, 6) and proteolytic enzymes, which may attack both cells and extracellular matrix.The virulence ~ of axenically cultured E. histolytica strains has been correlated with the presence of proteolytic enzymes found on the amoeba surface, in secretions, or in extracts of whole trophozoites (9-14). Unfortunately, as none of these proteinases has been purified to homogeneity, important questions remain as to how many are present and how they may contribute to the pathogenesis of amoebiasis.To determine what role secreted proteinases may play in tissue invasion, we assayed the degradation of extracellular matrix by live trophozoites and their secretory products, using an in vitro model of extracellular matrix successfully used to study other invasive parasites (15-18). These studies allowed us to For axenic amoebae in culture, "virulence" is defined in terms of ability to induce lesions in animals (7) or cytopathic effect on cell monolayers (8).

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A protracted outbreak of Escherichia coli O157:H7 infections was caused by consumption of unpasteurized ("raw") milk sold at Oregon grocery stores. Although it never caused a noticeable increase in reported infections, the outbreak was recognized because of routine follow-up interviews. Six of 16 Portland-area cases reported between December 1992 and April 1993 involved people who drank raw milk from dairy A. By pulsed-field gel electrophoresis (PFGE), E. coli O157:H7 isolates from these cases and from the dairy A herd were homologous (initially, 4 of 132 animals were E. coli O157:H7-positive). Despite public warnings, new labeling requirements, and increased monitoring of dairy A, retail sales and dairy-associated infections continued until June 1994 (a total of 14 primary cases). Seven distinguishable PFGE patterns in 3 homology groups were identified among patient and dairy herd E. coli O157:H7 isolates. Without restrictions on distribution, E. coli O157:H7 outbreaks caused by raw milk consumption can continue indefinitely, with infections occurring intermittently and unpredictably.

The investigation identified fresh strawberries as a novel vehicle for E. coli O157:H7 infection, implicated deer feces as the source of contamination, and highlights problems concerning produce contamination by wildlife and regulatory exemptions for locally grown produce. A comprehensive hypothesis-generating questionnaire enabled rapid identification of the implicated product. Good agricultural practices are key barriers to wildlife fecal contamination of produce.

To monitor risk factors for illness, we conducted a case-control study of sporadic Shiga toxin-producing Escherichia coli O157 (STEC O157) infections in 1999-2000. Laboratory-confirmed cases of STEC O157 infection were identified through active laboratory surveillance in all or part of seven states. Patients and age-matched controls were interviewed by telephone using a standard questionnaire. Information was collected on demographics, clinical illness, and exposures to food, water, and animals in the 7 days before the patient's illness onset. During the 12-month study, 283 patients and 534 controls were enrolled. STEC O157 infection was associated with eating pink hamburgers, drinking untreated surface water, and contact with cattle. Eating produce was inversely associated with infection. Direct or indirect contact with cattle waste continues to be a leading identified source of sporadic STEC O157 infections.