Diarrhea, Acute

Figure 73.1. Electron photomicrograph of <italic>Vibrio cholerae</bold>.

Figure 73.3. Model of cholera toxin showing the five binding subunits surrounding a single active (<italic>A</bold>) subunit.

Clostridial diseases. Clostridia in the vegetative form inhabit the gastrointestinal tract of humans and animals. Spores pass in the feces, contaminate soil and plant materials, and are ingested or enter sites of penetrating wounds. Under anaerobic conditions they revert to vegetative forms. Plasmids in the vegetative forms elaborate toxins that cause several clostridial diseases. Food poisoning and necrotizing enteritis. Meat dishes left to cool at room temperature grow large numbers of cl...

<bold>FIGURE 16-2</bold> <bold>The pathogenesis of cholera and enterotoxigenic <i>Escherichia coli</i> (ETEC) infections.</bold> The organisms colonize the mucosal surface via microbial adhesins—for example, colonization factor antigen (Cfa) of enterotoxigenic <i>E. coli.</i> The factor that binds <i>V. cholerae</i> to cells is not clearly defined, but a toxin coregulated pilus (Tcp) causes the organisms to adhere to one another and form mic...

<bold>FIGURE 16-3</bold> <bold>The pathogenesis of enteropathogenic <i>Escherichia coli</i> (EPEC).</bold> First, the organism attaches to the small bowel epithelial cell via a bundle-forming pilus (BfpA). Subsequently, a type III secretion system bridges to the cell and delivers a membrane receptor protein, Tir, and other effectors to the host cell. In a third stage, intimin on the bacterial surface mediates intimate adherence to the cell by binding to the newly d...

<bold><italic>Figure 15-20</bold> Mechanisms of bacterial enterocolitis.</bold> Diarrhea can be caused by (<bold>A</bold>) bacterial toxin formed in food before ingestion, (<bold>B</bold>) toxin formed in the intestinal tract after infection, or (<bold>C</bold>) direct invasion of infective organisms in the bowel wall.