tion by villus tip cells, resulting in loss of electrolyte-rich fluid, which appears clinically as watery diarrhea.
E. coli heat-stable toxin is a small polypeptide that activates guanylate cyclase activity, leading to an accumulation of cyclic GMP. This alters the enterocyte membrane function, resulting in net secretion and diarrhea.
Enterotoxigenic E. coli have accessory virulence properties in addition to LT or ST that are important factors in their ability to cause disease. The best-characterized accessory virulence properties are colonization factors that allow the E. coli to adhere to specific receptors on enterocytes of the proximal small intestinal mucosa. These colonization factors have been identified as fimbriae found on the surface of bacteria. There are at least three distinct types of adhesion fimbriae detected in enterotoxigenic E. coli of human origin, including colonization factor antigen (CFA) I, CFA II, and E8775 fimbriae. Several other fimbriae that may serve as colonization factors of E. coli also have been described.
Persons with illness caused by enterotoxigenic E. coli develop both serum and intestinal secretory IgA (SIgA) antibody responses to the homologous O antigen. The serum antibody against the O antigen is predominantly in the IgM class and peaks approximately 10 days after the onset of illness. In addition, persons who have diarrhea due to LT-producing strains of E. coli manifest significant rises in serum antitoxin. Increases in the level of secretory IgA antitoxin in intestinal fluid also have been detected after infection with LT-producing E. coli. Persons infected and ill with E. coli that produce only ST do not appear to develop neutralizing or binding antitoxin to ST. After infection with strains producing colonization factor antigens, rises in serum IgG and intestinal secretory IgA antibodies have been demonstrated (Levine et al., 1983).
Enterotoxigenic E. coli have been shown to cause diarrhea worldwide, but seem to be far more common as a cause of diarrhea in developing countries (Dupont, 1982).
The disease burden estimates for enterotoxigenic E. coli assuming the current level of intervention are shown in Table D-2.1. Table D-2.2 shows the disease burden estimates based on a scenario in which oral rehydration therapy prevents 50 percent of enterotoxigenic E. coli