Pathology

A basic prerequisite for infection by enteric pathogens is attachment to the intestinal lining by the pathogenic microorganism. The mechanism of the attachment varies from a highly specific receptor-ligand interaction, as seen for enterotoxigenic E. coli, to a nonspecific type of attachment, as is seen for the protozoan Giardia, which possess sucking disks for intestinal adherence. Variable degrees of intestinal damage can be seen in enteric infection. No anatomic or structural alterations are found in infection by enterotoxigenic E. coli or V. cholerae, where intestinal secretion and watery diarrhea occur secondary to cyclic nucleotide stimulation.

In shigellosis and campylobacteriosis, extensive inflammation with microabscess formation is seen. Small bowel pathogens (rotavirus, Norwalk viruses, and Giardia) may lead to depletions of intestinal disaccharidases and lactose (milk) intolerance. Malnutrition, which is common in areas where diarrhea is highly endemic, leads to a more prolonged disease of greater severity, although malnutrition does not predispose to the occurrence of diarrhea.

The synergy between the effects of malnutrition and diarrhea is an important reason why death from diarrhea is so common in Third World countries. Diarrheal illnesses have adverse effects on growth and contribute to malnutrition. There is a 20 to 60 percent decrease in body caloric intake during a bout of diarrhea. Ways in which malnutrition contributes to more severe or prolonged diarrhea may include decreased gastric acidity, impaired intestinal immunity, greater exposure to a contaminated environ-

ment, delayed recovery of intestinal mucosa, and persistent lactase deficiency. The agents producing the greatest frequency of dehydration are V. choieras, enterotoxigenic E. coli, and rotavirus. Rotavirus is the major cause of death in infants with diarrhea.

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