The incidence of colonization by enteropathogenic, enterotoxigenic, enteroinvasive, and enterohemorrhagic Escherichia coli (detected by DNA hybridization with specific radiolabeled probes), Salmonella sp., Shigella sp., Campylobacter jejuni, and rotavirus was related to the presence of diarrhea in a cohort of 75 rural infants followed longitudinally during the first year of life. The study was carried out between August 1985 and February 1987 in the village of Lugar Sobre la Tierra Blanca, in the state of Morelos, 180 km southwest of Mexico City. Intestinal colonization by specific enteropathogens was followed with fecal cultures taken every fortnight and every time a child had diarrhea. Pathogens isolated from cultures taken in the 48 hours prior to the initiation of the diarrheal episode were considered to be associated with the disease. Diarrhea was detected in 82% of the children with initial isolation of enterohemorrhagic E. coli and in 64% of the children with enteropathogenic E. coli or Shigella sp. The risk of diarrhea associated with the initial isolation of other pathogens was lower, at 41% for rotavirus and approximately 25% for enterotoxigenic E. coli, Salmonella sp., and C. jejuni. Initial colonization by the enteropathogens studied, whether or not they were associated with diarrhea, prevented disease, but not colonization by the same organism, when the children were reinfected during the first year of life. Enteropathogenic E. coli adherence factor, human or porcine heat-stable enterotoxins, fimbrial colonization factor antigens, and Shiga-like toxins I and II were important pathogenic characteristics related to the presence of diarrhea and to protection against subsequent infection by the same organisms.
Helicobacter pylori is the most abundant bacterium in the gastric epithelium, and its presence has been associated with the risk of developing gastric cancer. As of 15 years ago, no other bacteria were associated with gastric epithelial colonization; but thanks to new methodologies, many other non-H. pylori bacteria have been identified. It is possible that non-H. pylori may have a significant role in the development of gastric cancer. Here, we discuss the specific role of H. pylori as a potential trigger for events that may be conducive to gastric cancer, and consider whether or not the rest of the gastric microbiota represent an additional risk in the development of this disease.
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