More than 60% of episodes of symptomatic URI among young children were complicated by AOM and/or OME. Young age and specific virus types were predictors of URI complicated by AOM. For young children, the strategy to prevent OM should involve prevention of viral URI. The strategy may be more effective if the priority is given to development of means to prevent URI associated with adenovirus and respiratory syncytial virus.

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Competitive interactions between bacteria differ by number and species present; thus, vaccination and treatment strategies may alter nasopharyngeal flora and disease susceptibility.

Helicobacter pylori infection is associated with altered gastric epithelial cell turnover. To evaluate the role of oxidative stress in cell death, gastric epithelial cells were exposed to various strains of H. pylori, inflammatory cytokines, and hydrogen peroxide in the absence or presence of antioxidant agents. Increased intracellular reactive oxygen species (ROS) were detected using a redox-sensitive fluorescent dye, a cytochrome c reduction assay, and measurements of glutathione. Apoptosis was evaluated by detecting DNA fragmentation and caspase activation. Infection with H. pylori or exposure of epithelial cells to hydrogen peroxide resulted in apoptosis and a dose-dependent increase in ROS generation that was enhanced by pretreatment with inflammatory cytokines. Basal levels of ROS were greater in epithelial cells isolated from gastric mucosal biopsy specimens from H. pylori-infected subjects than in cells from uninfected individuals. H. pylori strains bearing the cag pathogenicity island (PAI) induced higher levels of intracellular oxygen metabolites than isogenic cag PAI-deficient mutants. H. pylori infection and hydrogen peroxide exposure resulted in similar patterns of caspase 3 and 8 activation. Antioxidants inhibited both ROS generation and DNA fragmentation by H. pylori. These results indicate that bacterial factors and the host inflammatory response confer oxidative stress to the gastric epithelium during H. pylori infection that may lead to apoptosis.Helicobacter pylori infection has been implicated in the pathogenesis of gastritis, peptic ulcer disease, gastric carcinoma, and gastric lymphoma (10, 18), but the mechanisms leading from chronic active gastritis to other disease manifestations remain unclear. Various bacterial factors as well as the host response are believed to contribute to the outcome of infection with H. pylori (25). Strains bearing the cag pathogenicity island (PAI) (15), which includes the cagA gene, have been shown to be associated with increased gastric inflammation (57), increased bacterial load, and both peptic ulcer disease and gastric cancer (11). Increased induction of gastric epithelial cytokines that recruit and activate immune/inflammatory cells is also observed with these strains (17,41,55,67). Although the full functions of genes included in the cag PAI remain unclear, it is known that cag PAI-positive strains activate specific transcription factors and cell signaling pathways (37,41,52,55,66).Bacterial and host factors can damage the gastric mucosal barrier and lead to alterations of epithelial cell growth and differentiation. H. pylori infection is associated with increased cellular proliferation in vivo (13, 43) although most in vitro studies demonstrate bacterial inhibition of cell growth (76), suggesting that factors other than H. pylori regulate cell growth in the complex milieu of the infected gastric mucosa. Increased numbers of apoptotic cells are found in the gastric epithelium of infected patients (36,45,50,58), suggesting that induction of apoptosis may b...

Infants and young children are prone to developing upper respiratory tract infections, which often result in bacterial complications such as acute otitis media and sinusitis. We evaluated 623 upper respiratory tract infection episodes in 112 children (6-35 months of age) to determine the proportion of upper respiratory tract infection episodes that result in acute otitis media or sinusitis. Of all upper respiratory tract infections, 30% were complicated by acute otitis media and 8% were complicated by sinusitis. The rate of acute otitis media after upper respiratory tract infection declined with increasing age, whereas the rate of sinusitis after upper respiratory tract infection peaked in the second year of life. Risk for acute otitis media may be reduced substantially by avoiding frequent exposure to respiratory viruses (eg, avoidance of day care attendance) in the first year of life.