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OBJECTIVE: Helicobacter pylori (H. pylori) is a recognized pathogen, but it may also have a protective effect for gastroesophageal reflux disease (GERD). We compared the prevalence of potential virulence factors (cagA, cagE, vacA genotypes) in GERD to other upper gastrointestinal diseases and controls. METHODS: A total of 405 patients underwent gastroscopy with H. pylori isolation and serum testing. Patient diagnostic subgroups were prospectively defined. Genotypes were determined by amplification using polymerase chain reaction. CagA antibodies were determined by western blot, enzyme-linked immunosorbent, and flow microsphere immunofluorescent assays. RESULTS: Patients were grouped as follows: nonulcer dyspepsia (26%), GERD (20%), gastric ulcer (17%), duodenal ulcer (12%), gastric cancer (6%), or controls (19%). The cagA gene was present in 94–97% of subjects in all categories, but the cagA antibody was less prevalent in nonulcer dyspepsia (69%, 95% CI: 48–86%, p = 0.02) and GERD (69%, CI: 39–91%, p CONCLUSIONS: The cagE and vacA S1 genotypes are more prevalent in patients with peptic ulcer or gastric cancer, suggesting a potential function in virulence for these genes. However, the vacA S1 genotype was also more prevalent in controls than GERD, suggesting a potential protective effect against GERD.

The in-vitro activities of omeprazole and three antimicrobial agents against 89 clinical isolates of Helicobacter pylori from a population with duodenal ulcer disease were determined by an agar dilution method. Resistance rates were 20% for metronidazole (MIC > 8 mg/L), 1% for clarithromycin (MIC > 2 mg/L) and zero for ampicillin (MIC > 8 mg/L). Omeprazole was relatively active against H. pylori in vitro (MIC < or = 8 mg/L).

It has long been suspected that Canadian Inuit children suffer from frequent severe lower respiratory tract infections (LRTIs), but the causes and risk factors have not been documented. This study assessed the infectious causes and other epidemiologic factors that may contribute to the severity of LRTI in young Inuit children on Baffin Island.A prospective case study was carried out at the Baffin Regional Hospital in Iqaluit, Nunavut, of infants less than 6 months of age, who were admitted to hospital between October 1997 and June 1998 with a diagnosis of LRTI. Immunofluorescent antibody testing was used to identify respiratory viruses, and enzyme immunoassay (EIA) and polymerase chain reaction (PCR) were used to test for Chlamydia trachomatis. Demographic and risk factor data were obtained through a questionnaire.The annualized incidence rate of admission to hospital for bronchiolitis at Baffin Regional Hospital was 484 per 1000 infants who were less than 6 months of age; 12% of the infants were intubated. Probable pathogens were identified for 18 of the 27 cases considered in our study. A single agent was identified for 14 infants: 8 had respiratory syncytial virus, 2 adenovirus, 1 rhinovirus, 1 influenza A, 1 parainfluenza 3 and 1 had cytomegalovirus. For 4 infants, 2 infectious agents were identified: these were enterovirus and Bordetella pertussis, adenovirus and enterovirus, cytomegalovirus and respiratory syncytial virus, and respiratory syncytial virus and adenovirus. C. trachomatis was not identified by either EIA or PCR. All infants were exposed to maternal smoking in utero, second-hand smoke at home and generally lived in crowded conditions.Inuit infants in the Baffin Region suffer from an extremely high rate of hospital admissions for LRTI. The high frequency and severity of these infections calls for serious public health attention.

To determine whether omeprazole eradicates Helicobacter pylori infection of the gastric antrum, six adolescents and one adult with H. pylori colonization of the antrum were entered into a clinical, open trial of medical therapy. Histologic evidence of antral gastritis and three complementary methods to document H. pylori colonization of the stomach (silver stain, urease testing, and culture of antrum) were obtained before and after an 8-week course of omeprazole. In vitro susceptibility to omeprazole and restriction endonuclease analysis were performed on H. pylori isolates obtained from patients before and after omeprazole therapy. Each of the seven patients treated with omeprazole had continued active inflammation in the antrum and one or more features indicative of persisting H. pylori colonization. Minimum inhibitory concentrations and DNA fingerprints of H. pylori isolated after therapy were identical to those of the pre-treatment bacterial isolates in each of the four subjects examined. We conclude that omeprazole therapy alone did not eradicate H. pylori infection of the human antrum. Continued bacterial colonization was not related to either acquired bacterial resistance to the drug or reinfection of the stomach with a different H. pylori strain.

Host hypoferremic responses occur during infection with Trypanosoma cruzi, presumably through the transfer of iron to the sites of intracellular parasite replication. Depletion of host intracellular iron stores reduces parasite pathogenicity. It has therefore been hypothesized that T. cruzi requires iron for optimal growth in host cells and that, unlike extracellular pathogens, T. cruzi may benefit from host hypoferremic responses. These hypotheses were examined by the in vitro infection of peritoneal macrophages with T. cruzi. Various doses of desferrioxamine or referrated desferrioxamine were added to the culture medium, and parasite growth was monitored. The influence of treatment on uninfected macrophage morphology, function, and iron content was also verified. Desferrioxamine reduced the rate of amastigote replication in a dose-dependent fashion, whereas referrated desferrioxamine did not. The iron content of desferrioxamine-treated macrophages was decreased by 55% without provoking significant morphological or functional changes. Thus, amastigotes used host cell iron stores for optimal growth, and desferrioxamine reduced growth by depleting host cell iron. Hence, it was suggested that depletion of host intracellular iron stores may protect against T. cruzi and, furthermore, that host responses which transfer iron to the intracellular sites of T. cruzi replication may enhance parasite pathogenicity.

The in vitro activities of omeprazole and eight antimicrobial agents against 18 clinical strains of Helicobacter pylori isolated from a pediatric population were determined by an agar dilution method. Ampicillin and erythromycin were the most active agents in vitro. All strains were susceptible to azithromycin, ciprofloxacin, doxycycline, metronidazole, and tinidazole. One isolate demonstrated resistance to cefixime (MIC, greater than or equal to 4 micrograms/ml). H. pylori was inhibited by the proton pump inhibitor omeprazole.