BACKGROUND:The effectiveness of Helicobacter pylori eradication regimens is influenced by antibiotic susceptibility of infecting strains. Data concerning antibiotic resistance in children are limited. We report the evolution of primary and secondary resistance in a series of Belgian children during the last 12 years. PATIENTS AND METHODS:From 1989 through 2000, H. pylori gastritis was diagnosed in 569 children, and antibiotic susceptibility tests were performed in 555. Eradication, using different schemes, failed in 128 of 457 treated children. After eradication failure antibiotic susceptibility determination was performed in 87 of 128. Comparison of antibiotic susceptibility of strains isolated from the gastric body and from the antrum was performed in 238 samples. RESULTS:Resistance to amoxicillin was not observed. The rate of primary resistance to nitroimidazole derivatives was 18.0% (101 of 555) and remained constant throughout this period, whereas primary resistance to macrolides increased from an average of 6.0% (range, 0 to 10%) before 1995 to 16.6% (range, 10 to 25%, P < 0.001) thereafter. Antibiotic consumption in Belgium, especially macrolides, did not show important fluctuations during the study period. Secondary resistance developed in 39 of 87 patients (46%). Strains isolated from different gastric locations show identical susceptibility testing in all but 5 of 238. CONCLUSIONS:Resistance of H. pylori to macrolides increased in our pediatric population which did not appear to correlate with macrolides prescription habits in our country. After eradication failure acquired secondary resistance was observed in one-half of the patients.

Incidence ofGI side effects inGroup 1versus Group 2 tonly G1 side effects significantly decreased; *p<0.05anti-HP therapy.Therefore

33 Efficacy of Helicobacter pylori (HP) eradication treatment is influenced by the primary resistance rate of the infecting strains. In a previous study over a 9-year period, we found 119/401 (30 %) strains resistant to at least one antibiotic before any treatment, steadily increasing in the last 4 years. Although the treatment regimen can be adapted to the results of the antibiogram, failure of eradication can be due to secondary resistance acquired during treatment. Aim: to evaluate the effect of secondary resistance on the eradication rate of HP strains in children. Methods: through 1993-97, in a series of 294 children (mean age 12.5 ± 5.3 years) with HP gastritis, 244 children were treated with several combinations of antibiotics according to the indications of an antibiogram and the efficacy of the treatment duly checked with the non invasive 13C-urea breath test. A second endoscopy with biopsies for culture and antibiogram was proposed before commencing a second treatment. Results: follow-up was not available in 24/244 (10%) children; among the 220 others 140/220 (64%) were cured and 80/220 (36%) remained infected. From these 80 children, HP strains could be isolated and cultured in 55 out of the 58 who underwent a second endoscopy. Resistance to at least one antibiotic was found in 34/55 (62%) HP strains. In 30/55 (54%) the antibiogram remained unchanged whereas in 4/55, the primary resistance was no more detected and, in 21/55 (38%), an acquired resistance against the last antibiotic used was found. Conclusions: 1) following treatment acquired secondary resistance of HP strains is a frequent mechanism that can account for failure of eradication 2) the emerging of a secondary resistance in 38% and the loss of resistance in 8% of HP strains, implies that children can probably be infected with multiple strains bearing different phenotypes.

BACKGROUND:Indirect noninvasive methods, such as the 13C-urea breath test and serology, can be useful for the detection of Helicobacter pylori infection in children. We analyzed retrospectively the diagnostic accuracy of these two methods.PATIENTS AND METHODS:Between September, 1989, and October, 1996, H. pylori status was determined in 139 children by means of culture and histologic study of gastric biopsies. We performed 146 13C-urea breath tests and serologic assays (Cobas core; Roche).RESULTS:H. pylori infection was detected in 91 of 139 (65%) children. The 13C-urea breath test was discordant with H. pylori status in 4 of 146 tests; serology was discordant in 24 and indeterminate in 7 of 146. The 13C-urea breath test was more sensitive than serology (98% vs. 79%, P < 0.01) but comparable in specificity (96% vs. 92%). The serology yielded false negative results more often in children younger than 5 years of age (P < 0.05).CONCLUSIONS:The 13C-urea breath test is more reliable than serology for the detection of active H. pylori infection in children. Below 10 years of age serology is insufficiently sensitive for clinical purposes, whereas the 13C-urea breath test remains a reliable test.

A new automated amplification method, Ligase Chain Reaction (LCx MTB), was evaluated for direct detection of Mycobacterium tuberculosis in respiratory specimens from 208 patients and its performance was compared with culture and direct smears. Out of 226 specimens, 28 LCx MTB and 15 cultures were found positive for M. tuberculosis After resolution of clinical history, the sensitivity of LCx MTB and culture was respectively 89.3% and 53.6% with a specificity of 98.5% and 100%. However, samples coming from untreated patients presented similar results between culture and LCx MTB (sensitivity 75% and 83.3% for culture and LCx MTB).

BXL).Age, gender, body size and weight distributions were similar in the three regions of the country and very close to the data from the National Institute for Statistics.Results: Overall, 28.1% of the population experienced heartburn, at least once a week in 11.3% and daily in 4.1%, with some striking differences between the three regions:

ABSTRACT In 1995, the rate of isolation of Enterobacter aerogenes in the Saint-Pierre University Hospital in Brussels, Belgium, was higher than that in the preceding years. A total of 45 nosocomial E. aerogenes strains were collected from 33 patients of different units during that year, and they were isolated from 19 respiratory specimens, 13 pus specimens, 7 blood specimens, 4 urinary specimens, 1 catheter specimen, and 1 heparin vial. The strains were analyzed to determine their epidemiological relatedness and were characterized by their antibiotic resistance pattern determination, plasmid profiling, and genomic fingerprinting by macrorestriction analysis with pulsed-field gel electrophoresis (PFGE). The majority of the strains (82%) were multiply resistant to different commonly used antibiotics. Two major plasmid profiles were found: most strains (64%) harbored two plasmids of different sizes, whereas the others (20%) contained a single plasmid. PFGE with Spe I and/or Xba I restriction enzymes revealed that a single clone (80%) was responsible for causing infections or colonizations throughout the year, and this result was concordant with those obtained by plasmid profiling, with slight variations. By comparing the results of these three methods, PFGE and plasmid profiling were found to be the techniques best suited for investigating the epidemiological relatedness of E. aerogenes strains, and they are therefore proposed as useful tools for the investigation of nosocomial outbreaks caused by this organism.

Since the recognition of Helicobacter pylori as a pathogen involved in chronic gastritis, peptic ulcers and gastric cancer, many studies have shown that clinical manifestations of H. pylori infection occur only in a minority of infected patients. Studies of the genomic diversity of this bacterium show relations of some bacterial characteristics with pathology. Imbalanced host response to infection may also play a major role in the clinical expression of H. pylori infection. Gastric epithelial cells are involved in the process, as well as lymphocytes and other immune cells of the underlying gastric tissue. A better understanding of the immunopathogenesis of H. pylori infection is required to understand the exact role of both the strain and the host.