Susceptibilities to clarithromycin and metronidazole of 444 Helicobacter pylori isolates cultured from antral biopsies of 444 dyspeptic patients were determined by disc diffusion tests (15 mu g disc for clarithromycin, 5 mu g disc for metronidazole). Susceptibility of 46 of these isolates to erythromycin (5 mu g disc) was also tested. Minimal inhibitory concentrations (MICs) of clarithromycin for 42 selected isolates were determined by a plate dilution method. A zone diameter of 30 mm was defined as a 'cut-off' size differentiating susceptibility and resistance of the organism to clarithromycin, by comparing results obtained with the two methods. Of the 444 isolates, 424 (95.5%) were highly sensitive to clarithromycin, with zone diameters ranging from 30 to 98 mm. Twenty isolates (4.5%) were defined as resistant to clarithromycin, with zone diameters ranging between 6 and 28 mm. The incidence of clarithromycin resistance was similar in men and women and in different age groups, and was not significantly different between patients with peptic ulcer and non-ulcer dyspepsia. Among the 444 isolates, 168 (37.8%) were metronidazole resistant. There was cross resistance between clarithromycin and erythromycin, but not between clarithromycin and metronidazole. Stability of clarithromycin resistance was evaluated by the disc diffusion test and confirmed by the plate dilution method. Among the 20 clarithromycin-resistant isolates, nine (45%) reverted to be sensitive after 25 subcultures on drug-free agar. The findings in this study indicate that the incidence of clarithromycin-resistant H. pylori in untreated dyspeptic patients is low. Cross-resistance occurs between macrolides and resistance to clarithromycin in some strains is reversible.

Nitroimidazoles, including metronidazole and tinidazole, have been used in multiple antimicrobial therapy strategies to eradicate Helicobacterpylori in peptic ulcer patients and nonulcer dyspeptic patients (1, 19). However, emergence of primary resistance and acquired resistance to these kind of drugs in H. pyloni may lead to treatment failure (3,7,10,11,21,27). Thus, evaluation of H. pylotn susceptibility to metronidazole before treatment appears to be important. Metronidazole resistance rates from 6.4 to 84% have been reported throughout the world (2,11,13,22

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Cultures of Helicobacter pylori on chocolate agar slants in biou bottles and on chocolate agar plates inside BBL Campy Pouches were mailed from Dublin to Galway, Ireland; Bordeaux, France; and Beijing, China. Both systems maintained viability of H. pylori for at least 4 days under mailing conditions. Ninety percent of the isolates on the slants survived for 6 days, but only 30%o of the isolates in the pouches survived. When the slants were stored at 4°C after arrival, 50%o of the isolates were recoverable 10 days after mailing. Failure of recovery was due to coccoid formation by the organisms. Contamination was not a problem in either system. Chocolate agar slants are considered the more suitable system for transporting H. pylori cultures, especially when transport time longer than 4 days is expected.

regulation of CD44 and ICAM-I expression on gastric epithelial cells by H. pylori. APMIS 103: 744-748, 1995. Interaction between lymphocytes and epithelial cells may play a key role in Helicobacter pylori ( H . pyfori)-associated gastric mucosal inflammation. This interaction process is at least partially mediated by various cell adhesion molecules. The aims of the present study were to assess using flow cytometric analysis whether H. pyfori directly or supernatants from H. pyfori-activated peripheral blood mononuclear cells (PBMC) can affect the expression of adhesion molecules on the gastric epithelial cell line AGS in vitro. The results showed that resting AGS cells expressed CD44 and ICAM-1. Co-culture of AGS with H. pylori or cytokine-rich supernatants from H. pylori-activated PBMC resulted in upregulation of expression of CD44 and ICAM-1 on AGS cells. These data suggest that H. pylori directly and indirectly through inflammatory cytokines may contribute to alternations in adhesion molecule expression on gastric epithelial cells. This may be of pathological significance in H . pyloriassociated gastric mucosal inflammation and carcinogenesis.

Recurrence of Helicobacter pylori infection after successful eradication occurs and is associated with relapse of gastroduodenal diseases. The aims of this paper were to assess the incidence and identify the nature and possible causes of recurrence of the infection. A broad-based Medline search was performed to identify all related publications addressing recurrence of the infection between 1986 and 1995. The 12-month recurrence rate varied among the different studies from 0 to 41.5%. A few studies showed 18- to 24-month recurrence rates, which ranged between 0 and 21.4%. Limited data, obtained using molecular fingerprinting techniques, have shown that in most cases recurrence is due to recrudescence of the original strain; a few cases appear to be due to reinfection with a new strain. Recrudescence is most likely during the first 12 months after apparent eradication. Despite the high sensitivity and specificity of the available individual tests for detecting H. pylori infection in untreated patients, no technique alone is sensitive enough to monitor eradication when the four-week-rule definition for eradication is used. A combination of two or more techniques increases sensitivity. Sensitivity and specificity are increased when biopsies are taken from both gastric antrum and corpus. The best treatments have the lowest recurrence rates and recurrence is rare when the eradication rate is over 90%. Individual susceptibility and reexposure to H. pylori are suggested as two major causes of reinfection.

There has been a significant increase in the prevalence of H. pylori resistance to metronidazole in recent years, while clarithromycin resistance is still relatively rare. In this study we assessed: (1) the effect of primary H. pylori resistance to metronidazole and clarithromycin on the clinical efficacy of a one-week regimen consisting of omeprazole, metronidazole, and clarithromycin; and (2) the rate of acquisition of secondary antimicrobial resistance after treatment failure. Eighty-seven patients with duodenal ulceration or nonulcer dyspepsia were included in the study. The primary metronidazole and clarithromycin resistance rates were 35.6% and 3.4%, respectively (all three pretreatment clarithromycin resistant strains had concurrent metronidazole resistance). H. pylori was eradicated in 81.6% of patients. The eradication rate for fully sensitive isolates was 98.2% (55/56) but was significantly reduced to 57.1% (16/28) for isolates that were resistant to metronidazole alone and 0% (0/3) in cases of dual resistance (P < 0.001). Secondary resistance to clarithromycin was acquired in 58.3% of cases of treatment failure. In areas of high prevalence of primary metronidazole resistance, this is a significant cause of treatment failure with this triple therapy regimen. This leads to the selection of strains with dual resistance that are difficult to eradicate and may contribute to an increase in the prevalence of clarithromycin resistance. In such areas an alternative first-line treatment should be prescribed.