This study identified pathogenicity genes in 40 Helicobacter pylori clinical isolates. The cagA, vacA, and iceA genes were detected in 65%, 97.5%, and 97.5% of the isolates, respectively. The cagA, iceA1, and vacAs1a/m1 genes were related to erosive gastritis, whereas the vacAs2/m2 and iceA2 genes were associated with enanthematous gastritis.Helicobacter pylori is considered the major etiologic agent of chronic active gastritis, an essential catalyst in the emergence of peptic ulcer, and a risk factor for the development of gastric cancer (17). Studies indicate that the evolution of the infection depends in part on the expression of specific bacterial pathogenicity genes, such as cagA (cytotoxin-associated gene A), vacA (vacuolating cytotoxin), and iceA (induced by contact with epithelium) (2).The cagA gene is considered to be a marker for the presence of a cagA pathogenicity island (8). The cagA-positive H. pylori strains increase interleukin-8 production and gastric inflammation (5). The vacA gene encodes a vacuolating cytotoxin able to induce the formation of cytoplasmic vacuoles in epithelial cells (11). This gene comprises two variable regions: the signal region, with two alleles, s1 (subtypes s1a, s1b, and s1c) and s2, and the middle region, with the alleles m1 and m2 (3, 28). In general, the s1/m1 strains produce large amounts of vacuolating cytotoxin, the s1/m2 strains produce moderate amounts, and the s2/m2 strains produce little or none (3). The iceA gene has two alleles: iceA1 and iceA2. The iceA1 allele is associated with peptic ulcer, and iceA2 is related to asymptomatic gastritis (24,29).This study analyzed the presence of cagA, vacA, and iceA genes in clinical isolates and correlated these findings with the endoscopic diagnosis. Forty isolates of H. pylori were obtained from biopsy specimens of the gastric antrum collected from dyspeptic patients admitted to the upper gastrointestinal endoscopic ward in the Hospital of the Federal University of Rio Grande, Rio Grande do Sul, Brazil. This study was approved by the ethics committee of our university. Informed consent was obtained from all patients.After collection, the biopsy specimens were kept in brain heart infusion broth (Acumedia, United States) with 20% glycerol and refrigerated (4 to 8°C) for a maximum of 4 h (22). This broth was thereafter vortexed, and 200 l was added to medium Columbia agar (Oxoid, United Kingdom), supplemented with 7% sheep blood and with a selective mixture for Helicobacter species isolation (Cefar, Brazil). The agar plates were incubated under microaerophilic conditions (5 to 15% O 2 and 10% CO 2 ) at 37°C for 4 to 10 days (14). The identification of H. pylori was performed using catalase, oxidase, and urease tests, microscopy, and ureA gene detection (12,19).The DNA extraction was performed after 48 h of bacterial growth. Colonies were collected and resuspended in 500 l of 1ϫ TE buffer. The suspension was centrifuged at 10,000 ϫ g for 5 min, and the supernatant was thereafter discarded. The DNA from the clinical isolat...