To study the virulence of H. Pylon infected native people and the distribution of cagA gene in H. Pylon. Methods: Typing of H. pylori was determined by PCR in 74 clinical isolates by using one primer set for the cagA ...To study the virulence of H. Pylon infected native people and the distribution of cagA gene in H. Pylon. Methods: Typing of H. pylori was determined by PCR in 74 clinical isolates by using one primer set for the cagA gene. The rapid-urease test, histological examinations and ELISA were also employed. Results: Prevalence of cagA gene in H. Pylon isolates was 90. 5%,the positive rate of cagA gene in peptic ulcer patients was 94. 9%, higher than that in chronic gastritis patients (85. 7% ), though the difference was insignificant. BOth type Ⅰ (cagA+ )and type Ⅱ (cagA- )isolates led to chronic inflammation of antrum, though the former caused more severe inflammation than the latter. There was no significant difference in seventy of active gastritis, intestinal metaplasia, atrophy and lymph folliciles. Conclusion: High prevalence of cagA gene in H. Pylon isolates from native patients indicates that cagA gene is common in H.pylori strains, and therefore is not reliable as a single marker for the discrimination of H. pylori strains with respect to a specific disease. However, owing to the high sensitivity and specificity, detecting cagA gene of H. Pylon by PCR may be considered as a helpful method in epidemiologic research.展开更多
文摘To study the virulence of H. Pylon infected native people and the distribution of cagA gene in H. Pylon. Methods: Typing of H. pylori was determined by PCR in 74 clinical isolates by using one primer set for the cagA gene. The rapid-urease test, histological examinations and ELISA were also employed. Results: Prevalence of cagA gene in H. Pylon isolates was 90. 5%,the positive rate of cagA gene in peptic ulcer patients was 94. 9%, higher than that in chronic gastritis patients (85. 7% ), though the difference was insignificant. BOth type Ⅰ (cagA+ )and type Ⅱ (cagA- )isolates led to chronic inflammation of antrum, though the former caused more severe inflammation than the latter. There was no significant difference in seventy of active gastritis, intestinal metaplasia, atrophy and lymph folliciles. Conclusion: High prevalence of cagA gene in H. Pylon isolates from native patients indicates that cagA gene is common in H.pylori strains, and therefore is not reliable as a single marker for the discrimination of H. pylori strains with respect to a specific disease. However, owing to the high sensitivity and specificity, detecting cagA gene of H. Pylon by PCR may be considered as a helpful method in epidemiologic research.
