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Biotype and molecular fingerprints of metronidazole-resistant strains of Helicobacter pylori from antral gastric mucosa

R. J. Owen, G. D. Bell^*, M. Desai, M. Moreno, P. W. Gant, P. H. Jones and D. Linton

National Collection of Type Cultures, Central Public Health Laboratory, 61 Colindale Avenue, London NW9 5HT

^*Department of Medicine, The Ipswich Hospital, Heath Road Wing

Public Health Laboratory, The Ipswich Hospital, Heath Road Wing.

Received February 18, 1992 Revision received April 13, 1992.
Accepted April 13, 1992

Biotypes, ribosomal RNA gene restriction patterns (ribopatterns), whole-cell protein patterns and plasmid profiles of paired Helicobacter pylori isolates from 17 patients were examined. Each pair comprised a pre- and a post-treatment isolate; nine of the 17 post-treatment isolates were obtained after treatment with tripotassium dicitrate bismuthate (DeNol) and metronidazole. All strains of H. pylori had identical biotypes, but exhibited diversity between pairs in their molecular fingerprints. Each of the 17 strain pairs had unique ribopatterns; the pre- and post-treatment isolates in most pairs (16 of 17) were similar or identical, irrespective of metronidazole susceptibility. DNA subtype variants were detected in three patient sets. Although nine post-treatment isolates had acquired resistance to metronidazole, most (six of nine) resembled the pre-treatment isolates in their ribopattern, protein and plasmid profiles. No significant correlation was observed between metronidazole resistance and plasmid content in these H. pylori isolates. Emergence of post-treatment metronidazole-resistant isolates of H. pylori isolates. Emergence of post-treatment metronidazole-resistant isolates of H. pylori was associated only rarely with colonisation by a novel strain or acquisition of a plasmid and, in most patients, probably resulted from spontaneous emergence of resistance in the original infecting strain.

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