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Title: Tetracycline Resistance in Helicobacter Pylori Requires Multiple Mutations

URL: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=R
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Antimicrob Agents Chemother 2002;46(12):3940-3946. "Emergence of Tetracycline Resistance in Helicobacter pylori: Multiple Mutational Changes in 16S Ribosomal DNA and Other Genetic Loci."
12/02/2002 11:00:48 AM
By Robert Short

Multiple mutations are needed to produce tetracycline resistance in [Helicobacter pylori. This is probably why such resistance is rare. These were the conclusions of Dr. D. Dailidiene, at the Department of Molecular Microbiology and Genetics, Washington University Medical School, St Louis, Missouri, United States, and colleagues. The researchers based their beliefs on the results of studying six tetracycline-resistant strains of H. pylori among 159 clinical isolates from El Salvador, Lithuania, and India. They found that tetracycline resistance in H. pylori results from an accumulation of changes that may affect tetracycline-ribosome affinity and/or other functions. The authors suggest that these other functions affected may include perhaps the porin or efflux pumps. Said Dr Dailidiene, "We suggest that the rarity of tetracycline resistance among clinical isolates reflects this need for multiple mutations and perhaps also the deleterious effects of such mutations on fitness." The investigators postulate that equivalent mutations with small but additive effects could contribute to traits such as host specificity and virulence and to the large genetic diversity seen in H. pylori. Five out of six tetracycline-resistant isolates contained one or two nucleotide substitutions in one part of the primary tetracycline binding site in 16S rRNA (AGA(965-967) [Escherichia coli coordinates] changed to gGA, AGc, guA or gGc. (The lowercase letters indicate the base changes). The sixth tetracycline-resistant isolate (isolate Ind75) retained AGA (965-967). Polymerase chain reaction products containing mutant 16S ribosomal-DNA alleles transformed recipient strains to tetracycline-resistant phenotypes. However, transformants containing alleles with single substitutions were less resistant than their tetracycline-resistant parents. Each of 10 tetracycline resistant mutants of reference strain 26695 ( in which mutations were induced with metronidazole, a mutagenic anti-H. pylori agent) contained the normal AGA(965-967) sequence. Transformant derivatives of Ind75 and one of the tetracycline resistant 26695 mutants that had acquired mutant ribosomal-DNA alleles were resistant to tetracycline at levels higher than those to which either parent strain was resistant.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=R
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