Furazolidone- and Nitrofurantoin-Resistant
            <i>Helicobacter pylori</i>
            : Prevalence and Role of Genes Involved in Metronidazole Resistance

Kwon, Dong H.; Lee, Mi-Ae; Kim, J. J.; Kim, J. G.; El-Zaatari, F. A. K.; Osato, Michael S.; Graham, David Y.

doi:10.1128/aac.45.1.306-308.2001

Cited by 52 publications

(47 citation statements)

References 19 publications

(23 reference statements)

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“…For example, it is likely that the [2Fe-2S]ferredoxin, which is expressed at levels similar to those of the 2[4Fe-4S]ferredoxin (unpublished data), is also a source of electrons to reduce nitro groups of antigiardial drugs (28,51,57,90). It is possible that the transfer of electrons from ferredoxin to metronidazole and furazolidone is catalyzed by oxygen-insensitive nitroreductases in giardia organisms, as has been described for H. pylori and E. coli, respectively (30,46,90,94). It remains to be determined whether the ferredoxin-nitroreductase, which may be an oxygen-sensitive nitroreductase because of the iron-sulfur group, is also involved in the reduction of nitro groups and the activation of drugs against giardia organisms, amebae, and clostridia.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Evidence for Lateral Transfer of Genes Encoding Ferredoxins, Nitroreductases, NADH Oxidase, and Alcohol Dehydrogenase 3 from Anaerobic Prokaryotes to Giardia lamblia and Entamoeba histolytica

et al. 2002

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Giardia lamblia and Entamoeba histolytica are amitochondriate, microaerophilic protists which use fermentation enzymes like those of bacteria to survive anaerobic conditions within the intestinal lumen. Genes encoding fermentation enzymes and related electron transport peptides (e.g., ferredoxins) in giardia organisms and amebae are hypothesized to be derived from either an ancient anaerobic eukaryote (amitochondriate fossil hypothesis), a mitochondrial endosymbiont (hydrogen hypothesis), or anaerobic bacteria (lateral transfer hypothesis). The goals here were to complete the molecular characterization of giardial and amebic fermentation enzymes and to determine the origins of the genes encoding them, when possible. A putative giardia [2Fe-2S]ferredoxin which had a hypothetical organelle-targeting sequence at its N terminus showed similarity to mitochondrial ferredoxins and the hydrogenosomal ferredoxin of Trichomonas vaginalis (another luminal protist). However, phylogenetic trees were star shaped, with weak bootstrap support, so we were unable to confirm or rule out the endosymbiotic origin of the giardia [2Fe-2S]ferredoxin gene. Putative giardial and amebic 6-kDa ferredoxins, ferredoxin-nitroreductase fusion proteins, and oxygen-insensitive nitroreductases each tentatively supported the lateral transfer hypothesis. Although there were not enough sequences to perform meaningful phylogenetic analyses, the unique common occurrence of these peptides and enzymes in giardia organisms, amebae, and the few anaerobic prokaryotes suggests the possibility of lateral transfer. In contrast, there was more robust phylogenetic evidence for the lateral transfer of G. lamblia genes encoding an NADH oxidase from a gram-positive coccus and a microbial group 3 alcohol dehydrogenase from thermoanaerobic prokaryotes. In further support of lateral transfer, the G. lamblia NADH oxidase and adh3 genes appeared to have an evolutionary history distinct from those of E. histolytica.

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Section: Discussionmentioning

confidence: 99%

“…Furazolidone-resistant giardia or-ganisms have also been selected in vitro, but the mechanism of resistance has not been characterized (87). It is not known whether giardia organisms have nitroreductases which enzymatically activate metronidazole and furazolidone, as described for Helicobacter pylori and Escherichia coli, respectively (30,41,46,94).…”

mentioning

confidence: 99%

Evidence for Lateral Transfer of Genes Encoding Ferredoxins, Nitroreductases, NADH Oxidase, and Alcohol Dehydrogenase 3 from Anaerobic Prokaryotes to Giardia lamblia and Entamoeba histolytica

et al. 2002

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“…This antibiotic has demonstrated a high antimicrobial activity against H pylori if given as a single drug [175] , and the majority of first-line furazolidone-based combination therapies revealed eradication rates above 80% [92] . Primary resistance to furazolidone is virtually absent [158,176,177] , and its potential to develop resistance is as low as for bismuth compounds or amoxicillin [178] . Moreover, this drug has no cross-resistance potential to metronidazole [176] .…”

Section: Furazolidone-based Rescue Regimensmentioning

confidence: 99%

“Rescue” regimens after Helicobacter pylori treatment failure

Gisbert¹

2008

WJG

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Helicobacter pylori (H pylori ) infection is the main cause of gastritis, gastroduodenal ulcer disease, and gastric cancer. After more than 20 years of experience in H pylori treatment, in my opinion, the ideal regimen to treat this infection is still to be found. Currently, apart from having to know first-line eradication regimens well, we must also be prepared to face treatment failures. Therefore, in designing a treatment strategy we should not focus on the results of primary therapy alone, but also on the final (overall) eradication rate. The choice of a "rescue" treatment depends on which treatment is used initially. If a clarithromycinbased regimen was used initially, a subsequent metronidazole-based treatment (quadruple therapy) may be used afterwards, and then a levofloxacinbased combination would be a third "rescue" option. Alternatively, it has recently been suggested that levofloxacin-based rescue therapy constitutes an encouraging second-line strategy, representing an alternative to quadruple therapy in patients with previous PPI-clarithromycin-amoxicillin failure, with the advantage of efficacy, simplicity and safety. In this case, a quadruple regimen may be reserved as a third-line rescue option. Finally, rifabutin-based rescue therapy constitutes an encouraging empirical fourthline strategy after multiple previous eradication failures with key antibiotics such as amoxicillin, clarithromycin, metronidazole, tetracycline, and levofloxacin. Even after two consecutive failures, several studies have demonstrated that H pylori eradication can finally be achieved in almost all patients if several rescue therapies are consecutively given. Therefore, the attitude in H pylori eradication therapy failure, even after two or more unsuccessful attempts, should be to fight and not to surrender.

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“…Strains resistant to furazolidone are rare and have no cross-resistance to metronidazole [18] . Furthermore, its potential to develop resistance is low [19] .…”

Section: Discussionmentioning

confidence: 99%

Furazolidone, amoxicillin, bismuth and rabeprazole quadruple rescue therapy for the eradication of Helicobacter pylori

Cheng

Hu²

2009

WJG

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AIM:To compare the efficacy and side effect profiles of three furazolidone and amoxicillin-based quadruple rescue therapies for the eradication of Helicobacter pylori (H pylori ). METHODS:Patients who failed in the H pylori eradication therapy for at least one course were randomly allocated into three groups. Group A received rebaprazole 10 mg + amoxicillin 1 g + furazolidone 100 mg, and bismuth subcitrate 220 mg, twice daily for 1 wk; group B received the same regimen of group A but for 2 wk; and group C received the same regimen of group B, but furazolidone was replaced by furazolidone 100 mg three times daily. To record the side effect profiles at the end of the treatment, H pylori eradication was assessed with 13 C-urea breath test 4 wk after therapy. RESULTS:Sixty patients were enrolled including 28 males, and 20 patients in each group. The average age of the patients was 49.2 years, ranging from 18 to 84 years. H pylori eradication rates with per-protocol analysis were 82%, 89% and 90% in the three groups, respectively. Side effects were found in 11 patients, including mild dizziness, nausea, diarrhea and increased bowel movement. None of the 11 patients needed treatment for their side effects. CONCLUSION:One-or two-week furazolidone and amoxicillin-based quadruple rescue therapy with a low dose furazolidone (100 mg bid ) for the eradication of H pylori is effective. Extending the antibiotic course to 14 d could improve the eradication rates.

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Furazolidone- and Nitrofurantoin-Resistant Helicobacter pylori : Prevalence and Role of Genes Involved in Metronidazole Resistance

Cited by 52 publications

References 19 publications

Evidence for Lateral Transfer of Genes Encoding Ferredoxins, Nitroreductases, NADH Oxidase, and Alcohol Dehydrogenase 3 from Anaerobic Prokaryotes to Giardia lamblia and Entamoeba histolytica

Evidence for Lateral Transfer of Genes Encoding Ferredoxins, Nitroreductases, NADH Oxidase, and Alcohol Dehydrogenase 3 from Anaerobic Prokaryotes to Giardia lamblia and Entamoeba histolytica

“Rescue” regimens after Helicobacter pylori treatment failure

Furazolidone, amoxicillin, bismuth and rabeprazole quadruple rescue therapy for the eradication of Helicobacter pylori

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