Skip to main content
  • ASM
    • Antimicrobial Agents and Chemotherapy
    • Applied and Environmental Microbiology
    • Clinical Microbiology Reviews
    • Clinical and Vaccine Immunology
    • EcoSal Plus
    • Eukaryotic Cell
    • Infection and Immunity
    • Journal of Bacteriology
    • Journal of Clinical Microbiology
    • Journal of Microbiology & Biology Education
    • Journal of Virology
    • mBio
    • Microbiology and Molecular Biology Reviews
    • Microbiology Resource Announcements
    • Microbiology Spectrum
    • Molecular and Cellular Biology
    • mSphere
    • mSystems
  • Log in
  • My alerts
  • My Cart

Main menu

  • Home
  • Articles
    • Current Issue
    • Accepted Manuscripts
    • COVID-19 Special Collection
    • Archive
    • Minireviews
  • For Authors
    • Submit a Manuscript
    • Scope
    • Editorial Policy
    • Submission, Review, & Publication Processes
    • Organization and Format
    • Errata, Author Corrections, Retractions
    • Illustrations and Tables
    • Nomenclature
    • Abbreviations and Conventions
    • Publication Fees
    • Ethics Resources and Policies
  • About the Journal
    • About AAC
    • Editor in Chief
    • Editorial Board
    • For Reviewers
    • For the Media
    • For Librarians
    • For Advertisers
    • Alerts
    • AAC Podcast
    • RSS
    • FAQ
  • Subscribe
    • Members
    • Institutions
  • ASM
    • Antimicrobial Agents and Chemotherapy
    • Applied and Environmental Microbiology
    • Clinical Microbiology Reviews
    • Clinical and Vaccine Immunology
    • EcoSal Plus
    • Eukaryotic Cell
    • Infection and Immunity
    • Journal of Bacteriology
    • Journal of Clinical Microbiology
    • Journal of Microbiology & Biology Education
    • Journal of Virology
    • mBio
    • Microbiology and Molecular Biology Reviews
    • Microbiology Resource Announcements
    • Microbiology Spectrum
    • Molecular and Cellular Biology
    • mSphere
    • mSystems

User menu

  • Log in
  • My alerts
  • My Cart

Search

  • Advanced search
Antimicrobial Agents and Chemotherapy
publisher-logosite-logo

Advanced Search

  • Home
  • Articles
    • Current Issue
    • Accepted Manuscripts
    • COVID-19 Special Collection
    • Archive
    • Minireviews
  • For Authors
    • Submit a Manuscript
    • Scope
    • Editorial Policy
    • Submission, Review, & Publication Processes
    • Organization and Format
    • Errata, Author Corrections, Retractions
    • Illustrations and Tables
    • Nomenclature
    • Abbreviations and Conventions
    • Publication Fees
    • Ethics Resources and Policies
  • About the Journal
    • About AAC
    • Editor in Chief
    • Editorial Board
    • For Reviewers
    • For the Media
    • For Librarians
    • For Advertisers
    • Alerts
    • AAC Podcast
    • RSS
    • FAQ
  • Subscribe
    • Members
    • Institutions
Mechanisms of Resistance

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

Dong H. Kwon, Miae Lee, J. J. Kim, J. G. Kim, F. A. K. El-Zaatari, M. S. Osato, D. Y. Graham
Dong H. Kwon
Department of Medicine and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Miae Lee
Department of Medicine and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
J. J. Kim
Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
J. G. Kim
Guro Hospital, Korea University, Seoul, Korea
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
F. A. K. El-Zaatari
Department of Medicine and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
M. S. Osato
Department of Medicine and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
D. Y. Graham
Department of Medicine and
Division of Molecular Virology, Baylor College of Medicine and Veterans Affairs Medical Center, Houston, Texas 77030, and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
DOI: 10.1128/AAC.45.1.306-308.2001
  • Article
  • Figures & Data
  • Info & Metrics
  • PDF
Loading

ABSTRACT

The prevalence of furazolidone, nitrofurantoin, and metronidazole resistance among Helicobacter pylori strains was assessed with 431 clinical isolates. Fifty-two percent were metronidazole resistant, compared to 2% (7 of 431) with resistance to furazolidone and nitrofurantoin. All seven furazolidone- and nitrofurantoin-resistant isolates were also metronidazole resistant.rdxA, frxA, and fdxB knockouts did not result in furazolidone or nitrofurantoin resistance. These data suggest that furazolidone and nitrofurantoin may be good alternatives to metronidazole for treating H. pylori infection.

H. pylori infection is one of the most common infections worldwide and is etiologically related to chronic gastritis, duodenal ulcer, gastric ulcer, gastric adenocarcinoma, and primary gastric lymphoma (3, 17, 18). Approximately one in six H. pylori-infected persons develop peptic ulcer disease. Patients with peptic ulcer disease experience pain and reduced quality of life and risk ulcer complications (1, 19). Cure of H. pylori infection prevents ulcer recurrence, heals gastritis, and also prevents progression from mild superficial gastritis to chronic atrophic gastritis (the precursor lesion to gastric cancer), which may reduce the risk, or prevent, gastric cancer (1, 15). Clinical experience has demonstrated that cure of H. pylori infection is difficult due to lack of compliance with the drug regimens and development of antibiotic-resistant H. pylori (8, 15). Metronidazole has been widely used as a critical component of combination therapies for H. pylori infection. Monotherapy with metronidazole results in more than 50% of H. pyloriisolates acquiring resistance (13), and current metronidazole-containing triple therapies are being undermined by development of resistance (4). Because of the high rate of metronidazole resistance in H. pylori, furazolidone and nitrofurantoin have been recommended as alternative agents (2, 9, 21).

Although furazolidone, nitrofurantoin, and metronidazole are classified as nitroheterocyclic and nitroaromatic compounds, it is not known whether the drug actions and the resistance mechanisms are similar. Metronidazole resistance among H. pylori strains has been reported worldwide with variable frequencies (6, 13, 16). The mechanism of metronidazole resistance among H. pyloristrains has been related to alterations in gene products having metronidazole nitroreductase activity, including oxygen-insensitive NAD(P)H nitroreductase (RdxA), NAD(P)H flavin oxidoreductase (FrxA), and ferredoxin-like protein (FdxB) (7, 12). This study asked whether furazolidone or nitrofurantoin susceptibility and resistance shared common features with metronidazole susceptibility and resistance.

We evaluated the prevalence of metronidazole, furazolidone, and nitrofurantoin resistance among H. pylori strains isolated from 431 patients, including 297 males and 134 females (median age, 45 years; range, 16 to 82 years) presenting at Guro Hospital in Seoul, Korea, between September 1993 and September 1999. The endoscopic diagnoses were chronic gastritis (101 patients), peptic ulcer diseases (85 patients with gastric ulcer disease and 128 patients with duodenal ulcer disease), and gastric cancer (117 patients). H. pyloriwas isolated from gastric mucosal biopsies that were plated onto selective (containing 1% nalidixic acid, 0.5% trimethoprim, 0.3% vancomycin, and 0.2% amphotericin) and nonselective brain heart infusion (BHI) agar plates containing 5% defibrinated horse blood. All plates were incubated under microaerobic conditions at 37°C for up to 14 days. H. pylori was identified by colony morphology, Gram staining, and catalase, urease, and oxidase reactions. MIC measurements were performed by agar dilution as described previously (12). Only 48% of the strains were susceptible to metronidazole. The MICs for 224 resistant strains ranged from ≥8 to 256 μg of metronidazole per ml; those for 172 strains (40% of the total) ranged from ≥16 to 256 μg of metronidazole per ml. Only 7 of the 431 strains (1.6%) required a MIC of 4 μg of furazolidone per ml. The same seven strains also required a MIC of 4 μg of nitrofurantoin per ml, and all seven strains with furazolidone and nitrofurantoin resistance also showed low-level metronidazole resistance (MICs of 8 or 16 μg/ml) (Table1). All other strains (424 of 431) required MICs of ≤0.5 μg of furazolidone or nitrofurantoin per ml. Similar findings (i.e., low frequency with low-level MICs and cross-resistance of furazolidone and metronidazole) have been recently reported for clinical H. pylori isolates from Brazil (14).

View this table:
  • View inline
  • View popup
Table 1.

Comparisons of MICs of metronidazole, furazolidone, and nitrofurantoin among 431 clinical H. pylori isolates

We evaluated the rate of spontaneous development of low-level furazolidone or nitrofurantoin resistance (MIC of 4 μg/ml) usingH. pylori ATCC 700392. Two-day-old H. pyloricells from two 89-mm-diameter plates were harvested and suspended in 4 ml of 5% horse serum–BHI broth. The cells were adjusted to approximately 109 cells and spread onto 5% horse blood–BHI agar plates supplemented with 2 μg of furazolidone or nitrofurantoin per ml or 8 μg of metronidazole per ml. The plates containing the cells were incubated at 37°C under microaerobic conditions for 6 days. No colonies grew on plates supplemented with furazolidone or nitrofurantoin. However, 253 colonies appeared on plates supplemented with metronidazole. These results suggest that furazolidone and nitrofurantoin resistance occurs spontaneously at a much lower frequency than metronidazole resistance. The ease of selection of spontaneous metronidazole-resistant colonies and the difficulty of selecting spontaneous furazolidone- or nitrofurantoin-resistant colonies could be related to clinical observations of high frequencies of metronidazole resistance but low furazolidone or nitrofurantoin resistance among H. pyloristrains.

It was already established that the resistance mechanism for metronidazole is different from that for furazolidone and nitrofurantoin (7, 12, 20). To confirm that the resistance mechanisms for metronidazole and for furazolidone and nitrofurantoin are indeed different, susceptibilities to these drugs were measured inrdxA-, frxA-, and fdxB-inactivated (knockout) H. pylori strains. We used 92 single and/or dual knockout H. pylori strains, including a positive control (furazolidone- and nitrofurantoin-resistant clinical isolate requiring a MIC of 4 μg/ml, as mentioned above) and a negative control (H. pylori ureB knockout strain) to measure MICs of furazolidone and nitrofurantoin. The 92 strains were isolated in the United States and were also used to measure MICs of metronidazole as reported previously (12). None of the parental, knockout, or negative control strains grew on 5% horse blood–BHI plates containing 2 μg of either furazolidone or nitrofurantoin per ml, while the positive controls grew on the same plates. These results were confirmed using five additional clinical isolates from Korea, which are susceptible to furazolidone and nitrofurantoin (MIC of 0.5 μg/ml), including H. pylori ATCC 43629, in which rdxA,frxA, and fdxB were knocked out as described previously (12). The MICs of metronidazole, furazolidone, and nitrofurantoin in these strains were evaluated as described previously (12). As shown in Table2, the metronidazole MICs forrdxA and frxA knockout strains increased from 1 to 32 μg/ml (ATCC 43629, KH220, and KH278) and from 8 to 128 μg/ml (KH259 and KH261). The metronidazole MICs for fdxB knockout strains, however, were unchanged for strains ATCC 43629, KH220, KH278 but increased from 8 to 64 μg/ml for KH259 and from 8 to 32 μg/ml for KH261. In contrast, the furazolidone and nitrofurantoin MICs for all the knockout strains were unchanged (0.5 μg/ml) from those for the parental strains. These results are consistent with those from the 92 knockout strains and confirm the previous data regarding the involvement of these genes in metronidazole resistance. In addition, these results indicate that the genes (rdxA,frxA, and fdxB) are unlikely to be directly involved in furazolidone and nitrofurantoin resistance in H. pylori.

View this table:
  • View inline
  • View popup
Table 2.

Effects of the rdxA, frxA, andfdxB genes on metronidazole, furazolidone, and nitrofurantoin susceptibilities in H. pylori

Although the modes of drug action of all three antibiotics are similar and nitroreduction is required for activation, the mechanisms of resistance to metronidazole and to furazolidone and nitrofurantoin may not be the same (20). Nitroreduction of furazolidone and nitrofurantoin may be exerted by nitroreductases other than RdxA, FrxA, and FdxB in H. pylori as described by Whiteway et al. (20) for E. coli, in which nitroreduction of 5-nitrofuran derivatives is exerted by the nsfA andnfsB products. It is possible that the nitroreductase for furazolidone and nitrofurantoin may be essential for H. pylori survival and that resistance may be acquired by partial inactivation of the nitroreductase. Candidates for furazolidone and nitrofurantoin nitroreductases include pyruvate:flavodoxin oxidoreductase (PorCDAB) and 2-oxoglutarate oxidoreductase (OorDABC). The lethal effect and possible metronidazole nitroreductase activity of the porCDAB and oorDABC products have been shown for H. pylori (10, 11). In this view, we postulate that furazolidone and nitrofurantoin may be more specific to PorCDAB and/or OorDABC, while metronidazole may be more specific to RdxA, FrxA, and FdxB, as substrate molecules. Therefore, strains with knocked-out rdxA, frxA, or fdxB were still sensitive to furazolidone and nitrofurantoin because of the existence of fully functional porCDAB and oorDABCgenes. In contrast, partially functional porCDAB andoorDABC genes that confer low-level furazolidone and nitrofurantoin resistance also confer low-level metronidazole resistance, as shown in this study. We are currently testing this hypothesis by purifying PorCDAB and OorDABC from H. pyloriand measuring the nitroreductase activities for furazolidone and nitrofurantoin.

Furazolidone- or nitrofurantoin-containing therapeutic regimens forH. pylori infection have been suggested for use instead of metronidazole to overcome the high frequency of metronidazole resistance among H. pylori strains. The ideal antibiotic forH. pylori therapy would have high efficacy without the development of antibiotic resistance. Several reports published recently indicate that furazolidone or nitrofurantoin is efficacious inH. pylori therapy, although details of the best therapy have not yet been defined (2, 9, 21). The results reported here suggest that furazolidone and nitrofurantoin may be good alternatives, especially in areas where metronidazole resistance is common.

ACKNOWLEDGMENTS

This work was supported in part by the Department of Veterans Affairs.

FOOTNOTES

    • Received 12 May 2000.
    • Returned for modification 20 August 2000.
    • Accepted 3 October 2000.
  • Copyright © 2001 American Society for Microbiology

REFERENCES

  1. 1.↵
    1. Buckley J. M.,
    2. Deltenre M.
    Therapy of Helicobacter pylori infection. Curr. Opin. Gastroenterol. 13 1997 56 62
    OpenUrl
  2. 2.↵
    1. Coudron P. E.,
    2. Stratton C. W.
    In-vitro evaluation of nitrofurantoin as an alternative agent for metronidaszole in combination antimicrobial therapy against Helicobacter pylori. J. Antimicrob. Chemother. 42 1998 657 660
    OpenUrlCrossRefPubMed
  3. 3.↵
    1. Crump M.,
    2. Gospodarowicz M.,
    3. Shepherd F. A.
    Lymphoma of the gastrointestinal tract. Semin. Oncol. 26 1999 324 337
    OpenUrlPubMedWeb of Science
  4. 4.↵
    1. de Boer W. A.,
    2. Tytgat G. N.
    The best therapy for Helicobacter pylori infection: should efficacy or side-effect profile determine our choice? Scand. J. Gastroenterol. 30 1995 401 407
    OpenUrlPubMedWeb of Science
  5. 5.
    1. Dore M. P.,
    2. Osato M. S.,
    3. Kwon D. H.,
    4. Graham D. Y.,
    5. El-Zaatari F. A. K.
    Demonstration of unexpected antibiotic resistance of genotypically identical Helicobacter pylori isolates. Clin. Infect. Dis. 27 1998 84 89
    OpenUrlCrossRefPubMedWeb of Science
  6. 6.↵
    1. Glupczynski Y.
    Antimicrobial resistance in Helicobacter pylori: a global overview. Acta Gastroenterol. Belg. 61 1998 357 366
    OpenUrlPubMed
  7. 7.↵
    1. Goodwin A.,
    2. Kersulyte D.,
    3. Sisson G.,
    4. Veldhuyzen van Zanten S. J. O.,
    5. Berg D. E.,
    6. Hoffman P. S.
    Metronidazole-resistance in Helicobacter pylori is due to null mutations in a gene (rdxA) that encodes an oxygen-insensitive NAD(P)H nitroreductase. Mol. Microbiol. 28 1998 383 393
    OpenUrlCrossRefPubMedWeb of Science
  8. 8.↵
    1. Graham D. Y.,
    2. de Boer W. A.,
    3. Tytgat G. N.
    Choosing the best anti-Helicobacter pylori therapy: effect of antimicrobial resistance. Am. J. Gastroenterol. 91 1996 1072 1076
    OpenUrlPubMedWeb of Science
  9. 9.↵
    1. Graham D. Y.,
    2. Osato M. S.,
    3. Hoffman J.,
    4. Opekun A. R.,
    5. Anderson S.,
    6. El-Zimaty H. M.
    Furazolidone combination therapies for Helicobacter pylori infection in the United States. Aliment. Pharmacol. Ther. 14 2000 211 215
    OpenUrlCrossRefPubMed
  10. 10.↵
    1. Hughes N. J.,
    2. Clayton C. L.,
    3. Chalk P. A.,
    4. Kelly D. J.
    Helicobacter pylori porCDAB and oorDABC genes encode distinct pyruvate:flavodoxin and 2-oxoglutarate:acceptor oxidoreductases which mediate electron transport to NADP. J. Bacterol. 180 1998 1119 1128
    OpenUrlAbstract/FREE Full Text
  11. 11.↵
    1. Kaihovaara P.,
    2. Hook-Nikanne J.,
    3. Uusi-Oukari M.,
    4. Kosunen T. U.,
    5. Salaspuro M.
    Flavodoxin-dependent pyruvate oxidation, acetate production and metronidazole reduction by Helicobacter pylori. J. Antimicrob. Chemother. 41 1998 171 177
    OpenUrlCrossRefPubMedWeb of Science
  12. 12.↵
    1. Kwon D.-H.,
    2. El-Zaatari F. A. K.,
    3. Kato M.,
    4. Osato M. S.,
    5. Reddy R.,
    6. Yamaoka Y.,
    7. Graham D. Y.
    Analysis of an rdxA gene and involvement of additional genes encoding NADPH flavin oxidoreductase (FrxA) and ferredoxin-like protein (FdxB) in metronidazole resistance of Helicobacter pylori. Antimicrob. Agents Chemother. 44 2000 2133 2142
    OpenUrlAbstract/FREE Full Text
  13. 13.↵
    1. Megraud F.
    Helicobacter pylori resistance to antibiotics Helicobacter pylori: basic mechanisms to clinical cure. Hunt R. H., Tytgat G. N. 1994 570 583 Kluwer Academic Publishers Dordrecht, The Netherlands
  14. 14.↵
    1. Mendonca S.,
    2. Ecclissato C.,
    3. Sartori M. S.,
    4. Godoy A. P.,
    5. Guerzoni R. A.,
    6. Degger M.,
    7. Pedrazzoli J. Jr.
    Prevalence of Helicobacter pylori resistance to metronidazole, clarithromycin, amoxicillin, tetracycline, and furazolidone in Brazil. Helicobacter 5 2000 79 83
    OpenUrlCrossRefPubMedWeb of Science
  15. 15.↵
    National Cancer Institute Cancer statistics review, 1973–1992 1995 2789 National Institutes of Health Bethesda, Md
  16. 16.↵
    1. Osato M. S.,
    2. Reddy R.,
    3. Graham D. Y.
    Metronidazole and clarithromycin resistance amongst Helicobacter pylori isolates from a large metropolitan hospital in the United States. Int. J. Antimicrob. Agents 12 1999 341 347
    OpenUrlCrossRefPubMedWeb of Science
  17. 17.↵
    1. Parsonnet J.
    Helicobacter pylori. Infect. Dis. Clin. N. Am. 12 1998 185 197
    OpenUrlCrossRefPubMedWeb of Science
  18. 18.↵
    1. Parsonnet J.
    Helicobacter pylori: the size of the problem. Gut 43 (Suppl. 1) 1998b S6 S9
    OpenUrlFREE Full Text
  19. 19.↵
    1. Soll A. H.
    Gastric, duodenal, and stress ulcer Gastrointestinal disease 5th ed. Sleisenger M., Fordtran J. 1993 580 679 W. B. Saunders Philadelphia, Pa
  20. 20.↵
    1. Whiteway J.,
    2. Koziarz P.,
    3. Veall J.,
    4. Sandhu N.,
    5. Kumar P.,
    6. Hoecher B.,
    7. Lambert I. B.
    Oxygen-insensitive nitroreductases: analysis of the roles of nfsA and nfsB in development of resistance to 5-nitrofuran derivatives in Escherichia coli. J. Bacteriol. 180 1998 5529 5539
    OpenUrlAbstract/FREE Full Text
  21. 21.↵
    1. Xiao S. D.,
    2. Liu W. Z.,
    3. Hu P. J.,
    4. Xia D. H.,
    5. Tytgat G. N.
    High cure rate of Helicobacter pylori infection using tripotassium dicitrato bismuthate, furazolidone and clarithromycin triple therapy for 1 week. Aliment. Pharmacol. Ther. 13 1999 311 315
    OpenUrlCrossRefPubMed
View Abstract
PreviousNext
Back to top
Download PDF
Citation Tools
Furazolidone- and Nitrofurantoin-ResistantHelicobacter pylori: Prevalence and Role of Genes Involved in Metronidazole Resistance
Dong H. Kwon, Miae Lee, J. J. Kim, J. G. Kim, F. A. K. El-Zaatari, M. S. Osato, D. Y. Graham
Antimicrobial Agents and Chemotherapy Jan 2001, 45 (1) 306-308; DOI: 10.1128/AAC.45.1.306-308.2001

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Print

Alerts
Sign In to Email Alerts with your Email Address
Email

Thank you for sharing this Antimicrobial Agents and Chemotherapy article.

NOTE: We request your email address only to inform the recipient that it was you who recommended this article, and that it is not junk mail. We do not retain these email addresses.

Enter multiple addresses on separate lines or separate them with commas.
Furazolidone- and Nitrofurantoin-ResistantHelicobacter pylori: Prevalence and Role of Genes Involved in Metronidazole Resistance
(Your Name) has forwarded a page to you from Antimicrobial Agents and Chemotherapy
(Your Name) thought you would be interested in this article in Antimicrobial Agents and Chemotherapy.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Share
Furazolidone- and Nitrofurantoin-ResistantHelicobacter pylori: Prevalence and Role of Genes Involved in Metronidazole Resistance
Dong H. Kwon, Miae Lee, J. J. Kim, J. G. Kim, F. A. K. El-Zaatari, M. S. Osato, D. Y. Graham
Antimicrobial Agents and Chemotherapy Jan 2001, 45 (1) 306-308; DOI: 10.1128/AAC.45.1.306-308.2001
del.icio.us logo Digg logo Reddit logo Twitter logo CiteULike logo Facebook logo Google logo Mendeley logo
  • Top
  • Article
    • ABSTRACT
    • ACKNOWLEDGMENTS
    • FOOTNOTES
    • REFERENCES
  • Figures & Data
  • Info & Metrics
  • PDF

KEYWORDS

Anti-Infective Agents, Urinary
Antitrichomonal Agents
furazolidone
Helicobacter pylori
metronidazole
nitrofurantoin

Related Articles

Cited By...

About

  • About AAC
  • Editor in Chief
  • Editorial Board
  • Policies
  • For Reviewers
  • For the Media
  • For Librarians
  • For Advertisers
  • Alerts
  • AAC Podcast
  • RSS
  • FAQ
  • Permissions
  • Journal Announcements

Authors

  • ASM Author Center
  • Submit a Manuscript
  • Article Types
  • Ethics
  • Contact Us

Follow #AACJournal

@ASMicrobiology

       

ASM Journals

ASM journals are the most prominent publications in the field, delivering up-to-date and authoritative coverage of both basic and clinical microbiology.

About ASM | Contact Us | Press Room

 

ASM is a member of

Scientific Society Publisher Alliance

 

American Society for Microbiology
1752 N St. NW
Washington, DC 20036
Phone: (202) 737-3600

Copyright © 2021 American Society for Microbiology | Privacy Policy | Website feedback

Print ISSN: 0066-4804; Online ISSN: 1098-6596