Cited by 500Antibiotic Use and ResistanceAntibiotic Resistance in BacteriaUrinary Tract Infections Management

Resistance to Trimethoprim-Sulfamethoxazole

Eliopoulos, G. M., Huovinen, P.·2001·Clinical Infectious Diseases

Abstract

Sulfonamides have a glorious history. In 1935, they were the first class of true antimicrobial agents with life-saving potency. Today, 66 years later, increased bacterial resistance to sulfonamides and to trimethoprim (TMP), a synthetic antimicrobial agent that is 30 years younger than sulfonamides, has limited their use to only a few indications. In the treatment and prophylaxis of patients with urinary tract infections, trimethoprim-sulfamethoxazole (TMP-SMZ) or TMP alone is still considered the first-line drug of choice, although increased bacterial resistance to these agents has been linked with treatment failure. TMP-SMZ has a possible role as a second- or third-line treatment for patients who have respiratory tract infections. In the developing world, where this inexpensive drug is widely used as first-line treatment, bacterial resistance has caused problems, especially with regard to the treatment of patients with severe respiratory tract infections. Use of TMP-SMZ as prophylaxis for Pneumocystis carinii infection has rapidly increased the multidrug resistance of bacterial pathogens found in human immunodeficiency virus-infected patients. Today, detailed and reliable knowledge on the resistance of bacterial pathogens to both TMP-SMZ and TMP is an essential requirement for the safe and effective use of these drugs in all clinical settings.

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Crossref · 10.1086/320532

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42 of 42 references verified0 citation errors · 0 not checkable

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  • Chromosomal mutations in the DHPS locus can lead to resistance.

    “Chromosomal mutations in the DHPS locus—such as point mutations, insertions of duplicate amino acids, or larger sequence alterations as a result of recombination—can also lead to resistance (8).”
  • Promoter mutations that increase production of DHFR or DHPS overwhelm the ability of TMP-SMX to inhibit folate production and permit bacterial survival.

    “These mutations result in the production of increased quantities of the above enzymes, “overwhelming” the ability of TMP-SMX to inhibit folate production and permitting bacterial survival (82, 83).”

    From Mechanisms of Antibiotic Resistance (2016) · cites this paper as [83]

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Authors
Eliopoulos, G. M., & Huovinen, P.
Corresponding author
Huovinen, P.
Venue
Clinical Infectious Diseases
Published
2001-06-01
Volume
32
Issue
11
Pages
1608-1614
ISSN
  • 1058-4838 (ISSN-L)
  • 1537-6591
OpenAlex
W2096526472
Cited by
500
References
42
Citations by year
2026: 25 · 2025: 39 · 2024: 34 · 2023: 30 · 2022: 26 · 2021: 35 · 2020: 33 · 2019: 42 · 2018: 25 · 2017: 29 · 2016: 28 · 2015: 27 · 2014: 17 · 2013: 12 · 2012: 10
FWCI
1.29
Type
journal article
Language
en
Open access
closed
Locations
  • Clinical Infectious Diseases (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Applied Microbiology and Biotechnology › Antibiotic Use and Resistance
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Medicine › Antibiotic Resistance in Bacteria
  • Health Sciences › Medicine › Epidemiology › Urinary Tract Infections Management
Keywords
trimethoprim-sulfamethoxazole, trimethoprim, sulfonamide resistance, bacterial antimicrobial resistance, urinary tract infection, respiratory infections, developing countries
MeSH terms
Drug Resistance, Microbial, Humans, Trimethoprim Resistance, Trimethoprim, Sulfamethoxazole Drug Combination

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