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Colistin

Drugs and Chemicals · NLM MeSH · updated 2026-10-31 · version 1

Citations verified against PubMedNot yet clinician-reviewed10 referencesApproximately 4 min read

Cyclic polypeptide antibiotic from Bacillus colistinus.

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

Definition and research guide

This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.

Content available: 4 complete abstracts (801 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.

Definition

Cyclic polypeptide antibiotic from Bacillus colistinus. It is composed of Polymyxins E1 and E2 (or Colistins A, B, and C) which act as detergents on cell membranes. Colistin is less toxic than Polymyxin B, but otherwise similar; the methanesulfonate is used orally.

Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.

Also known as: Colimycin; Colisticin; Polymyxin E; Colistin Sulfate; Sulfate, Colistin; Totazina; Coly-Mycin.

Where it fits in the MeSH classification

Broader topics
Polymyxins

Research landscape

PubMed indexes 6,756 records tagged with the MeSH heading “Colistin” (counts retrieved 2026-10-31). 2,392 of them (35.4%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 2,438 records.

Reviews account for 429 records (6.3%) and meta-analyses for 63. Randomized controlled trials number 133 (2.0%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.

PubMed records by publication periodthrough 1999: 1,501 records; 2000-2009: 425 records; 2010-2019: 2,438 records; 2020 onward: 2,392 records1,501through 19994252000-20092,4382010-20192,3922020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 19991,501
2000-2009425
2010-20192,438
2020 onward2,392
Share of records by publication typeReviews: 6.3 percent; Meta-analyses: 0.9 percent; Randomized controlled trials: 2.0 percentReviews6.3% (429)Meta-analyses0.9% (63)Randomized controlled trials2.0% (133)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 6,756 PubMed records
TypeRecordsShare
Reviews4296.3%
Meta-analyses630.9%
Randomized controlled trials1332.0%

Method: PubMed query "Colistin"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.

Reading the evidence in drugs and chemicals

Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.

Evidence from open-access studies

These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.

Study comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
Antibiotic Resistance during COVID-19: A Systematic Review
Sulayyim HJA, Ismail R, Hamid AA, Ghafar NA
2022Systematic review
Design not recorded in structured metadata
82cc by
PMID 36231256 · DOI · PMC9565540
Resolving colistin resistance and heteroresistance in Enterobacter species
Doijad SP, Gisch N, Frantz R, Kumbhar BV, Falgenhauer J, Imirzalioglu C, et al.
2023Research article
Design not recorded in structured metadata
57cc by
PMID 36627272 · DOI · PMC9832134
Regulatory fine-tuning of mcr-1 increases bacterial fitness and stabilises antibiotic resistance in agricultural settings
Ogunlana L, Kaur D, Shaw LP, Jangir P, Walsh T, Uphoff S, et al.
2023Research article
Design not recorded in structured metadata
45cc by
PMID 37723338 · DOI · PMC10579358
Resistance, heteroresistance, and fitness costs drive colistin treatment failure during Acinetobacter baumannii pneumonia
Hernandez-Bird J, He B, VanOtterloo LM, Billings EB, Huo W, Teodoro GIC, et al.
2026Research article
Design not recorded in structured metadata
6cc by
PMID 41461032 · DOI · PMC12773716

Antibiotic Resistance during COVID-19: A Systematic Review [1]

Systematic review Sulayyim HJA, Ismail R, Hamid AA, Ghafar NA · · 2022 · cited 82 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
One of the public health issues faced worldwide is antibiotic resistance (AR).
Closing excerpt
Antibiotics' prescription should be strictly implemented, relying on the Antimicrobial Stewardship Program (ASP) and guidelines from the World Health Organization (WHO) or Ministry of Health (MOH).
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (212 words)

One of the public health issues faced worldwide is antibiotic resistance (AR). During the novel coronavirus (COVID-19) pandemic, AR has increased. Since some studies have stated AR has increased during the COVID-19 pandemic, and others have stated otherwise, this study aimed to explore this impact. Seven databases-PubMed, MEDLINE, EMBASE, Scopus, Cochrane, Web of Science, and CINAHL-were searched using related keywords to identify studies relevant to AR during COVID-19 published from December 2019 to May 2022, according to PRISMA guidelines. Twenty-three studies were included in this review, and the evidence showed that AR has increased during the COVID-19 pandemic. The most commonly reported resistant Gram-negative bacteria was Acinetobacterbaumannii, followed by Klebsiella pneumonia, Escherichia coli, and Pseudomonas aeruginosa. A. baumannii and K. pneumonia were highly resistant to tested antibiotics compared with E. coli and P. aeruginosa. Moreover, K. pneumonia showed high resistance to colistin. Commonly reported Gram-positive bacteria were Staphylococcus aureus and Enterococcus faecium. The resistance of E. faecium to ampicillin, erythromycin, and Ciprofloxacin was high. Self-antibiotic medication, empirical antibiotic administration, and antibiotics prescribed by general practitioners were the risk factors of high levels of AR during COVID-19. Antibiotics' prescription should be strictly implemented, relying on the Antimicrobial Stewardship Program (ASP) and guidelines from the World Health Organization (WHO) or Ministry of Health (MOH).

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36231256 · DOI · PMC9565540

Resolving colistin resistance and heteroresistance in Enterobacter species [2]

Research article Doijad SP, Gisch N, Frantz R, Kumbhar BV, Falgenhauer J, Imirzalioglu C, et al. · · 2023 · cited 57 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Species within the Enterobacter cloacae complex (ECC) include globally important nosocomial pathogens.
Closing excerpt
To minimize therapeutic failures, we developed an assay that accurately detects colistin resistance levels for any ECC isolate.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (173 words)

Species within the Enterobacter cloacae complex (ECC) include globally important nosocomial pathogens. A three-year study of ECC in Germany identified Enterobacter xiangfangensis as the most common species (65.5%) detected, a result replicated by examining a global pool of 3246 isolates. Antibiotic resistance profiling revealed widespread resistance and heteroresistance to the antibiotic colistin and detected the mobile colistin resistance (mcr)-9 gene in 19.2% of all isolates. We show that resistance and heteroresistance properties depend on the chromosomal arnBCADTEF gene cassette whose products catalyze transfer of L-Ara4N to lipid A. Using comparative genomics, mutational analysis, and quantitative lipid A profiling we demonstrate that intrinsic lipid A modification levels are genospecies-dependent and governed by allelic variations in phoPQ and mgrB, that encode a two-component sensor-activator system and specific inhibitor peptide. By generating phoPQ chimeras and combining them with mgrB alleles, we show that interactions at the pH-sensing interface of the sensory histidine kinase phoQ dictate arnBCADTEF expression levels. To minimize therapeutic failures, we developed an assay that accurately detects colistin resistance levels for any ECC isolate.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36627272 · DOI · PMC9832134

Regulatory fine-tuning of mcr-1 increases bacterial fitness and stabilises antibiotic resistance in agricultural settings [3]

Research article Ogunlana L, Kaur D, Shaw LP, Jangir P, Walsh T, Uphoff S, et al. · · 2023 · cited 45 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Antibiotic resistance tends to carry fitness costs, making it difficult to understand how resistance can be maintained in the absence of continual antibiotic exposure.
Closing excerpt
Our study shows how regulatory evolution and plasmid transfer can combine to stabilise resistance and limit the impact of reducing antibiotic consumption.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (160 words)

Antibiotic resistance tends to carry fitness costs, making it difficult to understand how resistance can be maintained in the absence of continual antibiotic exposure. Here we investigate this problem in the context of mcr-1, a globally disseminated gene that confers resistance to colistin, an agricultural antibiotic that is used as a last resort for the treatment of multi-drug resistant infections. Here we show that regulatory evolution has fine-tuned the expression of mcr-1, allowing E. coli to reduce the fitness cost of mcr-1 while simultaneously increasing colistin resistance. Conjugative plasmids have transferred low-cost/high-resistance mcr-1 alleles across an incredible diversity of E. coli strains, further stabilising mcr-1 at the species level. Regulatory mutations were associated with increased mcr-1 stability in pig farms following a ban on the use of colistin as a growth promoter that decreased colistin consumption by 90%. Our study shows how regulatory evolution and plasmid transfer can combine to stabilise resistance and limit the impact of reducing antibiotic consumption.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37723338 · DOI · PMC10579358

Resistance, heteroresistance, and fitness costs drive colistin treatment failure during Acinetobacter baumannii pneumonia [4]

Research article Hernandez-Bird J, He B, VanOtterloo LM, Billings EB, Huo W, Teodoro GIC, et al. · · 2026 · cited 6 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Acinetobacter baumannii is an Enterococcus, Staphylococcus, Klebsiella, Acinetobacter, Pseudomonas, and Enterobacter species (ESKAPE) pathogen linked to healthcare-associated diseases.
Closing excerpt
baumannii.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (256 words)

Acinetobacter baumannii is an Enterococcus, Staphylococcus, Klebsiella, Acinetobacter, Pseudomonas, and Enterobacter species (ESKAPE) pathogen linked to healthcare-associated diseases. Due to evolved resistance, last-resort antibiotics such as the lipooligosaccharide (LOS)-targeting colistin are increasingly used to treat multidrug-resistant isolates. To track the evolution of colistin resistance within a host, we performed sequential oropharyngeal infections in immunocompetent or immune-depleted mice in the presence of inhaled colistin. Both resistant and heteroresistant A. baumannii strains emerged with pmrB mutations that efficiently competed with the susceptible parent in the presence of colistin. These pmrB mutants had a fitness cost in the absence of colistin treatment but retained their ability to colonize the host. In contrast, LOS-deficient A. baumannii mutants removed the target of colistin, but such mutants were unable to colonize the lung. The two pathogenic pmrB mutants showed clear evidence of LOS modification, which was linked to increased transcription of LOS modification enzymes, including the product of the cryptic eptA gene. Spontaneous insertion mutations that caused hyperexpression of eptA allowed the heteroresistant mutant to develop clinically significant colistin resistance. Insertion mutations upstream of the eptA gene or those disrupting hns, which encodes a small histone-like protein, resulted in increased eptA transcript, linking expression of this protein to clinically significant resistance. A resistant variant derived from the heteroresistant parent was stable in the absence of drug, but continued passaging selected for colistin-resensitized pseudorevertants that were largely due to disruption of the LOS modification enzymes. Therefore, colistin heteroresistance is an early stage in the stepwise acquisition of stable colistin resistance in A. baumannii.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41461032 · DOI · PMC12773716

Key reviews and meta-analyses

The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.

  • Research article Colistin: the revival of polymyxins for the management of multidrug-resistant gram-negative bacterial infections [5]
    Falagas ME, Kasiakou SK · Clin Infect Dis · 2005 · cited 1,265 times (Europe PMC)
  • Research article Colistin: the re-emerging antibiotic for multidrug-resistant Gram-negative bacterial infections [6]
    Li J, Nation RL, Turnidge JD, Milne RW, Coulthard K, Rayner CR, et al. · Lancet Infect Dis · 2006 · cited 1,043 times (Europe PMC)
  • Research article International Consensus Guidelines for the Optimal Use of the Polymyxins: Endorsed by the American College of Clinical Pharmacy (ACCP), European Society of Clinical Microbiology and Infectious Diseases (ESCMID), Infectious Diseases Society of America (IDSA), International Society for Anti-infective Pharmacology (ISAP), Society of Critical Care Medicine (SCCM), and Society of Infectious Diseases Pharmacists (SIDP) [7]
    Tsuji BT, Pogue JM, Zavascki AP, Paul M, Daikos GL, Forrest A, et al. · Pharmacotherapy · 2019 · cited 796 times (Europe PMC)
  • Research article Colistin and its role in the Era of antibiotic resistance: an extended review (2000-2019) [8]
    El-Sayed Ahmed MAE, Zhong LL, Shen C, Yang Y, Doi Y, Tian GB · Emerg Microbes Infect · 2020 · cited 566 times (Europe PMC)
  • Research article Colistin: an update on the antibiotic of the 21st century [9]
    Biswas S, Brunel JM, Dubus JC, Reynaud-Gaubert M, Rolain JM · Expert Rev Anti Infect Ther · 2012 · cited 426 times (Europe PMC)
  • Research article Evaluation of colistin as an agent against multi-resistant Gram-negative bacteria [10]
    Li J, Nation RL, Milne RW, Turnidge JD, Coulthard K · Int J Antimicrob Agents · 2005 · cited 407 times (Europe PMC)

References

  1. Sulayyim HJA, Ismail R, Hamid AA, Ghafar NA. Antibiotic Resistance during COVID-19: A Systematic Review. . 2022. PMID 36231256 · DOI · PMC9565540
  2. Doijad SP, Gisch N, Frantz R, Kumbhar BV, Falgenhauer J, Imirzalioglu C, et al.. Resolving colistin resistance and heteroresistance in Enterobacter species. . 2023. PMID 36627272 · DOI · PMC9832134
  3. Ogunlana L, Kaur D, Shaw LP, Jangir P, Walsh T, Uphoff S, et al.. Regulatory fine-tuning of mcr-1 increases bacterial fitness and stabilises antibiotic resistance in agricultural settings. . 2023. PMID 37723338 · DOI · PMC10579358
  4. Hernandez-Bird J, He B, VanOtterloo LM, Billings EB, Huo W, Teodoro GIC, et al.. Resistance, heteroresistance, and fitness costs drive colistin treatment failure during Acinetobacter baumannii pneumonia. . 2026. PMID 41461032 · DOI · PMC12773716
  5. Falagas ME, Kasiakou SK. Colistin: the revival of polymyxins for the management of multidrug-resistant gram-negative bacterial infections. Clin Infect Dis. 2005. PMID 15825037 · DOI
  6. Li J, Nation RL, Turnidge JD, Milne RW, Coulthard K, Rayner CR, et al.. Colistin: the re-emerging antibiotic for multidrug-resistant Gram-negative bacterial infections. Lancet Infect Dis. 2006. PMID 16931410 · DOI
  7. Tsuji BT, Pogue JM, Zavascki AP, Paul M, Daikos GL, Forrest A, et al.. International Consensus Guidelines for the Optimal Use of the Polymyxins: Endorsed by the American College of Clinical Pharmacy (ACCP), European Society of Clinical Microbiology and Infectious Diseases (ESCMID), Infectious Diseases Society of America (IDSA), International Society for Anti-infective Pharmacology (ISAP), Society of Critical Care Medicine (SCCM), and Society of Infectious Diseases Pharmacists (SIDP). Pharmacotherapy. 2019. PMID 30710469 · DOI · PMC7437259
  8. El-Sayed Ahmed MAE, Zhong LL, Shen C, Yang Y, Doi Y, Tian GB. Colistin and its role in the Era of antibiotic resistance: an extended review (2000-2019). Emerg Microbes Infect. 2020. PMID 32284036 · DOI · PMC7241451
  9. Biswas S, Brunel JM, Dubus JC, Reynaud-Gaubert M, Rolain JM. Colistin: an update on the antibiotic of the 21st century. Expert Rev Anti Infect Ther. 2012. PMID 23030331 · DOI
  10. Li J, Nation RL, Milne RW, Turnidge JD, Coulthard K. Evaluation of colistin as an agent against multi-resistant Gram-negative bacteria. Int J Antimicrob Agents. 2005. PMID 15620821 · DOI

About this article

Sources
NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
Verification
Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
Review state
automated source verified; no human expert review has been recorded yet.
Version
1, last updated 2026-10-31.

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At a glance

6,756
PubMed records on this heading
35%
published since 2020
429
review articles
133
randomized trials
10
verified references below

Counts come from PubMed on 2026-10-31; they show how much has been written, not how strong the evidence is.

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