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 (624 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
An antibiotic produced by the soil actinomycete Streptomyces griseus. It acts by inhibiting the initiation and elongation processes during protein synthesis.
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: Streptomycin Sulfate; Streptomycin Sulphate; Streptomycin Sulfate (2:3) Salt; Estreptomicina CEPA; Estreptomicina Clariana; Estreptomicina Normon; Strepto-Fatol; Strepto Fatol.
Where it fits in the MeSH classification
- Broader topics
- Aminoglycosides
- Narrower topics
- Dihydrostreptomycin Sulfate
Research landscape
PubMed indexes 22,819 records tagged with the MeSH heading “Streptomycin” (counts retrieved 2026-10-31). 409 of them (1.8%) were published from 2020 onward, and the busiest period so far is through 1999 with 20,566 records.
Reviews account for 512 records (2.2%) and meta-analyses for 26. Randomized controlled trials number 148 (0.6%) 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.
Show the data
| Period | Records |
|---|---|
| through 1999 | 20,566 |
| 2000-2009 | 915 |
| 2010-2019 | 929 |
| 2020 onward | 409 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 512 | 2.2% |
| Meta-analyses | 26 | 0.1% |
| Randomized controlled trials | 148 | 0.6% |
Method: PubMed query "Streptomycin"[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 / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Evolution of high-level resistance during low-level antibiotic exposure | 2018 | Research article Design not recorded in structured metadata | 348 | cc by PMID 29686259 · DOI · PMC5913237 |
| Transferable plasmid-mediated resistance to streptomycin in a clinical isolate of Yersinia pestis | 2001 | Research article Design not recorded in structured metadata | 181 | cc by PMID 11266293 · DOI · PMC2631670 |
| Urgently seeking efficiency and sustainability of clinical trials in global health | 2021 | Review article Design not recorded in structured metadata | 48 | cc by PMID 33865473 · DOI · PMC8424133 |
| Three genes controlling streptomycin susceptibility in Agrobacterium fabrum | 2023 | Research article Design not recorded in structured metadata | 4 | cc by PMID 37695858 · DOI · PMC10521367 |
Evolution of high-level resistance during low-level antibiotic exposure [1]
Abstract reading summary — source excerpts
- Opening excerpt
- It has become increasingly clear that low levels of antibiotics present in many environments can select for resistant bacteria, yet the evolutionary pathways for resistance development during exposure to low amounts of antibiotics remain poorly defined.
- Closing excerpt
- These results demonstrate how the strength of the selective pressure influences evolutionary trajectories and that even weak selective pressures can cause evolution of high-level resistance.
- 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 (146 words)
It has become increasingly clear that low levels of antibiotics present in many environments can select for resistant bacteria, yet the evolutionary pathways for resistance development during exposure to low amounts of antibiotics remain poorly defined. Here we show that Salmonella enterica exposed to sub-MIC levels of streptomycin evolved high-level resistance via novel mechanisms that are different from those observed during lethal selections. During lethal selection only rpsL mutations are found, whereas at sub-MIC selection resistance is generated by several small-effect resistance mutations that combined confer high-level resistance via three different mechanisms: (i) alteration of the ribosomal RNA target (gidB mutations), (ii) reduction in aminoglycoside uptake (cyoB, nuoG, and trkH mutations), and (iii) induction of the aminoglycoside-modifying enzyme AadA (znuA mutations). These results demonstrate how the strength of the selective pressure influences evolutionary trajectories and that even weak selective pressures can cause evolution of high-level resistance.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29686259 · DOI · PMC5913237
Transferable plasmid-mediated resistance to streptomycin in a clinical isolate of Yersinia pestis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Plasmid-mediated high-level resistance to multiple antibiotics was reported in a clinical isolate of Yersinia pestis in Madagascar in 1997.
- Closing excerpt
- pestis represents a critical public health problem since this antibiotic is used as the first-line treatment against plague in many countries.
- 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 (116 words)
Plasmid-mediated high-level resistance to multiple antibiotics was reported in a clinical isolate of Yersinia pestis in Madagascar in 1997. We describe a second Y. pestis strain with high-level resistance to streptomycin, isolated from a human case of bubonic plague in Madagascar. The resistance determinants were carried by a self-transferable plasmid that could conjugate at high frequencies to other Y. pestis isolates. The plasmid and the host bacterium were different from those previously associated with multiple-drug resistance, indicating that acquisition of resistance plasmids is occurring in this bacterial species. Emergence of resistance to streptomycin in Y. pestis represents a critical public health problem since this antibiotic is used as the first-line treatment against plague in many countries.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 11266293 · DOI · PMC2631670
Urgently seeking efficiency and sustainability of clinical trials in global health [3]
Abstract reading summary — source excerpts
- Opening excerpt
- This paper shows the scale of global health research and the context in which we frame the subsequent papers in the Series.
- Closing excerpt
- Finally, we discuss the importance of collaborative work in global health research towards generating sustainable and culturally appropriate research environments.
- 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 (147 words)
This paper shows the scale of global health research and the context in which we frame the subsequent papers in the Series. In this Series paper, we provide a historical perspective on clinical trial research by revisiting the 1948 streptomycin trial for pulmonary tuberculosis, which was the first documented randomised clinical trial in the English language, and we discuss its close connection with global health. We describe the current state of clinical trial research globally by providing an overview of clinical trials that have been registered in the WHO International Clinical Trial Registry since 2010. We discuss challenges with current trial planning and designs that are often used in clinical trial research undertaken in low-income and middle-income countries, as an overview of the global health trials landscape. Finally, we discuss the importance of collaborative work in global health research towards generating sustainable and culturally appropriate research environments.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33865473 · DOI · PMC8424133
Three genes controlling streptomycin susceptibility in Agrobacterium fabrum [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Streptomycin (Sm) is a commonly used antibiotic for its efficacy against diverse bacteria.
- Closing excerpt
- fabrum.
- 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 (215 words)
Streptomycin (Sm) is a commonly used antibiotic for its efficacy against diverse bacteria. The plant pathogen Agrobacterium fabrum is a model for studying pathogenesis and interkingdom gene transfer. Streptomycin-resistant variants of A. fabrum are commonly employed in genetic analyses, yet mechanisms of resistance and susceptibility to streptomycin in this organism have not previously been investigated. We observe that resistance to a high concentration of streptomycin arises at high frequency in A. fabrum, and we attribute this trait to the presence of a chromosomal gene (strB) encoding a putative aminoglycoside phosphotransferase. We show how strB, along with rpsL (encoding ribosomal protein S12) and rsmG (encoding a 16S rRNA methyltransferase), modulates streptomycin sensitivity in A. fabrum. IMPORTANCE The plant pathogen Agrobacterium fabrum is a widely used model bacterium for studying biofilms, bacterial motility, pathogenesis, and gene transfer from bacteria to plants. Streptomycin (Sm) is an aminoglycoside antibiotic known for its broad efficacy against gram-negative bacteria. A. fabrum exhibits endogenous resistance to somewhat high levels of streptomycin, but the mechanism underlying this resistance has not been elucidated. Here, we demonstrate that this resistance is caused by a chromosomally encoded streptomycin-inactivating enzyme, StrB, that has not been previously characterized in A. fabrum. Furthermore, we show how the genes rsmG, rpsL, and strB jointly modulate streptomycin susceptibility in A. fabrum.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37695858 · DOI · PMC10521367
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 SPERMIDINE, SPERMINE, AND RELATED AMINES [5]
- Research article Aminoglycoside uptake and mode of action--with special reference to streptomycin and gentamicin. I. Antagonists and mutants [6]
- Research article Dissemination of the strA-strB streptomycin-resistance genes among commensal and pathogenic bacteria from humans, animals, and plants [7]
- Research article Streptomycin and alternative agents for the treatment of tularemia: review of the literature [8]
- Research article A-factor as a microbial hormone that controls cellular differentiation and secondary metabolism in Streptomyces griseus [9]
- Research article Aminoglycoside uptake and mode of action-with special reference to streptomycin and gentamicin. II. Effects of aminoglycosides on cells [10]
References
- Wistrand-Yuen E, Knopp M, Hjort K, Koskiniemi S, Berg OG, Andersson DI. Evolution of high-level resistance during low-level antibiotic exposure. . 2018. PMID 29686259 · DOI · PMC5913237
- Guiyoule A, Gerbaud G, Buchrieser C, Galimand M, Rahalison L, Chanteau S, et al.. Transferable plasmid-mediated resistance to streptomycin in a clinical isolate of Yersinia pestis. . 2001. PMID 11266293 · DOI · PMC2631670
- Park JJH, Grais RF, Taljaard M, Nakimuli-Mpungu E, Jehan F, Nachega JB, et al.. Urgently seeking efficiency and sustainability of clinical trials in global health. . 2021. PMID 33865473 · DOI · PMC8424133
- Howarth RE, Pattillo CM, Griffitts JS, Calvopina-Chavez DG. Three genes controlling streptomycin susceptibility in Agrobacterium fabrum. . 2023. PMID 37695858 · DOI · PMC10521367
- TABOR H, TABOR CW. SPERMIDINE, SPERMINE, AND RELATED AMINES. Pharmacol Rev. 1964. PMID 14211123 · DOI
- Hancock RE. Aminoglycoside uptake and mode of action--with special reference to streptomycin and gentamicin. I. Antagonists and mutants. J Antimicrob Chemother. 1981. PMID 6795174 · DOI
- Sundin GW, Bender CL. Dissemination of the strA-strB streptomycin-resistance genes among commensal and pathogenic bacteria from humans, animals, and plants. Mol Ecol. 1996. PMID 9147689 · DOI
- Enderlin G, Morales L, Jacobs RF, Cross JT. Streptomycin and alternative agents for the treatment of tularemia: review of the literature. Clin Infect Dis. 1994. PMID 7948556 · DOI
- Horinouchi S, Beppu T. A-factor as a microbial hormone that controls cellular differentiation and secondary metabolism in Streptomyces griseus. Mol Microbiol. 1994. PMID 7934895 · DOI
- Hancock RE. Aminoglycoside uptake and mode of action-with special reference to streptomycin and gentamicin. II. Effects of aminoglycosides on cells. J Antimicrob Chemother. 1981. PMID 7037727 · 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.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.