Glossary · PeptideU · 7 min read

What Is Streptogramin B? Definition and What Research Reports

The short answer

Streptogramin B is a family of cyclic depsipeptide (peptide-like) antibiotics produced by Streptomyces bacteria, with pristinamycin IA, virginiamycin S and the semisynthetic derivative quinupristin as the best-known members. In the literature the term appears most often inside the acronym MLSB — macrolide, lincosamide, streptogramin B — which names a shared bacterial resistance pattern driven mainly by erm genes. Published studies are overwhelmingly microbiological: they characterise resistance genes, phenotypes and their distribution across staphylococci, streptococci and other clinical isolates.

Definition

Streptogramin B is the name given to one of the two structurally distinct halves of the streptogramin antibiotic family: a group of cyclic hexadepsipeptides — peptide-like rings that contain both amide and ester bonds — produced as secondary metabolites by soil bacteria of the genus Streptomyces. Named members include pristinamycin IA, virginiamycin S and the semisynthetic derivative quinupristin. Because the ring is assembled by non-ribosomal peptide synthetases rather than by the ribosome, streptogramin B molecules contain unusual and non-proteinogenic residues and are conventionally classified as natural-product peptides rather than as conventional linear peptides. In most published work the phrase does not appear alone: it appears inside the compound acronym MLS_B (macrolide–lincosamide–streptogramin B), which describes a resistance phenotype shared across three otherwise unrelated antibiotic classes.

Where the Molecule Comes From

Streptogramins are fermentation products of Streptomyces species. Every streptogramin-producing organism makes two chemically unrelated groups at once: group A (polyunsaturated macrolactones, which are not peptides) and group B (the cyclic depsipeptides described here). Quinupristin, a semisynthetic streptogramin B derivative, is paired with dalfopristin, a streptogramin A derivative, in a licensed injectable antibiotic product; virginiamycin has a separate history in veterinary and agricultural settings. This page is definitional and does not describe clinical use, regimens or administration of any of these products.

Streptogramin A Versus Streptogramin B

Feature	Streptogramin A	Streptogramin B
Chemical class	Polyunsaturated macrolactone (non-peptide)	Cyclic hexadepsipeptide (peptide-like)
Example members	Pristinamycin IIA, virginiamycin M, dalfopristin	Pristinamycin IA, virginiamycin S, quinupristin
Source organism	Streptomyces spp.	Streptomyces spp.
Appears in the acronym MLS_B?	No	Yes

How the Term Is Used in Research

Streptogramin B compounds are grouped together with macrolides and lincosamides because those three classes converge on an overlapping binding region of the bacterial 50S ribosomal subunit, and that shared target is the reason a single resistance mechanism can affect all three at once — the logic behind the MLS_B nomenclature used throughout the clinical-isolate literature (PMID 33510520). The dominant mechanism described in that literature is ribosomal RNA methylation encoded by erm (erythromycin ribosome methylase) genes; researchers characterising a novel plasmid-borne gene in Staphylococcus xylosus designated it erm(48) and reported that it conferred the MLS_B resistance pattern (PMID 28438941). A separate group described another new gene, erm(56), in Trueperella pyogenes and likewise reported an MLS_B phenotype (PMID 37417762). For a reader encountering "streptogramin B" in a paper, the term is therefore usually a label on a resistance axis rather than a description of a compound being tested.

Constitutive Versus Inducible Phenotypes

Laboratory reports routinely split MLS_B resistance into constitutive (cMLS_B) and inducible (iMLS_B) forms, the latter detected with a disc-approximation or "D-test". Investigators studying methicillin-resistant Staphylococcus aureus isolates in Chile combined phenotypic testing with genotyping and reported both constitutive and inducible MLS_B patterns among the clinical isolates examined (PMID 35892390). A study of clinical Staphylococcus isolates that examined MLS_B phenotypes alongside the ketolide telithromycin similarly reported phenotype distributions across the collection (PMID 25052113).

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What the Published Literature Reports

Resistance genes and their spread

Much of the verified literature is descriptive gene-hunting. The Staphylococcus xylosus work located erm(48) on a novel plasmid the researchers named pJW2311, a finding reported as evidence that MLS_B determinants continue to appear on mobile elements (PMID 28438941). The Trueperella pyogenes report added erm(56) to the same catalogue (PMID 37417762). A survey of clinical staphylococci reported on the distribution of MLS_B resistance genes among the isolates collected (PMID 33510520), and a study of streptococci recovered from human and animal clinical specimens combined phenotypic and genotypic antimicrobial-resistance characterisation across both host sources (PMID 37256427).

Regulation and unusual phenotypes

Several papers examined how erm expression is controlled rather than simply whether the gene is present. Work on the emergent emm92 type of group A Streptococcus investigated regulation of the erm(T) MLS_B phenotype and reported on how expression of that determinant was governed in the lineage (PMID 39843607). Another group described group B streptococcal isolates that were erythromycin-susceptible yet clindamycin-resistant and reported that this unexpected combination was associated with an IS1216E insertion within ermB (PMID 31257242). Earlier phenotypic and genotypic characterisation of group B streptococcal isolates in southern Brazil reported resistance patterns across that collection (PMID 20881175).

Induction by other agents

One study asked whether a newer macrolide could itself trigger the phenotype, and the researchers reported that solithromycin specifically induced MLS_B resistance under the conditions tested (PMID 32216609). Older work in Clostridium difficile examined the prevalence of MLS_B resistance and reported an association with resistance to moxifloxacin in the isolates studied (PMID 12615860). A 2025 population analysis of Streptococcus suis serotype 14 characterised the serotype as a non-negligible zoonotic population and reported on its antimicrobial resistance features (PMID 40901540).

Streptogramin B and the Peptide Literature

Streptogramin B is included in peptide reference material for a structural reason, not a physiological one. It is a textbook example of a non-ribosomal peptide: a cyclic depsipeptide assembled enzymatically, containing ester linkages and non-standard residues, and stable in ways that linear ribosomal peptides generally are not. That places it in the same broad chemical neighbourhood as other microbial depsipeptides, and it is why the compound is sometimes referenced in discussions of peptide natural products, macrocyclisation chemistry and non-ribosomal peptide synthetase biosynthesis. It is not a metabolic, regulatory or signalling peptide, and it bears no relationship to the growth-factor or hormone-analogue peptides that dominate other glossary entries.

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Human Safety and Adverse Events: What Studies Report

The verified literature summarised on this page is microbiological and epidemiological. These reports characterised resistance genes, phenotypes and isolate collections — for example the novel gene descriptions in Staphylococcus xylosus and Trueperella pyogenes (PMID 28438941, PMID 37417762) and the phenotype surveys in staphylococci and streptococci (PMID 35892390, PMID 37256427). None of them reported human dosing regimens, tolerability outcomes or adverse-event rates for streptogramin B compounds, so no such figures are stated here. Safety and prescribing information for any licensed streptogramin-containing product sits with its regulatory labelling and with treating clinicians, not with this reference entry.

Quick Reference

Class: cyclic hexadepsipeptide (non-ribosomal peptide) antibiotic group.
Source: Streptomyces fermentation; co-produced with the non-peptide streptogramin A group.
Named members: pristinamycin IA, virginiamycin S, quinupristin (semisynthetic).
Usual context in papers: the MLS_B resistance acronym.
Main resistance determinant described: erm-encoded rRNA methylases, including newly named variants such as erm(48) and erm(56) (PMID 28438941, PMID 37417762).

This page is for educational purposes only and is not medical advice; consult a licensed physician or qualified healthcare professional about any medical question, and note that PeptideU summarises published research without recommending any compound, product or course of action.

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References

Frequently asked questions

Is streptogramin B a peptide?▾

It is peptide-like. Streptogramin B compounds are cyclic hexadepsipeptides — rings built from amino-acid-derived residues joined by both amide and ester bonds and assembled by non-ribosomal peptide synthetases rather than by the ribosome. That makes them natural-product peptides in the chemical sense, but they are antibiotics, not signalling or metabolic peptides, and they are not related to hormone-analogue peptides.

What does the acronym MLSB mean?▾

MLSB stands for macrolide, lincosamide and streptogramin B — three antibiotic classes that share an overlapping binding region on the bacterial 50S ribosomal subunit, which is why one resistance mechanism can affect all three (PMID 33510520). Papers commonly split the pattern into constitutive and inducible forms, as reported in clinical MRSA isolates from Chile (PMID 35892390).

Which genes are linked to streptogramin B resistance in the literature?▾

Most reports centre on erm genes encoding ribosomal RNA methylases. Researchers described a novel plasmid-borne gene, erm(48), on the plasmid pJW2311 in Staphylococcus xylosus (PMID 28438941), and a separate group reported a new gene, erm(56), conferring the MLSB phenotype in Trueperella pyogenes (PMID 37417762). Surveys of clinical staphylococci have reported the distribution of such genes (PMID 33510520).

Where do streptogramins come from?▾

Streptogramins are fermentation products of Streptomyces soil bacteria. Producing organisms make two chemically distinct groups simultaneously: group A polyunsaturated macrolactones, which are not peptides, and group B cyclic depsipeptides. Named group B members include pristinamycin IA, virginiamycin S and the semisynthetic derivative quinupristin. This entry is definitional and does not describe clinical administration of any streptogramin-containing product.

Can other antibiotics trigger MLSB resistance?▾

One published study examined this directly and the researchers reported that solithromycin specifically induced macrolide-lincosamide-streptogramin B resistance under the conditions tested (PMID 32216609). Separate work in Clostridium difficile reported an association between MLSB resistance and resistance to moxifloxacin among the isolates examined (PMID 12615860). These are laboratory and isolate-level findings, not treatment guidance.

Do the cited studies report human doses or side effects?▾

No. The verified literature summarised here is microbiological and epidemiological: it characterises resistance genes, expression regulation and phenotype distributions in bacterial isolates, such as erm(T) regulation in emm92 group A Streptococcus (PMID 39843607) and resistance profiling in streptococci from human and animal specimens (PMID 37256427). None of these papers reported human dosing regimens or adverse-event rates.

Why do some isolates look susceptible to erythromycin but resistant to clindamycin?▾

Investigators reported group B streptococcal isolates with exactly that combination and linked it to an IS1216E element inserted within the ermB gene, which altered the expected phenotype (PMID 31257242). Earlier characterisation of group B streptococcal isolates in southern Brazil also reported phenotype and genotype patterns across a clinical collection (PMID 20881175). Discrepancies like these are why laboratories pair phenotypic with genotypic testing.

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References

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18+ · Educational purposes only
This page summarises published research for education — it is not medical advice, and nothing here is a recommendation to use, purchase, or dose any substance. Study parameters described are what researchers reported, not instructions. Consult a qualified clinician before any health decision.