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Article ; Online: Bacteria can compensate the fitness costs of amplified resistance genes via a bypass mechanism.

Pal, Ankita / Andersson, Dan I

2024 Volume 15, Issue 1, Page(s) 2333

Abstract: Antibiotic heteroresistance is a phenotype in which a susceptible bacterial population includes a small subpopulation of cells that are more resistant than the main population. Such resistance can arise by tandem amplification of DNA regions containing ... ...

Abstract	Antibiotic heteroresistance is a phenotype in which a susceptible bacterial population includes a small subpopulation of cells that are more resistant than the main population. Such resistance can arise by tandem amplification of DNA regions containing resistance genes that in single copy are not sufficient to confer resistance. However, tandem amplifications often carry fitness costs, manifested as reduced growth rates. Here, we investigated if and how these fitness costs can be genetically ameliorated. We evolved four clinical isolates of three bacterial species that show heteroresistance to tobramycin, gentamicin and tetracyclines at increasing antibiotic concentrations above the minimal inhibitory concentration (MIC) of the main susceptible population. This led to a rapid enrichment of resistant cells with up to an 80-fold increase in the resistance gene copy number, an increased MIC, and severely reduced growth rates. When further evolved in the presence of antibiotic, these strains acquired compensatory resistance mutations and showed a reduction in copy number while maintaining high-level resistance. A deterministic model indicated that the loss of amplified units was driven mainly by their fitness costs and that the compensatory mutations did not affect the loss rate of the gene amplifications. Our findings suggest that heteroresistance mediated by copy number changes can facilitate and precede the evolution towards stable resistance.
MeSH term(s)	Anti-Bacterial Agents/pharmacology ; Anti-Bacterial Agents/therapeutic use ; Tobramycin ; Bacteria/genetics ; Gene Amplification ; Gentamicins ; Microbial Sensitivity Tests ; Drug Resistance, Bacterial/genetics
Chemical Substances	Anti-Bacterial Agents ; Tobramycin (VZ8RRZ51VK) ; Gentamicins
Language	English
Publishing date	2024-03-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-46571-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Interspecies interaction reduces selection for antibiotic resistance in Escherichia coli.

Nair, Ramith R / Andersson, Dan I

Communications biology

2023 Volume 6, Issue 1, Page(s) 331

Abstract: Evolution of microbial traits depends on the interaction of a species with its environment as well as with other coinhabiting species. However, our understanding of the evolution of specific microbial traits, such as antibiotic resistance in complex ... ...

Abstract	Evolution of microbial traits depends on the interaction of a species with its environment as well as with other coinhabiting species. However, our understanding of the evolution of specific microbial traits, such as antibiotic resistance in complex environments is limited. Here, we determine the role of interspecies interactions on the dynamics of nitrofurantoin (NIT) resistance selection among Escherichia coli. We created a synthetic two-species community comprised of two variants of E. coli (NIT susceptible and resistant) and Bacillus subtilis in minimal media with glucose as the sole carbon source. We show that the presence of B. subtilis significantly slows down the selection for the resistant E. coli mutant when NIT is present and that this slowdown is not due to competition for resources. Instead, the dampening of NIT resistance enrichment is largely mediated by extracellular compounds produced by B. subtilis with the peptide YydF playing a significant role. Our results not only demonstrate the impact of interspecies interactions on the evolution of microbial traits but also show the importance of using synthetic microbial systems in unravelling relevant interactions and mechanisms affecting the evolution of antibiotic resistance. This finding implies that interspecies interactions should be considered to better understand and predict resistance evolution in the clinic as well as in nature.
MeSH term(s)	Humans ; Escherichia coli/genetics ; Nitrofurantoin ; Escherichia coli Proteins ; Escherichia coli Infections ; Drug Resistance, Bacterial/genetics
Chemical Substances	Nitrofurantoin (927AH8112L) ; Escherichia coli Proteins
Language	English
Publishing date	2023-03-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-023-04716-2
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Article ; Online: Antibiotic resistance begets more resistance: chromosomal resistance mutations mitigate fitness costs conferred by multi-resistant clinical plasmids.

Nair, Ramith R / Andersson, Dan I / Warsi, Omar M

Microbiology spectrum

2024 , Page(s) e0420623

Abstract: Plasmids are the primary vectors of horizontal transfer of antibiotic resistance genes among bacteria. Previous studies have shown that the spread and maintenance of plasmids among bacterial populations depend on the genetic makeup of both the plasmid ... ...

Abstract	Plasmids are the primary vectors of horizontal transfer of antibiotic resistance genes among bacteria. Previous studies have shown that the spread and maintenance of plasmids among bacterial populations depend on the genetic makeup of both the plasmid and the host bacterium. Antibiotic resistance can also be acquired through mutations in the bacterial chromosome, which not only confer resistance but also result in changes in bacterial physiology and typically a reduction in fitness. However, it is unclear whether chromosomal resistance mutations affect the interaction between plasmids and the host bacteria. To address this question, we introduced 13 clinical plasmids into a susceptible
Language	English
Publishing date	2024-03-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2807133-5
ISSN	2165-0497 ; 2165-0497
ISSN (online)	2165-0497
ISSN	2165-0497
DOI	10.1128/spectrum.04206-23
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Article: Gruff och knuff på krogen. Skador i samband med dans och restaurangbesök.

Björnstig, U / Björnstig, J / Andersson, P

Lakartidningen

1998 Volume 95, Issue 39, Page(s) 4250, 4253

Title translation	Rows and fighting in taverns. Injuries in connection with dancing and patronage of restaurants.
MeSH term(s)	Accidents ; Adolescent ; Adult ; Alcohol Drinking/adverse effects ; Dancing/injuries ; Female ; Humans ; Incidence ; Leisure Activities ; Male ; Restaurants ; Sweden/epidemiology ; Wounds and Injuries/diagnosis ; Wounds and Injuries/epidemiology ; Wounds and Injuries/etiology
Language	Swedish
Publishing date	1998-09-23
Publishing country	Sweden
Document type	Journal Article
ZDB-ID	391010-6
ISSN	1652-7518 ; 0023-7205
ISSN (online)	1652-7518
ISSN	0023-7205
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Ua VI Zs.411: Show issues

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Article ; Online: Pervasive Selection for Clinically Relevant Resistance and Media Adaptive Mutations at Very Low Antibiotic Concentrations.

Pereira, Catia / Warsi, Omar M / Andersson, Dan I

Molecular biology and evolution

2023 Volume 40, Issue 1

Abstract: Experimental evolution studies have shown that weak antibiotic selective pressures (i.e., when the antibiotic concentrations are far below the minimum inhibitory concentration, MIC) can select resistant mutants, raising several unanswered questions. ... ...

Abstract	Experimental evolution studies have shown that weak antibiotic selective pressures (i.e., when the antibiotic concentrations are far below the minimum inhibitory concentration, MIC) can select resistant mutants, raising several unanswered questions. First, what are the lowest antibiotic concentrations at which selection for de novo resistance mutations can occur? Second, with weak antibiotic selections, which other types of adaptive mutations unrelated to the antibiotic selective pressure are concurrently enriched? Third, are the mutations selected under laboratory settings at subMIC also observed in clinical isolates? We addressed these questions using Escherichia coli populations evolving at subMICs in the presence of either of four clinically used antibiotics: fosfomycin, nitrofurantoin, tetracycline, and ciprofloxacin. Antibiotic resistance evolution was investigated at concentrations ranging from 1/4th to 1/2000th of the MIC of the susceptible strain (MICsusceptible). Our results show that evolution was rapid across all the antibiotics tested, and selection for fosfomycin- and nitrofurantoin-resistant mutants was observed at a concentration as low as 1/2000th of MICsusceptible. Several of the evolved resistant mutants showed increased growth yield and exponential growth rates, and outcompeted the susceptible ancestral strain in the absence of antibiotics as well, suggesting that adaptation to the growth environment occurred in parallel with the selection for resistance. Genomic analysis of the resistant mutants showed that several of the mutations selected under these conditions are also found in clinical isolates, demonstrating that experimental evolution at very low antibiotic levels can help in identifying novel mutations that contribute to bacterial adaptation during subMIC exposure in real-life settings.
MeSH term(s)	Anti-Bacterial Agents/pharmacology ; Nitrofurantoin ; Fosfomycin/pharmacology ; Drug Resistance, Microbial/genetics ; Escherichia coli/genetics ; Microbial Sensitivity Tests ; Mutation ; Drug Resistance, Bacterial/genetics
Chemical Substances	Anti-Bacterial Agents ; Nitrofurantoin (927AH8112L) ; Fosfomycin (2N81MY12TE)
Language	English
Publishing date	2023-01-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	998579-7
ISSN	1537-1719 ; 0737-4038
ISSN (online)	1537-1719
ISSN	0737-4038
DOI	10.1093/molbev/msad010
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Zs.A 2137: Show issues

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Article ; Online: Evolutionary history of Staphylococcus aureus influences antibiotic resistance evolution.

Fait, Anaëlle / Andersson, Dan I / Ingmer, Hanne

Current biology : CB

2023 Volume 33, Issue 16, Page(s) 3389–3397.e5

Abstract: Antibiotic resistance often confers a fitness cost to the resistant cell and thus raises key questions of how resistance is maintained in the absence of antibiotics and, if lost, whether cells are genetically primed for re-evolving resistance. To address ...

Abstract	Antibiotic resistance often confers a fitness cost to the resistant cell and thus raises key questions of how resistance is maintained in the absence of antibiotics and, if lost, whether cells are genetically primed for re-evolving resistance. To address these questions, we have examined vancomycin-intermediate Staphylococcus aureus (VISA) strains that arise during vancomycin therapy. VISA strains harbor a broad spectrum of mutations, and they are known to be unstable both in patients and in the laboratory. Here, we show that loss of resistance in VISA strains is correlated with a fitness increase and is attributed to adaptive mutations, leaving the initial VISA-adaptive mutations intact. Importantly, upon a second exposure to vancomycin, such revertants evolve significantly faster to become VISA, and they reach higher resistance levels than vancomycin-naive cells. Further, we find that sub-lethal concentrations of vancomycin stabilize the VISA phenotype, as do the human β-defensin 3 (hBD-3) and the bacteriocin nisin that both, like vancomycin, bind to the peptidoglycan building block, lipid II. Thus, factors binding lipid II may stabilize VISA both in vivo and in vitro, and in case resistance is lost, mutations remain that predispose to resistance development. These findings may explain why VISA infections often are re-occurring and suggest that previous vancomycin adaptation should be considered a risk factor when deciding on antimicrobial chemotherapy.
MeSH term(s)	Humans ; Staphylococcus aureus/genetics ; Vancomycin/pharmacology ; Vancomycin/therapeutic use ; Vancomycin Resistance/genetics ; Anti-Bacterial Agents/pharmacology ; Staphylococcal Infections/drug therapy
Chemical Substances	Vancomycin (6Q205EH1VU) ; Anti-Bacterial Agents
Language	English
Publishing date	2023-07-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1071731-6
ISSN	1879-0445 ; 0960-9822
ISSN (online)	1879-0445
ISSN	0960-9822
DOI	10.1016/j.cub.2023.06.082
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Zs.A 3208: Show issues

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Article ; Online: Mechanisms and therapeutic potential of collateral sensitivity to antibiotics.

Roemhild, Roderich / Andersson, Dan I

PLoS pathogens

2021 Volume 17, Issue 1, Page(s) e1009172

MeSH term(s)	Anti-Bacterial Agents/pharmacology ; Bacteria/drug effects ; Bacteria/growth & development ; Drug Collateral Sensitivity ; Drug Design ; Drug Resistance, Multiple, Bacterial/drug effects ; Humans
Chemical Substances	Anti-Bacterial Agents
Language	English
Publishing date	2021-01-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1009172
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Article ; Online: Interspecies interaction reduces selection for antibiotic resistance in Escherichia coli

Ramith R. Nair / Dan I. Andersson

Communications Biology, Vol 6, Iss 1, Pp 1-

2023 Volume 9

Abstract: B. subtilis dampens nitrofurantoin resistance enrichment in E. coli through producing extracellular compounds such as YydF peptide. ...

Abstract	B. subtilis dampens nitrofurantoin resistance enrichment in E. coli through producing extracellular compounds such as YydF peptide.
Keywords	Biology (General) ; QH301-705.5
Language	English
Publishing date	2023-03-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: High prevalence of heteroresistance in Staphylococcus aureus is caused by a multitude of mutations in core genes.

Heidarian, Sheida / Guliaev, Andrei / Nicoloff, Hervé / Hjort, Karin / Andersson, Dan I

PLoS biology

2024 Volume 22, Issue 1, Page(s) e3002457

Abstract: Heteroresistance (HR) is an enigmatic phenotype where, in a main population of susceptible cells, small subpopulations of resistant cells exist. This is a cause for concern, as this small subpopulation is difficult to detect by standard antibiotic ... ...

Abstract	Heteroresistance (HR) is an enigmatic phenotype where, in a main population of susceptible cells, small subpopulations of resistant cells exist. This is a cause for concern, as this small subpopulation is difficult to detect by standard antibiotic susceptibility tests, and upon antibiotic exposure the resistant subpopulation may increase in frequency and potentially lead to treatment complications or failure. Here, we determined the prevalence and mechanisms of HR for 40 clinical Staphylococcus aureus isolates, against 6 clinically important antibiotics: daptomycin, gentamicin, linezolid, oxacillin, teicoplanin, and vancomycin. High frequencies of HR were observed for gentamicin (69.2%), oxacillin (27%), daptomycin (25.6%), and teicoplanin (15.4%) while none of the isolates showed HR toward linezolid or vancomycin. Point mutations in various chromosomal core genes, including those involved in membrane and peptidoglycan/teichoic acid biosynthesis and transport, tRNA charging, menaquinone and chorismite biosynthesis and cyclic-di-AMP biosynthesis, were the mechanisms responsible for generating the resistant subpopulations. This finding is in contrast to gram-negative bacteria, where increased copy number of bona fide resistance genes via tandem gene amplification is the most prevalent mechanism. This difference can be explained by the observation that S. aureus has a low content of resistance genes and absence of the repeat sequences that allow tandem gene amplification of these genes as compared to gram-negative species.
MeSH term(s)	Humans ; Staphylococcus aureus/genetics ; Vancomycin ; Daptomycin ; Linezolid/therapeutic use ; Teicoplanin/therapeutic use ; Prevalence ; Anti-Bacterial Agents/pharmacology ; Anti-Bacterial Agents/therapeutic use ; Staphylococcal Infections/genetics ; Staphylococcal Infections/drug therapy ; Oxacillin/therapeutic use ; Mutation ; Gentamicins
Chemical Substances	Vancomycin (6Q205EH1VU) ; Daptomycin (NWQ5N31VKK) ; Linezolid (ISQ9I6J12J) ; Teicoplanin (61036-62-2) ; Anti-Bacterial Agents ; Oxacillin (UH95VD7V76) ; Gentamicins
Language	English
Publishing date	2024-01-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	2126776-5
ISSN	1545-7885 ; 1544-9173
ISSN (online)	1545-7885
ISSN	1544-9173
DOI	10.1371/journal.pbio.3002457
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Zs.A 6193: Show issues

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Article ; Online: Within-species variability of antibiotic interactions in Gram-negative bacteria.

Tang, Po-Cheng / Sánchez-Hevia, Dione L / Westhoff, Sanne / Fatsis-Kavalopoulos, Nikolaos / Andersson, Dan I

mBio

2024 Volume 15, Issue 3, Page(s) e0019624

Abstract: Treatments with antibiotic combinations are becoming increasingly important even though the supposed clinical benefits of combinations are, in many cases, unclear. Here, we systematically examined how several clinically used antibiotics interact and ... ...

Abstract	Treatments with antibiotic combinations are becoming increasingly important even though the supposed clinical benefits of combinations are, in many cases, unclear. Here, we systematically examined how several clinically used antibiotics interact and affect the antimicrobial efficacy against five especially problematic Gram-negative pathogens. A total of 232 bacterial isolates were tested against different pairwise antibiotic combinations spanning five classes, and the ability of all combinations in inhibiting growth was quantified. Descriptive statistics, principal component analysis (PCA), and Spearman's rank correlation matrix were used to determine the correlations between the different combinations on interaction outcome. Several important conclusions can be drawn from the 696 examined interactions. Firstly, within a species, the interactions are in general conserved but can be isolate-specific for a given antibiotic combination and can range from antagonistic to synergistic. Secondly, additive and antagonistic interactions are the most common observed across species and antibiotics, with 87.1% of isolate-antibiotic combinations being additive, 11.6% antagonistic, and only 0.3% showing synergy. These findings suggest that to achieve the highest precision and efficacy of combination therapy, not only isolate-specific interaction profiling ought to be routinely performed, in particular to avoid using drug combinations that show antagonistic interaction and an expected associated reduction in efficacy, but also discovering rare and potentially valuable synergistic interactions.IMPORTANCEAntibiotic combinations are often used to treat bacterial infections, which aim to increase treatment efficacy and reduce resistance evolution. Typically, it is assumed that one specific antibiotic combination has the same effect on different isolates of the same species, i.e., the interaction is conserved. Here, we tested this idea by examining how several clinically used antibiotics interact and affect the antimicrobial efficacy against several bacterial pathogens. Our results show that, even though within a species the interactions are often conserved, there are also isolate-specific differences for a given antibiotic combination that can range from antagonistic to synergistic. These findings suggest that isolate-specific interaction profiling ought to be performed in clinical microbiology routine to avoid using antagonistic drug combinations that might reduce treatment efficacy.
MeSH term(s)	Humans ; Anti-Bacterial Agents/pharmacology ; Drug Synergism ; Bacterial Infections/drug therapy ; Drug Combinations ; Gram-Negative Bacteria ; Microbial Sensitivity Tests
Chemical Substances	Anti-Bacterial Agents ; Drug Combinations
Language	English
Publishing date	2024-02-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mbio.00196-24
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