Special Issue "Antibiotic Resistance"

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A special issue of Antibiotics (ISSN 2079-6382).

Deadline for manuscript submissions: closed (31 January 2013)

Special Issue Editor

Guest Editor
Prof. Dr. Dan I. Andersson (Website)

Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala Biomedicinska Centrum BMC, Husarg. 3, 751 23 Uppsala, Sweden
Interests: antibiotic resistance mechanisms; antibiotic action; bacterial genetics; molecular and experimental evolution

Special Issue Information

Dear Colleagues,

This call for manuscripts (original research work and reviews) to the recently started journal ANTIBIOTICS is aimed at the area of Antibiotic Resistance. Even though evolution is a process typically submitted to many unexpected factors and therefore thought by many to be essentially unpredictable, much of microbiological research applied to public health is based on the implicit belief that microbial variation leading to infectious diseases and antibiotic resistance is predictable and therefore can be controlled and prevented before causing clinical problems. Thus, to rationally and effectively deal with antibiotic resistance we need to understand the evolutionary origin of different types of resistance mechanisms and which factors are influencing the emergence and spread of these resistance mechanisms into human and animal bacterial pathogens. We also need to have conceptual as well as methodological tools available for prediction of when, where and how resistance will develop when antibiotic pressures are applied. Furthermore, we need to explore novel approaches with regard to how to rationally choose drug targets and drugs with minimized risk of resistance development.
Thus, the scope of this special issue is antibiotic resistance with a special focus on resistance mechanisms, their emergence and transmission and factors that influence the rate and trajectory of the evolution of various types of resistance mechanisms within and outside human hosts. Mechanisms include both mutational and laterally transferred resistance mechanisms, and we are interested in both experimental and theoretical work.

Prof. Dr. Dan I. Andersson
Guest Editor

Submission

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antibiotics is an international peer-reviewed Open Access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 300 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.

Keywords

  • antibiotic resistance
  • mechanisms of resistance
  • evolution
  • prediction
  • mathematical modeling
  • resistome
  • emergence
  • mutation
  • horizontal gene transfer
  • plasmids
  • transposons
  • integrons
  • transmission
  • virulence
  • mutator

Published Papers (5 papers)

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Review

Open AccessReview Multiple Pathways of Genome Plasticity Leading to Development of Antibiotic Resistance
Antibiotics 2013, 2(2), 288-315; doi:10.3390/antibiotics2020288
Received: 7 March 2013 / Revised: 21 May 2013 / Accepted: 23 May 2013 / Published: 30 May 2013
Cited by 3 | PDF Full-text (557 KB) | HTML Full-text | XML Full-text
Abstract
The emergence of multi-resistant bacterial strains is a major source of concern and has been correlated with the widespread use of antibiotics. The origins of resistance are intensively studied and many mechanisms involved in resistance have been identified, such as exogenous gene [...] Read more.
The emergence of multi-resistant bacterial strains is a major source of concern and has been correlated with the widespread use of antibiotics. The origins of resistance are intensively studied and many mechanisms involved in resistance have been identified, such as exogenous gene acquisition by horizontal gene transfer (HGT), mutations in the targeted functions, and more recently, antibiotic tolerance through persistence. In this review, we focus on factors leading to integron rearrangements and gene capture facilitating antibiotic resistance acquisition, maintenance and spread. The role of stress responses, such as the SOS response, is discussed. Full article
(This article belongs to the Special Issue Antibiotic Resistance)
Open AccessReview Phenotypic Resistance to Antibiotics
Antibiotics 2013, 2(2), 237-255; doi:10.3390/antibiotics2020237
Received: 4 February 2013 / Revised: 22 March 2013 / Accepted: 9 April 2013 / Published: 18 April 2013
Cited by 8 | PDF Full-text (493 KB) | HTML Full-text | XML Full-text
Abstract
The development of antibiotic resistance is usually associated with genetic changes, either to the acquisition of resistance genes, or to mutations in elements relevant for the activity of the antibiotic. However, in some situations resistance can be achieved without any genetic alteration; [...] Read more.
The development of antibiotic resistance is usually associated with genetic changes, either to the acquisition of resistance genes, or to mutations in elements relevant for the activity of the antibiotic. However, in some situations resistance can be achieved without any genetic alteration; this is called phenotypic resistance. Non-inherited resistance is associated to specific processes such as growth in biofilms, a stationary growth phase or persistence. These situations might occur during infection but they are not usually considered in classical susceptibility tests at the clinical microbiology laboratories. Recent work has also shown that the susceptibility to antibiotics is highly dependent on the bacterial metabolism and that global metabolic regulators can modulate this phenotype. This modulation includes situations in which bacteria can be more resistant or more susceptible to antibiotics. Understanding these processes will thus help in establishing novel therapeutic approaches based on the actual susceptibility shown by bacteria during infection, which might differ from that determined in the laboratory. In this review, we discuss different examples of phenotypic resistance and the mechanisms that regulate the crosstalk between bacterial metabolism and the susceptibility to antibiotics. Finally, information on strategies currently under development for diminishing the phenotypic resistance to antibiotics of bacterial pathogens is presented. Full article
(This article belongs to the Special Issue Antibiotic Resistance)
Open AccessReview Molecular Mechanisms and Clinical Impact of Acquired and Intrinsic Fosfomycin Resistance
Antibiotics 2013, 2(2), 217-236; doi:10.3390/antibiotics2020217
Received: 11 March 2013 / Revised: 5 April 2013 / Accepted: 8 April 2013 / Published: 16 April 2013
Cited by 9 | PDF Full-text (1062 KB) | HTML Full-text | XML Full-text
Abstract
Bacterial infections caused by antibiotic-resistant isolates have become a major health problem in recent years, since they are very difficult to treat, leading to an increase in morbidity and mortality. Fosfomycin is a broad-spectrum bactericidal antibiotic that inhibits cell wall biosynthesis in [...] Read more.
Bacterial infections caused by antibiotic-resistant isolates have become a major health problem in recent years, since they are very difficult to treat, leading to an increase in morbidity and mortality. Fosfomycin is a broad-spectrum bactericidal antibiotic that inhibits cell wall biosynthesis in both Gram-negative and Gram-positive bacteria. This antibiotic has a unique mechanism of action and inhibits the initial step in peptidoglycan biosynthesis by blocking the enzyme, MurA. Fosfomycin has been used successfully for the treatment of urinary tract infections for a long time, but the increased emergence of antibiotic resistance has made fosfomycin a suitable candidate for the treatment of infections caused by multidrug-resistant pathogens, especially in combination with other therapeutic partners. The acquisition of fosfomycin resistance could threaten the reintroduction of this antibiotic for the treatment of bacterial infection. Here, we analyse the mechanism of action and molecular mechanisms for the development of fosfomycin resistance, including the modification of the antibiotic target, reduced antibiotic uptake and antibiotic inactivation. In addition, we describe the role of each pathway in clinical isolates. Full article
(This article belongs to the Special Issue Antibiotic Resistance)
Open AccessReview Rifampicin Resistance: Fitness Costs and the Significance of Compensatory Evolution
Antibiotics 2013, 2(2), 206-216; doi:10.3390/antibiotics2020206
Received: 1 February 2013 / Revised: 28 March 2013 / Accepted: 28 March 2013 / Published: 3 April 2013
PDF Full-text (184 KB) | HTML Full-text | XML Full-text
Abstract
Seventy years after the introduction of antibiotic chemotherapy to treat tuberculosis, problems caused by drug-resistance in Mycobacterium tuberculosis have become greater than ever. The discovery and development of novel drugs and drug combination therapies will be critical to managing these problematic infections. [...] Read more.
Seventy years after the introduction of antibiotic chemotherapy to treat tuberculosis, problems caused by drug-resistance in Mycobacterium tuberculosis have become greater than ever. The discovery and development of novel drugs and drug combination therapies will be critical to managing these problematic infections. However, to maintain effective therapy in the long-term and to avoid repeating the mistakes of the past, it is essential that we understand how resistance to antibiotics evolves in M. tuberculosis. Recent studies in genomics and genetics, employing both clinical isolates and model organisms, have revealed that resistance to the frontline anti-tuberculosis drug, rifampicin, is very strongly associated with the selection of fitness compensatory mutations in the different subunits of RNA polymerase. This mode of resistance evolution may also apply to other drugs, and knowledge of the rates and mechanisms could be used to design improved diagnostics and by tracking the evolution of infectious strains, to inform the optimization of therapies. Full article
(This article belongs to the Special Issue Antibiotic Resistance)
Open AccessReview Bacterial Responses and Genome Instability Induced by Subinhibitory Concentrations of Antibiotics
Antibiotics 2013, 2(1), 100-114; doi:10.3390/antibiotics2010100
Received: 8 February 2013 / Revised: 4 March 2013 / Accepted: 5 March 2013 / Published: 14 March 2013
Cited by 8 | PDF Full-text (433 KB) | HTML Full-text | XML Full-text
Abstract
Nowadays, the emergence and spread of antibiotic resistance have become an utmost medical and economical problem. It has also become evident that subinhibitory concentrations of antibiotics, which pollute all kind of terrestrial and aquatic environments, have a non-negligible effect on the evolution [...] Read more.
Nowadays, the emergence and spread of antibiotic resistance have become an utmost medical and economical problem. It has also become evident that subinhibitory concentrations of antibiotics, which pollute all kind of terrestrial and aquatic environments, have a non-negligible effect on the evolution of antibiotic resistance in bacterial populations. Subinhibitory concentrations of antibiotics have a strong effect on mutation rates, horizontal gene transfer and biofilm formation, which may all contribute to the emergence and spread of antibiotic resistance. Therefore, the molecular mechanisms and the evolutionary pressures shaping the bacterial responses to subinhibitory concentrations of antibiotics merit to be extensively studied. Such knowledge is valuable for the development of strategies to increase the efficacy of antibiotic treatments and to extend the lifetime of antibiotics used in therapy by slowing down the emergence of antibiotic resistance. Full article
(This article belongs to the Special Issue Antibiotic Resistance)

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