Environmental selection of antibiotic resistance genes. Minireview (original) (raw)
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Frontiers in microbiology, 2013
Antibiotics and antibiotic resistance determinants, natural molecules closely related to bacterial physiology and consistent with an ancient origin, are not only present in antibioticproducing bacteria. Throughput sequencing technologies have revealed an unexpected reservoir of antibiotic resistance in the environment. These data suggest that co-evolution between antibiotic and antibiotic resistance genes has occurred since the beginning of time. This evolutionary race has probably been slow because of highly regulated processes and low antibiotic concentrations. Therefore to understand this global problem, a new variable must be introduced, that the antibiotic resistance is a natural event, inherent to life. However, the industrial production of natural and synthetic antibiotics has dramatically accelerated this race, selecting some of the many resistance genes present in nature and contributing to their diversification. One of the best models available to understand the biological impact of selection and diversification are β-lactamases. They constitute the most widespread mechanism of resistance, at least among pathogenic bacteria, with more than 1000 enzymes identified in the literature. In the last years, there has been growing concern about the description, spread, and diversification of β-lactamases with carbapenemase activity and AmpC-type in plasmids. Phylogenies of these enzymes help the understanding of the evolutionary forces driving their selection. Moreover, understanding the adaptive potential of β-lactamases contribute to exploration the evolutionary antagonists trajectories through the design of more efficient synthetic molecules. In this review, we attempt to analyze the antibiotic resistance problem from intrinsic and environmental resistomes to the adaptive potential of resistance genes and the driving forces involved in their diversification, in order to provide a global perspective of the resistance problem.
Antibiotic resistance in microbes
Cellular and Molecular Life Sciences (CMLS), 1999
The treatment of infectious disease is com-disseminated among bacterial populations by several promised by the development of antibiotic-resistant processes, but principally by conjugation. Thus the overall problem of antibiotic resistance is one of genetic strains of microbial pathogens. A variety of biochemical processes are involved that may keep antibiotics out of ecology and a better understanding of the contributing parameters is necessary to devise rational approaches to the cell, alter the target of the drug, or disable the reduce the development and spread of antibiotic resis-antibiotic. Studies have shown that resistance determitance and so avoid a critical situation in therapy-a nants arise by either of two genetic mechanisms: mutation and acquisition. Antibiotic resistance genes can be return to a pre-antibiotic era.
2007
The extended spectrum -lactamase (ESBL) production and multidrug resistant of Klebsiella pneumoniae in children below 5 years of ages are investigated. The K. pneumoniae strains isolated from patients suffering from intestinal and extra intestinal infection between the 0- 5 year’s ages of children showed resistant to the three antibiotics (ceftazidime, cefotaxime, ceftriaxone), and coexist with non -lactam resistance and ESBL production. All the strains were susceptibility to the antibiotic, imipenem. Out off 110 strains only 9 strains produced ESBL. The plasmid responsible for the antibiotic resistance and ESBL production can be transferred to recipient Escherichia coli strain. Key words: Klebsiella pneumoniae, drug resistance, ESBL production.
Impact #378 THE “EVOLUTION” OF ANTIBIOTIC RESISTANCE
2004
An increase in the frequency of antibiotic resistance in bacteria since the 1950s has been observed for all major classes of antibiotics used to treat a wide variety of respiratory illnesses, skin disorders, and sexually transmitted diseases. Is this resistance the result of bacteria evolving new genes in response to the presence of antibiotics, or are antibiotic-resistant bacteria selected for in the environment by possessing antibiotic resistance genes beforehand? To answer these questions a discussion of several factors involved in antibiotic resistance will show that resistance is a designed feature of pre-existing genes enabling bacteria to compete with the antibiotic producers in their environment. A brief look at an example of penicillin resistance reveals the increase in the frequency of antibiotic-resistant organisms since the time when antibiotic use became common. Penicillin is an antibiotic produced by the common bread mold Penicillium that was discovered accidentally in...
The emergence of antibiotic resistance by mutation
Clinical Microbiology and Infection, 2007
The emergence of mutations in nucleic acids is one of the major factors underlying evolution, providing the working material for natural selection. Most bacteria are haploid for the vast majority of their genes and, coupled with typically short generation times, this allows mutations to emerge and accumulate rapidly, and to effect significant phenotypic changes in what is perceived to be real-time. Not least among these phenotypic changes are those associated with antibiotic resistance. Mechanisms of horizontal gene spread among bacterial strains or species are often considered to be the main mediators of antibiotic resistance. However, mutational resistance has been invaluable in studies of bacterial genetics, and also has primary clinical importance in certain bacterial species, such as Mycobacterium tuberculosis and Helicobacter pylori, or when considering resistance to particular antibiotics, especially to synthetic agents such as fluoroquinolones and oxazolidinones. In addition, mutation is essential for the continued evolution of acquired resistance genes and has, e.g., given rise to over 100 variants of the TEM family of b-lactamases. Hypermutator strains of bacteria, which have mutations in genes affecting DNA repair and replication fidelity, have elevated mutation rates. Mutational resistance emerges de novo more readily in these hypermutable strains, and they also provide a suitable host background for the evolution of acquired resistance genes in vitro. In the clinical setting, hypermutator strains of Pseudomonas aeruginosa have been isolated from the lungs of cystic fibrosis patients, but a more general role for hypermutators in the emergence of clinically relevant antibiotic resistance in a wider variety of bacterial pathogens has not yet been proven.
2018
Author(s): Mira, Portia Mae | Advisor(s): Barlow, Miriam; Meza, Juan C | Abstract: Antibiotic resistance continues to be a major challenge we face today. Scientists and medical professionals are competing against a microbial evolutionary time bomb. The alarming increase in the number of deaths caused by multi-drug resistant infections (1) and the decrease in development of reliable treatment regimens is disturbing. Historically, most studies focus on the effects of fatal concentrations of antibiotics on the evolution of antibiotic resistance (2). Focusing on high antibiotic concentrations limits our understanding of antibiotic resistance and how its evolution is established. Especially since it has been shown that there is a greater selection of resistant bacteria at sub-lethal concentrations of antibiotics (3). Our main goal is to further investigate the impacts of sub-inhibitory concentrations of antibiotics on antibiotic resistance evolution. To do this, we studied two genes that...
Environmental and genetic modulation of the phenotypic expression of antibiotic resistance
FEMS microbiology reviews, 2017
Antibiotic resistance can be acquired by mutation or horizontal transfer of a resistance gene, and generally an acquired mechanism results in a predictable increase in phenotypic resistance. However, recent findings suggest that the environment and/or the genetic context can modify the phenotypic expression of specific resistance genes/mutations. An important implication from these findings is that a given genotype does not always result in the expected phenotype. This dissociation of genotype and phenotype has important consequences for clinical bacteriology and for our ability to predict resistance phenotypes from genetics and DNA sequences. A related problem concerns the degree to which the genes/mutations currently identified in vitro can fully explain the in vivo resistance phenotype, or whether there is a significant additional amount of presently unknown mutations/genes (genetic 'dark matter') that could contribute to resistance in clinical isolates. Finally, a very i...