Breakthroughs in bacterial resistance mechanisms and the potential ways to combat them

2016 ◽  
Vol 95 ◽  
pp. 32-42 ◽  
Author(s):  
Bahman Khameneh ◽  
Roudayna Diab ◽  
Kiarash Ghazvini ◽  
Bibi Sedigheh Fazly Bazzaz
Keyword(s):  
Bacterial Resistance ◽  
Resistance Mechanisms

Assessment of the correctness of identification and determination of antimicrobial susceptibility of Streptococcus pneumoniae in microbiological laboratories in Poland

2020 ◽  
Vol 55 (4) ◽  
pp. 271-276
Author(s):  
Ewa Młodzińska ◽  
Waleria Hryniewicz
Keyword(s):  
Quality Control ◽  
Antimicrobial Susceptibility ◽  
Bacterial Resistance ◽  
External Quality Assessment ◽  
Resistance Mechanisms ◽  
Medical Problems ◽  
External Quality ◽  
External Quality Assessment Scheme ◽  
Reliable Identification

The increase in bacterial resistance to antimicrobials is one of the most serious medical problems, therefore reliable identification in microbiological laboratories is important. The Polish National External Quality Assessment Scheme in Microbiological Diagnostics – POLMICRO programme is organized by the Centre of Quality Control in Microbiology (CQCM) enables the assessment of the competence of Polish microbiological laboratories in the field of identification, determination of susceptibility and detection of drug resistance mechanisms. This work presents the assessment of the results of identification and determination of S. pneumoniae antimicrobial susceptibility obtained by Polish laboratories during the 20 years of experience of the POLMICRO programme.

Bacterial Resistance to Antibiotics: Mechanisms and Prevalence in Hospitals and Nursing Homes

DICP ◽  
1989 ◽  
Vol 23 (7-8) ◽  
pp. 556-561 ◽  
Author(s):  
John A. Bosso
Keyword(s):  
Nursing Homes ◽  
Bacterial Resistance ◽  
Resistance Mechanisms ◽  
Resistance To Antibiotics

Bacterial resistance to antibiotics has become an increasingly distressing problem over the last few decades. In this article, known resistance mechanisms are reviewed and the extent of the problem in both hospitals and nursing homes is addressed. Suggestions for preventing the further spread of this problem are presented.

scholarly journals Analisis Mutasi pada Kodon 531 Pada Gen Rpob Mycobacterium tuberculosis Penyebab Resistensi Rifampisin

2017 ◽  
Vol 15 (2) ◽  
pp. 140
Author(s):  
Yatnita Parama Cita ◽  
Dwi Hilda Putri
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Bacterial Resistance ◽  
Rpob Gene ◽  
Resistance Mechanisms ◽  
Primer Design ◽  
Reference Sequence ◽  
Multi Drug Resistance ◽  
Accession Number ◽  
Chemotherapy Agent ◽  
Primer Design Program

Tuberculosis (TB) is a serious disesase in the world. According to the WHO, it is estimated more than 3 million people die every year as a result of this infectious disease. One factor that causes diffi culty handling TB chemoteraphy is not effective against the bacteria Mycobacterium tuberculosis that causes TB . Effectiveness of treatment is often hampered by the emergence of bacterial resistance against M. Tuberculosis chemotherapy agents are given. From some research found that bacterial resistance may occur in more one type of chemotherapy agent also known as multi-drug resistance (MDR). Mycobacterium tuberculosis develop resistance mechanisms that are different from other bacteria in general. In prokaryotes, resistance is generally due to the transfer of genetic, either through plasmids,transposons and other. Reference sequence beta sub unit of RNAP protein M. Tuberculosis with accession number NP_215181.1 and M. tucerculosis rpoB gene with accession number NC_000962.3 used to obtain preliminary information from the data base www.ncbi.nlm.gov and www.uniprot.org . Mutation done according to several studies literature. Analysis of the composition, profi le, location and structure of protein using www.expasy.org, TMHMM and http://bioinf.cs.ucl.ac.uk/psipred. The primer design is done with Primer Design Program. Based on the analysis of mutation in the beta subunit of RNAP protein M. Tuberculosis, codon 531 (Ser ->Leu), it is known that mutations cause changes in some properties and structure of proteins. Possible changes affecting the nature of bacterial resistance to antibiotics rifampicin. However, further analysis needs to be done with the analysis of the docking technique.

scholarly journals Experimental Induction of Bacterial Resistance to the Antimicrobial Peptide Tachyplesin I and Investigation of the Resistance Mechanisms

2016 ◽  
Vol 60 (10) ◽  
pp. 6067-6075 ◽  
Author(s):  
Jun Hong ◽  
Jianye Hu ◽  
Fei Ke
Keyword(s):  
Antimicrobial Peptide ◽  
Bacterial Resistance ◽  
Antimicrobial Agents ◽  
Resistance Mechanisms ◽  
Cross Resistance ◽  
Antibacterial Drug ◽  
Cationic Antimicrobial Peptide ◽  
Content Type ◽  
Tachyplesin I

ABSTRACTTachyplesin I is a 17-amino-acid cationic antimicrobial peptide (AMP) with a typical cyclic antiparallel β-sheet structure that is a promising therapeutic for infections, tumors, and viruses. To date, no bacterial resistance to tachyplesin I has been reported. To explore the safety of tachyplesin I as an antibacterial drug for wide clinical application, we experimentally induced bacterial resistance to tachyplesin I by using two selection procedures and studied the preliminary resistance mechanisms.Aeromonas hydrophilaXS91-4-1,Pseudomonas aeruginosaCGMCC1.2620, andEscherichia coliATCC 25922 and F41 showed resistance to tachyplesin I under long-term selection pressure with continuously increasing concentrations of tachyplesin I. In addition,P. aeruginosaandE. coliexhibited resistance to tachyplesin I under UV mutagenesis selection conditions. Cell growth and colony morphology were slightly different between control strains and strains with induced resistance. Cross-resistance to tachyplesin I and antimicrobial agents (cefoperazone and amikacin) or other AMPs (pexiganan, tachyplesin III, and polyphemusin I) was observed in some resistant mutants. Previous studies showed that extracellular protease-mediated degradation of AMPs induced bacterial resistance to AMPs. Our results indicated that the resistance mechanism ofP. aeruginosawas not entirely dependent on extracellular proteolytic degradation of tachyplesin I; however, tachyplesin I could induce increased proteolytic activity inP. aeruginosa. Most importantly, our findings raise serious concerns about the long-term risks associated with the development and clinical use of tachyplesin I.

scholarly journals Paving the Way to Unveil the Diversity and Evolution of Phage Genomes

Viruses ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 905
Author(s):  
Alejandro Reyes ◽  
Martha J. Vives
Keyword(s):  
Molecular Evolution ◽  
Host Range ◽  
Molecular Mechanisms ◽  
Bacterial Resistance ◽  
Viral Pathogenesis ◽  
Resistance Mechanisms ◽  
Molecular Tools ◽  
Special Issue ◽  
Bacterial Host ◽  
Host Interactions

Phage biology has been developing for the last hundred years, and the potential of phages as tools and treatments has been known since their early discovery. However, the lack of knowledge of the molecular mechanisms coded in phage genomes hindered the development of the field. With current molecular methods, the last decade has been a resurgence of the field. The Special Issue on “Diversity and Evolution of Phage Genomes” is a great example with its 17 manuscripts published. It covers some of the latest methods to sample and characterize environmental and host associated viromes, considering experimental biases and computational developments. Furthermore, the use of molecular tools coupled with traditional methods has allowed to isolate and characterize viruses from different hosts and environments with such diversity that even a new viral class is being proposed. The viruses described cover all different phage families and lifestyles. However, is not only about diversity; the molecular evolution is studied in a set of manuscripts looking at phage-host interactions and their capacity to uncover the frequency and type of mutations behind the bacterial resistance mechanisms and viral pathogenesis, and such methods are opening new ways into identifying potential receptors and characterizing the bacterial host range.

scholarly journals Some approaches to new antibacterial agents

2007 ◽  
Vol 79 (12) ◽  
pp. 2143-2153 ◽  
Author(s):  
John B. Bremner
Keyword(s):  
Bacterial Resistance ◽  
Efflux Pump ◽  
Transmembrane Protein ◽  
Resistance Mechanism ◽  
Resistance Mechanisms ◽  
Target Site ◽  
Resistant Bacteria ◽  
General Strategy ◽  
Dual Action ◽  
Hybrid Drugs

Bacteria use a number of resistance mechanisms to counter the antibacterial challenge, and one of these is the expression of transmembrane protein-based efflux pumps which can pump out antibacterials from within the cells, thus lowering the antibacterial concentration to nonlethal levels. For example, in S. aureus, the NorA pump can pump out the antibacterial alkaloid berberine and ciprofloxacin. One general strategy to reduce the health threat of resistant bacteria is to block a major bacterial resistance mechanism at the same time as interfering with another bacterial pathway or target site. New developments of this approach in the context of dual-action prodrugs and dual-action (or hybrid) drugs in which one action is targeted at blocking the NorA efflux pump and the second action at an alternative bacterial target site (or sites) for the antibacterial action are discussed. The compounds are based on a combination of 2-aryl-5-nitro-1H-indole derivatives (as the NorA efflux pump blocking component) and derivatives of berberine. General design principles, syntheses, antibacterial testing, and preliminary work on modes of action studies are discussed.

scholarly journals Impact of an Intervention to Control Imipenem-Resistant Acinetobacter baumannii and Its Resistance Mechanisms: An 8-Year Survey

2021 ◽  
Vol 11 ◽  
Author(s):  
Lida Chen ◽  
Pinghai Tan ◽  
Jianming Zeng ◽  
Xuegao Yu ◽  
Yimei Cai ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Acinetobacter Baumannii ◽  
Bacterial Resistance ◽  
Efflux Pump ◽  
Resistance Mechanism ◽  
Resistance Mechanisms ◽  
Multi Drug Resistance ◽  
Minimal Inhibitory Concentrations ◽  
Resistance Rates ◽  
The Impact

BackgroundThis study aimed to examine the impact of an intervention carried out in 2011 to combat multi-drug resistance and outbreaks of imipenem-resistant Acinetobacter baumannii (IRAB), and to explore its resistance mechanism.MethodsA total of 2572 isolates of A. baumannii, including 1673 IRAB isolates, were collected between 2007 and 2014. An intervention was implemented to control A. baumannii resistance and outbreaks. Antimicrobial susceptibility was tested by calculating minimal inhibitory concentrations (MICs), and outbreaks were typed using pulsed-field gel electrophoresis (PFGE). Resistance mechanisms were explored by polymerase chain reaction (PCR) and whole genome sequencing (WGS).ResultsFollowing the intervention in 2011, the resistance rates of A. baumannii to almost all tested antibiotics decreased, from 85.3 to 72.6% for imipenem, 100 to 80.8% for ceftriaxone, and 45.0 to 6.9% for tigecycline. The intervention resulted in a decrease in the number (seven to five), duration (8–3 months), and departments (five to three) affected by outbreaks; no outbreaks occurred in 2011. After the intervention, only blaAMPC (76.47 to 100%) and blaTEM–1 (75.74 to 96.92%) increased (P < 0.0001); whereas blaGES–1 (32.35 to 3.07%), blaPER–1 (21.32 to 1.54%), blaOXA–58 (60.29 to 1.54%), carO (37.50 to 7.69%), and adeB (9.56 to 3.08%) decreased (P < 0.0001). Interestingly, the frequency of class B β-lactamase genes decreased from 91.18% (blaSPM–1) and 61.03% (blaIMP–1) to 0%, while that of class D blaOXA–23 increased to 96.92% (P < 0.0001). WGS showed that the major PFGE types causing outbreaks each year (type 01, 11, 18, 23, 26, and 31) carried the same resistance genes (blaKPC–1, blaADC–25, blaOXA–66, and adeABC), AdeR-S mutations (G186V and A136V), and a partially blocked porin channel CarO. Meanwhile, plasmids harboring blaOXA–23 were found after the intervention.ConclusionThe intervention was highly effective in reducing multi-drug resistance of A. baumannii and IRAB outbreaks in the long term. The resistance mechanisms of IRAB may involve genes encoding β-lactamases, efflux pump overexpression, outer membrane porin blockade, and plasmids; in particular, clonal spread of blaOXA–23 was the major cause of outbreaks. Similar interventions may also help reduce bacterial resistance rates and outbreaks in other hospitals.

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