Antimicrobial Resistance: Introduction, types and mechanism

Antimicrobial Resistance

Introduction of Antimicrobial Resistance

Antimicrobial Resistance (AMR)can be defined as the temporary or permanent ability of an organism and its progeny to remain viable or multiply under environmental conditions that would destroy or inhibit other cells. An antibiotic is said to be resistant when that antibiotic in prescribed amount and concentration, is unable to kill/ suppress the growth of the pathogens.

Types of Antimicrobial Resistance

It is of following types and they are-

  1. Environmentally mediated antimicrobial resistance
  2. Genetic Basis of Antimicrobial Resistance
  3. Biochemical basis of antimicrobial resistance. 

Environmentally mediated antimicrobial resistance

It directly results from physical or chemical characteristics of the environment that either directly alter the antimicrobial agent or alter the microorganism’s normal physiological response to the drug. Examples of environmental factors include pH, anaerobic atmosphere, cation concentration and thymine – thymidine content. Antibacterial activities of erythromycin and aminoglycosides diminish with decreasing pH while the activity of tetracycline decreases with increasing pH. Aminoglycoside activity requires intracellular uptake across the cell membrane, much of which is driven by oxidative processes so that in the absence of oxygen, uptake and hence activity is substantially diminished. Microorganism mediated antimicrobial resistance: It refers to antimicrobial resistance that is due to genetically encoded traits of the microorganism and is the type of resistance that in vitro susceptibility testing methods are targeted to detect. Organisms based resistance can be divided into two subcategories: intrinsic or inherent resistance and acquired resistance.

  1. Antimicrobial resistance resulting from the normal genetic, structural or physiological state of a microorganism is referred to as intrinsic resistance, e.g., aminoglycosides against Enterococcus and Vancomycin against gram negative bacteria.
  2. Antibiotic resistance that results from altered cellular physiology and structure caused by change in a microorganism’s usual genetic makeup is called acquired resistance.

Genetic Basis of Antimicrobial Resistance

Conjugation: In conjugation, there is physical contact between two genetically different bacterial cells of the same or closely related species. There is no exchange of genetic material during conjugation, only unilateral transfers occur.Genetic material that mediates resistance is most often transferred as plasmids or transposons. Resistance may therefore, pass between species, from commensals to pathogens, and vice versa.

Transduction: Transduction is the transfer of genetic information between bacteria by bacteriophages. In the clinical setting, transduction may be more important in spreading resistance among gram positive bacteria than gram negative cells.

Transformation: It is a process in which free Deoxyribonucleic acid (DNA) molecule is transferred from a donor to a recipient bacterium. The DNA released from the donor cell upon cell lysis may be absorbed by competent cells and integrated into their genomes.

Biochemical basis of antimicrobial resistance

Conversion of an active drug to an inert derivative by enzyme produced by the resistant cells will result into drug resistant. For examples β- Lactamases (Penicillinases, including ESBLs,Metallo β- lactamaseAmpC enzymes and Oxacillinase)

References

  1. Rossolini G, Docquier J, editors. Metallo-beta-lactamases: a last frontier for beta-lactams. 15th European Congress of Clinical Microbiology and Infectious Diseases, Copenhagen/Denmark; 2005.
  2. Forbes BA, Sahm DF, Weissfeld AS, Trevino E. Bailey & Scott’s diagnostic microbiology, Mosby. Inc, St Louis. 2002.
  3. Anthonamma K, Prasad S, Rajasekhar D, Swapna N, Prasad M. In vitro antimicrobial efficacy of solvent extracts of seeds of Albizzia lebbeck (L.) Benth. International Journal of Advances in Pharmaceutical Sciences. 2010;1(3).
  4. Hawkey PM. The origins and molecular basis of antibiotic resistance. British Medical Journal. 1998;317(7159):657.
  5. Reddy P, Malczynski M, Obias A, Reiner S, Jin N, Huang J, et al. Screening for extended-spectrum β-lactamase-producing Enterobacteriaceae among high-risk patients and rates of subsequent bacteremia. Clinical infectious diseases. 2007;45(7):846-52.
  6. Bedenić B. [Beta-lactamases in laboratory and their role in resistance Part I.: Evolution of bacterial resistance mediated by beta-lactamases]. Lijecnicki vjesnik. 2003;126(11-12):314-24.
  7. Giedraitienė A, Vitkauskienė A, Naginienė R, Pavilonis A. Antibiotic resistance mechanisms of clinically important bacteria. Medicina (kaunas). 2011;47(3):137-46.
  8. Bradford PA. Extended-spectrum β-lactamases in the 21st century: characterization, epidemiology, and detection of this important resistance threat. Clinical microbiology reviews. 2001;14(4):933-51.
  9. Samaha-Kfoury JN, Araj GF, Anwar R. Recent developments in [beta] lactamases and extended spectrum [beta] lactamases. British Medical Journal. 2003;327(7425):1209.

 

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