Talk:Antibiotic resistance

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Parking original content for subsequent reinsertion. --Ashcraft - (reply) 19:45, 18 November 2015 (EST)

Schematic representation of how antibiotic resistance arises via natural selection.

Antibiotic resistance or antimicrobial resistance is a form of drug resistance so that some sub-populations of a particular microorganism, most commonly one or more strains of bacteria are able to survive exposure to one or more antibiotics. This can be acquired via: transformation, conjugation, transduction and mutation. Horizontal gene transfer is the primary reason for bacterial antibiotic resistance.[1][2][3] One of its mechanisms is bacterial conjugation, a process in which a bacterial cell transfers genetic material to another cell by cell-to-cell contact exchanging DNA that can add a new function to the recipient cell such as antibiotic resistance.[4]

Approximately about 20 years after the first sale of penicillin a new discovery emerged: Antibiotic resistance.[5] Resistance to antibiotics is considered an modern example of evolution in response to the widespread use of antibiotics but in a new report it was reported the discovery that resistance to antibiotics was already well built in organisms even before antibiotics were invented.[6]


Mechanisms of antibiotic resistance

Are known several ways of appearance of antibiotic resistance in bacteria[7]:

  • Reduced drug accumulation by decreasing drug permeability.
  • Reduced drug accumulation by increasing active efflux (pumping out) of the drugs across the cell surface.[8]
  • Alteration of target site eliminating or reducing binding of antibiotic.
  • Enzymatic deactivation - Enzymes, that by modification, inactive the antibiotic. This can occur for Hydrolysis or Derivation.
  • Sequestration of antibiotic by protein binding.
  • Alteration of metabolic pathway - Metabolic bypass of inhibited reaction.
  • Binding of specific immunity protein to antibiotic.
  • Overproduction of antibiotic target (titration).
  1. ↑ Kay E, Vogel TM, Bertolla F, Nalin R, Simonet P (July 2002). "In situ transfer of antibiotic resistance genes from transgenic (transplastomic) tobacco plants to bacteria". Appl. Environ. Microbiol. 68 (7): 3345–51. PMC 126776. PMID 12089013. http://aem.asm.org/cgi/pmidlookup?view=long&pmid=12089013. 
  2. ↑ Koonin EV, Makarova KS, Aravind L (2001). "Horizontal gene transfer in prokaryotes: quantification and classification". Annu. Rev. Microbiol. 55: 709–42. PMID 11544372. http://arjournals.annualreviews.org/doi/full/10.1146/annurev.micro.55.1.709?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed. 
  3. ↑ Nielsen KM (1998). "Barriers to horizontal gene transfer by natural transformation in soil bacteria". APMIS Suppl. 84: 77–84. PMID 9850687. 
  4. ↑ Tortora, Gerard J.; Funke, Berdell R.; Case, Christine L. (2010). Microbiology: An Introduction (10th ed.). San Francisco: Benjamin Cummings. p. 84. ISBN 978-0-321-55007-1. 
  5. ↑ Maczulak (2011). Encyclopedia of Microbiology. New York: Facts on File. p. 41. ISBN 978-0-8160-7364-1. 
  6. ↑ Oard, Michel J. (2012). "Fossil Ranges Continue to Expand". Journal of Creation (Jerlström, Pierre) 26 (1): 15. ISSN 1036-2916. 
  7. ↑ Madsen, Eugene (2008). "8-Special and Applied Topics in Environmental Microbiology". Environmental Microbiology:From Genomes to Biogeochemistry. Malden, MA/Oxford: Blackwell Publishing. p. 427. ISBN 978-1-4051-3647-1. 
  8. ↑ Li, X; Nikadio, H (2009). "Efflux-Mediated Drug Resistance in Bacteria: an Update". Drug 69 (12): 1555–623. PMC 2847397. PMID 19678712. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2847397. 
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