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Issue Brief

How Antibiotic Resistance Happens


What is antibiotic resistance and how do bacteria develop it?

Frequent, low doses of antibiotics that are not strong enough to kill all bacteria encourage some bacteria to develop means of survival, or to become “resistant.” Bacteria can develop ways to fight off antibiotics by: preventing antibiotics from reaching their target cells (e.g., changing the permeability of cell walls or pumping the drugs out of the cells); changing the structure of target cells or entirely replacing them; or producing enzymes that destroy antibiotics.

Bacteria may gain resistance by getting copies of resistance genes from other bacteria. Bacteria acquire resistance genes from other bacteria when:

  • Microorganisms join together and transfer DNA to each other;
  • Free-floating DNA pieces (called plasmids) are picked up, which can carry resistance to a number of antibiotics;
  • Small pieces of DNA jump from one DNA molecule to another, and then are incorporated; and
  • DNA remnants are scavenged from dead or degraded bacteria.

Once a resistance gene is picked up and added to a bacterium’s DNA, the bacterium can dominate other bacteria, and pass the resistance gene on to all of its descendants. Resistance is magnified because bacteria multiply rapidly.

Date added:
Feb 24, 2010
Project:
Pew Campaign on Human Health and Industrial Farming
Topic:
Antibiotics in Food Animal Production
Related Expert:
Laura Rogers
References:
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References:

1 Mellon, Margaret, Charles Benbrook, & Karen Lutz Benbrook. 2001. Hogging It! Estimates of Antimicrobial Abuse in Livestock. Cambridge, MA: Union of Concerned Scientists.
2 World Health Organization. Revised January 2002. Fact Sheet number 194, “Antimicrobial resistance.” Available at: http://www.who.int/mediacentre/factsheets/fs194/en/.
3 U.S. General Accounting Office (GAO). 2004. No. 04-490, Antibiotic Resistance: Federal Agencies Need to Better Focus Efforts to Address Risk to Humans from Antibiotic Use in Animals. See also: White, David G. et al. 2001. The Isolation of Antibiotic-Resistant Salmonella from Retail Ground Meats. The New England Journal of Medicine. 345(16): 1147-1154; Molbak, K. et al. 1999. An Outbreak of Multidrug-Resistant, Quinolone-Resistant Salmonella Enterica Serotype Typhimurium DT104. The New England Journal of Medicine, 341(19): 1420-1425; and Johnson, James R. et al. 2006. Similarity between Human and Chicken Escherichia coli Isolates in Relation
to Ciprofloxacin Resistance Status. Journal of Infectious Diseases 194(1): 71-78.
4 GAO, op. cit. See also: Price, Lance B. et al. 2007. Elevated Risk of Carrying Gentamicin-Resistant Escherichia coli among U.S. Poultry Workers. Environmental Health Perspectives 115(12): 1738-1742; and Smith, Tara C. et al. 2009. Methicillin-Resistant Staphylococcus aureus (MRSA) Strain ST398 Is Present in Midwestern U.S. Swine and Swine Workers. PLoS ONE 4(1): 1-6.
5 GAO, op. cit. See also: Chee-Sanford, J. C. et al. 2001. Occurrence and Diversity of Tetracycline Resistance Genes in Lagoons and Groundwater Underlying Two Swine Production Facilities. Applied and Environmental Microbiology 67(4): 1494-1502; Sapkota, A. R. et al. 2005. Antibiotic-Resistant Enterococci and Fecal Indicators in Surface Water and Groundwater Impacted by a Concentrated Swine Feeding Operation. Environmental Health Perspectives 115(7): 1041-1045; and Gibbs, Shawn G. et al. 2005. Isolation of Antibiotic-Resistant Bacteria from the Air Plume Downwind of a Swine Confined or Concentrated Animal Feeding Operation. Environmental Health Perspectives 114(7): 1032-1037.
6 Rule, Ana M., S. L. Evans, and E. K. Silbergeld. 2008. Food animal transport: A potential source of community exposures to health hazards from industrial farming (CAFOs). Journal of Infection and Public Health. 1: 33-39.

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