Multiple drug resistance

From Self-sufficiency
Jump to: navigation, search

Multiple drug resistance or Multidrug resistance is a condition enabling a disease-causing organism to resist distinct drugs or chemicals of a wide variety[1] of structure and function targeted at eradicating the organism. Organisms that display multidrug resistance can be pathologic cells, including bacterial and neoplastic (tumor) cells.

Bacterial resistance to antibiotics

Various microorganisms have survived for thousands of years by their being able to adapt to antimicrobial agents. They do so via spontaneous mutation or by DNA transfer. It is this very process that enables some bacteria to oppose the assault of certain antibiotics, rendering the antibiotics ineffective.[2] These microorganisms employ several mechanisms in attaining multidrug resistance:

  • No longer relying on a glycoprotein cell wall
  • Enzymatic deactivation of antibiotics
  • Decreased cell wall permeability to antibiotics
  • Altered target sites of antibiotic
  • Efflux mechanisms to remove antibiotics[3]
  • Increased mutation rate as a stress response[4]

Many different bacteria now exhibit multidrug resistance, including staphylococci, enterococci, gonococci, streptococci, salmonella, Mycobacterium tuberculosis and others. In addition, some resistant bacteria are able to transfer copies of DNA that codes for a mechanism of resistance to other bacteria, thereby conferring resistance to their neighbors, which then are also able to pass on the resistant gene.

To limit the development of antibiotic resistance, one should:

  • Use antibiotics only for bacterial infections
  • Identify the causative organism if possible
  • Use the right antibiotic; do not rely on broad-range antibiotics
  • Not stop antibiotics as soon as symptoms improve; finish the full course
  • Not use antibiotics for most colds, coughs, bronchitis, sinus infections, and eye infections, which are caused by viruses.

It is argued that government legislation will aid in educating the public on the importance of restrictive use of antibiotics, not only for human clinical use but also for treating animals raised for human consumption.

Neoplastic resistance

Cancer cells also have the ability to become resistant to multiple different drugs, and share many of the same mechanisms:

Because efflux is a significant contributor for multidrug resistance in cancer cells, current research is aimed at blocking specific efflux mechanisms.[5] Treatment of cancer is complicated by the fact that there is such a variety of different DNA mutations that cause or contribute to tumor formation, as well as myriad mechanisms by which cells resist drugs. There are also certain notable differences between antibiotic drugs and antineoplastic (anticancer) drugs that complicate designing antineoplastic agents. Antibiotics are designed to target sites that are specific and unique to bacteria, thereby harming bacteria without harming host cells. Cancer cells, on the other hand, are altered human cells; therefore they are much more difficult to damage without also damaging healthy cells.

Antifungal resistance

Scedosporium prolificans infections are almost uniformly fatal because of their resistance to antifungal agents. ([1] and [2] Combatting increasing resistance)

See also

References

  • Noble: Textbook of Primary Care Medicine, 3rd ed., Mosby, Inc. 2001.
  • Guminski, A. (2002). Scientists and clinicians test their metal-back to the future with platinum compounds. The Lancet Oncology 3(5).
  • Krishan, A. (2000). Monitoring of cellular resistance to cancer chemotherapy. Hematol Oncol Clin North Am. 16(2): 357-72.

Cite error: Invalid <references> tag; parameter "group" is allowed only.

Use <references />, or <references group="..." />

External links

de:Multiple Drug Resistance

he:נשאים רב תרופתיים id:Multidrug resistance

ja:多剤耐性
  1. MeSH Drug+Resistance,+Multiple
  2. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  3. Li, X, Nikadio H (2009). "Efflux-mediated drug resistance in bacteria: an update". Drug. 69 (12): 1555–623. doi:10.2165/11317030-000000000-00000. PMID 19678712. 
  4. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  5. http://www.wipo.int/pctdb/en/wo.jsp?IA=WO2002076439&DISPLAY=DESC p-gp modulation