Multiple drug resistance

Source: Wikipedia, the free encyclopedia.
This article is about multiple drug resistance in microorganisms. For multiple drug resistance in tumor/cancer cells, see antineoplastic resistance.
Not to be confused with
Multidrug tolerance
.

Multiple drug resistance (MDR), multidrug resistance or multiresistance is

antibiotics; other types include MDR viruses, parasites (resistant to multiple antifungal, antiviral, and antiparasitic drugs of a wide chemical variety).[2]

Recognizing different degrees of MDR in bacteria, the terms extensively drug-resistant (XDR) and pandrug-resistant (PDR) have been introduced. Extensively drug-resistant (XDR) is the non-susceptibility of one bacteria species to all antimicrobial agents except in two or less antimicrobial categories. Within XDR, pandrug-resistant (PDR) is the non-susceptibility of bacteria to all antimicrobial agents in all antimicrobial categories.[1] The definitions were published in 2011 in the journal Clinical Microbiology and Infection and are openly accessible.[1]

Common multidrug-resistant organisms (MDROs)

Common multidrug-resistant organisms, typically bacteria, include:[3]

Overlapping with MDRGN, a group of

Gram-negative bacteria of particular recent importance have been dubbed as the ESKAPE group (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa and Enterobacter species).[4]

Bacterial resistance to antibiotics

Main article:
Antibiotic resistance

Various microorganisms have survived for thousands of years by their ability to adapt to

DNA transfer. This process enables some bacteria to oppose the action of certain antibiotics, rendering the antibiotics ineffective.[5]
These microorganisms employ several mechanisms in attaining multi-drug resistance:

Many different bacteria now exhibit multi-drug resistance, including

streptococci, salmonella, as well as numerous other Gram-negative bacteria and Mycobacterium tuberculosis. Antibiotic resistant bacteria are able to transfer copies of DNA that code for a mechanism of resistance to other bacteria even distantly related to them, which then are also able to pass on the resistance genes, resulting in generations of antibiotics resistant bacteria.[11] This initial transfer of DNA is called horizontal gene transfer.[12]

Bacterial resistance to bacteriophages

Phage-resistant bacteria variants have been observed in human studies. As for antibiotics, horizontal transfer of phage resistance can be acquired by plasmid acquisition.[13]

Antifungal resistance

Yeasts such as Candida species can become resistant under long-term treatment with azole preparations, requiring treatment with a different drug class. Lomentospora prolificans infections are often fatal because of their resistance to multiple antifungal agents.[14]

Antiviral resistance

HIV is the prime example of MDR against antivirals, as it mutates rapidly under monotherapy.

valacyclovir, usually in immunosuppressed patients.[15]

Antiparasitic resistance

The prime example for MDR against antiparasitic drugs is

sulfadoxine-pyrimethamine resistant a few decades ago, and as of 2012 artemisinin-resistant Plasmodium falciparum has emerged in western Cambodia and western Thailand.[16]
Toxoplasma gondii can also become resistant to artemisinin, as well as atovaquone and sulfadiazine, but is not usually MDR[17]
Antihelminthic resistance is mainly reported in the veterinary literature, for example in connection with the practice of livestock drenching[18]
and has been recent focus of FDA regulation.

Preventing the emergence of antimicrobial resistance

To limit the development of antimicrobial resistance, it has been suggested to:[citation needed]

  • Use the appropriate antimicrobial for an infection; e.g. no antibiotics for viral infections
  • Identify the causative organism whenever possible
  • Select an antimicrobial which targets the specific organism, rather than relying on a broad-spectrum antimicrobial
  • Complete an appropriate duration of antimicrobial treatment (not too short and not too long)
  • Use the correct dose for eradication; subtherapeutic dosing is associated with resistance, as demonstrated in food animals.
  • More thorough education of and by prescribers on their actions' implications globally.

The medical community relies on education of its prescribers, and self-regulation in the form of appeals to voluntary antimicrobial stewardship, which at hospitals may take the form of an antimicrobial stewardship program. It has been argued that depending on the cultural context government can aid in educating the public on the importance of restrictive use of antibiotics for human clinical use, but unlike narcotics, there is no regulation of its use anywhere in the world at this time. Antibiotic use has been restricted or regulated for treating animals raised for human consumption with success, in Denmark for example.[19]

Infection prevention is the most efficient strategy of prevention of an infection with a MDR organism within a hospital, because there are few alternatives to antibiotics in the case of an extensively resistant or panresistant infection; if an infection is localized, removal or excision can be attempted (with MDR-TB the lung for example), but in the case of a systemic infection only generic measures like boosting the immune system with immunoglobulins may be possible. The use of bacteriophages (viruses which kill bacteria) is a developing area of possible therapeutic treatments.[20]

It is necessary to develop new antibiotics over time since the selection of resistant bacteria cannot be prevented completely. This means with every application of a specific antibiotic, the survival of a few bacteria which already got a resistance gene against the substance is promoted, and the concerning bacterial population amplifies. Therefore, the resistance gene is farther distributed in the organism and the environment, and a higher percentage of bacteria means they no longer respond to a therapy with this specific antibiotic. In addition to developing new antibiotics, new strategies entirely must be implemented in order to keep the public safe from the event of total resistance. New strategies are being tested such as UV light treatments and bacteriophage utilization, however more resources must be dedicated to this cause.

See also

References

  1. ^ a b c d A.-P. Magiorakos, A. Srinivasan, R. B. Carey, Y. Carmeli, M. E. Falagas, C. G. Giske, S. Harbarth, J. F. Hinndler et al. Multidrug-resistant, extensively drug-resistant and pandrug-resistant bacteria... Archived 6 December 2017 at the Wayback Machine. Clinical Microbiology and Infection, Vol 8, Iss. 3 first published 27 July 2011 [via Wiley Online Library]. Retrieved 16 August 2014.
  2. ^ Drug+Resistance,+Multiple at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
  3. PMID 32255576. Archived
    from the original on 18 October 2022. Retrieved 15 December 2023.
  4. PMID 19035777.{{cite journal}}: CS1 maint: multiple names: authors list (link
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  11. ^ Hussain, T. Pakistan at the verge of potential epidemics by multi-drug resistant pathogenic bacteria (2015). Adv. Life Sci. 2(2). pp: 46-47
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  16. ^ Dondorp, A., Nosten, F., Yi, P., Das, D., Phyo, A., & Tarning, J. et al. (2009). Artemisinin Resistance in Plasmodium falciparum Malaria. New England Journal Of Medicine, 361, 455-467.
  17. ^ Doliwa C, Escotte-Binet S, Aubert D, Velard F, Schmid A, Geers R, Villena I. Induction of sulfadiazine resistance in vitro in Toxoplasma gondii.Exp Parasitol. 2013 Feb;133(2):131-6.
  18. ^ Laurenson YC, Bishop SC, Forbes AB, Kyriazakis I.Modelling the short- and long-term impacts of drenching frequency and targeted selective treatment on the performance of grazing lambs and the emergence of antihelmintic resistance.Parasitology. 2013 Feb 1:1-12.
  19. PMID 24892505
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  20. PMID 28807909
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Further reading

External links
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