Cross-resistance

Cross-resistance is when something develops resistance to several substances that have a similar mechanism of action. For example, say a certain type of bacteria develops resistance to one antibiotic. That bacteria then also has resistance to several other antibiotics that target the same protein or use the same route to get into the bacterium. A real example of cross-resistance occurred for nalidixic acid and ciprofloxacin, which are both quinolone antibiotics. When bacteria developed resistance to ciprofloxacin, they also developed resistance to nalidixic acid because both drugs work by inhibiting topoisomerase, a key enzyme in DNA replication.[1] Due to cross-resistance, antimicrobial treatments like phage therapy can quickly lose their efficacy against bacteria.[2]

Definition

How cross-resistance is defined varies per field of research. In pest management for instance it is defined as the development of resistance by pest populations to multiple pesticides within a chemical family.[3] In another case it is defined as the resistance of a virus to a new drug as a result of previous exposure to another drug.[4] Or in the context of microbes as the resistance to multiple different antimicrobial agents as a result of a single molecular mechanism.[5] So the precise definition of cross-resistance is not fixed and depends on the field of interest. In general the idea is that the development of resistance to one substance subsequently leads to resistance to one or more substances that can be resisted in a similar manner. It occurs when resistance is provided against multiple compounds through one single mechanism, like an efflux pump.[6] Which can keep concentrations of a toxic substance at low levels and can do so for multiple compounds. Increasing the activity of such a mechanism in response to one compound then also has a similar effect on the others.

To antibiotics

One context in which cross-resistance plays a role is the development of resistance by bacteria to antibiotics. This is an area of clinical relevance, because infectious diseases remain a big health issue. There is a continued increase in the development of multi-drug resistance in bacteria. This is partially due to the widespread use of antimicrobial compounds in diverse environments.[7] But resistance to antibiotics can arise in multiple ways. It is not necessarily the result of exposure to an antimicrobial compound. Cross-resistance can take place between compounds that are chemically similar, like antibiotics within similar and different classes.[8] But also between compounds that are structurally dissimilar. This is possible when antimicrobial agents have the same target, initiate cell death in a similar manner or have a similar route of access. An example is cross-resistance between antibiotics and disinfectants. Exposure to certain disinfectants can lead to the increased expression of genes that encode for efflux pumps that are able to maintain low levels of antibiotics. So the same mechanism that is used to clear the disinfectant compound from the cell can also be used to clear antibiotics from the cell.[9] Another example is cross-resistance between antibiotics and metals. As mentioned before compounds do not have to be similar in structure in order to lead to cross-resistance. It can also occur when the same mechanism is used to remove the compound from the cell. In the bacteria Listeria monocytogenes for instance a multi-drug efflux transporter was found that could export both metals and antibiotics.[10][11] Experimental work has shown that exposure to Zinc can lead to increased levels of bacterial resistance to antibiotics.[12] Several other studies have reported cross-resistance to various types of metals and antibiotics. These worked through several mechanisms, like drug efflux systems and disulphide bond formation systems. The possible implication of this is that not only the presence of antibacterial compounds can lead to the development of resistance against antibiotics, but also environmental factors like exposure to heavy metals.[6]

See also

References

  1. ↑ Périchon, B. "Cross Resistance". ScienceDirect. Encyclopedia of Microbiology. Retrieved 26 July 2021.
  2. ↑ Wright, Rosanna (3 October 2018). "Cross-resistance is modular in bacteria-phage interactions". PLOS Biology. 16 (10): e2006057. doi:10.1371/journal.pbio.2006057. PMC 6188897. PMID 30281587.
  3. ↑ Sarwar, Muhammad; Aslam, Roohi (2020-01-01), Awasthi, L. P. (ed.), "Chapter 23 - New advances in insect vector biology and virus epidemiology", Applied Plant Virology, Academic Press, pp. 301–311, doi:10.1016/b978-0-12-818654-1.00023-2, ISBN 978-0-12-818654-1, retrieved 2021-09-23
  4. ↑ Locarnini, Stephen; Bowden, Scott (2010-08-01). "Drug Resistance in Antiviral Therapy". Clinics in Liver Disease. Chronic Hepatitis B: An Update. 14 (3): 439–459. doi:10.1016/j.cld.2010.05.004. ISSN 1089-3261. PMID 20638024.
  5. ↑ Colclough, Abigail; Corander, Jukka; Sheppard, Samuel K.; Bayliss, Sion C.; Vos, Michiel (2019-01-28). "Patterns of cross‐resistance and collateral sensitivity between clinical antibiotics and natural antimicrobials". Evolutionary Applications. Wiley. 12 (5): 878–887. doi:10.1111/eva.12762. ISSN 1752-4571. PMC 6503891. PMID 31080502.
  6. 1 2 Pal, Chandan; Asiani, Karishma; Arya, Sankalp; Rensing, Christopher; Stekel, Dov J.; Larsson, D. G. Joakim; Hobman, Jon L. (2017-01-01), Poole, Robert K. (ed.), "Chapter Seven - Metal Resistance and Its Association With Antibiotic Resistance", Advances in Microbial Physiology, Microbiology of Metal Ions, Academic Press, 70: 261–313, doi:10.1016/bs.ampbs.2017.02.001, PMID 28528649
  7. ↑ Anes, João; McCusker, Matthew P.; Fanning, Séamus; Martins, Marta (2015-06-10). "The ins and outs of RND efflux pumps in Escherichia coli". Frontiers in Microbiology. 6: 587. doi:10.3389/fmicb.2015.00587. PMC 4462101. PMID 26113845.
  8. ↑ Sanders, C C; Sanders, W E; Goering, R V; Werner, V (1984). "Selection of multiple antibiotic resistance by quinolones, beta-lactams, and aminoglycosides with special reference to cross-resistance between unrelated drug classes". Antimicrobial Agents and Chemotherapy. American Society for Microbiology. 26 (6): 797–801. doi:10.1128/aac.26.6.797. ISSN 0066-4804. PMC 180026. PMID 6098219.
  9. ↑ Chapman, John S. (2003). "Disinfectant resistance mechanisms, cross-resistance, and co-resistance". International Biodeterioration & Biodegradation. Hygiene and Disinfection. Elsevier. 51 (4): 271–276. doi:10.1016/s0964-8305(03)00044-1. ISSN 0964-8305.
  10. ↑ Mata, M.T.; Baquero, F.; Pérez-Díaz, J.C. (2000). "A multidrug efflux transporter in Listeria monocytogenes". FEMS Microbiology Letters. 187 (2): 185–188. doi:10.1111/j.1574-6968.2000.tb09158.x. ISSN 0378-1097. PMID 10856655.
  11. ↑ Baker-Austin, Craig; Wright, Meredith S.; Stepanauskas, Ramunas; McArthur, J.V. (2006). "Co-selection of antibiotic and metal resistance". Trends in Microbiology. Cell Press. 14 (4): 176–182. doi:10.1016/j.tim.2006.02.006. ISSN 0966-842X. PMID 16537105.
  12. ↑ Peltier, Edward; Vincent, Joshua; Finn, Christopher; Graham, David W. (2010). "Zinc-induced antibiotic resistance in activated sludge bioreactors". Water Research. International Water Association (Elsevier). 44 (13): 3829–3836. doi:10.1016/j.watres.2010.04.041. ISSN 0043-1354. PMID 20537675.
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