Looking at the mechanisms of Antibiotic Resistance, they each have their own complicated process. First, the main two methods that bacteria use to gain resistance to antibiotics are horizontal gene transfer and mutational resistance. Horizontal gene transfer (HGT) has three subcategories, all of which allow antibiotic resistance to be transferred amongst bacteria. The first is phage mediated transduction. It does not require physical contact between the bacteria, and is the process by which a virus introduces foreign DNA from another eukaryote, in this case a bacteria, into another bacteria. The second is conjugative pili, which is the most likely to happen, and occurs through the process of bacterial conjugation. The last are integrons, a mechanism which allows bacteria to adapt and evolve rapidly to new DNA. Mutational resistance is a category above the three subcategories of HGT, and it is simply when, during gene transcription, there is an accidental mutation that leads to some level of resistance against antibiotics (Ventola 2015). 

From these four branches come the five mechanisms of resistance. The changes in the DNA that are brought upon by HGT and accidental mutations can do a number of things: change the gene encoding the target site for the antibiotic, overexpress the pumps that remove antibiotics from the bacteria, produce an enzyme that affects the bacteria, and more. The first method of resistance is when the bacteria produces an enzyme that chemically modifies the antibiotic so that it can do no harm to the bacteria. The second is when the bacteria produces an enzyme that completely destroys the antibiotic. The last three each have subcategories under theme for methods of stopping the antibiotic from completing its duty. The third method of antibiotic resistance is porin-mediated resistance, which is a method of modifying the porins on the cellular membrane so that they do not let the antibiotic into the cell in the first place by changing the level of porins, the function of the porins, or the type of porins on the membrane. This type of antibiotic resistance is especially important in gram negative bacteria, the bacteria which have a cellular membrane. The fourth method is efflux pumps—complex bacterial machines that extrude toxic compounds, thus stopping it from affecting the bacteria. They are located in the tet gene of the chromosome, and there are five major families of efflux pumps: MFS (major facilitator super), SMR (small multidrug resistance), RND (resistance nodulation cell division), ABC (ATP binding cassette), MATE (multidrug and toxic compound extrusion), each with a slightly different mechanism of extruding the compound. The last is through editing the antibiotic’s interaction with the target site on the DNA. This has three sub-methods. The first is to protect the target site using another ligand that acts as a direct antagonist to the antibiotic so that it cannot attach on. The second is by modifying the target site so that the antibiotic doesn’t fit into the target site or the binding affinity is reduced. The third method is when bacteria evolve a new target site with similar biochemical functions but aren’t inhibited by the antibiotic, which is targeting the defunct site (Munita & Arias 2016).

Resources:

Jose M. & Cesar A. (2016). Mechanisms of Antibiotic Resistance. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4888801/

C. Lee V. (2015). The Antibiotic Resistance Crisis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4378521/

Antibiotic Resistance. (2018, February 5). Retrieved from https://www.who.int/news-room/fact-sheets/detail/antibiotic-resistance