Darwinism and the Age of Antibiotics: Evolution in a Petri Plate (5)

Darwinism and the Age of Antibiotics: Evolution in a Petri Plate (5) Evolution in Petri We have already talked about the ancient origin of bacterial resistance to antibiotics, and all the evidence suggests that bacteria are resistant to most therapeutic antibiotics thousands – perhaps millions – of years before exposure, and the logic seems simple. If bacteria did not have this resistance from the beginning, it would be doomed. There is no question that some bacterial strains that were previously known to be sensitive to antibiotics are now immune to many different types of antibiotics. This increase in the proportion of resistant species has caused a therapeutic crisis and even a nightmare for doctors. In some cases, mutations may cause bacteria to acquire new resistance to an antibiotic, but as we will see in the next paragraphs, the use of "loss of sensitivity" is more appropriate than "gaining resistance." Bacteria have evolved with mechanisms similar to those discussed in Lenski's experiment, meaning that bacteria have not acquired a new trait or function, but that we have lost some of their existing functions. For example, the antibiotic ciprofloxacin works by targeting an enzyme known as Gyraz, an enzyme necessary for bacteria to reproduce and copy their DNA. The enzyme consists of two proteins encoded by two genes (gyrA, gyrB). Resistance to ciprofloxacin is caused by point mutations of these genes, and because of these mutations the two proteins that make up the enzyme change shape and lose its chemical affinity for the antibiotic and do not react with it. This process can be likened to a lock and a key. In order for the key to work and unlock, both the lock and the key must be suitable for each other, so that the key enters the lock and unscrews it, but if a deformation occurs in the lock form by breaking it, for example, the key will not work. But it does not explain anything about its origin in the first place. Thus, this mutation, although beneficial to bacteria by protecting them from antibiotics, only explains the loss of chemical familiarity and does not explain its origin from the beginning, and therefore has nothing to do with Darwinian evolution.1 Another example is resistance against streptomycin, streptomycin works by disrupting the cell's ability to make protein by corrupting the cell's protein factories, ribosomes, and as a result of some mutations that change the structure of the ribosome, the ribosome loses its ability to form chemical bonds with the antibiotic and becomes immune to it. E. coli naturally has pumps that it uses to expel antibiotics outside the cell and reduce their concentration below the lethal limit. Because of these pumps, E. coli can resist multiple types of antibiotics at once (multiple-drug-resistance), and the manufacture of bacteria for these pumps is influenced by the MarR protein, which inhibits their construction, so mutations that reduce or eliminate the inhibiting force of that protein increase the rate of manufacture of the pumps. We end with the antibiotic that is used to prevent bacteria from making their own DNA needed for cell replication, which is metronidazole. This antibiotic enters the cell in an inactive form and relies on an enzyme made by bacteria to function. This enzyme NADPH nitroreductase converts the antibiotic from the inactive state of the active state, without which it may have no effect on the bacteria. As a result of the enzyme losing its ability to reduce metronidazole, it remains inactive and has no effect on bacteria, which means that bacteria gain new resistance against it, but the reason for this resistance is not to gain new information and functions, but again as a result of the loss of a pre-existing function. If we examine the essence of these changes, in all examples we find mutations responsible for the loss of biological devices and machines already present in the bacterial cell, so that the role of mutations is limited to stopping the action of a gene, disrupting the elements that regulate the expression of a gene, or losing an enzyme to its chemical activity, a role that is not similar to the creative role that evolutionists have for the only mutations in evolution. (1) Barnard, F. M., & Maxwell, A. (2001). Interaction between DNA Gyrase and Quinolones: Effects of Alanine Mutations at GyrA Subunit Residues Ser83 and Asp87. Antimicrobial Agents and Chemotherapy, 45(7), 1994-2000. doi:10.1128/aac.45.7.1994-2000.2001 (2) Leclerc, D., Melancon, P., & Brakier-Gingras, L. (1991). Mutations in the 915 region of Escherichia coli16S ribosomal RNA reduce the binding of streptomycin to the ribosome. Nucleic Acids Research, 19(14), 3973-3977. doi:10.1093/nar/19.14.3973 (3) Oethinger, M., Podglajen, I., Kern, W. V., & Levy, S. B. (1998). Overexpression of the marA or soxS Regulatory Gene in Clinical Topoisomerase Mutants of Escherichia coli. Antimicrobial Agents and Chemotherapy, 42(8), 2089–2094. (4) Tankovic, J., D. Lamarque, J.-C. Delchier, C.-J. Soussy, A. Labigne, and P.J. Jenks. 2000. Frequent association between alteration of the rdxA gene and metronidazole resistance in French and North African isolates Helicobacter pylori. Antimicrobial Agents and Chemotherapy 44:608-613. - Management of the Brahin Center — Source: Brahin Center website - Published on 2018-01-15 (archived at the Internet Archive) https://braheen.com/articles/evolution-design/الداروينية-وعصر-المضادات-الحيوية-5