Marciniak, K., Tyczewska, A., & Grzywacz, K. (2024). Genetics of antibiotic resistance in methicillin-resistant Staphylococcus aureus (MRSA). Journal of Biotechnology, Computational Biology and Bionanotechnology, 105(2), 169–177. https://doi.org/10.5114/bta.2024.139756
The purpose of the study is to examine the genetic mechanism that contributes to the antibiotic resistance in methicillin-resistant Staphylococcus aureus (MRSA). Marciniak, Tyczewska, and Grzywacz (2024) break down how MRSA has become such a tough bacterium to treat. This was mainly due to its ability to pick up resistance genes through horizontal gene transfer. One key player is the mecA gene, which allows MRSA to survive methicillin and other β-lactam antibiotics by producing a special penicillin-binding protein (PBP2a) that regular antibiotics can’t block. The study also dives into how MRSA develops resistance to other drugs like fluoroquinolones and vancomycin, either through mutations in specific genes or by thickening its cell wall to keep antibiotics out, which is not easy to do. The authors emphasize that MRSA isn’t just resistant to one or two antibiotics. The bacteria has found ways to fight off over 20 different drugs. This makes it a serious global health threat, and they argue that new treatments, whether through modifying existing antibiotics or exploring alternative approaches like nanotechnology and plant-based compounds, are urgently needed to be able to continue to save lives.
Wickramage, I., Spigaglia, P., & Sun, X. (2021). Mechanisms of antibiotic resistance of Clostridioides difficile. Journal of Antimicrobial Chemotherapy, 76(12), 3077–3090. https://doi.org/10.1093/jac/dkab231
The purpose of the study is to examine the genetic mechanisms that contribute to antibiotic resistance in Clostridioides difficile (C-Diff). The authors explain that C-Diff is one of the top antibiotic-resistant threats in the U.S., with multidrug-resistant (MDR) strains becoming more common worldwide. The study explores how C-Diff develops resistance through multiple mechanisms, including altering antibiotic targets, modifying drugs, and using efflux pumps to remove antibiotics from the cell. The researchers also highlight the role of mobile genetic elements, such as transposons, which allow resistance genes to spread between different bacterial strains. C-diff is especially concerning because its spores and biofilm formation make it highly resilient, allowing it to persist in healthcare settings even after antibiotic treatment. The study emphasizes the need for better antibiotic oversight and surveillance of resistant strains, and new treatment strategies to fight this growing public health challenge. An uphill battle that some experts say that we are losing, something that this article highlights through demonstrating how good C-Diff is in combating efforts to fight it off.
MacLean, R. C., & amp; San Millan, A. (2019). The evolution of antibiotic resistance. Science, 365(6458), 1082–1083. https://doi.org/10.1126/science.aax3879
The purpose of the study is to explore how bacteria develop and spread antibiotic resistance (ABR), which is becoming a serious global health threat. MacLean and San Millan (2019) explain that bacteria gain resistance in two main ways: random mutations and sharing resistance genes through horizontal gene transfer (HGT). HGT is especially concerning because it allows bacteria to "borrow" resistance from other microbes, making them harder to treat. The study points out that only a few highly successful bacterial strains are responsible for most of the resistance spreading worldwide, making infections tougher to control. The authors argue that more real-world research is needed—most studies focus on lab experiments that don’t fully capture how resistance works in actual infections. They also discuss possible solutions, like using CRISPR-Cas technology to remove resistance genes or combining antibiotics in ways that make bacteria more vulnerable. Overall, the study highlights how urgent it is to tackle ABR before we run out of effective treatments.
Ragheb, M. N., Thomason, M. K., Hsu, C., Nugent, P., Gage, J., Samadpour, A. N. Merrikh, H. (2019). Inhibiting the evolution of antibiotic resistance. Molecular Cell, 73(1), 157– 165. https://doi.org/10.1016/j.molcel.2018.10.015
The purpose of the study is to explore ways to slow down the evolution of antibiotic resistance in bacteria. Ragheb et al. (2019) focus on a protein called Mfd, which plays a key role in increasing bacterial mutation rates and speeding up resistance development. Their research found that when Mfd is removed, bacteria mutate less frequently and struggle to develop resistance, even when exposed to antibiotics. The study suggests that targeting Mfd with "anti- evolution" drugs could be a new way to fight antibiotic resistance by preventing bacteria from quickly adapting to treatments. The authors argue that rather than just developing new antibiotics—which bacteria eventually find ways to resist—scientists should focus on stopping bacteria from evolving resistance in the first place. This approach could help preserve the effectiveness of existing antibiotics and slow the rise of drug-resistant infections. From this article I plan to use some of the graphic images that show antibiotics and the drug envolution. It is a simplistic images that makes understanding easier for those who are not up to date on the knowalls.
Knöppel, A., Näsvall, J., & amp; Andersson, D. I. (2017). Evolution of antibiotic resistance without antibiotic exposure. Antimicrobial Agents and Chemotherapy, 61(11), e01495-17. https://doi.org/10.1128/AAC.01495-17
Scientists have long known that using antibiotics too much leads to resistance, but this study by Knöppel, Näsvall, and Andersson (2017) takes things a step further by showing that bacteria can develop antibiotic resistance even without being exposed to antibiotics. The researchers evolved Escherichia coli and Salmonella enterica in different lab environments for hundreds of generations, focusing on their adaptation to specific growth conditions rather than antibiotic exposure. Surprisingly, some of the bacteria developed genetic mutations that also made them more resistant to multiple antibiotics, even though none were present. The study suggests that natural selection for other survival traits—like better metabolism or stress response—can incidentally make bacteria more resistant to antibiotics. This finding challenges the traditional view that resistance only emerges in response to antibiotic use and highlights how bacterial evolution in the real world, including in natural environments and hospitals, might be fueling the antibiotic resistance crisis in unexpected ways.