The present-day world faces many problems connected to various bacteria causing human diseases. At the time of pandemics such as COVID-19, these issues are clearly seen both by specialists and citizens. Since the major difficulty is related to the development of new properties by bacteria or, most importantly, their resistance to drugs over time, this field draws researchers’ special attention (Kapoor et al., 2017). In order to overcome it, they use various methods allowing them to deal with biochemical types of mechanisms that bacteria use when introducing new drugs (Kapoor et al., 2017). These mechanisms can explain the nature of the processes contributing to their increased resistance.
There are numerous reasons why drugs may selectively act on bacterial cells, and they can be considered from the aforementioned perspective. The most common way for bacteria to influence their operation is the so-called antibiotic inactivation when they change cells so that the drug no longer works (Kapoor et al., 2017). It is complemented by target modification and altered permeability, also resulting in drug inactivity (Kapoor et al., 2017). From this point of view, the selectiveness in the effects of antibiotics on bacterial cells is explained by the latter’s attempts to decrease their influence.
The current situation poses a threat to the world population since no effective methods allowing to resolve this issue exist. The defensiveness of bacteria not only leads to the selectiveness of drug effects but also contributes to the complications in the case of pandemics. Therefore, in order to fight microbes that are not yet known, the researchers need to find a mechanism that would make bacteria’s efforts to resist antibiotics inefficient. In this way, drugs will affect all of them and thereby help to avoid pandemics in the future.
Reference
Kapoor, G., Saigal, S., & Elongavan, A. (2017). Action and resistance mechanisms of antibiotics: A guide for clinicians. Journal of Anaesthesiology, Clinical Pharmacology, 33(3), 300-305. Web.