You may have heard of the concept of antibiotic resistance, but what exactly does it mean? It is caused by overuse of antibiotics in both humans and animals. Basically, resistance occurs when bacteria change their targets to resist the effects of an antibiotic. An example of this is the ability of E. coli to add a compound to its cell wall. This is called the mcr-1 gene. To learn more about antibiotic resistance, read the article below.
Mechanisms of bacterial resistance
Bacterial resistance to antibiotics can occur in two main ways: by mutation or by acquisition of new genetic material. Bacterial mutation is an inevitable process that occurs when cells divide, and is the cause of increased antibiotic resistance. Bacteria only have one chromosome, and the more times a cell replicates, the greater the chance for mutation. Acquisition of new genetic material is another common mechanism, which can be a contributing factor to bacterial resistance to antibiotics.
The emergence of resistant bacteria can be traced to the introduction of semi-synthetic penicillin, methicillin. The development of MRSA, or multi-drug-resistant bacteria, was the result of the widespread use of antibiotics. Bacterial genomes are extremely malleable, and their adaptive capacity is vast. Bacterial mutations are influenced by the presence of specific environmental factors such as nutrition, genetic diversification, or DNA exchange mechanisms. Bacterial genomes are constantly exposed to antibiotics, and many of these compounds are excreted unchanged. Because bacteria constantly experience antibiotics, they have become extremely resistant. There are four main mechanisms by which bacteria become resistant to antibiotics:
Horizontal gene transfer
One method used to determine whether horizontal gene transfer is a cause of antibiotic resistance is by studying the genetic code of bacteria. This method uses bioinformatics to identify atypical sequence signatures and strong discrepancies in evolutionary history, indicating that the transferred gene is likely related to genes from the same or neighboring species. In this way, a horizontal gene transfer is confirmed and can be implicated as a cause of antibiotic resistance.
The mechanism by which HGT occurs varies between bacteria of different species. It can occur between strains of the same species as well as across orders and families. The relationship between two bacteria plays a role in the success of the transfer, with closely related bacteria being more likely to transfer genetic material than less closely related ones. Horizontal gene transfer is an important cause of antibiotic resistance. To understand how horizontal gene transfer works, we must look at the different mechanisms that bacteria use to pass on their genes to each other.
Mutations in genes
The rate at which genes change to become resistant to antibiotics is regulated by gene specificity. In many cases, these mutations have no additional costs and the population remains resistant to antibiotics without selective pressure. However, in some cases, mutated genes do cause antibiotic resistance, and these mutations may be compensated by further mutations in other regions of the chromosome. This is a rare case. This study identifies two genes that are particularly important for the development of resistance to antibiotics.
The rate of mutation varies with antibiotic concentrations. The number of selectable mutations is dependent on the concentration and structure of the drug. The mutation rate decreases dramatically when the concentration of selectors is high. If the concentration of antibiotic is high enough, mutation rates increase, but they do not completely eliminate antibiotic resistance. Moreover, a single mutation is not enough to produce resistance. For a single antibiotic, multiple mutations must occur.
Global cell adaptive response
The global cell adaptive response to antibiotic resistance (GCR) has been poorly understood. This is largely due to incomplete understanding of the interplay between environmental conditions and the development of resistance in bacteria. This article explores the genetic, metabolic, and functional constraints of antibiotic resistance in GCR. In particular, we explore how metabolic changes lead to the acquisition of antibiotic resistance. We demonstrate that resistance to antibiotics is driven by the synthesis of different substances in the cell.
The study found that genes expressed during the generalised response to antibiotics include the stringent response, osmotic stress sigma factor sE, and ppGpp synthetase RelA. This data suggests that removing these genes reduces the level of resistance to vancomycin and bacitracin in E. coli. Identifying the genes involved in global cell adaptive response to antibiotics can provide a useful guide to detecting drug resistance in E. coli and other bacterial species.
While evolution occurs over geological time, the process is more rapid when an environment is subjected to a strong selective pressure. This is what happens in the environment of AMR. Antimicrobials have been applied widely in very high doses for many years, triggering a rapid selection pressure response that resulted in the spread of resistance genes and the production of new AMR-producing genes. Currently, the AMR crisis does not appear to have reached an irreversible state, but it remains an unresolved issue.
Antibiotic resistance can be reversed or reduced by using alternative methods of controlling bacteria. Alternative treatments for insect pests and hand-washing are among the methods that can slow evolution. Changing antibiotics or changing the dosage may help to delay the onset of full resistance to antibiotics. However, there is a fundamental arms race that still remains and costs lives. In the long run, no approach will be effective. Until then, the only way to combat the problem is to slow down the pace of evolution.