The adult human body consists of about 39 trillion bacteria cells, which is even more than the number of human cells of around 30 trillion (International Journal of Environmental Research and Public Health, 2022). Bacteria are microorganisms that were among the first to exist on Earth. Despite being single-celled, their total biomass exceeds that of all plants and animals combined; and live in almost every habitat, including terrestrial, marine, as well as human organs (Genomegov, 2019). Many of these bacteria are harmless with some even serving important roles in digestion and immunity. However, there are certain bacteria that can cause dangerous infections ranging from small illnesses to widespread epidemics. Luckily, there are various modern-day treatments available to combat bacterial infections– known as antibiotics.These antibiotics that are either synthesized from chemicals or found organically in nature like fungi or mold, neutralize and kill bacteria by destroying the bacteria’s cell wall or disrupting vital procedures like protein synthesis whilst keeping human cells unharmed. People started using antibiotics extensively during the twentieth century, which made many formerly deadly infections relatively treatable. However, due to the evolution of antibiotic resistance in bacteria, these aforementioned antibiotics are becoming more and more ineffective.
The Evolution of Antibiotic Resistance
Antibiotic resistance is a type of antimicrobial resistance that arises when a bacteria evolves to the extent that antibiotics fail to kill or hinder their growth, and causes bacterial infections to become more difficult to cure. Parasites, fungie, and viruses can all become antibiotic resistant; so, bacteria cells are the ones directly developing antibiotic resistance rather than the human body itself (World Health Organization, 2023). When this occurs, there will be less antibiotics that are effective in treating an infection against that certain bacteria. Although there may be other types of antibiotics that may help, it is critical to have a wider range of treatment options and begin effective therapy as soon as possible for infections that are severe. Thus, if it takes longer to discover or find another drug to treat an antibiotic-resistant illness, there may be far more severe and catastrophic consequences.
This problem does not lie within the antibiotics themselves, but with the bacteria’s natural instinct to survive. As shown in Figure 2, this phenomenon can be deciphered with Charles Darwin’s theory of evolution and natural selection. Bacteria reproduce asexually, and much like other living organisms, they also undergo mutations (ReAct, 2016). These mutations are often caused by random errors in DNA replication or exposure to mutagens like chemicals and radioactive substances. Spontaneous mutations occur at a rate of 1 out of 105 or 108, contributing to random variations within the population (PubMed, 2023). Many of these mutations have a positive or neutral effect on the human body, but occasionally, a mutation occurs that gives the bacteria a benefit to survive and fight off antibiotics. For example, certain bacteria evolved biochemical "pumps" that can expel antibiotics prior to them reaching their target, while others create enzymes that can deactivate antibiotics. In Mycobacterium tuberculosis, resistance is promoted by mutations impacting fluoroquinolone antibiotic resistance specifically, leading to multidrug-resistant strains (Missouri Department of Health and Senior Services, 2019). In this scenario, the bacterium gains significantly from a mutation that provides resistance to a specific antibiotic. When susceptible bacteria strains are eradicated in antibiotic-rich environments like hospitals, antibiotic-resistant bacteria get more resources and space to reproduce and pass on their advantageously changed genes to the next generation (Bitesize, 2018).
Bacteria multiply at a very fast rate, oftentimes under 20 minutes. As a result, antibiotic-resistant bacteria can quickly dominate a bacterial community. However, reproduction is not the only method of proliferation. For instance, bacterias release their DNA after death that is then absorbed by other bacteria in a process called transformation, while others use a mechanism known as conjugation in which they join via pili to exchange their genes. Through many more methods of horizontal gene transfer over time, resistance genes multiply, resulting in the creation of entire strains of resistant super bacteria (Biology LibreTexts, 2016). Furthermore, during DNA exchange, bacteria may simply exchange DNA segments across related and unrelated species. Antibiotic-resistant genes from one bacteria can be integrated into another and as a result, treating a bacterial infection with a single antibiotic may induce resistance to develop in both the targeted bacteria and other bacterial species (Missouri Department of Health and Senior Services, 2019).
Drivers of Antibiotic Resistance
In the field of medicine, there are over 100 antibiotics used to cure bacterial infection with different threat levels ranging from simple acne to pneumonia and sepsis (eMedicineHealth, 2021). However, overuse, misuse, and abuse of antibiotics while treating these infections are also the leading causes to antibiotic resistance through stress-induced mutagens. Overuse of antibiotics will increase the dynamics of antibiotic action on bacterial cells and increase its mutation rates. This is because, if the bacterial population is not effectively eliminated, the remaining cells will be under stress that can cause alterations in the expression of genes that affect the mutation rate, such as triggering error-prone DNA polymerases or suppressing DNA repair genes (Critical reviews in biochemistry and molecular biology, 2011). Additionally, if antibiotic treatment is stopped before the designated time or before completion of its full course, the lingering bacteria will continue to multiply and regrow the population; and it is very likely that the new population will develop antibiotic resistance. This prolongs the recovery period and also necessitates stronger, additional antibiotics to treat the infection instead (Cedars Sinai, 2022). Longer antibiotic courses increase the likelihood of antibiotic resistance at both individual and community levels. Increased antibiotic usage creates selective pressure that kills susceptible strains and allows resistant bacteria to flourish. This applies for illnesses when the goal of treatment is to kill all existing bacteria in the body, such as tuberculosis and gonorrhea, but not for infections caused by normal human flora, such as most skin and urinary tract infections. Some common cases of antibiotic resistance in medicine today include strains of Staphylococcus aureus that evolved into MRSA, which are resistant to beta-lactam antibiotics due to a gene that substitutes the targeted protein; and other bacteria such as Salmonella that produce enzymes that break down antibiotics, and E. coli which eject antibiotics such as quinolones to prevent their function (Journal of Infection and Public Health, 2021).
Bacteria multiply at a very fast rate, oftentimes under 20 minutes. As a result, antibiotic-resistant bacteria can quickly dominate a bacterial community. However, reproduction is not the only method of proliferation. For instance, bacterias release their DNA after death that is then absorbed by other bacteria in a process called transformation, while others use a mechanism known as conjugation in which they join via pili to exchange their genes. Through many more methods of horizontal gene transfer over time, resistance genes multiply, resulting in the creation of entire strains of resistant super bacteria (Biology LibreTexts, 2016). Furthermore, during DNA exchange, bacteria may simply exchange DNA segments across related and unrelated species. Antibiotic-resistant genes from one bacteria can be integrated into another and as a result, treating a bacterial infection with a single antibiotic may induce resistance to develop in both the targeted bacteria and other bacterial species (Missouri Department of Health and Senior Services, 2019).
Social and Medical Implications
Drug resistance of pathogens renders antibiotics and all other antimicrobial treatments ineffective, complicating infection treatment and raising the risk of severe illness spread, disability, and death. Antimicrobial resistance as a whole jeopardizes human and animal health, well-being, and even social equity. When normal treatment methods become ineffective, it forces the adoption of more potent, costly, and risky options that may not be as accessible to everyone in the community. Therefore, resistant infections increase both morbidity and mortality rates. According to recent estimates, drug-resistant infections caused 1.27 million deaths worldwide in 2019; and if this problem remains unregulated by 2050, there could be up to 10 million casualties. The most impoverished populations are disproportionately affected by AMR due to the fact that they lack access to advanced healthcare and efficient medications that can help decrease their susceptibility to resistant infections. Hence, if this problem is not better regulated, antimicrobial resistance may reduce GDP by $3.4 trillion per year and put 24 million more people into extreme poverty over the next decade (World Economic Forum, 2023).
Moreover, antibiotic resistance has a direct, detrimental influence on medicine and healthcare systems by raising infections, increasing expenses, disrupting hospital operations and restricting treatment alternatives. Resistant infections not only replace susceptible strains, but can lead to additional illnesses as well. For example, 100 susceptible infections might be divided into 90 susceptible plus 30 resistant infections, resulting in the addition of 20 additional infections. Some similar real-life cases that exhibit this are epidemic clones of vancomycin-resistant genus Acinetobacter and Enterococcus faecium– seeing as they caused nosocomial infections from previously innocuous sources. Increasing resistance also poses a threat towards surgical operations and immunosuppressive treatment. In the United States, 38.7% to 50.9% of microorganisms causing surgical site infection and 26.8% of those causing post-chemotherapy infections are the ones that are resistant to typical preventive antibiotics (European Journal of Hospital Pharmacy, 2022).
What Can You Do to Prevent the Growth of Antibiotic Resistance?
That being said, the most effective strategy to avoid antibiotic resistance among individuals is to use antibiotics responsibly and only when necessary. To help, do not use antibiotics for viral infections, do not save a course of antibiotics for later use, take antibiotics exactly as recommended by professionals without missing doses, and refrain from taking antibiotics prescribed for another individual. Healthcare practitioners may by administering antibiotics only if it is strictly required, targeting specific bacterias with the antibiotic as quickly as possible, and practicing good hygiene. Furthermore, limiting the usage of antibiotics in livestock by lowering the dosages or not using them for basic growth can help reduce new resistance forming and the possibility of it being passed on to humans (Cedars Sinai, 2022).
Scientists are currently racing to keep up with the fast evolution of bacteria. Despite the research of new antibiotics slowing down, the World Health Organization is now promoting new, innovative treatments as researchers are investigating alternate infection-prevention methods, such as therapeutic use of bacteriophages and vaccinations (World Health Organization, 2024). However, because antibiotic resistance can spread easily from one patient to another through direct contact, close proximity, or even poor hygiene, the collaboration of individuals around the world is also required in order to halt the spread and evolution of antibiotic resistance before it reaches critical levels.