Antibiotic resistant infections have become a serious problem in the medical community, killing and/or debilitating millions of people worldwide each year. Without a way to keep these bacteria in check, they can ravage the body, leading to amputations or death. “The modern medicine available to us today may very well be gone tomorrow if we don’t slow the development of antibiotic resistance,” says Dr. Robert Redfield, director of the U.S. CDC in Atlanta. (Cunningham, 12-7-2019)
In 2001, the FDA issued this ominous warning: “Unless antibiotic resistance problems are detected as they emerge, and actions are taken to contain them, the world could be faced with previously treatable diseases that have again become untreatable, as in the days before antibiotics were developed.” (McArale, 2011, p. 42)
How do bacteria develop antibiotic resistance?
Bacteria are evolution’s poster-child for adaptability. Because their life cycles are so much shorter, and their reproduction rates much higher, they can reproduce in as little as a few minutes to a few hours, depending on the strain. It’s possible for a single bacteria to create 16,777,216 offspring in a span of only 24 hours. (Miller, 2014, p. 212)
This high rate of reproduction makes it easy for them to pass on drug-resistant genes. Just like people, each new generation results in slight alterations to the genetic code. Some of these genetic alterations will be better equipped to tolerate certain antibiotics. If antibiotics work to kill 99.9% of harmful bacteria, but .01% prove resistant, those .01% of microbes are going to have better odds of surviving, passing these advantageous genes onto future generations.
When antibiotics are overused, infectious bacteria can rather quickly develop a resistance to them. Eventually these resistant “superbugs” emerge as the dominant strain for a particular infection, since they’re the ones with the best odds of surviving and reproducing. When a population of bacteria is exposed to antibiotics, resistance can occur in as little as a few days to a couple of weeks. Those antibiotic-resistant pathogens that survive can then be passed on to others. In some cases it’s possible for a pathogen to leap from as little as 1-2% immunity to a particular antibiotic to as much as 99% in a single year.
“Even worse, bacteria can become genetically resistant to antibiotics they have never been exposed to,” says G. Tyler Miller Jr. “When a resistant and a nonresistant bacterium touch one another (say, on a hospital bed sheet or in a human stomach), they can exchange a small loop of DNA called a plasmid. This enables them to transfer genetic resistance to a disease from one organism to another.” (Miller, 2014, p. 212)
Penicillin was first discovered in 1928, and saw medical use in the early 1940s. By 1955, penicillin-resistant strains of staph started turning up. Methicillin was introduced in 1959; by 1972 methicillin-resistant staphylococcus aureus had appeared. Vancomycin was introduced in 1972, but by the late 1980s, vancomycin-resistant bacteria had turned up as well. (Quommen, 2018)
What causes antibiotic resistance?
Antibiotic resistance is a naturally occurring phenomenon, but we humans are helping it along and speeding up the process through our overuse of antibiotics. There are a number of ways we are accelerating the rate of antibiotic resistance:
1. Careless use & over-use of antibiotics in humans
Antibiotics are massively over-used. They are often prescribed when a doctor isn’t certain about the cause of a particular illness, and therefore carelessly prescribed for conditions they can’t possibly treat. Antibiotics are often prescribed for viral infections, which they are completely useless against. Curbing the over-use of antibiotics for respiratory infections alone “could have a dramatic impact in curbing the rise of antibiotic resistance,” says pediatric infectious disease specialist Gregory Storch. (Barath, 2021)
We also resort to antibiotics far too quickly instead of allowing a patient’s immune system to clear the infection on its own. A patient feels sick and goes to the doctor expecting to walk out with a prescription. So the doctor prescribes an antibiotic that may shave a day or two off the illness. But using antibiotics for mild, everyday illnesses means they’re less effective in those serious situations when they’re most needed.
Antibiotic resistance can also be aided by careless or incorrect use of antibiotics. When a person doesn’t take the doses consistently, or when they stop taking them after a couple days because they feel better even though the infection hasn’t been completely cleared from their system, it allows the possibility that those few resistant bacteria will survive and re-start the infection. Their progeny will now carry this genetic resistance as they infect other people.
2. Antibiotic use among livestock
In the ‘what were they thinking?’ chapter of the book on humanity, we’ve been carelessly feeding livestock the same antibiotics we ourselves rely on. This is done to promote faster growth and keep them healthy in highly unsanitary conditions like feed lots. “The most conservative estimates,” says Dr. Alan Greene, “agree that more antibiotics are given in the United States to fatten food animals (not to treat their diseases) than all of the antibiotics used to treat every man, woman, and child in the United States.” (Greene, 2009, p. 205)
This creates a breeding ground for antibiotic resistant strains to emerge, and these pathogens can easily cross from animals to humans through close proximity contact, whether that’s the food we eat or the farmworkers and meat processers who harvest these animals. One study found that simply driving behind a truck transporting broiler chickens exposed people to drug-resistant bacteria, which were found in the air and on the surface both inside and outside the car. (Rule, Evans & Silbergeld, 2008)
In fact, many of the most serious infectious illnesses to have emerged in recent years come from cases where a pathogen that normally circulates among animals has crossed over to infect humans. There’s the H1N1 “Swine Flu” (pigs), H5N1 “Bird flu” (Poultry), HIV-AIDS (monkeys butchered for bush meat in Africa), SARS (bats), and Ebola (suspected to have come from bats), just to name a few. So creating a nursery for antibiotic resistant superbugs in the livestock we keep isn’t a very wise course of action.
3. Environmental contamination
Such widespread overuse of antibiotics ends up leeching these wonder drugs into the environment at low but persistent levels. We excrete them through our urine, and they wash from feed lots into streams and rivers. Which means our fields and waterways are steadily being covered in a dusting of antibiotics, allowing mild exposures that encourage pathogens to develop resistance. “When you put mild environmental pressure on billions of bacteria,” says Ron Najafi, CEO of Nova Bay, “there’ s enough genetic diversity that you can kill them all except one, and that one becomes the predominant player.” (Svoboda, 2009)
Traces of antibiotics can be found in just about every lake, river, and stream throughout the world. In 2008, for the first time ever, researchers testing multiple soil samples found bacteria that weren’t just resistant to the strongest antibiotics, but had evolved to live off them as their primary food source. (Dantas et al., 2008)
Can’t we just invent new antibiotics?
We certainly can, and a few people are working on this problem. But because of the profit-driven way in which modern health systems are run, there’s not a lot of advancements being made in this area. Antibiotics aren’t considered a profitable endeavor by pharmaceutical companies, since patients take them for a limited time only when especially sick. So they don’t pull in the type of obscene profits drug companies have become accustomed to. It’s yet another example of the perverse incentives that are rampant throughout modern health care systems, which focus on profit rather than health. Disease is profitable, health is not.
One area of promise is to develop a new class of antibiotics that destroy bacteria more immediately and thoroughly. “A drug like penicillin targets an enzyme, and it’s easy for an organism to develop a single mutation to get past that,” says Georgetown University immunologist Michael Zasloff. “But when a drug destroys a bacterium’s entire membrane, it’s difficult for the bacterium to redesign it.” (Svoboda, 2009) This could give us the upper hand in this evolutionary arms race. Unfortunately, such approaches are still being tested, and we’re not anywhere close to developing a new class of antibiotics that can actually work on this principle.