Antibiotics May Soon Become Useless | The Walrus
Antibiotics May Soon Become Useless | The Walrus
Doctors are looking to an experimental treatment for help
As living organisms, bacteria are encoded by DNA, and DNA occasionally mutates. Sometimes genetic mutations render a bacterium immune to an antibiotic’s chemical tactics. The few cells that might escape antibiotic pressure then have a sudden advantage: with their counterparts wiped out, resources abound, and the remaining antibiotic-resistant bacteria proliferate. It’s a problem not only for the host—you or me when we are treated with an antibiotic and develop a resistant strain—but also for anyone with whom we happen to share our resistant bacteria, say, on a door handle or keyboard. In fact, most resistant bacteria develop not in people but in livestock fed antibiotics to promote growth; these resistant bacteria infect people through contaminated animal products. This is how even antibiotic “naive” people come to be infected with resistant strains of bacteria.
I see this all the time as a family doctor. A woman has a urinary tract infection. I tell her that her bacteria are resistant to this or that antibiotic, and she says, “But I’ve never taken any of those.” Welcome to the global human soup.
We should have stopped irresponsible use of antibiotics decades ago.
But capitalism decided.
Patients also demand antibiotics even after the health care provider explains that they do no good. PCP’s are left with the choice of prescribing something or risk losing the patient.
So everyone gets a fun little z-pack for their viral infection, and then they get to post how the z-pack cleared things right up.
Australia what are you doing? https://ourworldindata.org/grapher/antibiotic-usage-in-livestock
I don't trust these figures at all. The USA's factory farming is gargantuan. Canada is similar to Australia. The only way I could see this chart making sense is if there were diminishing returns in antibiotics at a certain scale or density, which doesn't sound right either, or the winter climate reduced the need for antibiotics.
It’s impossible to know exactly what we don’t know. This is a big issue, but there are people taking it seriously. It seems likely new antibiotics which will work are going to be developed. For example: this new class that was discovered a couple months ago using AI.
The article discusses the 'newest' form of treatment ...
BACTERIOPHAGES, or phages for short, are viruses that attack bacteria and kill them; the two organisms have been involved in an evolutionary cat-and-mouse game for millions of years. Phages are ever present in the environment, from sea water to barnyard waste—anywhere bacteria are found in high numbers.
oh, great
You can't cheat evolution.
People often cite evolution for antibiotic resistance, but that's not the case.
There's an inverse relation between bacteriophage resistance and antibiotic resistance. Antibiotic resistance requires more efflux pumps and less strong cell walls, and bacteriophage resistance requires stronger cell walls and less efflux pumps.
What's happening is allele drift within colonies towards better antibiotic resistance, but these colonies are also very susceptible to bacteriophages.
This is no different than the frequency of spots on deer in a population group increasing our decreasing over generations.
I know many people call that evolution, but I think it's important to be precise with our definitions. These traits for antibiotic or bacteriophage resistance are already present within the genome. They each just get expressed under different conditions, and the phenotypic strength of each is inversely proportional to the expression of the other.
This isn't a simple or straightforward relationship. Genetics are always incredibly complex, but this relationship is confirmed.
I understand what you're saying about drift, but I'm not sure that feels sufficient to explain the prevalence of anti-biotic resistance. You're right to highlight that the genes for antibiotic resistance already exist and it's just a question of how prevalent they are in different populations/generations, but I don't think this excludes it from being evolution. I would consider the human use of antibiotics in medicine and agriculture to be a selective pressure that is increasing the prevalence of antibiotic resistant genes in bacteria, especially in combination with human activities that facilitate the global spread of antimicrobial resistance.
I agree that "evolution" is a pretty muddy term though, which is made trickier by the fact that with how language evolves, some people use it in a different sense than what is probably strictly "correct". I'm a biochemist, for example, and I don't know if I could give a strictly correct definition for evolution. Along those lines, I realise I may be misinterpreting your point.
Separate to all that, it sounds like you're well versed on the bacteriophage stuff, are there any articles that you think cover the topic well? I'm more of a protein structure gal myself, so I only have patchy, undergrad level knowledge of microbiology stuff.
Your comment is confusing. Yes, genetic drift is evolution, so saying "people cite evolution" and then dismissing it is not a good approach.
Perhaps you mean it isn't natural selection, but then the trait being under balancing selection (a tradeoff between phage resistance and antibiotic resistance) is still under selection. And the presence of antibiotics shifts the balance heavily in favor of resistance even if that means decreasing resilience in the absence of antibiotics.
You say the traits are already there and just need to be expressed, so perhaps it's mutation you think is not happening. That's often the case, but it still took mutation to create the means of resistance to begin with. Some of it is passed around on plasmids, but they the traits had to evolve in the first place. In addition, once resistance becomes dominant, there is enough diversity to select for compensatory mutations that increase the fitness of the resistant bacteria. Things like compensating for cell wall weaknesses or pumps that were initially favored despite their drawbacks.
You are reporting one side of a three-sided coin. You can find instances of phage resistance linked to increased antibiotic susceptibility, decreased antibiotic susceptibility, and in most cases no change in antibiotic susceptibility. Studies linking phage resistance to increased antibiotic susceptibility are based on in vitro selections resulting in genetic disruptions that would never arise in a host, and are likely due to the relaxation of selective pressures when bacteria are grown in rich broth. For example, phage that use LPS as a receptor cannot infect cells with LPS defects, but those cells are so sick and mucoid that they become susceptible to just about any other stress, including antibiotics. We never isolate bacteria with LPS defects in the wild because they would go extinct in any competitive environment.
The real lessons we need to learn from phages and other antibacterial systems is that resistance is inevitable. These systems have built in flexibility and modularity to accommodate changes and mutate rapidly. Almost all of these systems follow a similar pattern: bind to target cell, get inside target cell, destroy target cell. There are many ways to accomplish each of those steps, and these systems are set up to rapidly evolve new ways accomplish each. This evolution is not limited to the slow single mutations we often associate with evolution. We often observe recombination where another target cell binding domain can be swapped in to generate a new functional system.
Modern phage therapy advocates suggest combination therapies, where multiple antibacterial agents are deployed to substantially lower the rate of resistance. But we will never get that number to zero. Also phage therapy is limited in efficacy based on the site of infection (phage do not penetrate tissues like small molecule antibiotics do) Instead of evolution being a brick wall for therapy, we need to play the game. We need to get off of broad-spectrum antibiotics, focus on functional modules (like cell entry, cell toxicity, etc), and reform our regulatory structure to enable mixing and matching of these modules in regimented phases in response to the resistance that we know will arise. Phage therapy is not the answer; the phage evolutionary cycle is the answer.
Ive nearly shit myself to death over the last 2 weeks thanks to antibiotic resistant campylobacter. Hoping the 3rd and 4th antibiotics can help me get rid of this thing.
Another reason to become vegetarian.
vegetarians still support the egg and dairy industry, which use massive amounts of antibiotics. the solution is veganism.
I know, but seeing the number of downvotes, it seems that many people still prefer to deny the problems.
A vegetarian that eats eggs is a sith.
Lemmy hates vegetarians. Just look at all the pro meat propaganda posted. They're not even aware of that yet.
Which is surprising as becoming vegetarian is one of the best things you can do, as an individual, for the climate. It also tends to be quite healthy.
What are you talking about? Beans are totally vegetarian...
Another reason to regulate industry, as has already begun in the US and EU. Relying on individual behavioural changes to solve these types of systemic failures simply does not work.
But I'm glad it gives you a reason to feel morally superior.
I'd rather they don't. As long as others are dependent on meat, their total fitness shall remain lower than mine, giving me a very real competitive advantage.