Empirically, bacteria are very quick to rid themselves of genes once they’re no longer useful. For example, if you insert DNA into a bacteria that affords antibiotic resistance, it will keep those genes as long as antibiotics are around. But once you remove the antibiotics, it will jettison that DNA within a few hours.
So does this mean that when bacteria evolve antibiotic resistance in a new location (i.e. new hospital, new farm, etc), they have to do it de novo?
Good question! I don’t know, but I think that they don’t necessarily need to. Something I didn’t get into in the post but which is pretty important for understanding bacterial genomes is that they do horizontal gene transfer, which basically means that they trade genes between individuals rather than exclusively between parents and offspring.
From what I understand, this means that although on average the bacteria shed the unhelpful DNA if given the opportunity, so long as a few individuals within the population still have the gene, it can get rapidly reacquired when needed. I don’t know exactly how the math works out, but I’d guess that in big enough populations, if antibiotic encounters are somewhat common, then probably they don’t need to do it de novo each time?
This also means bacterial genomes are much more distributed than eukaryotic ones. So long as any individual bacteria has some gene, it’s “as if” the whole species has it. Which means their genomes are, in a sense, actually longer than they might naively seem. Being distributed has advantages: no single genome needs to be very long, yet the population can hold onto useful stuff. But it also has disadvantages: any adaptation that relies on genes being close together in a single genome is unlikely to develop (which includes e.g. all of the regulatory hierarchy stuff mentioned in the post). So I do still expect that the pressure towards short genomes meaningfully stunts bacterial complexity.
Good question! There’s a literature on the epidemiology of drug-resistant bacteria, and they do manage to get transmitted between hospitals and across international borders in the bodies of hosts.
Increasing antibiotic resistance is also caused by transmission of resistant bacteria within hospitals by cross colonisation of patients via the hands of healthcare staff and subsequent spread between hospitals by transfer of colonised patients
So unfortunately no, we can breed antibiotic resistant bacteria in one place and spread them around all over.
wait so is a viable strat re: antibiotic resistant infections to just go a while without any antibiotics, then restart? granted, the patient needs to survive, and ideally not spread the infection to others, but still. Is this a documented action suite?
I don’t know for sure. It seems important that most antibiotic resistant infections start in a patient who is not on antibiotics, suggesting there’s a clinically meaningful time delay before the bacterial population loses antibiotic resistance in the absence of selection pressure.
Hospitals have tried approaches of either using distinct antibiotics on different patients, or rigidly using one antibiotic at a time on all patients on a rotation, in order to avoid antibiotic resistance, and I know the efficacy of these approaches does get studied.
I think with antibiotic resistance, we see the doctors trying one drug after another on the patient until they see a response. For each drug, the bacteria in the patient will have gone at least the length of time since the patient’s infection started since last being exposed to it. Possibly a patient who responds to no drugs but who manages to be kept alive despite the infection could then find success if the doctors tried one of the old drugs again. My guess is this is just a rare circumstance. In most cases the patient will have recovered or died.
Think of it as exponential decay. If the half life of a completely non-functional gene is only 2 hours, then after a week only one in 10^25 bacteria have it—i.e. none. Trace amounts of functionality (like trace amounts of antibiotics) will slightly extend the half life—but this causes outsized effects at the tails. If the half life of an antibiotic resistance gene when there’s trace antibiotics gets extended to 3 hours, then after a week one in 10^17 bacteria still have it—i.e. still probably none, but maybe a few that can carry the gene from farm to farm or hospital to hospital.
One other mechanism that would lead to the persistence of e.g. antibiotic resistance would be when the mutation that confers the resistance is not costly (e.g. a mutation which changes the shape of a protein targeted by an antibiotic to a different shape that, while equally functional, is not disrupted by the antibiotic). Note that I don’t actually know whether this mechanism is common in practice.
So does this mean that when bacteria evolve antibiotic resistance in a new location (i.e. new hospital, new farm, etc), they have to do it de novo?
Good question! I don’t know, but I think that they don’t necessarily need to. Something I didn’t get into in the post but which is pretty important for understanding bacterial genomes is that they do horizontal gene transfer, which basically means that they trade genes between individuals rather than exclusively between parents and offspring.
From what I understand, this means that although on average the bacteria shed the unhelpful DNA if given the opportunity, so long as a few individuals within the population still have the gene, it can get rapidly reacquired when needed. I don’t know exactly how the math works out, but I’d guess that in big enough populations, if antibiotic encounters are somewhat common, then probably they don’t need to do it de novo each time?
This also means bacterial genomes are much more distributed than eukaryotic ones. So long as any individual bacteria has some gene, it’s “as if” the whole species has it. Which means their genomes are, in a sense, actually longer than they might naively seem. Being distributed has advantages: no single genome needs to be very long, yet the population can hold onto useful stuff. But it also has disadvantages: any adaptation that relies on genes being close together in a single genome is unlikely to develop (which includes e.g. all of the regulatory hierarchy stuff mentioned in the post). So I do still expect that the pressure towards short genomes meaningfully stunts bacterial complexity.
Good question! There’s a literature on the epidemiology of drug-resistant bacteria, and they do manage to get transmitted between hospitals and across international borders in the bodies of hosts.
So unfortunately no, we can breed antibiotic resistant bacteria in one place and spread them around all over.
wait so is a viable strat re: antibiotic resistant infections to just go a while without any antibiotics, then restart? granted, the patient needs to survive, and ideally not spread the infection to others, but still. Is this a documented action suite?
I don’t know for sure. It seems important that most antibiotic resistant infections start in a patient who is not on antibiotics, suggesting there’s a clinically meaningful time delay before the bacterial population loses antibiotic resistance in the absence of selection pressure.
Hospitals have tried approaches of either using distinct antibiotics on different patients, or rigidly using one antibiotic at a time on all patients on a rotation, in order to avoid antibiotic resistance, and I know the efficacy of these approaches does get studied.
I think with antibiotic resistance, we see the doctors trying one drug after another on the patient until they see a response. For each drug, the bacteria in the patient will have gone at least the length of time since the patient’s infection started since last being exposed to it. Possibly a patient who responds to no drugs but who manages to be kept alive despite the infection could then find success if the doctors tried one of the old drugs again. My guess is this is just a rare circumstance. In most cases the patient will have recovered or died.
Think of it as exponential decay. If the half life of a completely non-functional gene is only 2 hours, then after a week only one in 10^25 bacteria have it—i.e. none. Trace amounts of functionality (like trace amounts of antibiotics) will slightly extend the half life—but this causes outsized effects at the tails. If the half life of an antibiotic resistance gene when there’s trace antibiotics gets extended to 3 hours, then after a week one in 10^17 bacteria still have it—i.e. still probably none, but maybe a few that can carry the gene from farm to farm or hospital to hospital.
One other mechanism that would lead to the persistence of e.g. antibiotic resistance would be when the mutation that confers the resistance is not costly (e.g. a mutation which changes the shape of a protein targeted by an antibiotic to a different shape that, while equally functional, is not disrupted by the antibiotic). Note that I don’t actually know whether this mechanism is common in practice.