Is a shorter course of antibiotics OK? + Genetic risk of fibromyalgia

[MUSIC PLAYING] FLORA LICHTMAN: Hey, it’s Flora, and you’re listening to Science Friday. You’ve probably been warned that you’d better finish that course of antibiotics, because if you don’t, you could find yourself battling antibiotic-resistant bacteria. Well, guess what? Apparently, there is more to this story. In fact, a growing body of research suggests that the exact opposite might be true.

So what does this mean for you and your next sinus infection? Here to tell us more is Dr. Amy Mathers, medical director of Antimicrobial Stewardship and an associate professor of medicine and pathology at the University of Virginia. Amy, thanks for being here.

AMY MATHERS: Thank you, Flora. Thanks for having me.

FLORA LICHTMAN: OK, this seems like a big shift from what I have always heard.

AMY MATHERS: Yeah, so there was this dogma that finish the course, or you will develop resistant bacteria. And it comes from long ago, before we really understood how resistant bacteria worked. Not finishing the course sometimes would cause relapse.

However, what we now understand is that a lot of relapse infections that were assumed to be because of resistant bacteria were actually more complicated than that. They may be a new infection, or they may have been that the first infection didn’t get completely cleared out. But it didn’t necessarily mean that the bacteria was resistant. For example, strep that causes strep throat doesn’t have any resistance to penicillin, and that’s never been described. So it’s not resistance that’s driving it. It’s something else if you have a relapse.

FLORA LICHTMAN: I thought the logic was that if you don’t take the full course, you might not fully wipe out the bacteria causing the infection. And then the ones that weren’t eliminated are ones that are likely to be resistant to that antibiotic. And then they could go forth and multiply. So what’s wrong with that picture?

AMY MATHERS: You’re on the right track for sure. Because what happens is, is antibiotics actually target the infecting organism, but they also target a lot of other stuff and flora. And so the only bacteria that are left–

FLORA LICHTMAN: Flora like microflora, you mean.

AMY MATHERS: Yeah, like microflora, like healthy bacteria that live in your gut, that use up nutrients and probably don’t carry resistance. And so when you expose all of those bacteria to an antibiotic, you may wipe all of those out, leaving behind only the resistant organisms. And so the next time you have an infection, if you get a new infection, say, in your bladder or in your sinus, it may develop resistance to antibiotics the next time you try to treat it.

So you’re not actually wrong. The issue is, is the longer you’re exposed to them, the more you’re getting rid of that healthy flora and selecting for resistant bacteria. So what a lot of people and a lot of clinical trials have been doing lately is seeing what the shortest course possible is to decrease the collateral damage while still treating the infecting organism effectively.

FLORA LICHTMAN: So the upshot here is that a longer course of antibiotics might actually make you more likely to develop antibiotic resistant bacteria inside of you.

AMY MATHERS: That is correct. The longer you’re on the antibiotic, the more selective pressure you put on your microbiome, and therefore, the more likely you are to have resistant bacteria.

FLORA LICHTMAN: Have we measured that, how much bacteria you lose after seven days versus 14 days?

AMY MATHERS: So some of that research is emerging. And depending on the antibiotic in the situation, not all of that’s been filled out completely. But there is a dose effect. And some scientists have shown the longer you’re on an antibiotic or the more broad spectrum the antibiotic, that may have a different impact on your gut flora. So some antibiotics that might be more targeted won’t cause as much selection for resistance as other antibiotics. And the duration, we know, makes a difference.

It also can select for other infections, such as C. diff, which may be a microbe that you select for when you kill everything else off. C. diff is left behind and can cause a gut infection. Because your normal flora is not there taking up the nutrients, C. diff has a chance to get a foothold in and overgrow and then cause a bad colon infection. There’s definite research saying that almost every day of antibiotic that you take puts you at higher risk for C. diff, depending on whether or not you’re at risk for that infection.

FLORA LICHTMAN: Really? Every day– it’s that granular. I mean, do we have a sense of what the Goldilocks zone is for different antibiotics and different infections?

AMY MATHERS: Yeah, so there’s a lot of really great research coming out about it. And for example, there was a clinical trial last year that looked at seven days versus 14 days for even bloodstream infections and showed that seven days was adequate. So now physicians should be treating most bloodstream infections with seven days of antibiotics, instead of 14. There’s studies in pneumonia, urinary tract infections.

Having said that, it’s not a panacea, and not all conditions have been studied. And there are some situations where shorter course was not necessarily equivalent. And so you really need to talk to your doctor about, do I need this antibiotic? And do I need to take it for this long? And so making sure that your physician’s up on the most current research of what has actually been studied for a shorter course, so that you can kill off the infecting bacteria as soon as possible and decrease unnecessary days of antibiotics.

FLORA LICHTMAN: I mean, are doctors up to date on this?

AMY MATHERS: Well, there’s a lot of people in antibiotic stewardship that are trying to make sure that everybody is up on the literature. And so I think within hospitals, in the last decade, the duration of antibiotic prescribing has changed completely for hospitalized patients. So in our hospital for pneumonia, for example, most patients are getting five days, and if it’s a more complicated pneumonia, seven days, instead of the old 14 days, which was a decade ago.

FLORA LICHTMAN: Are there guidelines somewhere? I don’t how prescriptions work, like if the AMA puts out guidelines around this. But if doctors aren’t reading the literature, would they know that those standards have changed?

AMY MATHERS: Yeah, so the Infectious Disease Society of America puts out guidelines around how long to treat. And so, for example, the urinary tract infection guidelines have recently been updated to reflect the shorter courses, and who needs a longer course and who needs a shorter course. So hopefully physicians are getting that message and shortening the course. Yeah, there’s a lot of nuance in psychology in the way that antibiotics get prescribed. And I think getting the message out that if you don’t need an antibiotic at all, don’t take it, and understanding some of the downsides of antibiotics, I think, is just really important, getting the word out.

FLORA LICHTMAN: What do you mean there’s psychology involved?

AMY MATHERS: So we know from studies that when doctors score more tired, they’re more likely to prescribe antibiotics.

FLORA LICHTMAN: When doctors are more tired, they are more likely to prescribe antibiotics?

AMY MATHERS: Because, well, when you go to your doctor, a lot of times, people want something done. If you’re feeling terrible, you went to the doctor to have something done. And so sometimes patient satisfaction scores can be linked to getting an antibiotic. And so having that long, nuanced discussion, like you and I are having, may not be easy when a doctor is in a rush and a patient is feeling bad. And so that time is well spent in that if you don’t need an antibiotic, we now understand so many of the downsides of taking antibiotics we don’t need, supporting both you, as a patient, not getting an antibiotic you don’t need, as well as not demanding an antibiotic that you don’t need if a physician is trying to tell you, I think this is a virus, I think this will get better without antibiotics.

FLORA LICHTMAN: Yeah. Yeah, so ask your doctor. And also, ask your doctor about duration.

AMY MATHERS: That’s right.

FLORA LICHTMAN: That sounds like that’s the message, too.

AMY MATHERS: 100%. And so just say, 14 days seems like a really long time. Is this the typical duration for antibiotics at this point?

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FLORA LICHTMAN: It’s great advice. OK, thank you, Amy.

AMY MATHERS: Thank you so much, Flora.

FLORA LICHTMAN: Dr. Amy Mathers is the medical director of Antimicrobial Stewardship and an associate professor of medicine and pathology at the University of Virginia. Don’t go away. We have to take a break. But when we come back, a new large-scale study about the genes associated with fibromyalgia– what does this result tell us about this illness?

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FLORA LICHTMAN: Fibromyalgia is a condition that can cause debilitating chronic pain and brain fog. But what causes it has been something of a mystery. For patients, imaging and blood work often turn up normal, and as a result, patients have historically often felt dismissed by doctors. Now, a new large-scale study has identified a group of genes that are associated with the disease, a breakthrough that may help doctors understand people’s risk of developing it, but also may reveal something about the nature of this mysterious illness.

NASA SINNOTT-ARMSTRONG: Joining me now is one of the study’s lead authors. Dr. Nasa Sinnott-Armstrong is an assistant professor of Computational Biology and Public Health at Fred Hutch Cancer Center. Nasa, welcome to Science Friday.

NASA SINNOTT-ARMSTRONG: Thanks so much for having me.

FLORA LICHTMAN: I mean, for people with fibromyalgia, this must be such a gratifying result, to have something tangible.

NASA SINNOTT-ARMSTRONG: Yeah, I agree. I think it’s been a really long time coming for us to understand better what are the biological processes that drive fibromyalgia risk. And this is just one step in that journey.

FLORA LICHTMAN: I mean, did we already know that fibromyalgia had a genetic component or that it ran in families?

NASA SINNOTT-ARMSTRONG: There has been evidence in other studies that there were familial associations. For example, twins have higher risk of developing fibromyalgia if their other twin has fibromyalgia. But there hadn’t been any specifically known genetic risk factors. And this study started off the process of trying to look at that more.

FLORA LICHTMAN: So how many genes did you identify? And how much is the risk increased if you have these variants?

NASA SINNOTT-ARMSTRONG: Yeah, so overall, in our huge study, we found a total of 26 different genetic variants that increase or decrease risk of fibromyalgia. And overall, these explain a pretty small fraction of risk. If you look at all of the genetic variants that we were able to identify in the study, it’s a total of about 10% increased or decreased risk. So this isn’t saying that genetics means that you will or will not have fibromyalgia, but rather, it helps us understand better the process of the disease and the consequences of that on your health.

FLORA LICHTMAN: I mean, 10% feels low still. Does that mean that we’re still looking for other gene variants or that the environment plays a big role? What does that tell you?

NASA SINNOTT-ARMSTRONG: I think both are true. I think that probably there are other genetic variants that increase risk of fibromyalgia. And I think that probably some of the factors that we haven’t identified aren’t genetics at all, that there’s a lot of factors that we already know about related to individual environmental exposures. And those differences matter a lot, too.

FLORA LICHTMAN: I mean, do the variants that you found, do they tell us anything about the nature of fibromyalgia, something we didn’t know before?

NASA SINNOTT-ARMSTRONG: Yeah, I think the biggest thing that we identified in this study is that a lot of the genetics of fibromyalgia is attributable to the nervous system. So there are factors in the genes that act in the nervous system that are close to these genetic variants. And what that means is that probably some of the biology of fibromyalgia is biology of the nervous system. And that can take many different forms. But I think that that’s probably the biggest thing that we learned.

And then the other big thing that is part of the story is that the factors that we identified for the genetics of fibromyalgia don’t seem to be sex-specific. So individuals, regardless of sex, have the same risk from a genetic perspective that we understand for developing fibromyalgia.

FLORA LICHTMAN: I know that there have been hypotheses that there’s an immune system link to fibromyalgia. Does this finding rule that out?

NASA SINNOTT-ARMSTRONG: It does not rule out that possibility. There’s definitely still the possibility of an immune link. And a lot of different immune factors could be relevant, both to the environment or to genetic factors that we haven’t identified as closely as the ones that were presented in this study.

FLORA LICHTMAN: I know that one of the genes you found is also associated with Huntington’s disease. How do you interpret that? What do you make of that?

NASA SINNOTT-ARMSTRONG: I think that the gene being associated with Huntington’s is something that can help us learn about biological processes, but it doesn’t tell us that individuals with fibromyalgia have an increased risk of developing Huntington’s disease. All it means is that some of the stuff that we’ve learned about how Huntington’s works can now help us hopefully learn more about how fibromyalgia does as well.

FLORA LICHTMAN: I know that fibromyalgia often requires some kind of trigger to come on, like a physical trauma or severe stress or an infection. Does anything about your findings help explain why that is?

NASA SINNOTT-ARMSTRONG: I think that our study suggests that fibromyalgia does have a component related to nociplastic pain, or how people experience pain. And that nociplastic component could be related to all of these different types of triggers. But our study, because it was looking mostly at genetic factors and not across all of the different possible ways that people might develop or that they could have risk contributed for fibromyalgia, because we weren’t looking at all of those at the same time, we can’t say, necessarily, which ones might be more specific to the genetics versus to other parts of the development of the disease.

FLORA LICHTMAN: Are there any implications for screening now?

NASA SINNOTT-ARMSTRONG: I think in the immediate term, it could teach us how we want to do screening, but there’s not a specific– you wouldn’t want to take a genetic test to determine if you had fibromyalgia. What this study does is it more helps us understand ways that people might benefit from different types of treatments, or the ways in which additional research could be done to better understand how and when fibromyalgia develops.

FLORA LICHTMAN: Let’s talk about that. How could this lead to better treatments?

NASA SINNOTT-ARMSTRONG: So I think one of the big opportunities that this study reveals is that there’s actually a lot of known genes that are being presented as part of the findings that we had in this work. So one of the big ones that we’re really excited about is looking more into GPR52. That’s a gene that’s associated with some of this Huntington’s disease biology that we previously described and some of the other findings within the study. And there’s already an investigational drug being used to treat Huntington’s that acts through the GPR52 gene.

So what that means is that maybe some of what we’re learning about fibromyalgia could be applied in the context of this GPR52 variant. And we might be able to use drugs that target GPR52 to help with fibromyalgia. I don’t know if that’s necessarily going to work, but I do think that hopefully we’ll get to a point where we’ll be able to understand better if it might.

FLORA LICHTMAN: So where do you go from here?

NASA SINNOTT-ARMSTRONG: Well, I think definitely some of that work in GPR52 and some of our other target genes to say, are these going to improve care, are there ways in which we could develop new drugs against some of the targets here, how can we think about the role of nociplastic pain in the development of fibromyalgia, or how people experience pain, I think all of those are important directions to look at.

And I think that the other big direction that we should go in is trying to identify whether or not these risk factors are relevant for everybody with fibromyalgia, or maybe there’s different subsets of people where some of these risk factors are more or less important. And I think those are both important directions to go in.

FLORA LICHTMAN: Dr. Nasa Sinnott-Armstrong is an assistant professor of Computational Biology and Public Health at Fred Hutch Cancer Center. Nasa, thanks for being here.

NASA SINNOTT-ARMSTRONG: Thanks so much for having me. It was great talking about this.

FLORA LICHTMAN: This episode was produced by Shoshannah Buxbaum. If you’re already listening to the podcast, check out our social media accounts or our newsletter, sciencefriday.com/newsletter. I’m Flora Lichtman. We’ll catch you next time.

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