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

Shorter courses of antibiotics may reduce antimicrobial resistance. Plus, a new study finds a group of genes associated with fibromyalgia.

Speaker names marked ? are inferred from speaking time and the show’s known hosts — they are not voice-verified.

• 0:00Speaker 00

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• 0:17Flora 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.

• 0:55Speaker 02

  Thank you, Flora. Thanks for having me.

• 0:58Flora Lichtman?

  Okay. This seems like a big shift from what I have always heard.

• 1:03Speaker 02

  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,

• 1:45Speaker 02

  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.

• 1:55Flora Lichtman?

  You know, 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 have, to be resistant to that antibiotic. And then they could, you know, go forth and multiply. So what's wrong with that picture?

• 2:17Speaker 02

  You're on the right track for sure, because what happens 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-

• 2:32Flora Lichtman?

  Flora, like microflora.

• 2:33Speaker 02

  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, 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.

• 3:16Speaker 02

  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.

• 3:31Flora 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.

• 3:41Speaker 02

  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.

• 3:55Flora Lichtman?

  Have we measured that? You know, how much bacteria you lose after seven days versus 14 days?

• 4:03Speaker 02

  So some of that research is emerging. And depending on the antibiotic and 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,

• 4:48Speaker 02

  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.

• 5:09Flora 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?

• 5:21Speaker 02

  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?

• 6:05Speaker 02

  And do I need to take it for this long? And so making sure that you, 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.

• 6:26Flora Lichtman?

  I mean, are doctors up to date on this?

• 6:30Speaker 02

  Well, you know, 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.

• 6:58Flora Lichtman?

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

• 7:13Speaker 02

  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 and 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.

• 7:55Flora Lichtman?

  What do you mean, there's psychology involved?

• 7:57Speaker 02

  So we know from studies that when doctors score more tired, they're more likely to prescribe antibiotics.

• 8:08Flora Lichtman?

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

• 8:12Speaker 02

  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's 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,

• 8:56Speaker 02

  as well as, you know, not demanding an antibiotic that you don't need if a physician's trying to tell you, I think this is a virus. I think this will get better without antibiotics.

• 9:08Flora Lichtman?

  Yeah, yeah. So ask your doctor, and also ask your doctor about duration.

• 9:12Speaker 02

  That's right.

• 9:12Flora Lichtman?

  It sounds like that's a message, too.

• 9:13Speaker 02

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

• 9:23Flora Lichtman?

  That's great advice. Okay, thank you, Amy.

• 9:25Speaker 02

  Thank you so much, Flora.

• 9:26Flora 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?

• 9:55Flora Lichtman?

  Hey, everybody. If you like Science Friday, I want to recommend another podcast I know you'll love, too. Science Versus. From peptides to protein-maxing, Science Versus takes on fads and trends and the opinionated mob I know you know what I mean, to find out what is fact, what is not, and what's something in between. And they're the only podcast with better pun game than us. So check them out, Science Versus, wherever you get your podcasts.

• 10:29Flora 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. Joining me now is one of the study's lead authors. Dr. Nasa Sinat-Armstrong is an assistant professor of computational biology and public health at Fred Hutch Cancer Center. Nasa, welcome to Science Friday.

• 11:13Speaker 03

  Thanks so much for having me.

• 11:16Flora Lichtman?

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

• 11:22Speaker 03

  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.

• 11:35Flora Lichtman?

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

• 11:42Speaker 03

  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 kind of started off the process of trying to look at that more.

• 12:04Flora Lichtman?

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

• 12:12Speaker 03

  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.

• 12:43Flora 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?

• 12:54Speaker 03

  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.

• 13:14Flora 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?

• 13:21Speaker 03

  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 kind of 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.

• 14:08Flora Lichtman?

  You know, I know that there have been hypotheses that there's an immune system link to fibromyalgia. Does this finding rule that out?

• 14:16Speaker 03

  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.

• 14:32Flora 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?

• 14:41Speaker 03

  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.

• 15:07Flora Lichtman?

  You know, 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?

• 15:21Speaker 03

  I think that our study suggests that fibromyalgia does have a component related to nocicepastic pain or how people experience pain. And that nocicepastic 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.

• 15:58Flora Lichtman?

  Are there any implications for screening now?

• 16:03Speaker 03

  I think in the immediate term, it could teach us how we want to do screening. But there's not a specific, like, 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.

• 16:26Flora Lichtman?

  Let's talk about that. How could this lead to better treatments?

• 16:30Speaker 03

  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.

• 17:14Speaker 03

  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.

• 17:28Flora Lichtman?

  So where do you go from here?

• 17:31Speaker 03

  Well, I think definitely some of that work in GPR52 and some of our other target genes to say, like, 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 nocicepastic 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 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.

• 18:08Flora Lichtman?

  Dr. Nasa Sinat-Armstrong is an assistant professor of computational biology and public health at Fred Hutch Cancer Center. Nasa, thanks for being here.

• 18:17Speaker 03

  Thanks so much for having me. It was great talking about this.

• 18:21Flora Lichtman?

  This episode was produced by Shoshana Buxbaum. If you're already listening to the podcast, check out our social media accounts or our newsletter, sciencefriday.com/newsletters. I'm Flora Lipton. We'll catch you next time.