Pod Insights Short Wave These bacteria may be key to the fight against antibiotic resistance About this episode In 1928, a chance contaminant in Scottish physician Alexander Fleming’s lab experiment led to a discovery that would change the field of medicine forever: penicillin. Since then, penicillin and other antibiotics have saved millions of lives. With one problem: the growing threat of antibiotic resistance. Today on Short Wave, host Regina G. Barber https://www.npr.org/people/1082526815/regina-g-barber talks to biophysicist Nathalie Balaban https://nano.huji.ac.il/people/nathalie-questembert-balaban from Hebrew University about the conundrum — and a discovery her lab has made in bacteria that could turn the tides.
Check out our episodes on extreme bacteria in Yellowstone https://www.npr.org/2025/02/05/1229167010/yellowstone-bacteria-hot-springs-microbes-relationship and the last universal common ancestor https://www.npr.org/2025/01/17/1225172117/life-species-luca-ancestors.
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Transcript Speaker names marked ? are inferred from speaking time and the show’s known hosts — they are not voice-verified.
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0:18 Regina Barber? You're listening to Short Wave from NPR.
0:26 Regina Barber? In 1928, the Scottish physician Alexander Fleming made a discovery that would change the field of medicine forever. He was studying bacteria on auger plates in the lab when he noticed something odd. There weren't any bacteria growing around a spot of mold that had contaminated a part of the plate. It turns out, he discovered a medical super compound: penicillin. Since then, penicillin and other antibiotics have saved millions of lives with one problem: the growing threat of antibiotic resistance.
0:59 Speaker 02 Antibiotic resistance means that somehow the bacterium usually acquired a mutation. For example, the penicillin is there, but it doesn't do its job. And therefore, the bacterium grows happily and it's resistant to penicillin.
1:15 Regina Barber? This is Natalie Balaban, a biophysicist at the Hebrew University in Jerusalem. And she says more and more bacteria are becoming resistant to all of our antibiotics, which could spell a major problem. One day, all of our antibiotics could stop working unless scientists can find a major weakness in bacteria.
1:38 Regina Barber? Recently, Natalie's lab may have done just that by hacking dormant bacteria. Because antibiotics, they work by killing off growing bacteria. But sometimes, bacteria don't grow. They shut down. And in that case, antibiotics like our guy penicillin are rendered useless.
1:57 Speaker 02 The penicillin will kill all the growing one, but the ones that are non-growing are going to persist. And this is what is called persistence.
2:07 Regina Barber? Today on the show, antibiotic persistence, what it is and how it can help scientists discover new ways to combat a growing bacterial threat. I'm Regina Barber. You're listening to Shorewave, the science podcast from NPR.
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3:46 Regina Barber? OK, Natalie, antibiotic resistance is definitely a problem. We talked about that. But there's another way bacteria evade antibiotics, which is what you study, right? Like, what is that term?
3:58 Speaker 02 Right, so we study antibiotic persistence. And it's different from resistance because persistent bacteria, they just survive during the antibiotic treatment because they turn on to a dormant form. They just arrest their growth. And when bacteria arrest their growth, then many antibiotics don't work because antibiotics typically need active growth in order to kill the bacteria.
4:31 Regina Barber? And then those dormant bacteria can come back once the antibiotic is gone. These are the persisters. So it seems like this dormancy is the key. What did scientists know about this dormant state before you looked into this?
4:47 Speaker 02 So it was it was known for a long time that when bacteria do not grow, they are not targeted by many antibiotics. They protect themselves from all kinds of stresses. So usually, when you starve them, they arrest their growths and then they go into this dormant, protected form. But it was not realized that these dormant forms, once they grow again, they can really lead to the speedup of the evolution of antibiotic resistance.
5:20 Regina Barber? When we were prepping for this episode, our team learned that clinicians really don't look at persistence in people. They just kind of focus on resistance.
5:29 Speaker 02 So definitely, resistance is a major problem. And usually, if you have a good immune system and you are given the correct antibiotics, these persister bacteria, they are there. But your system is the one that is going to take care of them.
5:47 Regina Barber? OK.
5:48 Speaker 02 So the antibiotics never kill all the bacteria. This we already know. But it's enough in a healthy patient, it's enough for the antibiotic to kill most of the bacteria or even just to arrest the growth of bacteria.
6:05 Speaker 02 But of course, in immunocompromised persons or in a part of the body where the immune system doesn't work or in elderly patients, persistence leads to resistance. And these resistance strains actually can go and infect other people.
6:26 Regina Barber? Antibiotic persistence can lead to antibiotic resistance.
6:30 Speaker 02 Yes, actually, we saw that when bacteria are more persistent, they have a higher probability of becoming, at the end of the day, resistant. So, in other words, persistence, antibiotic persistence, is really a stepping stone for antibiotic resistance. And it means that any new drug that you put on the market, if you are not taking care also of the persistent bacteria, then they will eventually evolve to be resistant to this drug and then this drug will not be as effective as it was.
7:08 Regina Barber? And you published a paper this year in 2026 about how these bacteria can persist in this dormancy state to then become resistant to antibiotics. What did you find in that study?
7:20 Speaker 02 What we found is something that changed the way we look at dormancy.
7:26 Speaker 02 So in the lab, we can use, for example, these antibiotics that just arrest the bacteria. You can also use all kinds of heat stress or pH stress. So there are different stresses and will create bacteria, will make them enter a state of growth arrest or dormancy that protects them from different types of antibiotics. Many, many times, it was more, you know, you haven't parked your car and this is why your car is not on the road. It's just, you know, by accident. You just, you had a car crash.
8:05 Speaker 02 And now your car is not moving.
8:08 Regina Barber? It's not, it's not because you're actually stopped because you wanted to.
8:11 Speaker 02 Exactly. This car crash didn't kill them, but it made them stop their growth. And now this crash, instead of being bad for this bacteria, it turned out to be beneficial because now the antibiotics comes and they happen to be non-growing and therefore they happen to survive the antibiotic treatment.
8:31 Regina Barber? So what would be like an example of a car crash in this situation?
8:37 Speaker 02 So in the body, it can be a meeting with an immune cell that is trying to to kill the bacteria, but doesn't succeed, right?
8:47 Regina Barber? Hmm.
8:47 Speaker 02 Then I would would go into this arrest.
8:51 Regina Barber? They're just putting them in dormant states.
8:53 Speaker 02 They are putting them in dormant state, but what we find out in the lab is that it's not an organized dormant state. It's this car crash type of dormant state.
9:03 Regina Barber? What does it mean for bacteria to be in this more chaotic dormant state? Like, how does that change how they behave or respond?
9:11 Speaker 02 So when they are in this chaotic state, instead of being, you know, this bacteria that when you, when they see an external signal, they they have a very organized response. Now they are trapped into this state that they didn't plan to enter.
9:28 Regina Barber? Hmm.
9:29 Speaker 02 And it means that now their recovery is going to be very, very long, extremely long, in the context of infection. It means that if you had a persistent bacteria that was in this chaotic state, now you stop the antibiotics. You may not see anything, but after a day or a few days, this chaotic bacteria will start growing again, and then you'll have a reinfection. So the chaos that is governing the recovery time of this bacteria is also actually dictating how long the treatment should be,
10:10 Speaker 02 because, you know, you need to keep the treatment on for as long as they are in this chaotic state.
10:18 Regina Barber? Yeah. How could knowing this chaotic, this like dysregulated state, like that it exists? How can it help us with future antibiotic treatment?
10:28 Speaker 02 So it really has changed the way we thought about tackling persistent bacteria, because what we find out in this recent work is that their membrane is more permeable.
10:44 Regina Barber? Oh, OK.
10:46 Speaker 02 This chaotic state. And now there are all kinds of ideas of how to take advantage of this increased membranal permeability to actually use all kinds of compounds that can kill them.
11:02 Regina Barber? How could this like, search for these, these new types of drugs, change the trajectory of treating antibiotic resistance?
11:09 Speaker 02 So I think it's, it really realizing that in order to prevent the evolution of resistance, there are many things to do. One of them is to prevent these persisto bacteria from reemerging in these very long infections. And preventing from them from reemerging means treating them with this, probably with this membrane targeting components before we stop the antibiotic treatment completely. So, and then we've treated most of the bacteria. The only ones surviving are these chaotic bacteria.
11:51 Speaker 02 Now let's use a component that is specific against these chaotic bacteria, and then stop the treatment.
11:58 Regina Barber? Natalie, thank you so much for talking to me about antibiotic persistence.
12:04 Speaker 02 Thank you.
12:07 Regina Barber? If you liked this episode, listen to our shows on Extreme Bacteria in Yellowstone and The Last Universal Common Ancestor. We'll link to them in our show notes. And follow us on the iPOD app or wherever else you get your podcasts. This episode was produced by Burley McCoy and edited by our showrunner Rebecca Ramirez. It was fact checked by Tyler Jones. Jimmy Keely was the audio engineer. I'm Regina Barber. Thank you for listening to Short Wave from NPR.
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