Declining MMR Vaccination Rates Make West Texas Outbreak a Threat to Measles Elimination
High vaccination rates eliminated measles in the U.S. An outbreak that began in West Texas is threatening to overturn that status.
By , Lauren J. Young, Fonda Mwangi & Alex Sugiura
Rachel Feltman: For Scientific American 's Science Quickly, I'm Rachel Feltman.
More than 1,000 cases of measles have been confirmed in the U.S. since late January, including a cluster in West Texas that has caused one of the worst outbreaks in recent memory. These outbreaks are occurring even though measles was technically eliminated in the U.S. back in 2000. Here to explain what that means—and why that status could be at risk—is Lauren Young, associate editor for health and medicine at Scientific American.
Lauren, thanks so much for coming on to chat with us today.
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Lauren Young: No, thank you for having me.
Feltman: So to refresh our listeners' memories could you give us a brief overview of the current measles outbreaks of concern?
Young: Sure, so the situation continues to worsen in the U.S.; measles cases are continuing to rise. The current case count as of May 1 of the [Centers for Disease Control and Prevention's] report says 935 confirmed cases, which is growing at a pretty alarming rate. The initial outbreak began in West Texas, and now it's in 29 states, and we're also seeing cases and outbreak spread in Mexico and Canada.
So it's important to note, too, that nearly 70 percent of the confirmed cases [in the U.S.] have been in younger people, ages 19 and below, and a large proportion of those cases are in unvaccinated people ...
Feltman: Mm.
Young: Which—and this is a concern 'cause measles is very highly contagious. It's known for, you know, spreading via cough. It's also known for creating a rash, which is pretty uncomfortable, coughing and runny nose, but it could also cause severe complications: it could open up people to pneumonia, organ failure and death. There've been three people who've died so far from these outbreaks, one adult and two children, and all three have been unvaccinated ...
Feltman: Mm.
Young: So it's definitely concerning. I know a lot of public health experts are keeping an eye on this and trying to understand, too, the public health response that's going on.
Feltman: Sure, and just how abnormal is this compared to recent years?
Young: Right, so every year we do see cases of measles, and this often happens primarily due to travel—so when someone goes abroad to a place where measles is more common, they'll come back and reintroduce, you know, some cases. But they're usually relatively contained. What we're seeing now is the highest number of cases since 2019, when we had a pretty large outbreak that started in New York.
But, you know, experts are pretty much in agreement that the case counts right now probably are also underestimations. When these cases started in West Texas, for instance, it was highly concentrated in Gaines County, which is known to have a pretty high population of homeschool children. And so it's hard to understand fully the vaccination rates in kids, since, again, these outbreaks and the, the cases are highly concentrated in children, so yeah, public health experts are definitely keeping an eye on this and are concerned about what's gonna happen in the next few months, yeah.
Feltman: Yeah, I think a lot of folks get confused about the statement that we hear a lot lately that measles has been 'eliminated' in the United States. Could you explain what that status means and how we got it?
Young: Sure, so a disease gets 'elimination' status when its incidence is reduced to zero in a specific region for a set time frame. It's a little bit of a jargony, like, public health status thing, but the CDC and the World Health Organization define the status for measles as a period of 12 months with zero endemic cases, so that means there needs to be no continuous transmission of the disease over a 12-month period of time—so you can't link one case from another case.
The United States achieved its elimination status of measles in 2000, and we've been able to keep that status primarily through prevention measures, particularly through vaccination. And, as we know, the measles, mumps and rubella vaccination, which is how you get vaccinated for measles, is pretty highly effective and very safe.
Feltman: Yeah, do experts think that that elimination status is at risk right now?
Young: Yeah, so there were a few prominent experts in the field of vaccine science who spoke out about this recently. Peter Marks, who was a former [Food and Drug Administration] official and he's a prominent vaccine expert,said he's worried that we're on the way to losing this status. Also Katherine Wells, who is the public health director in Texas, said in March during a news briefing that she's anticipating that this outbreak could go a year long ...
Feltman: Mm.
Young: So that would definitely be pushing into that 12-month window for achieving that elimination status.
Feltman: As you mentioned, this isn't our first big outbreak since 2000, so what factors are coming together to put our elimination status at risk after, you know, 25 years of success?
Young: Yeah, so there's a few things that seem to be, you know, folding into play based off of what I'm just hearing from the experts that I've talked to. One, for sure, is: we've been seeing kind of this steady decline in vaccination rates, specifically in kids but, you know, just nationally as well, ever since the pandemic. A big part of that was: during the pandemic itself a lot of children missed their well appointments, where they would get their routine vaccinations. We did see, you know, some increase from that, but there's other things at play.
There's been a lot of anti-vaccine rhetoric that's been going on that's causing some of that increase to stagnate slightly, and, you know, experts are really highly concerned. We also have, you know, some public health officials in office right now who have a history of endorsing anti-vaccine rhetoric and are also endorsing studies to reevaluate things like autism and vaccines and that connection there.
So there's just this heightened concern around vaccines. And when we see things like a decline in vaccination rates it's very important for a disease like measles because it is so highly contagious. And for something like measles we need to see, as some experts have explained to me, very highly uniform vaccine coverage—in other words, high 'herd immunity,' which is basically the level of either natural immunity or vaccination immunity you need to have in order to stop the spread of disease. So for measles you need about a 95 percent vaccination rate, and any sort of, you know, even slight decline in that can cause these severe outbreaks.
So that's what we're seeing here, where, you know, we have a small pocketed community that had a lower vaccination rate and is, you know, spurring this particular outbreak. But we're seeing that also, too, in other places in the country where there might be even just a small dip in vaccination and it causes a disease to spread. And measles is kind of, as some experts have said, canary in a coal mine for vaccine-preventable diseases because it is so highly contagious, but if we continue to see this overall decrease in vaccinations for things like, you know, other eliminated diseases—like polio, for instance—that's also a little bit of concern for several experts.
We did a whole story about this—Tara Haelle, one of our contributors, did a really deep dive on what that exactly would look like. So this is on the forefront of a lot of people's minds, just the general interplay between vaccine recommendations from public health officials and also how that's playing out from, you know, past historical trends. It's all kind of coalescing together.
Feltman: Yeah, what do public health experts think we can do to keep measles from becoming endemic again?
Young: It seems maybe like a little bit beating a dead horse, but getting vaccinated, you know, I think is still an important thing to do. Listening to trusted health practitioners about treatment. Being active about, you know, going to the hospital or going and getting treatment if you're seeing any signs or symptoms—which, again, include the rash, coughing, and the runny nose and watery eyes.
Feltman: Lauren, thank you so much for coming on. Unfortunately, I'm sure this won't be the last time we talked to you about measles, but we really appreciate it.
Young: No, thank you for having me.
Feltman: That's all for today's episode. If you haven't already submitted your answers for the Science Quickly listener survey, go check it out at ScienceQuickly.com/survey. Your responses will help us steer the future of the show, and you might just win a fun prize for helping us out. We'll be back on Friday.
Science Quickly is produced by me, Rachel Feltman, along with Fonda Mwangi, Kelso Harper, Naeem Amarsy and Jeff DelViscio. This episode was edited by Alex Sugiura. Shayna Posses and Aaron Shattuck fact-check our show. Our theme music was composed by Dominic Smith. Subscribe to Scientific American for more up-to-date and in-depth science news.
For Scientific American, this is Rachel Feltman. See you next time!
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- Scientific American
Animal Lifespans Offer Clues about the Science of Aging
Could the spectrum of animal lifespans hold clues about the science of aging? By , Fonda Mwangi & Alex Sugiura Rachel Feltman: For Scientific American 's Science Quickly, I'm Rachel Feltman. In the animal kingdom lifespans can stretch from mere hours to entire centuries, but that's just the start. Some creatures deteriorate so slowly that we've never actually caught them dying of old age. Others don't seem to age at all. And some can apparently reset their biological clocks and bounce back to infancy to start all over again. Plenty of humans would like to figure out how that works—and potentially harness the ability for our own use. But science has a long way to go. The truth is that we barely understand why or how we age in the first place—let alone how we might stop it. On supporting science journalism If you're enjoying this article, consider supporting our award-winning journalism by subscribing. By purchasing a subscription you are helping to ensure the future of impactful stories about the discoveries and ideas shaping our world today. My guest today is João Pedro de Magalhães. He's the chair of molecular biogerontology at the University of Birmingham in England, and he's here to tell us all about the nascent science of aging. Thank you so much for coming on to chat today. João Pedro de Magalhães: My pleasure. Thank you for the invitation. Feltman: So I'm sure that all of our listeners know that different species have different lifespans, but could you start by giving us a sense of some of the extremes that are out there? Magalhães: Absolutely. It's been a mystery of biology for a very long time, ever since Aristotle noticed [these] differences in lifespan across species. And we know that some animals have very short lifespans; others have very long lifespans. And this happens even amongst closely related species like mammals. For example, hamsters live about two years; mice and rats can live up to three or four years; and, you know, of course, humans, we can live over 100 years. And then at the other end of the spectrum we have certain species of whales that have been estimated to live over 200 years ... Feltman: Mm. Magalhães: So it is quite remarkable how much of a variation in longevity there is. Feltman: Yeah, and then, besides mammals, I would assume that things get even more extreme when you're talking about less closely related species. Magalhães: Well, there's some very unusual animals. There's this type of jellyfish which appears to be immortal, or it appears to have the ability to rejuvenate, to go back in biological time, so adults can go back to earlier stages of development and start again their own lives. So it's not that they're immortal [in] that you can't kill them, but they are biologically immortal in the sense that biological time, for them, doesn't roll in one direction, like it happens for us. Feltman: Mm. Magalhães: So there's very unusual animals—again, we're talking invertebrates like rotifers or very simple animals—whose adults don't have mouths. Feltman: Mm. Magalhães: They don't have a way of feeding. So they're very clear examples of mechanical limitations that will result in the demise of organisms. So you have a very big variety in terms of not just longevity and paces of aging but even in aging phenotypes and how species degenerate and die. Feltman: And fundamentally, what is aging? Magalhães: So aging, we are all familiar with it—I tend to have a very broad definition of aging as a, a progressive and inevitable physiological degeneration, an increase in vulnerability and decrease in viability. Now, of course, there's many facets to aging. I mean, it involves physiological degeneration. I mean, our bodies get weaker. We become frailer with age. But there's also, of course, many cellular, molecular changes that occur as well. And then, of course, there's increased incidence of diseases: cancer, cardiovascular diseases, neurological diseases, and so on. So one of the hallmarks of aging is that once you reach about age 30 your chance of dying [doubles] roughly every eight years, and that's very consistent across populations. And that happens as well in animals, only in animals like mice, it varies a bit between strains, but it'll be something like every few months the chance of dying doubles. Feltman: Hmm, and what do we know about what causes aging? You know, why is it inevitable for most species, but then, you know, for some, like those jellyfish, it doesn't seem to be? Magalhães: Well, that's a big question, and we don't have a good answer yet. We don't have a good understanding why some species age very fast. So for example, mice and rats, as I mentioned, they only live up to three or four years, but they also age much faster than human beings. No matter how you take care of them, a mouse will age about 20, 25, 30 times faster than a human being. So we know there's a very big diversity, also, in rates of aging, but what's behind it is not well-understood. We know there must be genetic differences, again, because no matter how well you take care of your mouse or hamster or rat, it will age a lot faster than a human being. So, you know, you can let it watch Netflix all it wants, it will still age much faster than human beings, right? So there has to be genetic differences. It's not environment, it's not the diet; it has to be genetically determined—it has to be encoded in our genomes how fast we age. But then, of course, the question is, 'Okay, but what [are] the biochemical, molecular, cellular determinants?' That's something we don't understand well yet. Having said that, there are some hypotheses. For example, one idea that's been around for decades is the idea that damage to the DNA and mutations in the DNA accumulate gradually with age and then cause aging. And the hypothesis being that in mice, for example, [this] accumulation of mutations occurs much faster—for which there is some experimental evidence. So that is one hypothesis. And at the moment, however, it's still unproven or unknown, really, why human beings age. Feltman: Hmm, and are there any factors that long-living organisms have in common? Magalhães: There are multiple factors associated with long lifespans. I mean, the important point is that we are a product of our evolutionary history. Of course, we now have technology, and we have medicine, but we didn't evolve in these conditions; we evolved as, as [cavemen], you know, hundreds of thousands or millions of years ago. And the same for every other species. And so the major determinant of whether a species evolves a short lifespan or a long lifespan is extrinsic mortality, so how much they die of—in particular, predation. So if you have animals like—short-lived animals like mice, I mean, mice in the wild very rarely live more than one year, not just because of diseases but primarily because of predators ... Feltman: Mm-hmm. Magalhães: And because they have very short lifespans, even in the wild, then, you know, they have to grow very quickly, they have to develop very quickly, and they have to reproduce very quickly, and so everything happens very quickly. So it's a very fast life history, a very fast life that they live. On the other hand, humans or the Galápagos tortoise would be an example or big whales or underground, subterranean animals like mole rats, they're protected from predators. I mean, we are protected from predators, one, because we're relatively big for primates and, of course, because of our intelligence, which [allowed] us to escape predators when we were, of course, in the time of cavemen and when we were evolving. And that means that because we have fewer predators, we are top of the food chain, that means that we have more time to grow, to develop, and then, of course, that leads to a longer lifespan as well. So across species there's this pattern, of course, of, you know, we are a product of our evolution, and we have the life history and the longevity that fits our evolutionary history. Feltman: What kinds of tools are researchers using to try to answer all of these questions we have about aging and lifespan? Magalhães: So there's different types of tools we can use. I mean, one big technological breakthrough was DNA sequencing. We can sequence DNA relatively cheaply and relatively rapidly nowadays. I mean, the human genome sequencing cost billions of dollars, but nowadays you can sequence your own genome, anyone can sequence their genomes for [a] few hundred dollars. So it's relatively cheap to sequence genomes, which means we can also sequence the genomes of different species, species with different lifespans. So for example, our lab, we sequenced the genome of the bowhead whale, which is the longest-lived mammal, [which has] been estimated to live over 200 years, as well as naked mole rats and other long-lived, disease-resistant species. And there's now hundreds of genome [sequences] from many different species with different lifespans. And so what you can do with that trove of information is analyze it for patterns associated with the evolution of longevity. You can ask questions—so for example, you know, 'Do species that live a longer lifespan, do they have more DNA repair genes?' So you can use that information on the DNA to study the evolution of longevity, then try to find specific genes and pathways associated with it. Feltman: Mm. Magalhães: Now, the other approach we use to study aging, of course, is in model systems. I mean, unfortunately we cannot really study aging in human beings—or we can, but it's very difficult and time-consuming—and so we tend to use short-lived model systems like mice or fruit flies or worms. [Some] worms live a few weeks. We tend to use fruit flies, Drosophila, that live a few months. Mice can live up to three, four years. So we can study these animals to try to gather insights into the mechanisms of aging, hoping that some of these will be applicable to humans. I mean, there's some rationale for it because we know the basic biochemistry of life in a mouse is quite similar to humans. We can also manipulate aging to some degree in animal models, particularly at the genetic level. We can tweak genes in animals, including in mice, and extend their lifespan. In mice [it's] up to about 50 percent. But for example, in worms we can tweak a single gene in worms and extend by about 10 times ... Feltman: Mm. Magalhães: Which is quite remarkable. So we can do a lot of studies in animal models: we can manipulate aging to some degree in animals, and then we can do mechanistic studies. We can look at their molecules, we can look at their cells, we can look at their hormones and try to test mechanistic [hypotheses] of aging. Feltman: What do you think are the biggest questions that we should be tackling about human aging and human lifespans? Magalhães: Well, I suppose the big question is still why we age. I mean, why do human beings age? As I said, there's hypotheses like DNA damage and mutations, like oxidative damage, like loss of protein, homeostasis. There's different hypothesis, but we still don't know why we age, and I think that remains the big question in the field. There's other questions, of course: Can we manipulate human aging? Because although we can manipulate, to some degree, aging in animal models, we don't know if that's possible or not in human beings. We can manipulate, to some degree, our longevity by exercise, eating healthy, not smoking, not drinking too much alcohol, and so on. But whether, for example, can we develop a longevity drug? And there's a number of companies and labs trying to develop longevity pills, and—but whether they're gonna be effective in humans, that's still something that's up to discussion and will require, for example, clinical trials. Feltman: Mm. Magalhães: So one aspect that's quite fundamental and important in, in aging is that there are complex species—like some species of reptiles like the Galápagos tortoise; some species of fishes, like rockfishes; some species in salamanders, like the olm—that appear not to age at all. There's no mammals in this category, but there are complex vertebrates that, in studies spanning decades, do not exhibit increased mortality, do not exhibit increased physiological degeneration. So that is quite a fascinating observation, that some species—I mean, maybe they do age after a very long time, but at the very least they age much, much, much slower than human beings ... Feltman: Hmm. Magalhães: Which I think is a great inspiration as well. Because, so, for example, just like the Wright brothers took inspiration from birds: they saw birds—'Well, birds are heavier than air, and yet they can fly, so there's no reason to think we cannot build a machine that's heavier than air and can make us fly.' We can take inspiration [from] these animals. There's no physical limit that [holds] that every organism has to age. And so we can take [inspiration] from the species that appear not to age and think, 'Well, maybe with technology and, and therapeutics we can, at the very least, slow our aging process.' Feltman: Thank you so much for coming on to talk today. This has been great. Magalhães: Well, thank you. My pleasure. Feltman: That's all for today's episode. We'll be back on Friday. Science Quickly is produced by me, Rachel Feltman, along with Fonda Mwangi, Kelso Harper, Naeem Amarsy and Jeff DelViscio. This episode was edited by Alex Sugiura. Shayna Posses and Aaron Shattuck fact-check our show. Our theme music was composed by Dominic Smith. Subscribe to Scientific American for more up-to-date and in-depth science news.
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