When you're fighting off a cold or flu, it's easy to imagine the battle is being waged solely inside the confines of your body. But in order to spread, pathogens rely on nearly every aspect of our shared societies. Food and drink, social customs, our proximity to animals, urban design, income inequality: The science of epidemiology connects them all.
Patient Zero investigates the spaces where people and pathogens collide.
Coming August 15th from New Hampshire Public Radio.
Click here for a full transcript
For people lucky enough to grow up healthy, the procedures of Western medicine can be oddly reassuring. Lab coats, clipboards, and the roll of crinkly paper on the exam room table are all part of a system that seems tidy and well understood. But that, to some extent, is an illusion.
There are lots of diseases that leave us with more questions than answers. But when it comes to Lyme disease, the illusion seems especially thin, as though the guts of the system are exposed. It’s a place we’re calling Lymeworld.
Patient Zero, the name of the podcast, is a misnomer. It’s a term lifted from a CDC document during the AIDS crisis and its use became a complicated, homophobic mess.
The real phrase, used by scientists when identifying the first documented patient in an epidemiological investigation, is “index case,” but “patient zero” has become the pop culture equivalent.
The patient zero of Lymeworld was a woman from Connecticut who, in her own fashion, was the index case that started it all: Polly Murray.
To understand Polly’s story, though, it’s important to learn a little about epidemiology. Epidemiology is a study of patterns and pathogens: how does disease move through society? Who gets infected? And how do you stop an epidemic?
Epidemiologists are first and foremost investigators, like a medical Sherlock Holmes. But one of the big things that differentiates epidemiology from detective work is the scale.
If identifying a disease is akin to catching a criminal, then epidemiologists are studying crime as a whole because an outbreak can bring a city to its knees.
You may think about disease like a patient: you get sick, are tested, diagnosed, and treated. That’s what so many of us experience in the doctor’s office. But the way disease spreads, the way it moves through and between networks of human beings, touches literally every aspect of our shared lives.
And that’s where epidemiologists exist. They’re not simply investigating pathogens - they’re investigating the connections between pathogens and people.
(Sara Plourde, NHPR)
A very basic tool that scientists use for this purpose is the epidemiological triangle. One point is the agent - the disease. The second post is the host - that’s us. The third is the environment - everything from our proximity to animals and what we eat to whose hands we shake and the design of our city. It’s this point that makes everything more complicated.
Lyme, CT (Taylor Quimby, NHPR)
In the 1960s and 1970s, Polly Murray was raising her family in Lyme, Connecticut. She was an artist, capturing her children and the landscape in paintings and drawings. She was also capturing her family’s health, in detailed notes on her calendar.
Tracking her own symptoms, Polly became convinced that her various symptoms were connected.
Over several years, she saw a grab-bag of experts, who examined her for lupus, psoriasis, rheumatoid arthritis, thyroid problems, and hypoglycemia.
Some doctors were supportive, some were dismissive, but nobody had any answers. At least one doctor told her her symptoms were psychosomatic and she needed a psychotherapist. When Polly saw one, she was told that she was depressed… because she had a chronic illness that no one could identify.
But then, in the mid-1970s, there was a new development: other members of her family started to develop symptoms. Four out of six members of her family now had a similar, mysterious disease.
Above: Some of Polly Murray’s notes on her family’s symptoms and treatments
It was Polly’s son Todd who finally got what had eluded her: a diagnosis. Juvenile Rheumatoid Arthritis (JRA). Several other kids in town got the same diagnosis, too.
JRA affects about 1 in 10,000 children. Two cases in Lyme would have been unusual; Polly was seeing three or four cases on the same street.
Polly knew something was happening. But solving the mystery would take more than six years. How they figured it out, in episode 2.
FURTHER READING
What Is Epidemiology?, Centers for Disease Control and Prevention
“In Philadelphia 30 Years Ago, an Eruption of Illness and Fear,” Lawrence Altman, New York Times
“Legionnaires’ disease, once ‘the greatest epidemiological puzzle of the century,’ kills seven in N.Y.,” Sarah Kaplan, Washington Post
Bull’s Eye: Unraveling the Medical Mystery of Lyme Disease, Jonathan A. Edlow
BONUS
Taylor takes a drive to the former Murray residence in Lyme, CT
Click here for a full transcript.
Back in 1975, Polly Murray had been to doctor after doctor, trying to figure out what was happening to the children of Lyme, Connecticut.
Why did it take so long to figure out Lyme disease?
Science is, by definition, slow. It’s easy in 2019 to look back and say, well duh, Lyme disease is spread by ticks and is treated with antibiotics. But back in 1975, when researchers were first investigating the disease, they had to rule out all the possibilities. They had to check water supplies, investigate the local schools, collect and test mosquitoes, and count ticks, one by one.
To study a novel disease, you have to focus on something objective like symptoms that can be measured, tested, or observed with the naked eye. This is called a case definition. It’s incredibly important because a case definition outlines and focuses an epidemiological investigation so that it doesn’t go off the rails. Researchers start with the narrowest case definition possible, and work their way outwards.
Dr. Allen Steere (Yale archives)
Dr. Allen Steere is one of two doctors whose work is most commonly associated with Lyme disease today. Today, Dr. Steere is a researcher and professor of rheumatology at Harvard but back in 1975, he had just finished up two years with the Disease Detectives - The Epidemic Intelligence Service- and was starting a fellowship in rheumatology at Yale when he received a call about what was happening in Lyme with the large number of cases of Juvenile Rheumatoid Arthritis (JRA).
Dr. Steere began looking for children with JRA. He met with the school nurse and local doctors, and he met with Polly Murray.
Polly Murray had come prepared when she met with Dr. Steere. She’d been documenting her family’s health for years but over the past few months, she had become a veritable amateur epidemiologist interviewing neighbors and parents, conducting her own miniature investigation. She had names and contact information.
Above: Some of Polly Murray’s notes about others in her area experiencing similar symptoms. Phone numbers have been obscured.
But Dr. Steere was looking for children with arthritis and many of the contacts she provided did not qualify for Steere’s study. In fact, Polly herself did not qualify. Two of her sons did but her own symptoms were stranger and harder to pin down.
Dr. Steere began his investigation in December 1975. The following May, he wrote to participants about his as-of-yet unpublished findings: 39 children and 12 adults met their criteria, most of whom suffered bouts of arthritis, especially in the knees, preceded by a flu-like illness some time before.
There were other strange symptoms reported too - nerve pain, facial paralysis, trouble sleeping - but these were inconsistent, not as easily defined, and by design not the current focus of the investigation.
Science is compartmentalized by necessity. There’s too much to learn, so experts have to focus that knowledge in order to make progress.
Steere was a rheumatologist, so he focused on the one thing he knew best. He called the unknown disease Lyme Arthritis. He believed it was caused by a virus and that it would get better on its own, like the flu. He advised patients to treat pain and swelling with Aspirin.
At the same time, Yale scientists were collecting tens of thousands of mosquitoes and thousands of ticks as well, searching for the pathogen that might be causing Lyme Arthritis. Dr. Steere speculated that mosquitoes might be the cause.
But Dr. Steere’s theory was wrong: often, Lyme disease does not go away on its own, and it is not treated with aspirin. But that’s science. Steere was making an educated guess. And it didn’t pan out. But that’s science.
A few years later, the Yale researchers released a statement. They were no longer studying Lyme Arthritis; they were studying Lyme Disease, a multisystem illness that could invade the joints, the heart, the facial nerves, and the lining of the brain.
They had collected enough evidence to widen the case definition, and confirm what Polly Murray had believed all along - that the disease was more serious than originally thought.
And after years of recommending aspirin, they changed course. They started recommending antibiotic treatment for patients with a bullseye rash and unusual bouts of arthritis, but they didn’t know for sure which type of antibiotic was best, or for how long.
One thing was certain, though: Lyme disease wasn’t being spread by mosquitoes. Cases were coming from a number of states, roughly matching the geographic range of what we now call the blacklegged tick.
(Sara Plourde, NHPR)
Across the country in a lab in Montana, microbiologist Alan Barbour and medical entomologist Willy Burgdorfer found something unusual inside a batch of ticks from Long Island, New York: a spirochete.
Borellia burgdorferi, the spirochete responsible for Lyme disease (CDC Public Health Image Library)
A spirochete is bacteria that twists like a corkscrew. The most famous spirochete is the one that causes syphilis. But neither Barbour nor Burgdorfer recognized this one. They ran some tests and eventually managed to isolate the bacteria. It was an unknown pathogen, the causative agent of Lyme disease. They named it Borrelia burgdorferi, after Willy Burgdorfer.
In the years after the bacteria was identified, Polly Murray was invited to scientific conferences to speak about her experiences in Lyme. She collected piles and piles of medical journals and scientific papers about the disease.
In 1975, 51 people in Connecticut were diagnosed with what would later be known as Lyme Disease. Today, it’s the most common vector-borne disease in the United States.
But what exactly is the disease doing when it gets into your body? A trip into the tick and your body in episode 3.
SCIENCE EXTRA
Scientists at the Cary Institute for Ecosystem Studies in Millbrook, New York, have been studying the relationships between ticks, white-footed mice, and Lyme disease for decades.
They take samples of tissue, blood, urine, and feces, and count all of the ticks on every mouse they catch.
This is what science looks like: four people, sitting in white coveralls at a plastic poker table in the middle of the woods, counting ticks with tweezers.
All day. Every day.
This is the actual pace of the epidemiological progress, too, which is easy to forget when you’re the one waiting for answers.
(Photos by Taylor Quimby, NHPR)
Click here for a full transcript
Lyme disease is confusing. A lot of people don’t know what it is or what it can do to you, or how Lyme disease gets in to you in the first place.
After hatching, ticks need a blood meal at each stage of life in order to survive. Common hosts for tick larvae are small rodents & birds. Bacteria picked up at the larval stage from the primary host can be passed on to later hosts at the nymph - the highest risk to humans - and adult stages. (Sara Plourde, NHPR)
Let’s start with the humble blacklegged tick. Unlike insects, which have three body parts - the thorax, abdomen, and head - the black legged tick has a tear shaped body and... a thing on top. It’s not a face. It has no eyes; it’s totally blind. Scientists call it by a very gross and very memorable name: the mouthparts. These are the bits that work their way into your skin.
On the outside are the palps, which feel around for a good spot to bite. In between them are two sawed blades that rub themselves into the skin, and then flex backwards, pulling the most important part - a spiky tube - into your body.
Above: Images taken of ticks under a microscope (Willy Burgdorfer Archives)
That tube has backward facing barbs, sort of like a harpoon - so that once it’s embedded inside the skin, the tick can start secreting special chemicals through it like a straw to help prepare its meal.
(Sara Plourde, NHPR)
In the first 24 hours, ticks are not feeding on you. They are injecting you with antihistamines so you don’t get a welt that might tip you off to the fact that you have a tick inside you; with anticoagulants so your blood doesn’t clot; and with cementing agents that literally bond the tick’s mouthparts to the body. They are doing all of these things to cover their tracks, so you don’t know you’ve been bitten.
Once they’re done doing all of this - numbing you, gluing to you, medicating you - they start to drink in earnest. But they aren’t just drinking blood. They are also secreting saliva into your bloodstream. It’s the spit that the Lyme pathogen - Borrelia burgdorferi - uses to travel into your body
You won’t contract Lyme disease the second the tick burrows into your skin. Some refer to this as the “24 to 48 hour rule.” After the tick has done its meal prep, it starts drinking blood, which gives the tick and the bacteria a food source. The bacteria needs that food source to grow and multiply, so it takes time. The amount of time that takes is controversial - there are anecdotal stories of people who get Lyme after being bit just a few hours earlier - so 24 - 48 hours is more of a guideline than a hard and fast rule.
Borrelia spirochetes within the midgut of a tick (Willy Burgdorfer Archives)
The pathogen that causes Lyme, the spirochete, is a single celled organism shaped a little bit like a snake or a corkscrew. And it’s covered in textured spikes known as Outer Surface Proteins. Different strains of Borrelia have different protein structures, which is the reason that you can get Lyme disease more than once.
Many of the symptoms that people with Lyme experience come from the immune system trying to fight off infection, including the characteristic bullseye rash.
In a best case scenario, the disease is found and the doctor orders a round of antibiotics that doesn’t kill the bacteria but sabotages its production and stops it from multiplying.
If you’re one of the thousands who don’t get diagnosed, though, that little bacteria can outrun your immune response and lodge itself in your joints, in your brain, in your cells and start to do some real damage.
The worst case scenario…is coming in episode 4.
Click here for a full transcript
Here’s a simple question with a really complicated answer. How do you know if you have Lyme disease? Not how do you know if you’ve ever had it, but how do you know the bacteria is in your body… right… now?
The way different doctors answer that one question might be the single greatest contributor to the existence of Lymeworld.
Todd Murray pictured at a home he is renovating in Massachusetts, where he sat for an interview. (Taylor Quimby, NHPR)
Toward the end of 1994, Dr. Allen Steere, along with scientists from the CDC and other government agencies, met in Dearborn, Michigan to address a serious problem that had cropped up with the Lyme disease laboratory tests: namely, that they were terrible.
The first diagnostic tests for Lyme came out in the 1980s but the tests weren't standardized. Some of the tests used to diagnose Lyme disease are read visually - as in, a technician literally looks at a sample and interprets whether it’s positive. Depending on the person reading the slide, one might call it negative while another person might call it positive. Lyme antibodies can also look like antibodies for other diseases.
For these reasons, among others, people back in the 1980s and 1990s didn’t trust the tests - and studies showed that they had good reasons.
So the scientists who convened in Dearborn, Michigan, in 1994 sought to give Lyme testing uniformity, to agree, in essence, on what to call positive and what to call negative.
The approach was called the Dearborn Criteria, but a standardized approach didn’t put questions about testing to bed. Partly because the criteria, while more accurate, is confusing to patients because it’s two-tiered: meaning there are two tests used to get a positive diagnosis.
But also, the tests are not good in the first few weeks of an infection. Early on in an infection, patients haven’t yet developed antibodies for Lyme disease yet so results will come back negative. That’s alarming because a lot can happen in the first few weeks of Lyme disease.
The Dearborn Criteria was also more conservative about who tested positive, and that left a lot of patients feeling like the rug had been pulled out from under them.
After the meeting in Michigan, demand for alternative testing grew. And this is maybe the biggest reasons that the Dearborn meeting failed to solve the testing problem: labs don’t have to use it. A handful of labs have continued to use tests that aren’t endorsed by the CDC.
What most of these alternative tests do is run the same tests, but interpret the results differently. They move the cut-off point for what’s considered positive.
For the droves of people who get diagnosed and treated quickly, Lyme disease can be no big deal. But for those who don’t, Lyme can transform lives in dramatic ways, and cause a variety of nasty symptoms. In very rare cases, it can even end in death.
Do you have Lyme disease, or don’t you?
An algorithm for determining whether a subject is positive for Lyme/Lyme antibodies (Source: “The Past, Present, and (Possible) Future of Serologic Testing for Lyme Disease,” Elitza S. Theel, Mayo Clinic)
Diseases do not always appear the way they do in medical textbooks. Instead, they appear on a bell curve. Most people who get Lyme disease are in the center of the bell. Those on the left are patients who for some reason don’t get very sick. Those on the right are the patients that get much, much sicker.
In the days after a tick bite, the Lyme disease pathogen can slowly make its way from your skin into your bloodstream. From there, it can hitchhike through your circulatory system and get into all sorts of bad places.
It can wind up back in your skin and cause multiple rashes all over your body. It can wind up in your joints and cause pain and swelling. It can wind up in your nerves and cause tingling, pain, numbness, or weakness in the arms and legs, or even Bell’s Palsy
(Sara Plourde, NHPR)
If the Lyme pathogen snakes its way into your skull, it can cause inflammation in the meninges. That’s the area surrounding your brain, and swelling there can cause excruciating head and neck pain. Less than 2% of confirmed cases between 2001 and 2015 reported meningitis.
Even further on the bell curve are symptoms associated with sight. Lyme can burrow inside the optic nerve, and Inflammation there can cause double vision, or in very rare cases, blindness.
And most notably, Lyme can squeeze in between the cardiac tissues in your heart and slow the electrical signal that makes it beat correctly. Making up just 1% of confirmed US Lyme cases between 2001 and 2015, it’s a rare complication of Lyme but it is the one that can kill you.
Since 1985, the CDC has tracked nine deaths in the medical literature to heart infections associated with Lyme disease. This complication is called Lyme Carditis, and people who get it are less likely to have gotten a bull’s eye rash.
Rare as they are, symptoms like Bell’s Palsy and Lyme Carditis share an important quality: they can be measured using tools and tests like an echocardiogram or physical examination.
Part of what makes these symptoms so frightening is that they seem disconnected but there is one thing that pretty much unites them all: inflammation. In Lyme disease, the symptoms are caused by your own immune system as it attempts to hunt down and fight off the invaders.
Inflammation might also be the key to one of the biggest mysteries in Lyme disease: Post-Treatment Lyme Syndrome.
Post-Treatment Lyme Syndrome describes the 10 to 20% of Lyme patients that continue to have symptoms after treatment. It’s characterized by hard to measure symptoms like fatigue, general muscle and joint pain, and depression that can have a huge impact on your quality of life. It’s a condition that can take months or even years to resolve.
Mainstream medical authorities have acknowledged that they don’t know what’s happening with these people. One—very controversial, and as yet unproven—theory is that sufferers might have a persistent infection that is not responding to antibiotics. Equally controversial are the many doctors believe that patients with post-treatment symptoms are not actually suffering from Lyme disease, but something else entirely.
But there are other theories as well, such as the possibility that a long infection can lead to persistent inflammation, or auto-immune disorders.
Given the years of unreliable tests, the many years it took to discover the cause of Lyme Disease, and the mistakes that were made along the way, an understandable thicket of distrust has crept over Lyme disease.
The Dearborn Criteria is backed by the best science, but critics of the test have a point, too: that the best science still isn’t 100%. There is no perfect test for Lyme disease, and Post-Treatment Lyme Syndrome is real.
This is the sort of place where people are liable to be confused and desperate and angry. The perfect place for someone to step in and offer solutions that seem a little too good to be true - that’s in episode 5.
SCIENCE EXTRA
Willy Burgdorfer’s archive of Lyme-related research and correspondence is available in the public domain, and the producers of Patient Zero found it to be a rich trove of primary sources, test results, and original research notes. It is also a trove of Dr. Burgdorfer’s inscrutable handwriting. See below.
Click here for a full transcript
When patients feel like doctors have closed the door to proper healthcare because they’re unable or unwilling to help, another set of doors open. These doors sometimes lead to dubious providers, miracle cures, and untested treatments.
A meeting of a Lyme support group, where patients often discuss their symptoms and treatments (Taylor Quimby, NHPR)
Some Lyme therapies are discouraged or downright condemned by the Centers for Disease Control (CDC). Among these are colloidal silver. It’s a supplement that is literally particles of silver metal suspended in liquid, and while there are no studies to show it does anything helpful for Lyme disease (or anything else) there is evidence that it can screw up your liver. In fact, if you take enough of it, it can turn your skin blue (a condition called argyria). Another questionable treatment is malaria therapy, where people intentionally contract malaria as a way to fight symptoms of Lyme.
Rosemary Jacobs, “The Silver Woman,” whose argyria was caused by childhood use of colloidal silver nasal spray (not for Lyme)
On the other hand, there are things like transcranial magnetic stimulation, which is FDA approved for the treatment of depression, a common diagnosis among people who have suffered with a disease for an extended period of time. This therapy isn’t quackery and doesn’t have many risks associated with it.
And then there are lasers. This type of treatment is more specifically known as Low Level Light Therapy. Patients don’t feel much at all during treatment as the frequencies of the lasers are on the very low end of the spectrum. Low-level light devices are approved by the FDA for the treatment of aches and pains. Studies show that they have some mild effects in reducing inflammation and speeding up the healing process for minor injuries.
So how might lasers cure Lyme disease?
At the Lyme Laser Center in North Andover, Massachusetts, patients go through a treatment protocol involving several different therapies, including lasers. Dr. Doug Wine’s explanation for how lasers can treat Lyme disease rests on something called “biofilm.”
Some pathogens form a protective coating, called a biofilm, under which colonies of bacteria can grow untouched by antibiotics. It’s pretty common in species of bacteria that infect your mouth - dental plaque, for example, is basically a biofilm. One researcher has shown that Lyme bacteria can create biofilms but so far, it’s only been done in lab conditions; biofilms have never been seen in human or animals with Lyme. Dr. Wine says that biofilms explain persistent symptoms in post treatment and chronic Lyme patients, even though the science backing up this claim is flimsy.
Despite the progress of medical science in the last century, there are ways in which the line between healthcare and quackery is still thinner and more permeable than you might realize. Therapies are dismissed because their benefits are hard to measure or aren’t well understood. Conventional FDA approved drugs that perhaps aren’t as effective as we’d perhaps like to believe. But sometimes, there’s a nugget of truth hidden underneath a pile of questionable claims.
Take snake oil. In the mid-19th century, thousands of Chinese laborers came to the United States to build the Central Pacific Railroad across California and Nevada. It was hard work and at the end of a long day, some workers likely used snake oil, a traditional Chinese remedy, for their aches and pains. This oil, which came from Chinese water snakes, was rubbed on the skin topically. The oil was high in Omega 3 fatty acids, which studies have consistently shown can help reduce heart disease and inflammation, that sort that causes arthritis and pain in the joints.
Most of the snake oil that was sold in the 19th and early 20th centuries in the U.S. as a cure all, however, did not come from these special water snakes giving the term a dubious connotation. But the original snake oil, the Chinese remedy, may have had some positive effect.
The temptation is always to say that some therapy is either real evidence-based medicine or pure useless snake oil but sometimes therapies are a little bit of both.
The limits of science...coming up on episode 6.
SCIENCE EXTRA: REFUTING DR. WINE
As of this publication, the website for Lyme Laser Centers includes some dangerous claims, including the statements shown below like “don’t take antibiotics” and “don’t trust doctors.”
But that’s not the extent of inaccurate claims. We took a deeper look at some of the claims Dr. Wine made when we interviewed him.
Statement: “You will have to have [Lyme disease] for a minimum of nine months before you're ever going to test positive.”
It is true that when you are first bitten by a tick, you will test negative on the standard CDC recommended Lyme disease test. One study found that in the first week after a bullseye appears, less than 1 in 5 patients will have enough Lyme antibodies to register. However in the same study, by three weeks after the appearance of a bullseye, that number rises to 85 percent.
This is why the standard practice is to treat anyone presenting a bullseye rash immediately for Lyme disease. Testing is typically most useful for patients who have “disseminated” Lyme disease — usually months after a tick bite, after the bullseye rash and flu-like illness has disappeared and other symptoms begin to manifest. In patients who have cardiac symptoms, acute neurological symptoms, or the classic “Lyme arthritis” the tests have been found to be 85 to 99 percent accurate.
Statement: “70 percent of all ticks carry the Lyme spirochete.”
Charitably we could assume that Doug Wine omitted some words here, and intended to say “all blacklegged/deer ticks.” If that were the case, there is one spot in the country where Lyme infection rates among adult deer ticks approached those numbers: on Shelter Island — the place where the bacterium was first identified — approximately 66 percent carry Lyme. We also have to assume Dr. Wine is rounding up, to make this statement accurate.
Across the whole country, infection rates among blacklegged ticks are closer to 20 percent. Even in the Northeast, where the epidemic is most acute, only around 25 percent of ticks carry the disease. In a recent nationwide study, Connecticut took the top spot at 30 percent.
These numbers are only referring to infection rates in blacklegged ticks, as we start to include dog ticks, western blacklegged ticks, lone-star ticks, and the other ninety tick species found in North America, Doug Wine’s statement becomes even less accurate.
Statement: “The tick is, like, number 7 or 8 down the list of what is actually transmitting disease.”
One study has found Lyme in mosquitoes, deer flies and horse flies. However, the same researchers attempted to transmit the disease from the mosquitoes to hamsters in a lab, and it didn’t work. Dog ticks can also be found to be carrying the Lyme pathogen, but have never been documented as transmitting it.
Enough googling will yield a single “case study” from Finland in which a man believes he contracted Lyme after being bitten by a deer fly, however this single case could also be explained by a tick bite that the jogger never noticed.
Statement: “Now we know that [Lyme disease] is sexually transmitted. We know that it is transmitted by all bodily fluids. You kiss someone, you have sex with someone you're giving it or getting Lyme disease.”
We’ll start with sex, and get to saliva next.
The root of this particular fallacy is a 2014 study that found Lyme disease in vaginal and seminal fluids. Further, syphilis is a spirochete, and is transmitted sexually, so why not Lyme?
The short answer is that detection of a bacteria in a fluid is not the same as proving it has evolved to transmit via that fluid. Syphilis creates open sores or chancres in and around the mouth and sexual organs, which produce large numbers of bacteria in order to facilitate transmission.
A 1991 study on infected rats designed specifically to test this question found no transmission of Lyme occurred through sex. A 1995 study of infected hamsters found the same. To date, there has been no recorded case of Lyme passing from person to person via sex or saliva - though there have been a few documented cases of Lyme being transmitted from mother to child through the placenta.
Statement: “Drink out of one bottle and you forgot which one is yours and you pick up the other one and have a drink of beer, and that guy has Lyme... You just acquired Lyme. One drop of saliva will do it.”
This statement — again — seems to flow from the 2014 study, though we could find no research confirming the presence of borrelia burgdorferi in saliva, only comments from fearful patients at the bottom of blog posts. However, even if it were present — again — this is not enough to ensure transmission.
HIV can be present in saliva as well, but that does not mean that you can get it through kissing.
FURTHER LISTENING/READING
Sawbones podcast on fever, incl. discussion of malaria treatments
“Snake Oil Salesman Were on to Something,” Cynthia Graber, Scientific American
Marketplace of the Marvelous: The Strange Origins of Modern Medicine by Erika Janik
“Colloidal Silver Turns You Blue - But Can it Save Your Life?,” Mallory Pickett, Wired [Spoilers: No.]
Click here for a full transcript
Editor's Note: A previous version of this story identified Mary Curtain Pierce as a critical care nurse at Alice Peck Day Memorial Hospital at the time of her illness in 2016. This is incorrect. She was working at a different hospital in New Hampshire at that time. We apologize for the error.
Sometimes, it seems like there is a gulf between epidemiologists and health care providers, and the actual patients they’re trying to help. Two people, looking at the same information, and walking away with radically different conclusions.
Note: There are many complications to collecting Lyme data, and the maps above represent only the best data we have available, not all possible cases of Lyme. For more on the process behind and limitations of Lyme disease surveillance, read this documentation from the CDC.
Chronic Lyme is the central controversy of Lymeworld. But what is it? Where does it come from? And why is treating it, with long rounds of antibiotics, so controversial?
According to the experts that help set treatment guidelines, 14 days of doxycycline, a standard oral antibiotic, is supposed to cure most cases of non-complicated Lyme disease. New draft guidelines suggest even less - just 10 days. But some people don’t feel all the way better after treatment for Lyme disease. In 10 to 20% of Lyme cases, patients continue to have arthritis, or pain and fatigue, or cognitive problems.
For people who have a clear diagnosis of Lyme in the first place, authorities call these cases Post-Treatment Lyme Disease Syndrome. There is no CDC-official name for ambiguous cases, with weird symptoms, and unclear lab results, but many of these patients wind up calling it Chronic Lyme Disease.
There are a few theories about why people have persistent symptoms after treatment. The bacteria may have caused permanent damage to the joints, or triggered an auto-immune reaction that lasts even after the infection is treated. The chronic Lyme community have embraced another theory for their lingering symptoms: that the spirochete isn’t actually dead.
According to mainstream medical guidelines on Lyme, the toughest cases - hospitalized patients with Lyme carditis, or cases of Lyme-related meningitis - might require up to 28 days of IV antibiotics. Occasionally, if clear signs of infection re-emerge, another round of antibiotics might be warranted. And yet, more antibiotics are often what chronic Lyme patients end up getting.
When you’re covering Lyme disease, you’ll often hear people say something like:
When will people realize that chronic Lyme disease is a real disease?
But what is it that makes a disease “real?”
For patients, chronic symptoms are very real indeed. But how epidemiologists name and define disease is a moving target, and they argue that chronic Lyme might not be the best way to describe what people are experiencing. Lyme disease, for instance, used to be called Lyme arthritis. The name changed as more was learned about the disease.
Scientists and researchers are wary of the term chronic Lyme because it’s so ambiguous. The symptoms are so all over the place that it might turn out to be lots of different diseases and conditions that have accidentally been lumped into one.
Regardless of what we may discover in the future, in the present, patients with chronic Lyme and Post-Treatment Lyme are subjecting themselves to repeated rounds of long-term antibiotics, in some cases intravenously.
Antibiotics are serious drugs. Infectious disease experts are so alarmed by unnecessary or ambiguous antibiotic therapy because thousands of people die every year from infections acquired during treatments that aren’t actually helping.
And then there’s the possibility that hundreds of thousands of people will die because antibiotics won’t work anymore. Antibiotics are the only class of drugs that lose effectiveness over time. It’s like being put in a time machine where patients are dying of infections that a decade ago could have been treated with an antibiotic. Patients who gamble on antibiotics, when there is unclear evidence that they need them, aren’t just risking their own necks but are, in a small indirect way, contributing to antibiotic resistance.
Lyme disease is not the leading cause of antibiotic resistance. Far from it. Colds, bronchitis, and urinary tract infections are the bulk of problems that lead to unnecessary antibiotic use. This also isn’t a straightforward causal relationship. Taking long-term antibiotics does not mean that ten people will die from an infection.
But from a symbolic point of view, Lyme disease does present a particular problem. The treatments are being used despite minimal evidence of benefit and with no clear sense that the therapy will cure patients for lengths of time that are otherwise unheard of in medicine - years. This is why mainstream researchers are skeptical of chronic Lyme.
So this is where we are. Patients and advocates fight for the right to treat with long-term antibiotics. The medical establishment fight to stop the trend from going too far.
The answers aren’t easy. But you do have to hope that everybody is asking the important questions.
Because either way, the stakes are very, very high.
In episode 7, we zoom in to look at the ecological systems that spread Lyme, and zoom out to see how human society has helped to usher in this epidemic.
Click here for a full transcript
Lyme disease does a lot of things inside and to the body. But Lyme disease is part of a much larger ecosystem, and we now have the tools to alter that ecosystem - permanently.
Blacklegged ticks are not typically born carrying Lyme disease. They have to get it from something, and typically, they get it from feeding on a mouse during their very first blood meal.
(Sara Plourde, NHPR)
Think of it this way: mice are like mobile Lyme disease storage tanks scattered all over the forest floor. The ticks are delivery trucks carting around the bacteria, dumping it into empty storage tanks, and filling up from other ones along the way.
There are, roughly speaking, three main ingredients in the Lyme ecosystem: ticks, mice, and deer. But deer are what scientists call incompentent reservoirs, which means they don’t actually get infected with the bacteria that causes Lyme disease.
So if mice are storage tanks, and ticks are delivery trucks, the deer are more like the delivery truck factories because adult ticks literally reproduce on top of them, before dropping off to lay their eggs.
Gross as all these details may be, they present an opportunity. If all three of these are required to spread Lyme, that gives three potential avenues to interrupt the cycle and spread of the disease. Why not just remove one of the ingredients and see what happens?
Off the coast of Maine, Monhegan Island had an overabundance of deer and an abundance of ticks. So, in the 1990s, a proposal was made - to change the makeup of the island permanently by killing deer. The villagers hired a sharpshooter to do the job. They killed 72 that first winter; 35 the next year. For some reason, the number of ticks actually went up. And then, a final vote among residents: 31 to 23 in favor of complete eradication. The last 6 deer were killed in 1999. And a few years later, no infected ticks. It worked.
Biocontrol isn’t usually as clear cut as it was on Monhegan island - here’s just a handful of factors that can influence the tick population and spread of Lyme. Other factors, like the biodiversity of a specific location, can have a huge influence on how well any of these would work. (Sara Plourde, NHPR)
Islands are amazing places to do research because they are contained. The ocean is a natural border that limits the number of factors that can influence an experiment. So, if you want to see how change ripples through an environment, you’re more likely to see a direct cause and effect in an island ecosystem. You can introduce an element here, or take something away there and see what happens.
Nantucket is one of the worst affected areas for Lyme disease in the country. The island, located off Cape Cod in Massachusetts, is covered in beaches and salt marshes scrub oak and pine barrens, and tall grasses. But despite the beauty, it’s not actually quite as biologically diverse as the mainland. There are fewer species of plants, fewer species of animals.
Even though Nantucket is small, it’s many times the size of Monhegan and home to thousands of deer. Efforts to even cull the herd have been controversial so not only would it be logistically more difficult to eradicate them all, it’s politically unfeasible.
But there are two other organisms in the trifecta: two more opportunities to stop the cycle. Killing all the ticks is impossible for logistical reasons, which leaves mice. Scientists at MIT have come up with an idea to immunize the mice, a project called Mice Against Ticks. The plan would alter the genes of mice to block transmission of Lyme. Thousands of these modified mice would then be released onto the island.
But some of the very things that make islands wonderful places for research - fewer variables, fewer complications - are also drawbacks when applying these lessons to a mainland ecosystem with a dizzying number of variables.
Biodiversity is a huge part of whether and how Lyme rates increase and decrease in a given area, and it is just hard to measure. Lyme rates - in people - have been going up steadily since it was first discovered - but if you look year to year, there are booms and busts.
(Sara Plourde, NHPR)
Remember way back to episode 1 and the epidemiological triangle? The third point was the environment. And in the case of the Lyme epidemic, it’s the point that we have been unintentionally sharpening for hundreds of years.
From housing and transportation, to white flight and agriculture, a dizzying number of cultural factors have led us to maximize the number of deer : more than 30 million in America today. We’ve built homes and roads, cutting back into forests. Our communities leapfrog across natural areas and slice odd shapes into the landscape, fragmenting forests in a way that pushes away predators and increases the amount of forest edge next to homes. The edges of forests are where mice do best. In many ways, the risk of getting Lyme disease is higher in your yard than in remote parts of the Appalachian Trail.
Increasing development & deforestation means we are living closer to forest edges - along with mice and ticks. (Sara Plourde, NHPR)
This is the stage that was set for Lyme disease in 1975, when Polly Murray’s kids were out playing in the woods of Lyme, Connecticut.
Wherever the hosts go, the ticks go. But historically, that hasn’t always meant they’d survive. Previously, if a bird deposited a tick too far north, or it fell off on a beach or in a bog, the tick’s journey would come to an untimely end.
Different ticks prefer different environments but generally, they don’t like it too cold and they don’t like it too dry.
Because now, with global temperatures going up and many areas experiencing wetter weather, the ticks have more places to gain a foothold and survive the journey. This and other factors aren’t just spreading Lyme disease but are helping to spread all sorts of tick-borne pathogens. Some of these are very much like Lyme disease and others are more rare but more deadly.
In the forty plus years since Lyme disease was first recognized and named, we have learned so much about spirochetes, inflammation, symptoms, and society. But the best technology currently available for stopping ticks remains socks and pants.
Senior Producer Taylor Quimby on the boat from Nantucket, trying to capture ferry sounds (that never happened).
Nantucket as viewed from the ferry.
Nantucket as viewed from the ferry.
One of many signs on Nantucket warning residents about ticks.
Danica Connors, Lyme herbalist who offers shamanic wellness practices for islanders with Lyme and chronic Lyme.
Dr. Kevin Esvelt introducing Coq-Au-Vin on stage at the Mice Against Ticks meeting in August 2018.
Coq-Au-Vin performing at the Mice Against Ticks meeting, August 2018.
Dr. Kevin Esvelt of MIT, Mice Against Ticks meeting, August 2018
The New Yorker’s Michael Spector, Dr. Kevin Esvelt of MIT, and bioethicist Dr. Ruth Faden of Johns Hopkins, Mice Against Ticks meeting, August 2018.
Dr. Duane Wesemann of Harvard University and Dr. Sam Telford, disease ecologist from Tufts University
A full house at the Mice Against Ticks meeting.
Standing room only, Mice Against Ticks meeting.
Dr. Jen Karberg with the Nantucket Conservation Foundation.
A scene from Nantucket.
Nantucket habitat
Senior Producer Taylor Quimby, looking wistfully out at the Atlantic.
Above: Images from Taylor’s reporting trip to Nantucket, MA (Justine Paradis, NHPR)
