In the autumn of 1997, shortly after finishing college, I began experiencing peculiar sensations I referred to as "electric shocks." These were sharp, stabbing feelings that would course through my limbs each morning. They became so intense that during my walk to work from my basement apartment in the East Village, I frequently had to pause and rub my legs against a parking meter to alleviate the twitching and spasming that followed. My physician couldn't determine the cause, attributing it to dry skin, and eventually, these sensations disappeared. They reappeared a year later, only to subside again just when I was at my wit's end.

Over the years, these shocks, along with other baffling symptoms like vertigo, fatigue, joint pain, memory lapses, and tremors, would come and go. By 2002, I was waking up nightly in a drenched sweat, my legs covered in hives. A doctor suspected lupus based on test results, although I lacked several key indicators of the disease. In 2008, at age 32, I had surgery and physical therapy for diagnosed arthritis in my hips and neck, yet I remained inexplicably fatigued. The various doctors I consulted assured me that my tests were normal and that nothing serious was amiss.

In 2012, I was diagnosed with Hashimoto’s thyroiditis, a mild autoimmune disorder. Yet, despite my efforts to maintain a healthy lifestyle, I struggled with daily functioning. My doctor found it perplexing, as did I, when I frequently struggled to recall simple words. During a poetry class I taught at Princeton, I awkwardly explained, “the season that follows winter, when flowers bloom.” I was in almost constant pain, a plight I detailed in an essay for The New Yorker about living with chronic illness. Despite this, part of me wondered if this was merely the standard experience for those in their mid-30s—pain, fatigue, and mental fog.

One cold December night in 2012, after a holiday party in New Jersey, I found myself driving colleagues back to Brooklyn. As I glanced at the man beside me, a novelist I had known for years, I realized I couldn’t recall his name. The recognition was disconcerting; I knew I recognized him, but who was he? It took an hour to piece together that he was a friend. Upon returning home, I asked my partner, Jim, if he had ever experienced such confusion. He hadn’t. I sensed something was amiss.

By the following fall, even routine outings—teaching a class or attending a friend’s birthday dinner—could leave me bedridden for days afterward. I did my best to conceal my struggles. As my medical bills soared, I sought top specialists (most of whom didn’t accept insurance), including a neurologist who diagnosed me with neuropathy of unknown origin, and a rheumatologist who labeled my condition as “unspecified connective-tissue disease,” prescribing steroids and intravenous immunoglobulin infusions. I turned to acupuncturists and nutritionists, as well as expensive “integrative” physicians, who diagnosed me with overexertion and recommended IV vitamin drips. Many doctors appeared uncertain about my situation, questioning whether it was all in my head. One even suggested I visit a therapist, while another dismissed my complaints, stating, “We’re all tired.”

Despite having access to superior medical care, I felt profoundly isolated—until the fall of 2013 when I consulted yet another doctor with an interest in infectious diseases, who tested me for Lyme disease. Growing up on the East Coast, I had often camped and hiked, pulling many ticks off myself over the years. Although I had never developed the classic bull's-eye rash, this doctor ordered multiple tests for Lyme, and while the results were inconclusive, they led her to suspect I might have the infection.

As I researched further, I found other patients with similar issues—troublesome joint pain and neurological symptoms. Some had been on oral and intravenous antibiotics for years to manage their symptoms, a risky endeavor; one acquaintance was on her fifth or sixth course of IV treatment, the only remedy that seemed to preserve her cognitive abilities. I stumbled upon posts detailing debilitating exhaustion and memory loss, with some individuals so disoriented they struggled to find their homes, while others battled severe depression. Most had navigated a medical system that discredited their experiences and struggled to provide a diagnosis, often being referred from internists to psychiatrists. The narratives were disheartening.

After 15 years of unanswered questions, I finally had a potential explanation for my ailments. Yet instead of relief, I felt trapped in a nightmare. I questioned whether my illness was truly untreated Lyme disease. Even if it was, there was no consensus on how to treat someone like me—whose test results were inconclusive and who had received a late diagnosis—leaving me unsure if antibiotics would even help.

The journey ahead felt daunting. My doctor warned that the label “Lyme disease” could easily be attached to various symptoms due to the inaccuracy of tests. I understood; I had faced false hope before. My medical experiences led me to believe that specialists often interpreted my issues through their narrow perspectives—an autoimmune condition! a viral issue! or even a psychological problem! I feared that if I consulted a Lyme specialist, he might diagnose me without proper evidence.

In the absence of medical clarity, I had to choose my path. Would I become a Lyme patient? If so, whom could I trust, and how far would I go? One night, while deep in my research, I found a discussion thread among Lyme patients describing electric shocks that mirrored my own experiences. A chill ran down my spine. For nearly two decades, I had sought a doctor who would recognize my issue as more than dry skin. I had asked friends if they understood what I was feeling, but no one ever did. I had often felt like I was imagining things or overly sensitive—perhaps it was my fault. To see my struggle articulated with such painful precision jolted me into action.

I knew I needed to delve deeper into the complex reality of Lyme disease and confront the nearly insurmountable task of distinguishing what was known from what remained uncertain. I wasn't yet aware that by merely exploring the possibility of untreated Lyme disease as the source of my illness, I risked being labeled one of the “Lyme loonies”—patients who believed that a past tick bite was the root of their prolonged suffering. This term had been used in a 2007 email from the program officer overseeing Lyme grants at the National Institutes of Health. The infamous phrase highlighted the intense controversy surrounding the disease, which John Aucott, a physician and director of the Johns Hopkins Lyme Disease Clinical Research Center, later described as “one of the biggest controversies that medicine has seen.”

Lyme disease was first identified in Connecticut in the 1970s and has since emerged as a significant and escalating health threat, spreading far beyond its initial East Coast origins. Reported cases surged nearly fivefold from 1992 to 2017, with the Centers for Disease Control and Prevention estimating annual incidences at over 300,000—possibly exceeding 400,000. In parks across coastal Maine or Paris, ominous black and red signs warn of ticks that transmit Lyme disease. During summers in the eastern U.S., many parents I know take precautions, covering their children head to toe for hikes or trips to grassy playgrounds, regardless of the heat. On a recent visit to my brother’s new country home in Vermont, just weeks before his partner awoke with a distinct bull's-eye rash, I chased my young sons around, spraying them with tick repellent so often that they thought we were engaged in a special outdoor game.

Today, most people know someone who has been diagnosed with Lyme disease, and many are aware of the telltale rash (though many rashes are solid-colored lesions rather than the classic bull's-eye) and the need for prompt antibiotic treatment. For most who receive timely diagnosis and treatment, that is where the story ends. However, many Americans have also heard of individuals who remained unwell after their antibiotic courses, or of cases where no rash appeared, leading to late diagnoses and lasting damage. Others, upon discovering a tick, have encountered doctors hesitant to prescribe antibiotics for a potential Lyme infection, fearing overdiagnosis.

The level of alarm and confusion surrounding this long-standing public health issue is significant. The ramifications are profound, as Lyme disease has become an almost “unparalleled threat to regular American life,” according to Bennett Nemser, a former epidemiologist at Columbia University, who now manages the Cohen Lyme and Tickborne Disease Initiative at the Steven & Alexandra Cohen Foundation. “Anyone—regardless of age, gender, political affiliation, or wealth—can step into grass and get a tick on them.”

Despite changes in climate and land use contributing to a notable rise in Lyme and other tick-borne diseases, the American medical community remains embroiled in a debate over who qualifies as a Lyme disease patient and whether it can become chronic—and if so, why. This standoff has hindered research that could clarify how the elusive bacterium and its co-infections affect human health. After four decades in the public eye, Lyme disease still lacks a preventive vaccine, evades reliable testing, and continues to create friction between patients and doctors, as well as among researchers themselves. Upon receiving my inconclusive diagnosis, I knew better than to hope for a quick fix. Yet, I was unprepared for the extreme uncertainty that lay ahead.

Lyme disease first gained public attention during an outbreak of what seemed to be rheumatoid arthritis among children in Lyme, Connecticut. A young rheumatologist at Yale, Allen Steere, now conducting research at Massachusetts General Hospital, studied these children. In 1976, he named the mysterious illness after the town and described its primary symptoms: a bull's-eye rash, fevers, aches, Bell’s palsy (partial facial paralysis), and other neurological issues, as well as rheumatological manifestations such as knee swelling. After extensive research, Steere concluded that the black-legged ticks residing on mice and deer might carry a pathogen responsible for this outbreak. In 1981, medical entomologist Willy Burgdorfer identified the bacterium causing Lyme disease, which was subsequently named Borrelia burgdorferi.

B. burgdorferi is a corkscrew-shaped bacterium, known as a spirochete, that can infiltrate its host’s tissue, causing damage while morphing from corkscrew to cyst-like forms, and potentially to slimy “biofilm” structures. Due to this adaptability, researchers deem it an “immune evader.” Once in the human bloodstream, it alters its outer surface to evade immune responses and swiftly moves into tissues, complicating early detection. Difficult to find in the bloodstream and other bodily fluids, the B. burgdorferi spirochete is also challenging to culture, the standard method for definitively diagnosing bacterial infections. If left untreated, B. burgdorferi can invade joint fluid, the spinal cord, and even the brain and heart, potentially causing the life-threatening Lyme carditis.

The concept of chronic Lyme disease is viewed by the infectious disease community as a pseudoscientific diagnosis—a belief system rather than a biological reality.

By the mid-1990s, a mainstream consensus formed that Lyme disease was relatively easy to diagnose, thanks to the characteristic rash and flu-like symptoms, and straightforward to treat. Infectious diseases typically present clear-cut cases that our medical system handles well. Evidence indicated that the recommended treatment—several weeks of oral antibiotics, usually doxycycline—would resolve most early-stage cases, while advanced Lyme cases might require intravenous antibiotics for up to a month. This assessment, made by the Infectious Diseases Society of America (IDSA), shaped their treatment guidelines from 2006 until recently. (In late June, a revised draft proposed a shorter course—10 days—of doxycycline for early Lyme patients.)

However, the reality on the ground appeared much murkier. A significant number of individuals with Lyme symptoms later testing positive had never exhibited the telltale rash. Others displayed many characteristic symptoms but tested negative for the disease yet began treatment anyway. Most startling was that a portion of patients who received timely, definitive Lyme diagnoses and standard doxycycline treatment did not fully recover. As individuals from these groups failed to improve, they began labeling their conditions as “chronic Lyme disease,” believing that the bacterium remained deep within their bodies.

Frustrated with the medical system's apparent ineffectiveness, patients became an activist force, asserting that Lyme disease was more challenging to treat than the establishment acknowledged. Family physicians in endemic areas, faced with patients who weren’t improving, began experimenting with alternative treatment protocols, including long-term oral and intravenous antibiotics, sometimes extending for months or years. They also started rigorously testing for tick-borne co-infections that were emerging in some of the most ill patients. Many of these doctors rotated drugs in hopes of discovering a more effective regimen. Some patients responded positively; others did not. In 1999, these physicians formed the International Lyme and Associated Diseases Society (ILADS), highlighting issues with Lyme disease testing and citing early evidence suggesting that bacteria could persist in both animals and humans post-treatment. ILADS proposed an alternative care standard that defined the illness more broadly and permitted more extensive treatment.

However, some prominent Lyme disease researchers remained skeptical about the infection's persistence post-treatment, arguing that many chronic Lyme patients were being treated for infections they no longer had, while others had never had Lyme disease but had appropriated the diagnosis for symptoms with alternative causes. In the IDSA's view, chronic Lyme disease was a pseudoscientific diagnosis—an ideology rather than a biological reality. The IDSA contended that under the influence of this ideology, credulous patients were subjected to unnecessary and potentially dangerous IV antibiotics from irresponsible physicians (this concern intensified following the death of a Lyme patient in her 30s from an IV-related infection).

To support its stance, the IDSA referenced several studies indicating that long-term antibiotic treatment for ongoing symptoms was no more effective than placebo—evidence, in their eyes, that the bacterium was not responsible for the symptoms. The IDSA also highlighted statistics suggesting that the commonly cited chronic Lyme symptoms—persistent fatigue, brain fog, joint pain—occurred no more frequently in Lyme patients than in the general population. In the media, experts from this camp implied that patients believing they had suffered from Lyme disease for years were either deluded or mentally ill.

The animosity was “fierce and alienating for patients,” according to Brian Fallon, director of the Lyme and Tick-Borne Diseases Research Center at Columbia University Irving Medical Center. Tensions escalated not only between patients and experts but also between community physicians and academic doctors. In 2006, IDSA guidelines for patients and physicians asserted that “in many patients, post-treatment symptoms appear to be more related to the aches and pains of daily living rather than to either Lyme disease or a tick-borne co-infection.” This message resonated hollowly for many. “Researchers were suggesting, ‘Your symptoms are unrelated to Lyme. You have chronic fatigue syndrome, fibromyalgia, or depression,’” Fallon noted. “This was perplexing for patients who had been well until their Lyme infection, after which they became ill.”

By the time a doctor first suggested, in 2013, that I might have Lyme disease, my headaches, brain fog, and joint pain had intensified, and I had developed small bruises all over my arms and legs. I became so dizzy that I began to faint. A dark wave seemed to engulf me, preventing me from catching my breath. I felt as disconnected from the joys of life as a firefly trapped in a jar.

When I returned to the doctor’s office two weeks later for my test results, I was uncertain about what awaited me. Flawed diagnostics are central to the entire debate over Lyme disease. Standard Lyme tests—structured in two tiers to reduce false positives—struggle to identify early infections or determine whether an infection has been fully cleared. This is because the tests do not directly detect the “immune evader” itself—the B. burgdorferi spirochete—in the blood. Instead, they indirectly assess the presence of antibodies (the small proteins our bodies produce to combat infections) created in response to the bacteria. However, it takes time to produce antibodies, complicating early detection. Moreover, once generated, antibodies can linger for years, making it challenging to ascertain whether an infection has resolved or if a new one has developed. Additionally, antibodies for autoimmune and viral diseases can mimic those produced in response to Lyme.

To obtain comprehensive interpretations, some physicians send blood samples to multiple laboratories, which can yield inconsistent results. The CDC recommends that only a specific pattern of antibodies, established by experts in 1994, be deemed indicative of a positive test. They also suggest that when necessary, physicians should use their judgment to make what’s termed a “clinical diagnosis” based on symptoms, likelihood of exposure, and lab tests.

I was bewildered. My doctor presented mixed results from three labs. Two showed a positive response for one segment of the test but not the other, while the third returned negative results for both segments. Based on my medical history and specific test findings, she concluded that I likely had Lyme disease. However, she noted the presence of several troublesome viruses, including Epstein-Barr. Moreover, the tests might have detected autoimmune antibodies related to my earlier diagnosis.

At the suggestion of a science-writer friend, I sought out Richard Horowitz, a Lyme specialist in upstate New York who had gained a reputation as an exceptional diagnostician. Dr. H, as many of his patients call him, is a practicing Buddhist with bright blue eyes and an infectious enthusiasm. He was recently a member of the Tick-Borne Disease Working Group organized by the Department of Health and Human Services, which issued a report to Congress in 2018 highlighting the diagnostic and treatment challenges faced by Lyme patients.

I expressed my uncertainty about having Lyme disease, presenting a stack of lab results nearly half a foot thick—a paper trail that would deter many doctors. He meticulously examined every page, posed questions, and took notes. Finally, he looked up and said, “Based on your labs, your symptoms, and your historical test results, I highly suspect you have Lyme.” He pointed to a set of results from Stony Brook laboratory, noting, “These bands are specific for Lyme.”

In his waiting room, I had filled out an extensive questionnaire designed to differentiate Lyme patients from those with other multi-system illnesses (it has since been validated as a screening tool). Dr. H conducted a physical examination and ordered a variety of tests to rule out additional thyroid issues, diabetes, and other potential causes for my symptoms. Given my night sweats and the feeling of not being able to take a deep breath—known as “air hunger”—he proposed that I might have a co-infection of babesia, a malaria-like parasite also transmitted by ticks. I had always thought of Lyme primarily as an arthritic disease, while I had many neurological and cognitive symptoms. He explained that B. burgdorferi is now known to exist in different strains, which are thought to produce various types of disease.

“The interesting thing is, I believe you’re actually a very strong and healthy person, which is why you managed so well for so long,” he continued. “Now your body needs assistance.”

Dr. H prescribed a month of doxycycline and cautioned me about what I had read online. Upon starting the antibiotic, I might initially feel worse, as the bacteria die and release toxins, causing what is known as a Jarisch-Herxheimer reaction—a flu-like response common among Lyme patients. However, he assured me that I should begin to feel better over time. If not, we would need to reassess our approach.

That evening, I shared my reservations about taking antibiotics with Jim. I lacked a definitive positive Lyme test and was aware of the detrimental effects antibiotics can have on the microbiome. “What do you really have to lose?” he asked incredulously. “You’re sick, you’re suffering, and you’ve tried everything else.”

The next morning, I took my first dose of doxycycline, along with Plaquenil, which is believed to help the antibiotics penetrate cells more effectively. I took another dose that night with dinner. I went to bed and awoke feeling terrible. My throat was sore, and my head felt foggy. My neck burned as if it were on fire.

Two days later, we went out for lunch, but I still felt groggy and unwell. It was a heavy, gray day with low-hanging clouds. On our way home, I felt rain on my bare arms. I told Jim we should hurry inside.

“Why?” he asked.

“It’s raining!” I insisted.

“It’s not raining,” he replied. “It’s just cloudy.” I raised my arms to show him the raindrops. A dozen cold pips dotted my skin, but there was no rain. As we walked, the feeling of cold drops rushed over my body, as if a strange, violent water were purifying me.

Days later, I was excited about flying to a conference in Chicago rather than feeling exhausted by the prospect. For three more weeks, I adhered to Dr. H’s prescribed medications and supplements. The doxycycline made me sensitive to sunlight. One late spring morning, I neglected to apply sunblock to my right hand before taking a walk with a friend while holding a coffee cup. Even though it was only 9 a.m. and cloudy, by the time I returned home, my hand felt sore, and within days, a second-degree burn developed, blistering into an open wound.

After a month of antibiotics, I returned to Dr. H’s office for follow-up. On his questionnaire, I rated my symptoms as less severe than a month prior, yet my total score remained high. Dr. H adjusted my treatment plan, adding an antimalarial medication due to my continued night sweats and air hunger.

When I started the new regimen in June 2014, I felt nearly as sick as I had ever been. I traveled to Paris to teach at NYU’s summer writing program, but within two days of arriving, I could barely walk down the street. Violent electric shocks coursed through my skin, and patches of burning pain and numbness spread up my neck. I trembled and shivered for five days, during which panic intertwined with pain. How could I discern whether this was a herxheimer reaction indicating a positive response to the drugs as they eliminated bacteria, or a manifestation of the disease itself? Or were the weeks of antibiotics exacerbating my condition?

“I know you think you’re doing the right thing,” a concerned colleague remarked, “but aren’t you just making yourself worse?”

On the sixth day, I sat on the couch in my rented apartment, and the shocks felt so intense, racing along my forearms, thighs, and calves, that I contemplated jumping out the tall windows to escape the torment.

The next morning, I awoke to the same bright sunlight, feeling better than I had in ages. Astounded by my energy, I went for a run. I may not have sprinted down the sidewalk, but for the first time in years, I managed to run three miles in 40 minutes. As weeks passed, my condition improved. My relentless night sweats disappeared, the air hunger subsided, and I regained substantial energy. I continued taking antibiotics for several more months, and with each month, my symptoms diminished. After eight months, Dr. H decided I could discontinue treatment. It was spring 2015.

That autumn, at 39, I became pregnant. On Dr. H’s advice, I took antibiotics intermittently during my pregnancy. In the summer of 2016, I gave birth to a healthy baby boy.

By the time I began treatment, the acknowledgment that Lyme disease could cause ongoing symptoms in some patients could no longer be dismissed as mere figments of their imagination. A well-conducted longitudinal study by John Aucott at Johns Hopkins revealed the persistence of brain fog, joint pain, and related issues in approximately 10 percent of even those ideally treated—patients who exhibited the Lyme rash and received the recommended antibiotics. Other studies suggested these symptoms could affect up to 20 percent of patients. The condition, termed “post-treatment Lyme disease syndrome” (PTLDS), is now recognized by the CDC. (However, this term does not apply to patients like me, who lacked a rash or a clearly positive test.) Even so, the concept remains hotly contested, with many influential figures in the field—and the IDSA itself—still refusing to acknowledge it as an official diagnosis. Moreover, critical questions regarding the causes of ongoing symptoms remain unanswered, partly due to the decades-long standoff concerning the potential for chronic disease. As Sue Visser, the CDC’s associate director for policy in the Division of Vector-Borne Diseases, admits, “Many are understandably frustrated that it’s been decades and we still lack answers for certain patients.”

Recently, a multitude of new studies has begun to address many of these questions: Why do Lyme symptoms persist in only certain patients? What don’t we understand about the behavior of B. burgdorferi that might clarify the differences in patients’ responses?

Federal funding for Lyme disease research is scarce, and what little exists often focuses on prevention and transmission. (The NIH allocates only $768 for each new confirmed Lyme case, compared to $36,063 for each new case of hepatitis C.) Much of the financial support for investigating PTLDS has come from private foundations, such as the Steven & Alexandra Cohen Foundation, the Global Lyme Alliance, and the Bay Area Lyme Foundation. Recently, the CDC and NIH reached out to these organizations, motivated partly by the 2018 Tick-Borne Disease Working Group report to Congress, which outlined significant gaps in the scientific understanding of Lyme disease.

In a conversation I had with him, Bennett Nemser of the Cohen Foundation outlined some of the hypotheses currently being explored. The complexity is overwhelming. A patient with persistent symptoms may still harbor a Lyme infection and/or a lingering infection from another tick-borne illness. Alternatively, the original infection might have caused systemic damage, resulting in recurring issues like nerve pain and chronic inflammation. Another possibility is that the Lyme infection may have triggered an autoimmune response, wherein the immune system begins to attack the body’s tissues and organs. Or, a patient may be experiencing a combination of all three, compounded by unidentified triggers.

New research suggests that an intricate interplay between the infection and the immune system is at play in patients who do not recover. The immune response to the Lyme infection is “highly variable,” according to John Aucott. For instance, some research has indicated that ongoing symptoms may stem from an overactive immune response triggered by Lyme disease. However, a recent study co-authored by Aucott and scientists at Stanford revealed that in patients who developed PTLDS, the Lyme bacteria inhibited the immune response.

Accumulating evidence now indicates that B. burgdorferi can persist after antibiotic treatment in many mammals—prompting more scientists to investigate whether the bacteria can do the same in humans. In 2012, a team led by microbiologist Monica Embers at the Tulane National Primate Research Center discovered intact B. burgdorferi lingering in rhesus macaques months after treatment. Embers also reported that these macaques exhibited varying immune responses to the infection, possibly elucidating why active bacteria remained in some. The study faced criticism from proponents within the IDSA establishment, who argued it failed to prove that the bacteria remained biologically active. However, Embers informed me that this year, her team successfully cultured B. burgdorferi in mice, demonstrating its viability post-doxycycline treatment. New studies investigating potential bacterial persistence in humans, conducted by the National Institute of Allergy and Infectious Diseases (part of the NIH), are currently underway.

Meanwhile, several researchers, including Ying Zhang at the Johns Hopkins Bloomberg School of Public Health, have proposed another theory regarding how B. burgdorferi may persist following treatment: the existence of “persister bacteria,” similar to those found in challenging staph infections but long thought to be absent in Lyme disease. In the context of Lyme, persister bacteria are a subpopulation that enters a dormant state, enabling them to survive a normally lethal antibiotic assault. Zhang’s team discovered that these persister bacteria caused severe symptoms in mice, and the current single-antibiotic protocols for Lyme did not eradicate them—this is logical, as doxycycline primarily inhibits bacterial replication rather than directly kills them. Thus, it affects only actively dividing bacteria, relying on a healthy immune system to eliminate remaining B. burgdorferi.

The significant breakthrough is that when Zhang’s team treated the mice with a cocktail of three antibiotics, including a drug effective against persistent staph infections, the mice successfully cleared the persistent B. burgdorferi infection. “We now possess not only a plausible explanation but also a potential solution for patients suffering from persistent Lyme disease symptoms despite standard single-antibiotic treatment,” Zhang stated. Taking the next step, Kim Lewis at Northeastern University, who has had a distinguished career studying persister bacteria, is about to conduct a study—collaborating with Brian Fallon—examining whether a compound specifically targeting persister cells can assist patients with PTLDS.

Of course, even if active bacteria persist in some Lyme patients, they may not necessarily cause the symptoms, as many in the IDSA have long argued. Paul Auwaerter, clinical director of infectious diseases at Johns Hopkins School of Medicine and a former IDSA president, points out that Lyme bacteria can leave behind DNA “debris” that may trigger ongoing “low-grade inflammatory responses.” Lewis stated that the overarching question—“whether the pathogen is present and slowly causing damage, or has already vacated the body and wrecked the immune system”—remains unresolved. Nevertheless, he expressed optimism that he and others would discover a cure for PTLDS.

When my son was seven months old, my period of feeling energetic and largely symptom-free abruptly ended. He was not a good sleeper, and months of nighttime awakenings took a toll on me. In early April 2017, we both fell ill, and I couldn’t bounce back. My body hurt, and my mind felt foggy. My primary care physician noted that the Epstein-Barr virus was once again active in my system. Dr. H suggested that the Lyme infection might have resurfaced, necessitating another course of antibiotics, but I hesitated. I was unsure whether to believe that the Lyme infection could linger, attributing my decline to an autoimmune flare or post-viral fatigue. I delayed for months, but soon the electric shocks returned, zapping my limbs and turning life into a struggle. I began antibiotics. Within five days, my energy returned, and I felt almost completely well again. A month later, feeling healthier than I had in nearly 20 years, I became pregnant with my second son.

Could this recovery be attributed to the placebo effect? If so, it was the only placebo that had ever truly worked for me.

Meanwhile, my father, living in Connecticut, began to experience drenching night sweats, fatigue, and aches. His tests returned negative for Lyme but suggested ehrlichiosis, another tick-borne illness. His doctor—situated in Lyme's epicenter—opted to treat this plausible diagnosis and its co-infection. My father was prescribed doxycycline for five months but did not improve, which surprised me given my immediate positive response. Then, one day, my brother found him at home, close to collapse, and rushed him to the ER, where extensive testing revealed a different issue—he was suffering from Stage 4 Hodgkin’s lymphoma.

In 2018, my father passed away from pneumonia complications after recovering from cancer. I couldn’t help but wonder how those lost months may have cost him, as the cancer progressed and weakened him—all because Lyme seemed a sufficiently plausible explanation, and the testing was murky enough that his doctor did not pursue alternative diagnoses. Although promising new diagnostic technologies are emerging, we still cannot reliably distinguish between those with tick-borne diseases and those without.

On a brisk March day this year, one of those indecisive days between warmth and cold, I visited a research lab at Massachusetts General Hospital led by Allen Steere, the rheumatologist who discovered Lyme disease and helped establish its testing protocols. A slim, gray-haired man with an intense gaze, Steere has become, in the eyes of many Lyme patients, a symbol of the medical establishment’s indifference, as he has long suggested that some chronic Lyme patients were misdiagnosed from the start. He has been confronted at conferences and approached by individuals claiming to be journalists. Scientists who oppose his views have nonetheless acknowledged his commitment to Lyme research. I wanted to hear his thoughts on the disease and the ongoing debate after four decades of involvement.

While acknowledging that medicine can be humbling and that Lyme disease is complex, Steere spoke with a calmness reminiscent of a teacher correcting a child. He stressed that in many instances, Lyme disease can resolve without antibiotics, describing a disease in the U.S. that typically follows a specific progression of stages if left untreated: beginning with an early rash and fever, then neurological symptoms, and culminating in inflammatory arthritis. Although joint inflammation may persist for months or even years after antibiotic treatment, he does not believe this is due to the bacteria’s survival. His research on patients exhibiting ongoing arthritis symptoms has identified genetic susceptibility as one cause of persistent inflammation, leading to effective treatments for the long-term challenges of Lyme arthritis utilizing disease-modifying anti-rheumatic agents.

After I shared a bit about my experience, he spoke with a similar tone of earnest firmness. He indicated that he believes late-stage Lyme (which is what I had been diagnosed with) does not usually cause a lot of systemic symptoms, such as the fatigue and brain fog I had experienced. “I want you to liberate yourself from the Lyme ideology,” he advised. “You clearly benefited from antibiotic therapy. But I don’t support the notion that it was solely due to a spirochetal infection. Of course, there are other infectious agents,” he added, noting that some may trigger complex immune responses.

I left Steere’s office feeling unsettled, contemplating that if I had encountered a doctor with a similar perspective in 2014, I might never have started doxycycline and subsequently improved. Was it possible that I had an entirely different condition that merely responded to antibiotics? He was an expert who had devoted his career to unraveling the mechanics of the disease, while I was a patient, temperamentally both meticulous and excitable, driven by scientific curiosity and a desire for evidence.

That evening, I settled in with my computer and reread a 1976 New York Times article about the discovery of Lyme disease. New insights struck me, particularly Steere’s growing suspicion that bacteria might not be the root cause, as this microorganism wasn’t behaving like a traditional bacterium:

> “The bacterial infections known to cause arthritis leave permanent joint damage, and bacteria are easy to identify in bodily fluids and easily cultured in test tubes. All efforts to culture bacteria from fluids and tissues from the patients have failed.”

Steere had shifted his focus to a new possibility: “A virus is the most likely candidate,” he told the Times. “Just because we haven’t identified one yet doesn’t mean it isn’t present. We’ll keep searching.” In a recent correspondence, I inquired whether he felt he had been “fooled” by Lyme disease in the 1970s, and he reminded me how much he and others had learned about this novel infection in such a short span. He emphasized that scientific inquiry can lead to numerous “dead ends,” underscoring the importance of learning from these failures and persisting in our efforts.

“Anyone who claims to fully understand the pathophysiology at play is oversimplifying,” said Ramzi Asfour, a physician and member of the IDSA with notably open views on Lyme disease, during a phone conversation from his Bay Area office. Asfour has found that a one-size-fits-all approach to Lyme diagnosis and treatment often falls short for most patients in his practice. We still lack comprehensive knowledge about diseases characterized by abnormal immune activity, he asserted. However, alongside the typical standardized protocols, there is a pressing need for personalized medicine approaches, given the immune system's intricacy and individuality. For instance, autoimmune disorders can be triggered by stressors, including trauma or infection. Furthermore, standard lab reports may not always capture early disease stages. Listening to patients is vital.

“Being an infectious disease doctor is generally quite rewarding in the conventional sense,” Asfour explained. “The patient is in the ICU; you identify a bacteria, and you see it; then you provide a magic pill, and they recover and walk home. It’s incredibly satisfying.” The experiences of Lyme patients challenge this model. As surgeon Atul Gawande once wrote regarding the medical profession, “Nothing is more threatening to your self-image than a patient with a problem you cannot solve.”

The less we understand about a condition, as Susan Sontag argued in Illness as Metaphor, the more likely we are to psychologize or stigmatize it. Amidst the current debate over Lyme, I find myself reflecting on other illnesses that modern medicine misunderstood for years. Multiple sclerosis was once labeled hysterical paralysis, and ulcers were deemed “a disease of tense, nervous individuals leading strenuous and worrisome lives,” as one mid-20th-century medical manual stated, perpetuating a notion that persisted until the 1980s. In reality, ulcers are caused by bacteria—though when a researcher proposed this in 1983, he was nearly laughed out of a gathering of experts who staunchly believed the stomach was sterile. We now understand that not everyone carrying the bacteria develops an ulcer; its occurrence results from a complex interplay between the pathogen and the host, akin to post-treatment Lyme disease syndrome.

In a week, a month, or six months, I anticipate feeling unwell again. Sharp electric shocks will begin coursing through my legs and arms, lasting for minutes, then hours, then days.

Indeed, Lyme disease has evolved into a term that represents more than itself. If it is not an ideology, it serves as a metonym for all tick-borne illnesses, for the struggles of suffering, and for the ways medicine has faltered in its goal of doing no harm—specifically by dismissing and ridiculing afflicted patients. As Wendy Adams of the Bay Area Lyme Foundation remarked, “We now possess incontrovertible evidence demonstrating that these individuals are genuinely ill.” Just because a symptom is prevalent and subjective—like fatigue—does not mean that a patient cannot differentiate between its normal and pathological forms. After all, we can distinguish between a common cold and a case of the flu. When I was severely unwell, I felt like a zombie—more importantly, I felt fundamentally different from my true self. In contrast, today, while I experience aches and fatigue, I am predominantly “me.”

Recently, I reached out to Richard Horowitz and several other Lyme experts to ask once more whether they believed it likely that I had Lyme disease. “Meghan, you have Lyme disease,” Dr. H asserted. “You’ve had multiple Lyme-specific antibodies appear on your tests. You displayed all the symptoms leading to a clinical diagnosis. And you improved with antibiotics.” Others echoed his conclusion.

I navigate uncertainties, as poet John Keats articulated while succumbing to an infection once thought to signify a disease of sensitive souls, which we now recognize as tuberculosis. However, I am quite certain of one thing: In a week, a month, or six months, I will begin to feel unwell again. My head will grow foggier, my energy levels will plummet. Upon waking, I will have a severe headache. Sharp electric shocks will start racing through my legs and arms, lasting for minutes, then hours, then days. My older son will pause his breakfast and ask, “What’s wrong, Mommy?” And once again, I will reach out to Dr. H for antibiotics.