THE ATLANTIC SEPTEMBER 2019 59In 2018, my father died of complications from pneumonia,
after recovering from the cancer. I couldn’t help wondering how
much those lost months had perhaps cost him, as the cancer
advanced and weakened him—all because Lyme had seemed
like an obvious enough explanation, and the testing was suf-
ficiently murky, that his doctor did not pursue other diag noses.
Though promising new diagnostic technologies are on the hori-
zon, we still can’t reliably sort out who has a tick-borne disease
and who doesn’t.O
N A BRISK MARCH DAY THIS YEAR, the kind of
day that can’t decide whether it’s warm or cold, I vis-
ited a research laboratory at Massachusetts General
Hospital directed by Allen Steere, the rheumatologist
who discovered Lyme disease and helped establish the testing
parameters for it. A slim, gray-haired man with an intense gaze,
he has become, in the eyes of many Lyme patients, an embodi-
ment of the medical system’s indifference, because he has long
suggested that some chronic Lyme patients were incorrectly
diagnosed in the first place. He has been shouted down at con-
ferences and ambushed by people purporting to be journalistic
interviewers. Scientists who disagree with him had nonetheless
singled him out to me for his commitment to studying Lyme. I
wanted to hear his perspective on the disease and on the debate
after four decades of immersion in both.
While underscoring that medicine can be humbling, and that
Lyme disease is complex, Steere spoke with the calm air of some-
one setting a child straight. Emphasizing that in many people Lyme
disease can resolve on its own without antibiotics, he carefully
described a disease that in the United States frequently follows a
specific progression of stages if untreated, beginning with an early
rash and fever, then neurological symptoms, and culminating
later in inflammatory arthritis. The joint inflammation can con-
tinue for months or even years after antibiotic treatment, but not,
he believes, because the bacteria persist. His research on patients
who have these continuing arthritis symptoms has revealed one
cause to be a genetic susceptibility to an ongoing inflammatory
response. This discovery has led to effective treatment for thelonger-term challenges of Lyme arthritis, using what are called
disease- modifying anti-rheumatic agents.
After I told him a little about my case, he struck a note of
similarly solicitous firmness. He told me that in his view, late-
stage Lyme (which is what I had been diagnosed with) usuallydoes not cause a lot of “systemic symptoms,” such as the fatigue
and brain fog I had experienced. “I want you to free yourself
from the Lyme ideology,” he said. “You clearly were helped by
antibiotic therapy. But I don’t favor the idea that it was spiro-
chetal infection. Of course, there are other infectious agents,”
he continued, noting that some of them trigger complex
immune responses.
I left Steere’s office unnerved, thinking that if I had met a doc-
tor with some version of this view in 2014, I would never have
started doxycycline and gotten better. Could it really be that I
had some condition other than Lyme that turned out to respond
to anti biotics? He was an expert who had devoted his entire
career to studying the mechanics of the disease; I was a patient
who happens to be temperamentally both exacting and excitable,
and scientifically curious—a layperson craving evidence.
That night I curled up with my computer in my hotel room and
reread a 1976 Ne w York Times article about the discovery of Lyme.
New things struck me, in particular Steere’s growing suspicion
back then that bacteria couldn’t be the cause, because this micro-
organism wasn’t acting like a bacterium:The bacterial infections that are known to cause arthritis leave
permanent joint damage, and bacteria are easy to see in body flu-
ids and easy to grow in test tubes. Every effort to culture bacteria
from fluids and tissues from the patients has failed.Steere had moved on to a new possibility: “A virus is the most
likely candidate,” he told the Times. “Just because we haven’t
found one yet doesn’t mean it isn’t there. We’ll keep looking.”
When I recently wrote to ask him if he had been “fooled” by
Lyme disease back in the 1970s, he reminded me of how much
he and others had learned, in just a few years, about this then-
new infection. He went on to remind me that science can “lead
to one ‘dead end’ after another. One needs to learn from these
dead ends and continue trying.”“A
NY O NE WHO S AY S they really understand
the pathophysiology of what’s going on is over-
simplifying to some degree,” said Ramzi Asfour, a
physician and member of the Infectious Diseases
Society of America with notably open views on Lyme disease,
when I reached him on the phone in his Bay Area office. Asfour
has found that a one-size-fits-all approach to Lyme diagnosis
and treatment is inadequate for most patients in his medical
practice. We don’t know enough yet about diseases that are
characterized by abnormal activity of the immune system,
he emphasized. But, alongside the usual standardized proto-
cols, they clearly call for the tactics of personalized medicine,
because the immune system is so complex—and so individual-
ized. For example, autoimmune diseases can be triggered by
stressors that include trauma or infection. And standard lab
reports don’t always capture early stages of disease. Listening
to patients is crucial.
“Being an infectious-disease doctor is usually pretty reward-
ing in the conventional sense,” Asfour said. “The patient is in
the ICU; you grow a bacteria, and you see it; then you give them
a magic pill. They get better and walk home. It’s very satisfying.”
The experience of Lyme patients challenges that model. As the
surgeon Atul Gawande once wrote of the medical profession,
“Nothing is more threatening to who you think you are than a
patient with a problem you cannot solve.”In a week, or a month, or six months,
I will start feeling less well. Sharp
electric shocks will start runningalong my legs and arms, for minutes,
then hours, then days.