Almost ten years ago, on October 7th, 2013, Doc Gumshoe posted a piece about Lyme disease, with a couple of short bits about babesiosis and Erlichiosis/anaplasmosis. The clinical details about Lyme – the pathogen that carries the disease, the ticks that transmits the pathogen to the patient, the initial symptoms, the usual treatments – were correct. Where that posting came a bit short was in the discussion of those difficult and controversial cases where the patient had a number of strange symptoms that might or might not be associated with Lyme disease, but did not meet the specific criteria for a diagnosis of Lyme disease.

In that previous piece, I set the stage by introducing three fictitious young women, whom I cleverly named Maxine, Patty and LaVerne, after the Andrews Sisters, who were pretty famous about 80 years ago (thus identifying myself as a bona fide geezer). I described how they got exposed to the ticks, by going for a pleasant walk in the woods on a fine summer day.

“These young women are not dedicated hikers. They do not wear long pants tucked into their socks, they do not wear boots, they do not spray themselves with insect repellent. On the contrary, they wear nifty short shorts, sleeveless blouses, and cute open-toed sandals. They look like jazz babes, and they have a terrific time.”

Maxine’s story

Each of the three develop Lyme disease – Maxine first, then Patty about a year later, and finally LaVerne. Maxine’s case is the easiest to diagnose, since her symptoms emerge about a week after their walk in the woods. She has a headache, chills, and a temperature of about 102°. She feels genuinely lousy. Her sisters persuade her to go see a doctor, who quickly diagnoses her with Lyme disease.

Her doctor looks her over, and in the course of the physical examination, he notices several round reddish rashes on her upper legs and lower back. They are over an inch wide and show no signs of a bite. There are small reddish areas in centers of the rashes, surrounded by a lighter area, and then darker slightly raised red ring at the edges, making the rashes look like bulls-eyes.

The doctor then explains to Maxine how she came to be infected with Lyme disease and the particularly sneaky way the tick went about biting her. The tick bite did not sting or itch. The tick – Ixodes scapularis, also called a deer tick or a black-legged tick – infected her with a micro-organism, a spirochete called Borrelia burgdorferi. He explains that spirochetes are nasty little creatures, hard to eradicate, because they tend to travel far from the site where they enter the body and hide deep in the tissues where the antibiotics that are used to kill them don’t easily penetrate. A particularly dangerous spirochete is Treponema pallidum, the pathogen that causes syphilis, which – if not properly treated early on – can penetrate the tissues and cause dementia, cardiac damage, and liver damage, many, many years after the initial infection. The Lyme pathogen is thought by some to have the same potential, thus leading to those controversial cases which we’ll discuss further in this piece. That’s why early, aggressive treatment is crucial. A four week treatment with any of several oral antibiotics eliminates the Lyme pathogen most of the time.

The doctor does not do any further testing. Maxine’s symptoms and her bulls-eye rashes are enough to diagnose Lyme disease, and, in any case, the blood tests for Lyme depend on the formation of antibodies to the pathogen, and antibodies wouldn’t yet have formed. There’s no reason to delay treatment pending confirmation by a blood test, and every reason to start treatment right away, to kill those evil little pathogens before they further conceal themselves.

Maxine’s bull’s-eye rashes – known as erythema migrans – are not the sites of the tick bite, by the way. The tick probably landed on Maxine’s leg as she brushed against a bush on her walk. Then it wandered over her body until it found a nice spot to dig in, which might have taken a full day or even longer. Then the tick buried itself in Maxine’s tender flesh, feasted on her blood, and dropped off when it had had enough. Maxine would likely have felt nothing when the tick bit her – tick bites don’t sting or itch. As her doctor explained, if Maxine had felt the tick bite, she would have likely brushed the tick away, and the tick would have gotten no free lunch. Ticks are not quick, like mosquitoes, which can get their blood meal in a few seconds before you swat them.

Maxine’s doctor prescribes a 28-day course of a common antibiotic, probably doxycycline (although a number of other oral antibiotics work just as well – he checks first to see whether Maxine has demonstrated any allergies or sensitivity to doxycycline). And he firmly tells her that she must complete the full 28-day course, even if she feels perfectly fine after a week or so.

However, about a week later, Maxine develops another very distressing symptom. She feels numb on the left side of her face, and she has trouble fully closing her mouth on that side. In fact, she dribbles her food, and she’s afraid she’s had some kind of stroke.

She runs back to her doctor in a state of considerable concern. But her doctor reassures her: she has a touch of a temporary neurologic condition called Bell’s palsy. The emphasis here is on “temporary.” It will certainly pass in a couple of weeks, and she will be totally back to normal. Episodes of Bell’s palsy are quite common with Lyme disease, and Maxine should not worry.

Indeed, in a few days, the numbness in her face is gone, the bulls-eye rashes have disappeared, and Maxine is feeling like her old self again. The next time she’s invited to go for a walk in the woods, she will cover up and use insect repellant, resuming her more glamorous outfit when she’s on the boardwalk on Coney Island.

Patty’s story

About a year after Maxine’s bout of Lyme disease, her sister Patty began to have strange symptoms. She develops troubling pains in her knees. She racks her brain to try to remember anything she has done that would account for these pains, which seem to be a combination of soreness and stiffness. The pains are in both knees, and they seem to originate in the joint itself and to spread to the sides of the knees. They aren’t sharp pains, and they don’t really prevent her from doing anything she needs to do. But they slow her down, and, more than anything else, they are puzzling and disturbing. After all, she says to herself, I’ve just turned 40, and there’s no reason for me to be developing arthritis or anything like that.

So Patty goes to the doctor, and the doctor examines her and orders blood tests. The doctor explains that it’s possible, although unlikely, that Patty really is developing rheumatoid arthritis – women as young as their mid-30s sometimes develop rheumatoid arthritis – and it’s important to make sure Patty does not have this disease, because if she does, she needs to be treated quickly and aggressively to make sure the disease does not progress. There are also other possibilities that might need to be considered, including fibromyalgia, but the top priority is to rule out rheumatoid arthritis.

But at the same time, the doctor, remembering that Patty’s sister Maxine had Lyme disease the year before, decides to do a blood test for Lyme disease. (Note, if I had not cooked up the story of the three sisters and their woodlands stroll, and if Patty were just another unrelated character, it’s quite possible and even likely that the doctor would not have done the Lyme disease test, in which case Patty might have gone for a considerable time experiencing her knee pains with no clue as to the cause.)

The rheumatoid arthritis tests all come back negative. But the test for Lyme antibodies – the enzyme-linked immunosorbent assay, or ELISA – came back positive. ELISA is a type of test, and ELISA tests can be used for a very wide variety of conditions, or even just for the presence of a large number of proteins. The advantage of ELISA tests is that they are relatively quick and inexpensive. However, they are far from definitive. There can be false positives, meaning that they appear to identify an antibody when in fact that specific antibody is not present, but the test reagents have responded to a different antibody. And there can be false negatives, meaning that the reagents have failed to respond to an antibody that may be present, but perhaps at insufficient levels.

However, a positive ELISA for Lyme disease at least requires further investigation, so Patty’s doctor orders the next level of test, a Western blot test. This is a more complex and more expensive test, and it evaluates several immunoglobulin types, typically about 10 immunoglobulin M (IgM) bands and 3 immunoglobulin G (IgG) bands. According to the Centers for Disease Control, a Western blot test for Lyme disease is considered positive if either 5 of the 10 IgG bands or 2 of the 3 IgM bands are positive. Western blot bands are distinguished by the size of proteins that migrate through a series of gels, as measured in kiloDaltons (a kiloDalton is 1000 Daltons, one Dalton being equivalent to the weight of one nuclear particle). Some particular Western blot bands are thought to be specific to Lyme disease, while others are not considered to be specific.

In any case, the point of this perhaps unnecessarily technical blather is to make it clear that the positive identification of Lyme disease is not simple. For most infectious diseases, identifying the pathogen is relatively straightforward. A tissue or blood sample is cultured, and colonies of the pathogen grow out in the culture and are usually fairly easily identified microscopically, frequently with the aid of stains. But Borrelia burgdorferi doesn’t grow in cultures, or at least not quickly enough to diagnose and treat the patient, so clinicians and the lab folks are stuck with trying to identify the antibodies that the wicked little pathogens elicit as they go around making mischief. And identification of Lyme antibodies is not always absolutely accurate; the best the lab is able to do is track correlations. For example, proteins in the 39 kiloDalton band are found in the serum of patients with established Lyme disease frequently enough so that proteins of this size are thought to be specific indicators of Lyme. The sensitivity and specificity of Western blot ranges is in the low to mid 90%s, which is good, but not perfect.

No surprise, Patty’s Western blot test comes back positive, and her doctor now has to recommend a course of treatment. Available options include oral, intramuscular, and intravenous antibiotics. The doctor and Patty talk it over, and the decision is to try a course of oral treatment first and see if it leads to improvement. There are a number of antibiotic candidates, with no single candidate having an edge over the others. Patty sticks with her antibiotic regimen for the recommended 28 days, and gradually begins to feel better.

LaVerne’s story

And, about a year after Patty’s experience, LaVerne develops problems of her own. Only these problems are a good deal more complicated and troubling. Yes, she has pains in her joints. But she’s having other problems as well – headaches, problems with her memory, difficulty concentrating. She feels truly lousy and in a bad mood. And she’s definitely worried.

Her doctor, knowing about Maxine’s and Patty’s Lyme disease episodes, immediately suspects Lyme, even though, like Patty, LaVerne had none of the typical Lyme symptoms after that historic walk in the woods.

It’s only because this particular doctor was the one who treated Maxine and Patty that he even suspects Lyme disease as a possibility. As far as the doctor knows, LaVerne hasn’t been recently exposed to those crafty ticks. There’s a good chance that patients like LaVerne, whose symptoms take a considerable time to emerge, aren’t diagnosed with Lyme for years, and may never receive a Lyme diagnosis, but simply go on living with their symptoms and attempt to deal with them with a variety of stratagems, mostly ineffective. We’ll discuss that kind of situation further on in this piece.

But this particular doctor knows that many patients overlook the initial symptoms. The erythema migrans doesn’t always take on the bulls-eye appearance, and the other symptoms, even if the appeared at all, might have been so mild that LaVerne shrugged them off.

The doctor orders the standard Lyme disease tests, the ELISA and the Western blot. But they both come back negative. Or rather, the ELISA comes back negative, and the Western blot doesn’t meet the Centers for Disease Control standards for diagnosis of Lyme disease. Only one of the bands was positive, and it was not considered specific for Lyme.

LaVerne’s doctor still thinks that Lyme disease is a possibility; however, other possible sources of LaVerne’s symptoms need to be investigated and either confirmed or ruled out. So the doctor recommends to LaVerne that she consult with two other physicians – a neurologist and a rheumatologist.

The appointment with the rheumatologist comes up first. After reviewing LaVerne’s symptoms and her medical history, the rheumatologist orders blood tests to rule out rheumatoid arthritis, because RA, although unlikely, could be a real threat to LaVerne’s long-term health. LaVerne has tenderness and stiffness in several joints, and also at several points in her body which are not joints. While joint pain is characteristic of RA, the other pains that LaVerne is experiencing are not typical RA symptoms, so the rheumatologist thinks it’s not likely that LaVerne will turn out to have RA. But LaVerne should not take the risk of ignoring the possibility, since untreated RA can lead to permanent joint damage in as little as a few months. Fortunately for LaVerne, the RA blood tests – erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), rheumatoid factor (RF), and antinuclear antibody (ANA) all come back negative.

This leaves the rheumatologist to explore the possibility that LaVerne is suffering from fibromyalgia. This condition is genuinely difficult to diagnose precisely, and treatment is by no means straightforward. The causes are uncertain, and there are some who question whether fibromyalgia is a bona fide disease entity and not just a cluster of unrelated symptoms. A theory about the cause of this condition or syndrome that has many adherents is that fibromyalgia is brought about by low levels of serotonin. This is supported by the observation that women typically have lower levels of serotonin than men, and also that women, by a large ratio, are more susceptible to fibromyalgia than men. This has led to the use of drugs that boost serotonin levels, such as antidepressants of the selective serotonin reuptake inhibitor (SSRI) class – e.g., Prozac – and, indeed, these drugs do relieve some of the fibromyalgia symptoms in many cases.

LaVerne demonstrated some of the typical fibromyalgia symptoms, and the rheumatologist, in consultation with LaVerne’s main physician, suggests that LaVerne at least try a course of an SSRI. LaVerne agrees to give it a shot.

After about a month on the SSRI, LaVerne’s general mood, not surprisingly, improves. But the tender and painful areas in her body have not improved, and she is taking large doses of over-the-counter pain medications – non-steroidal anti-inflammatory drugs, or NSAIDs – just to get through the day. Her doctor does not think that long-term chronic NSAID use is a good option for LaVerne, and urges her to keep her appointment with the neurologist.

The neurologist, as the rheumatologist had done, examines LaVerne and reviews her medical history. Once again, the question of Lyme disease comes up. In spite of negative ELISA and Western blot results, the neurologist thinks that Lyme is a possibility. The other leading possibilities have been, if not entirely eliminated, reduced to “highly unlikely” status, and there’s no evidence of trauma or repetitive stress that could lead to LaVerne’s symptoms.

The neurologist recommends one more test – a spinal tap. The sample is sent for analysis to two different academic laboratories, and one of them reports identification of antibodies to the Lyme pathogen.

At this point, the treatment decision is fairly straightforward. LaVerne should be treated with intravenous infusions of an antibiotic that has optimal penetration, such as a cephalosporin. After consulting both with LaVerne’s primary care physician and an infectious disease specialist, a four-week course of ceftriaxone is recommended, and LaVerne should be closely monitored for signs of relapse.

A more complicated and vexing situation

These Andrews sisters all clearly had Lyme disease – Maxine, whose symptoms emerged about a week after her exposure, Patty, whose symptoms didn’t show up until a year after her exposure, but who tested positive for Lyme, and LaVerne, whose symptoms took even longer to appear and finally tested positive for Lyme based on a spinal tap and the identification of antibodies to the Borrelia burgdorferi pathogen. But what about persons – and there are lots of them – who have suspicious symptoms, but test negative on the usual tests?  LaVerne had a spinal tap because her doctor, who had treated Maxine and Patty, was aware of the possibility that LaVerne’s symptoms were caused by Lyme. Many – perhaps most – doctors would not have ordered a spinal tap, and many cases of Lyme disease would therefore go undetected.

There’s a contingent of clinicians out there that strongly hold the view that seronegative Lyme disease is a reality, and requires treatment. What is meant by “seronegative” is that no test, whether ELISA, Western blot, or spinal fluid analysis, reports the presence of Borrelia burgdorferi antibodies. The pathogens have the sneaky capacity to penetrate deep in the body’s tissues, generate protective coatings (called biofilms) and avoid triggering the formation of antibodies, thus preventing detection by available testing methods. The International Lyme Diseases and Associated Diseases Society (ILADS) has issued guidelines calling for antibiotic treatment of patients with symptoms associated with Lyme disease, regardless of whether their sera test positive for Lyme antibodies.

Here is their list of Lyme disease symptoms

• Fatigue
• Low grade fevers, “hot flashes” or chills
• Night sweats
• Sore throat
• Swollen glands
• Stiff neck
• Migrating arthralgias, stiffness and frank arthritis
• Myalgia
• Chest pain and palpitations
• Abdominal pain, nausea
• Diarrhea
• Sleep disturbance
• Poor concentration and memory loss
• Irritability and mood swings
• Depression
• Back pain
• Blurred vision and eye pain
• Jaw pain
• Testicular/pelvic pain
• Tinnitus
• Vertigo
• Headaches
• Lightheadedness
• Dizziness

ILADS is somewhat suspicious of laboratory findings as a basis for treatment when it comes to Lyme disease. Here’s what they say about that question:

“Treatment decisions should not be based routinely or exclusively on laboratory findings. The two-tier diagnostic criteria, requiring both a positive enzyme-linked immunosorbent assay (ELISA) and western blot, lacks sensitivity and leaves a significant number of individuals with Lyme disease undiagnosed and untreated. These diagnostic criteria were intended to improve the specificity of tests to aid in identifying well-defined Lyme disease cases for research studies. Though arbitrarily chosen, these criteria have been used as rigid diagnostic benchmarks that have prevented individuals with Lyme disease from obtaining treatment. Diagnosis of Lyme disease by two-tier confirmation fails to detect up to 90% of cases and does not distinguish between acute, chronic, or resolved infection.”

That’s definitely at odds with what the CDC says about Lyme disease testing for Lyme disease. Here’s the CDC’s statement:

“CDC currently recommends a two-step testing process for Lyme disease. Both steps are required and can be done using the same blood sample. If this first step is negative, no further testing is recommended. If the first step is positive or indeterminate (sometimes called “equivocal”), the second step should be performed. The overall result is positive only when the first test is positive (or equivocal) and the second test is positive (or for some tests equivocal).

Key points to remember

Most Lyme disease tests are designed to detect antibodies made by the body in response to infection.

Antibodies can take several weeks to develop, so patients may test negative if infected only recently.

Antibodies normally persist in the blood for months or even years after the infection is gone; therefore, the test cannot be used to determine cure.

Infection with other diseases, including some tick-borne diseases, or some viral, bacterial, or autoimmune diseases, can result in false positive test results.

Some tests give results for two types of antibody, IgM and IgG.  Positive IgM results should be disregarded if the patient has been ill for more than 30 days.”

And as for the Infectious Disease Society of America (IDSA), they limit their recommendations to cover persons who have experienced a tick bite. As far as I could see, they say nothing about Lyme disease tests for individuals who develop suggestive symptoms, but who are not known to have been attacked by a tick. Here’s what the IDSA has to say:

“Which diagnostic tests should be used following a tick bite?
(A) Diagnostic Tick Testing

1. We recommend submitting the removed tick for species identification (good practice statement).
2. We recommend against testing a removed Ixodes tick for B. burgdorferi (strong recommendation, moderate-quality evidence). Comment: The presence or absence of B. burgdorferi in an Ixodes tick removed from a person does not reliably predict the likelihood of clinical infection.

(B) Diagnostic Testing of Asymptomatic Patients Following Tick Bites

1. We recommend against testing asymptomatic patients for exposure to B. burgdorferi following an Ixodes spp. tick bite (strong recommendation, moderate-quality evidence).”

I could not find anything either in the CDC or IDSA material recommending testing for persons based on symptoms alone.

In my previous disquisition on Lyme disease, I expressed serious misgivings about ILADS pronouncement on the likelihood of Lyme disease in individuals who had no positive serologic tests. Here’s the ILADS statement and my response:

“A patient who has tested seronegative may have a clinical presentation consistent with Lyme disease, especially if there is no evidence to indicate another illness.

Although many individuals do not have confirmatory serologic tests, surveillance studies show that these patients may have a similar risk of developing persistent, recurrent, and refractory Lyme disease compared with the seropositive population.”

In other words, LaVerne’s likelihood of having Lyme disease is the same whether her lab tests were positive or negative? My warning antennae went up sharply!

That would imply that diagnosis of Lyme disease would rely on symptoms, and considering the long and complex list of symptoms, huge numbers of people could be deemed to have Lyme disease, and therefore to require antibiotic treatment, frequently for extended periods. That could pose a rather large problem – to the individuals in question, to the medical community, and to society.

A decision to treat so-called “seronegative Lyme disease” would likely lead to lengthy antibiotic treatment courses that might not be necessary and could produce definitely negative consequences. Such treatment would probably kill all or most of the beneficial micro-organisms in the GI tract, and lead to really troublesome opportunistic infections such as Clostridium difficile, which is nasty and difficult to deal with. And it could very well produce resistant strains of some of the bacteria that normally colonize our bodies, causing serious soft tissue and upper respiratory infections.

The controversy about Lyme disease has not gone away in the ten years since that first piece posted. On balance, at that time I tended to side with the established medical community and the IDSA. Here’s what my conclusion was:

“All of this said, it’s certainly possible that some people have seronegative Lyme disease. There’s no doubt that the pathogen is exceedingly elusive, and the antibody tests are far from perfect. Nevertheless, I don’t think that it’s remotely reasonable to conclude that there’s anything like an even chance that a person with some of the symptoms on that long list, whose Lyme tests are all negative, actually has Lyme disease. My guess is that an experienced and wise physician would go slowly in a situation of that kind, perhaps suggesting topical analgesics for pain. It might be nerve-wracking for the patient, but I doubt whether such a physician would initiate aggressive antibiotic treatment without some indication as to what pathogen was the culprit.”

The Ross Douthat factor

Ross Douthat is an opinion writer for the New York Times, generally tending slightly more conservative than the paper. He is highly intelligent and also deeply principled. Recently he came to our town to give a talk, which was mostly about his own experience with Lyme disease, which had lasted for years and had been very troubling.

Douthat and his wife lived in Washington, D.C., but were planning to move to Connecticut to a more rural location. While on a trip scouting their planned new home, Douthat was evidently bitten by a tick. The first Lyme disease symptoms didn’t emerge until he and his wife were back in D.C. When he noticed a painful red swelling on his neck, he went to a walk-in clinic where he was told it was “just a boil … nothing to worry about.” Exactly what he wanted to hear, especially since he had just learned that his wife was pregnant with their third child.

But mysterious symptoms kept coming – stiff and painful neck, a sensation that there was a vibration in his head, then a stabbing sensation in his mouth around his teeth. “…my whole body was just … wrong, haywire somehow, as though someone had twisted dials randomly in all my systems.” He wondered whether he was having a heart attack or a stroke. He went to the emergency room. The blood tests all came back normal, and the doctors suggested he was suffering from stress.

The pain that had started in his neck kept jumping around – to his spine, to his chest muscles. He went to a number of doctors and had many tests – blood, stool, urine, cranial and abdominal scans.

Then he read a story in New York Magazine by a doctor who had lived with undiagnosed Lyme disease for years, leading to a condition that required a heart transplant. The doctor’s symptoms sounded very much like his own. He had actually had a Lyme test, and when he looked at his copy of the test, he saw that one of the bands was positive. One band of course is not sufficient for a diagnosis of Lyme disease, but Douthat was wondering if indeed Lyme disease was the cause of his mysterious symptoms.

Douthat consulted a physician who was open to the possibility that he had Lyme disease and prescribed a ten-day course of doxycycline. He took it, felt a bit better for one day, and then started gagging and vomiting. His symptoms continued, and after a week he stopped taking the drug.

He kept having symptoms and kept going to different doctors, none of whom were able to pinpoint the cause of his symptoms. And then one doctor suggested to his wife that Douthat could benefit from having cognitive behavioral therapy. That particular doctor was essentially admitting that he/she had no notion of the cause of Douthat’s symptoms and suggesting that these symptoms were all really in Douthat’s mind – i.e., Douthat was a malade imaginaire.

Douthat was willing to give just about anything a try, so he followed that suggestion, and it helped, but just a little bit. His physical symptoms continued. He kept talking to people about his condition and went to numerous other doctors. He noticed a difference in how these doctors responded to his symptom recital. In part, their response varied with where they were practicing. The doctors in D.C. had heard of Lyme disease, but had very little experience with it, and did not give the Lyme diagnosis much consideration. More of the doctors in the wilds of Connecticut, where they had purchased a property, were familiar with Lyme and thought it was a possible – even likely! – diagnosis.

For a period lasting some years, Douthat tried a large number of treatment options, sometimes switching from one to another. He had several different antibiotics on hand, and, depending on the severity of his symptoms, he would dose himself with these. He became the kind of patient that would be enormously frustrating to most health-care professionals, since it would be almost impossible to link symptom relief to any single drug.

And it wasn’t just antibiotics. Douthat dosed himself extensively with vitamin C, at first orally, and then via intravenous infusions. He attempted a salt protocol for Lyme disease, the specifics of which are available in a three-ring binder from Amazon. He went through a period of therapy which consisted of fifteen flat magnets taped to the various spots on his body where he felt the symptoms.

The strangest but perhaps most effective treatment was delivered by a Rife machine. This machine was invented about 90 years ago by Royal Raymond Rife, who had worked on the development of several powerful microscopes. He claimed that certain frequencies could destroy micro-organisms, much the way a note sung by a skilled singer (a soprano, of course!) could shatter a wine-glass. This looks totally delusional, but there appears to be some real substance behind the claim.

In any case, Douthat acquired a Rife machine – a gift from his father – and began trying various frequencies on himself. The Rife machine came with a list of 873 pre-programmed channels, each linked to a specific ailment, plus another hundred frequencies contributed by users of the Rife machine. There were two channels listed for Lyme disease, each of which included dozens of frequencies. Douthat gave the Rife machine a try. It seemed to work. He continued his regimen of antibiotics in conjunction with Rife machine sessions. He improved steadily, and before long, his symptoms had disappeared.

Whether it was the antibiotics, the Rife machine, or a revitalization of his immune system, Douthat totally recovered from his symptoms. The process took several years. At no point is it entirely clear whether the underlying disease was Lyme or something else, some mysterious as yet undefined pathogen. My guess is that it was indeed Lyme, and that the Borrelia burgdorferri had burrowed deep into his tissues and escaped detection.

It seems evident that there are many, many such cases.

Douthat wrote a book about his experience which is, in my opinion, definitely worth a read – The Deep Places, from Convergent, New York,

* * * * * * *

As I said in the opening sentence of this piece, the original epistle had brief discussions of a couple of other tick-borne diseases – babesiosis and Erlichiosis/anaplasmosis. Since then a couple of other tick-borne diseases have demanded attention – Alpha-Gal syndrome and Rocky Mountain spotted fever. This piece is long enough anyway – perhaps too long! So discussion of those will have to wait. To all Gumshoe denizens, stay well and be of good cheer! Best to all and keep those comments coming! Michael Jorrin (aka Doc Gumshoe)

[ed note: Michael Jorrin, who I dubbed “Doc Gumshoe” many years ago, is a longtime medical writer (not a doctor) and shares his commentary with Gumshoe readers once or twice a month. He does not generally write about the investment prospects of topics he covers, but has agreed to our trading restrictions.  Past Doc Gumshoe columns are available here.]