Madison Area Lyme Support Group

Can you introduce yourself and share how did you got personally involved with Lyme disease? 

I am a professor of microbiology at SUNY Adirondack, which is a small State University of New York college located at the southern end of a 6.1 million acre state forest preserve known as the Adirondack Park. Prior to 2009, my program of undergraduate research focused mostly on environmental microbiology with an emphasis on small lake ecosystems, of which we have many here in the Adirondack region.

In 2009, my youngest daughter was a freshman in college and excelling both academically and athletically. In her first year, she had broken college records in her sport (swimming) and had just qualified as All-American in her first NCAA Nationals. Within a month of those achievements, she called to say she wasn’t feeling well and wanted to come home for the weekend. She went to bed that night, and didn’t get up again to fully return to her life for almost a year.

It was early spring when she got sick. There were no ticks to be seen, she did not have any kind of rash anywhere, and her physician never considered that her illness could be a tick-borne disease. She was referred to a rheumatologist (because she had profound joint and muscle pain), a cardiologist (because she had tachycardia and pain in her chest), and a neurologist (because she was having debilitating headaches, was constantly dizzy and had pain, tingling and on several occasions complete numbness and paralysis of her right arm and leg). After several rounds of blood tests, a CT scan, and a couple of MRI’s, there was still no diagnosis.

Then, in May, my husband attended a presentation at the school where he works given by one of his colleagues. The topic was Lyme disease, and after listening to the presentation and talking further with the presenter, he felt that our daughter’s condition could be related to Lyme disease.

We requested a blood test for Lyme disease, to which her physician reluctantly acquiesced. We were all surprised when it came back positive, and I remember at the time how relieved we all felt because at last, there was a diagnosis. Little did we know…

When the prescribed oral antibiotic was completed and she immediately relapsed, I realized that what I — as a microbiologist — thought I knew about this disease from textbooks and the CDC was wrong. So I started reading the scientific literature, and quickly realized that the dominant medical view of Lyme disease being a bacterial infection that was “hard to catch and easy to cure” was profoundly wrong, that the bacteria and the disease symptoms it caused were not like other bacterial illnesses, and that the CDC-recommended approach to diagnosis and treatment of this disease lagged well behind the science.

My struggles to pull my daughter out from under the weight of the chronic disease that had consumed her, made me realize that her experience mirrored that of hundreds of thousands of other people who were also being gaslighted by their physicians and marginalized by public health agencies. As my daughter’s condition improved, my attention turned first to educating the public about the dangers of ticks and the diseases they carry, followed by governmental advocacy to change the outdated and harmful health care policies of the CDC.

Along the way, I co-founded a 501-c-3 organization called Lyme Action Network, and now also serve as scientific advisor for two other organizations; Project Lyme which focuses on educating the public about ticks and tick-borne disease, and for the Focus On Lyme Foundation, which is raising funds for research toward better diagnostic tests and treatment for tick-borne diseases.

Focus On Lyme is also working to address one of the most significant roadblocks to scientific research on tick-borne diseases in humans, which is the lack of a readily accessible, no strings attached, biorepository of well-characterized human blood samples.

I (and many others) have come to realize that the path forward to accurate diagnostic tests and effective treatments will have to come from those who are most affected by the disease, through patient-centered (and often funded) projects such as this, because there is little to no leadership coming from governmental agencies on this issue.

You recently gave a testimony at the senate commission hearing of the State of New York and you gave a lecture at the Focus On Lyme 2017 conference about the science backing up Lyme and co-infections. What have you discovered?  Can you summarize your strong criticism of the mainstream assumptions surrounding Lyme in a way that everybody can understand?

Over the past 5 years, I believe it is safe to say I have read most if not all of the published science on borreliosis (the broad name for diseases caused by bacteria in the Borrelia genus).

It is very important for people to realize that when they hear medical or public health professionals proclaim that the medical guidelines dictating the practice of medicine and insurance reimbursement for Lyme disease are based on the best available science, such assertions are rhetorical hyperbole and little else.

The mainstream approach to medical practice for Lyme disease is currently guided by a relatively small number of clinical studies which are overly focused on one feature of this very protean disease – the appearance of a “bulls-eye” rash after a tick bite.

From 1977-1980, a team at Yale University headed by Alan Steere “discovered” and then defined a new disease, which he initially called Lyme arthritis. Steere noted in his early publications that approximately 25% of the people in his study cohorts had a very unique clinical feature – a rash called an erythema migrans or EM which resembles a bulls-eye – that sometimes accompanied other non-specific but debilitating symptoms (joint/muscle pain, headaches, peripheral nerve pain and sensations, fatigue).

As a newly minted “Epidemiology Fellow” of the CDC, he had been trained to look for clinical signs associated with disease symptoms, which could be “objectively” observed by a physician without relying on “subjective” reports by patients about what aches and pains they might be having. The unusual skin rash was just such a perfect, pathognomonic, feature.

Having noted and associated this unique rash with patients showing a similar cluster of subjective symptoms, his next studies set out to investigate the association of the rash with the disease. Steere’s subsequent studies were DESIGNED to CONFIRM what he wanted to be true – that the EM was a clinical sign of this new disease – as opposed to designing studies to impartially study the occurrence of the rash in people with the cluster of symptoms typical of people with Lyme disease. This is an example of a notable type of research bias, referred to as confirmation bias.

Steere also overemphasized the significance of joint swelling as a clinical sign of “Lyme arthritis,” because he was, after all, a rheumatologist, and therefore pain in a joint that was swollen could be taken as a “sign” of a disease process. Joint pain without obvious swelling was considered a nonspecific symptom that did not point to anything in particular.

The 1980s came along and New York decided that maybe they should look into this “new” disease since Long Island shares a body of water with Connecticut. SUNY Stony Brook on Long Island had a research team looking at ticks and diseases, so in 1982, the NYS Department of Health launched a study to find out just how many cases of this new disease there were in New York, to decide if the State should consider whether a public health response was needed.

The design of this study was for the Department of Health to alert New York State health care providers, through newsletter publications and also by sending letters to 300 primary care physicians, about the new disease and provide them with specific and detailed information and pictures about what to look for FIRST — a unique rash shaped like a perfect bulls-eye.

The letters directed health care providers to fill out a form for each patient seeking medical care for (in order of emphasis): a rash with a bulls-eye appearance; aseptic meningitis; facial paralysis (Bell’s Palsy); or large joint arthritis with swelling.

The inherent bias in the design of this research is obvious. The study directed a naïve population to be on the lookout for a new disease hallmarked by a specific type of rash shaped like a bulls-eye.

So what do you think got noticed by the physicians who participated in this study – the patients walking in the door with a bulls-eye rash, or the ones complaining about fatigue or headaches or pain in their non-swollen joints?

Before this investigation of the “Epidemiological Features of Lyme Disease in New York, the rate of association between an EM rash and Lyme disease symptoms ranged from 25-40%, as gleaned from a review of the published research from this period. In the New York study, 77% of the case reports were about people who exhibited an EM rash.

The perceived authority of this one study, published 33 years ago in 1984, serves as the ANCHOR for the misconception currently advanced by the CDC and other public health agencies, that 70-80% of the people who get Lyme disease will show a bulls-eye rash as a clear clinical sign.

Even though this assertion has been REPEATEDLY and REPRODUCIBLY shown to be false (with the true rate of association between and a bulls-eye shaped rash and a diagnosis of Lyme disease being only 10-40%), anchor bias perpetuates the myth that most people get an EM rash as a sign of “early” Lyme disease.

The bad news for patients is that since at least the late 1990s, the medical guidelines for diagnosing and treating Lyme disease patients have been based on clinical trials heavily influenced by this strong and pervasive anchor bias. Every research study that investigated the clinical course of Lyme disease in humans since the late 1970, used the appearance of a bull’s-eye rash as the main criteria for either inclusion in the study, or as an end point of the study.

Which means that all of the clinical research done to date has EXCLUDED from study 60-90% of people who actually have Lyme disease.

And even worse – a search of the NIH-funded clinical trials currently in the pipeline for Lyme disease returns with 20 studies currently enrolling or inviting participants. The “Inclusion Criteria” (to be eligible as a participant in the study) for these studies requires that a person must either meet the CDC case definition for Lyme disease, or meet the criteria set forth in the clinical practice guidelines developed by the Infectious Diseases Society of America, which are in practice one and the same. Briefly, those criteria are 1) the bulls-eye rash; and/or 2) “laboratory evidence” of infection.

“Laboratory evidence” is another way of saying “diagnostic test.” Diagnostic tests that would serve as laboratory evidence of an infectious disease like Lyme disease, either show direct evidence of infection with the bacteria causing the disease (such as growing the bacteria in culture or detecting their DNA or proteins in a blood sample), or indirectly demonstrate a past or present infection by measuring antibodies specific for the disease-causing agent in a person’s blood.

This latter method, called serology, is currently the ONLY type of laboratory testing recommended by the CDC for diagnosing a case of Lyme disease – even though serology has been REPEATEDLY and REPRODUCIBLY shown to be very inaccurate with a high rate of false negative tests (serology is falsely negative in 1 out of every 2 tests). A research paper just published takes it one step further and shows that serology is next to useless in persons who received antibiotic treatment before the test was done.

Ironically, a quote from the CDC website states: “Before CDC will recommend new tests, their performance must be demonstrated to be equal to or better than the results of the existing procedure, and they must be FDA approved.”

The explicit use of the term “FDA approved” by the CDC is interesting, because currently there are NO FDA APPROVED tests for Lyme disease, and that INCLUDES the serological tests the CDC recommends. Serology has been CLEARED by the FDA for marketing as a medical device, based on it being “substantially equivalent” to something already being marketed, which is, in essence serology itself, since serology was and is the only test in routine use across the globe.

FDA APPROVAL requires more than just a comparison to the existing standard, it requires additional evidence of the test’s safety and effectiveness. Serology, compared only to itself, has never actually gone through the FDA approval process.

This and other rhetorical twists of the existing science by the CDC has severely limited the use of any other test that could serve as “laboratory evidence” of Lyme disease, particularly ones which rely on the direct observation (such as culture or microscopic examination) or detection of biomolecules (such as DNA or RNA). Which is illogical, because direct detection of the microbe or molecules from it should yield no false positives, and therefore a person showing this type of laboratory evidence could be correctly diagnosed and treated.

What all this means is that we actually know next to nothing about the true nature of disease in persons infected with Borrelia or tick-borne coinfections, in the majority of persons who actually have Lyme disease. And if the status quo is maintained, we won’t be learning anything new from NIH-funded research on Lyme disease for the next 20 years.

If it was up to you to create an action plan for Lyme disease, what would you do? 

My action plan would start by making Lyme disease a national (and international) research priority, to the same extent that AIDS was prioritized in the 1980s. Given that there are annually more than 6 times the number of cases of Lyme disease as there are HIV/AIDS, with Lyme disease patients often experiencing a higher level of disability, this elevation in status is clearly warranted.

There are three areas related to tick-borne diseases that desperately need more research: diagnostics, treatment, and prevention. I would argue that diagnostics should be the first priority, because at this moment we are overly reliant on 40+ year old tests that are supposed to detect antibodies against a bacterium that can successfully “hide” from and even alter how and what types of antibodies are produced during an immune response to infection. There is currently no real way to differentiate between past or recent exposure to Borrelia in these tests, and no way to track the efficacy of treatments.

Once we have a way to directly detect infection – and I believe we are close to achieving that goal with several methods, including professor Laane’s work on a simple, direct method to detect the Borrelia with microscopy, direct detection of antigens, DNA sequencing, or nucleic acids from all tick-borne microbes – then it would be possible to reassess the existing dogma about the human course of this disease through well-designed, unbiased, hypothesis-driven research. Eva Sapi as another scientist using advanced microscopic methods for detection. This is the article describing her work on skin tissues.

The foundational research already exists – on bacteria grown in culture, and in animal models ranging from mice to dogs to non-human primates. Some of that research (new antibiotic dosing strategies, existing drugs with superior efficacy over the antibiotics currently medical guidelines recommend) is ready to advance to human clinical trials and only awaits funding.

Historically, research on preventing Lyme disease in humans has focused on vaccines and most recently, on a pre-exposure prophylactic (PrEP) that would render Borrelia burgdorferi incapable of causing an infection. The problem with this singular approach is that someone who is vaccinated or receives PrEP would NOT be protected against infection by other tick-borne microbes (such as other species of Borrelia, or Babesia, Bartonella, or Anaplasma) that also cause human diseases.

Existing research shows potential for a vaccine to prevent ticks from staying attached or transmitting microbes, and that type of vaccine deserves significantly more research attention, because it would reduce the human risk of acquiring any tick-borne disease, not just Lyme disease.

I would also argue that additional research is warranted to investigate other potential routes of transmission for the microbes labelled “tick-borne.” In the United States, CDC disease surveillance data reveals that Lyme disease is not just the “fastest growing vector borne disease,” it is the SECOND MOST COMMON infectious disease period, with only sexually-transmitted chlamydia causing more cases of disease per year. Gonorrhea comes in third.

Since there is scientific evidence of congenital transmission of Borrelia and research suggesting that sexual transmission occurs as well, it seems likely that Lyme disease is not all that “hard to catch” after all.

Professor Holly Ahern

Interviewer: Huib Kraaijeveld

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