The Zika virus commandeered the transmissive vector of the Aedes mosquito when junked tires filled with water, modifying the mosquitos’ breeding pattern, and allowing for a rapid spread of the virus. We change the environment; the environment changes us.
We are seeing an acceleration in the acquisition and presentation of several tick-borne diseases in the United States, thought in part to be a reflection of environmental and local climate changes. Several different diseases exist; Lyme is perhaps the most well recognized and most commonly diagnosed. Lyme is due to the Ixodes tick, which carries and transmits the spirochete (bacteria) Borrelia. The infection rate is region-dependent, but the environmental “cline” of the tick is spreading. Several current studies propose climate-related alterations of deer and rodent populations as potential vehicles for the dissemination of the disease.
Typically characterized by a bulls-eye rash that forms within a week of a tick bite, the initial infection is associated with fever, malaise, and joint pain. But a full 30-50% of people exposed don’t develop these symptoms. Initial symptoms in some of the other tick borne illnesses (which will not be covered here) tend to be severe. People tend to get really sick when infected by a bartonella or babesia species. Borrelia, the Lyme organism, tends to be a bit more covert, and sometimes it is a little less obvious. These are the more challenging cases.
If you are unfortunate to be infected by Borrelia, but fortunate enough to be treated within the first weeks to months of exposure, the cure rate with an extended course of the antibiotic doxycycline is pretty high. Things begin to get a bit tricky when one starts to consider whether or not, and the degree to which, borrelia can persist in the body and central nervous system (CNS). Studies of infected patients show that antibodies to the bacteria may persist in patients without symptoms, or be absent in patients that have persistent neurological symptoms. It’s hard to know exactly, and it’s hard to know if extended courses of intravenous antibiotics in Lyme specialty clinics really make any difference in the long run. To my knowledge there have been no clinical trials looking at any objective markers of the benefits of long term antibiotic administration, particularly via the intravenous route. Subjective improvement may be shown, but the human mind, and the power of placebo, is capricious.
It is hard for me to recommend such treatments without measurable clinical endpoints such as the elevated Cerebrospinal Fluid (CSF) white blood cells in the study quoted above, or other measurable confirmation of persistent disease. The CDC, in a 2006 expert opinion, specifically recommends against the use of long term IV antibiotics due to the lack of supporting data for its use. I am including a link to the manuscript here. It is a fairly comprehensive look at the biology, epidemiology and treatment recommendations for Lyme and the other tick borne diseases encountered in our country. Understand that this does not mean that there is no benefit of long term antibiotic use; it only means that a consensus of national experts, reviewing the published data by 2006, found no studies to support this practice.
A large, prospective, randomized and blinded trial (the “gold standard” of clinical studies) was published in the esteemed New England Journal of Medicine in 2016 looking at prolonged courses of oral antibiotics after initial Lyme treatment in almost 300 patients. The initial treatment protocol was pretty aggressive: two weeks of daily IV Ceftriaxone, followed by prolonged antibiotic treatments or placebo. In the end, there was no difference in detailed symptom scores between the groups, suggesting no improvement with prolonged treatment. By the CDC recommendations, initial treatment may include either oral or IV routes, with the IV route recommended for more severe, or neurological expressions of the disease. It is generally felt that when diagnosed early, and without severe neurological symptoms, Lyme can be treated with orally administered antibiotics.
Part of the problem with Lyme is inherent in how a diagnosis is made. As a rule the diagnosis is clinical, which means that it is not absolutely defined by a laboratory marker. If a person has a blood pressure of 200/140, there is no question that they are hypertensive. A person with a hematocrit of 20 is severely anemic (range 36-45); a person with a sodium of 120 is severely hyponatremic, and so on. The technology of looking for Lyme disease at this point is based on identifying enough distinguishing characteristics to make an overwhelming case of the bacteria’s presence. There is no single “ah-ha” marker; all possibilities occur along a spectrum. Let’s examine this more fully below.
When we are infected by an organism, our immune system responds to a portion of the organism, and an immune “memory” is initiated. In acute infections, our body makes high levels of the antibody IgM. This is a large antibody that is typically short lived, persisting typically for weeks to months. As the IgM wanes, our body starts to manufacture more numerous and enduring antibodies of the IgG variety. Did you have chickenpox at age 6? You will assuredly test positive for the IgG antibody to the varicella virus at ages 10, 40, 60 and 90. The same applies to the Borrelia bacteria, but without a single, seminal identifying marker. We have to rely on a constellation of markers from the IgM and IgG stables. But there is a catch.
The catch is that none of the markers are indisputably distinct for the bacteria responsible for Lyme disease. The proteins that are associated with, and measured for Lyme, are shared with a host of other bacteria. In all likelihood, we have been exposed to one or more of these “other” bacteria in the course of our lives, thus we may harbor an antibody “memory” of these exposures. The task is reminiscent of the blind men trying to identify an elephant. Individually a stout leg, floppy ear, and tufted tail may be associated with any number of other animals and things. A rhinoceros also has a stout leg; a large leaf could resemble an elephant’s ear. When several identifiers are assembled together there is agreement on “elephant”, but only then. And with more components that define “elephant”, perhaps adding a sharp tusk and wheezing trunk, there can be consensus that indeed there is an elephant. Making a diagnosis of Lymes is similar to this task.
An initial screen with high sensitivity is first made, known as an IFA study. This will likely not miss a diagnosis of Lyme, but in exchange for not missing any true cases is willing to accept some false positive diagnoses. At this point the usual screen reflexes to a series of tests known as Western Blots, a collection of several antibody markers (bands) against a tusk, a tufted tail, a stout leg or a floppy ear. According to the CDC, if 2 out of 3 of the IgM antibodies are positive, or 5 of the 10 IgG antibodies are positive, enough of these these markers, these bands, exist to define a diagnosis of Lyme. Enough markers, and the blind men agree on the consensus of “elephant”; enough bands confer a diagnosis of Lyme.
So if a patient presents with a “bulls-eye” rash, a history of a tick bite, and several weeks of low grade fevers and fatigue with 3 positive IgM markers and no IgG markers, they have Lyme disease and should be treated. Similarly a person with, say, one IgM marker, seven positive IgG bands, and a vague recollection of feeling bad after camping the prior year may similarly have a diagnosis of Lyme. Treatment is similarly merited, but success is somewhat diminished after time. The Neurology paper suggests that antibiotics can clear Lyme disease, but system persistence may still plague some patients. So what gives?
There is little debate that the Borrelia spirochete can cause significant disease, and that any significant stressor to the human body can wear us down and present with a wide array of symptoms. I am just not convinced that all post-Lyme symptoms are directly related to the original infection. In my personal practice I have seen significant arrays of dysfunction in numerous systems following an exposure: nutritional markers are low, the gut isn’t working well, cortisol is dysfunctional, hormones are off.
In this context, I work with my post-Lyme patients through the Health Pyramid. By addressing and optimizing the body’s systems, cleaning up the diet, normalizing cortisol, fixing the gut, removing immunogenic foods and balancing hormones, I believe that the majority of people suffering with “chronic Lyme Disease” will find that their symptoms abate over time.
In summary, I believe that Lyme Disease is a significant, evolving threat to our health, and many people may have had exposures. On one hand we may be underdiagnosing the disease, by simply failing to test for the spirochete. But I am additionally concerned by overdiagnosis and overtreatment, subjecting a patient to extensive, invasive, and potentially injurious interventions. As with so many things, the essence of health is found in a balance.
Yes, you may require antibiotics to treat Lyme Disease, and yes, there may be some poorly understood fallout from the initial infection. And yes, our understanding of the disease is still evolving, with clinical studies underway as I write. I do not claim to have all the answers; I am not sure anybody does. But rest assured that if the remainder of the Health Pyramid is not addressed in the wake of a tick-borne infection, it is unlikely that you will ever truly feel fully well again.
Complete health is found in addressing the body as a constellation of systems, including those found in the environment. This includes toxins, chemicals, foods, and in the case of Lyme, microbes.
 Neurology. 1993 Jan;43(1):169-75.Borrelia burgdorferi-specific intrathecal antibody production in neuroborreliosis: a follow-up study. This study remarkably looked at initial, and repeat studies of cerebrospinal fluid in 27 known Lyme-positive patients. Antibody testing confirmed neurological Lyme before treatment, and was repeated after treatment to see if the infection had cleared. It demonstrated that antibody production may persist, but without evidence of continued immunologic responses (persistently elevated white blood cells) to the infection. The conclusion was that antibody production may persist for years, without clinical signs of active disease.
 NEJM 2016 March 31; 374(13): 1209-20. Randomized Trial of Longer-Term Therapy for Symptoms of Lyme Disease.
Dr. Scott Resnick
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