Natural Treatments for Lyme Coinfections

Anaplasma, Babesia, and Ehrlichia

Stephen Harrod Buhner

• Publisher: Healing Arts Press
• Year: 2015
• ISBN:
  9781620552599
• Topic: Medicine
• Subtopic: Diseases & Allergies

A guide to the natural treatment of three coinfections of Lyme disease• Reviews the latest scientific research on Babesia, Ehrlichia, and Anaplasma• Reveals how these three conditions often go undiagnosed, complicate the treatment of Lyme disease, and cause symptoms from headache to seizures• Outlines effective natural treatments with herbs and supplements for specific symptoms and to combat overreactions of the immune system and the inflammation responseHarvard researchers estimate there are nearly 250, 000 new Lyme disease infections each year--only 10 percent of which will be accurately diagnosed. One of the largest factors in misdiagnosis of Lyme is the presence of other tick-borne infections, which mask or aggravate the symptoms of Lyme disease as well as complicate treatment. Three newly emergent Lyme coinfections are Babesia, Ehrlichia, and Anaplasma. Tens of thousands of people are known to be asymptomatically infected and at least ten percent will become symptomatic this year--with symptoms ranging from chronic headache and arthritis to seizures. Distilling the latest scientific research on Babesia, Ehrlichia, Anaplasma, and Lyme disease, Stephen Buhner examines the complex synergy between these infections and reveals how they can go undiagnosed or resurface after antibiotic treatment. He explains how these organisms create cytokine cascades in the body--essentially sending the immune system into an overblown, uncontrolled inflammatory response in much the same way rheumatoid arthritis or cancer can. Providing an in-depth guide for those suffering from Babesia, Ehrlichia, or Anaplasma infection as well as for clinicians who work with those infected by these organisms, Buhner details effective natural holistic methods centered on herbs and supplements, such as Ashwaganda and Chinese Skullcap, and reveals how to treat specific symptoms, interrupt the cytokine cascades, reduce inflammation, and bring the immune system back into balance. He explains how these natural methods not only complement conventional Lyme disease treatments involving antibiotics and other pharmaceuticals but also provide relief when other forms of treatment have failed.

1

Emerging Diseases and Coinfections

The New Epidemics

Hosts that are coinfected by multiple parasite species seem to be the rule rather than the exception in natural systems.

A. L. GRAHAM, I. M. CATTADORI,
J. O. LLOYD-SMITH, ET AL.,
“TRANSMISSION CONSEQUENCES OF COINFECTION:
CYTOKINES WRIT LARGE?”

Patients with immunocompromised systems are at greater risk for a more prolonged and severe course of illness, especially with multiple infectious etiologies, illustrated here with Lyme disease and babesia. In these patients, reasoning to the single most likely cause of illness may not be the best approach to diagnosis and empiric treatment. Familiarity with tick-borne diseases is important and may become more so as the habitats of humans and ticks increasingly intersect.

Y. ABRAMS,
“COMPLICATIONS OF COINFECTION WITH BABESIA AND LYME DISEASE AFTER SPLENECTOMY”

Coinfections could, thus, increase vulnerability to the emergence of new parasites by facilitating species jumps, if the coinfected portion of a population provides favourable conditions for an emerging parasite to adapt to a new host species.

A. GRAHAM, I. M. CATTADORI,
J. O. LLOYD-SMITH, ET AL.,
“TRANSMISSION CONSEQUENCES OF COINFECTION:
CYTOKINES WRIT LARGE?”

I first became interested in bacterial diseases in the early 1990s after reading about the emergence of resistant bacteria in hospitals. Having studied mathematics, I well understood what an exponential growth curve meant. I could see as well as anyone that we had only a short period of time in which to begin to address the problem.

As I studied more deeply, I began to be aware not only of resistant bacteria, the majority of which flow from hospital settings (and large, commercial farms) into the general community, but also of diseases emerging in the human population due to overpopulation and the environmental disruption that causes. Lyme was among the earliest of the emerging diseases that caught my attention and, as time went on, the coinfections that accompany Lyme (initially thought to be extremely uncommon) did so as well.

It became clear, the more I learned, that many of these emerging diseases were difficult to treat with conventional technological medicine, that the diagnostic tests were often unreliable, and that many of the organisms did not respond well to antibiotics. As well, and most regrettably, it slowly became obvious that many physicians had little knowledge of, or much interest in, these diseases.

I have been deeply immersed in the study of emerging and resistant bacteria for over two decades now. It is clear that while technological medicine still has a role to play, sometimes an important one, evolutionary changes are occurring that make many of our assumptions about such diseases and their treatment obsolete.

I was born in 1952 into an extended family that included many physicians, among them a surgeon general of the United States. For my family, “modern” medicine was the way to approach disease—the only way. Penicillin had become widely available in 1946, just after World War II, and new antibiotics were being discovered (seemingly) every day. Vaccines, too, were making history. The year I was born there were 58,000 new cases of polio, more than 3,000 of those infected with the disease died, and many of the others were permanently disabled—some terribly so. The next year, Jonas Salk announced the successful testing of his vaccine against polio. Then, in 1962, Albert Sabin introduced his oral vaccine, something that made mass vaccination easily possible. I still remember that long walk to the lunch room in elementary school, the long wait in line, and the sugar cube in the tiny, white paper cup.

The excitement of those days is very hard to explain to newer generations, but for people then, it seemed as if infectious diseases were going to be permanently eradicated. In fact, many researchers and physicians in the late 1950s and early 1960s, including my great-uncle Lee Burney, then surgeon general of the United States, and my grandfather David Cox, president of the Kentucky Medical Association, went so far as to loudly proclaim that the end of all infectious disease was upon us. A 1963 statement by the Australian physician Sir F. Macfarlane Burnet, a Nobel laureate, is typical. By the end of the twentieth century, he said, humanity would see the “virtual elimination of infectious disease as a significant factor in societal life” (Levy 1992, 3). And in 1970, one of my great-uncle’s successors, Surgeon General William Stewart, testified to Congress that “it was time to close the book on infectious diseases” (Levy 1992, 3). With satisfaction, physician David Moreau observed in a 1976 article in Vogue magazine that “the chemotherapeutic revolution has reduced nearly all non-viral disease to the significance of a bad cold” (Griggs 1991, 261).

They were wrong, of course, the victims of their own hubris and a deep lack of understanding of the natural world, most especially of bacteria. By the time Moreau’s comments appeared resistant bacterial diseases were already on the rise. A short 30 years later, with infectious diseases from resistant bacterial strains become rampant, the world came to face the specter of epidemic disease outbreaks more dangerous than any known in history. As bacterial resistance researcher and physician David Livermore recently put it, “It is naive to think we can win” (Bosley 2010).

There are two factors that have stimulated the emergence of potent bacterial disease organisms. The first is the tremendous overuse of antibiotics over the past 70 years. The second is the severe ecological disruption that increasing human population is causing.

In an extremely short period of geologic time the earth has been saturated with hundreds of millions of tons of nonbiodegradable, often biologically unique pharmaceuticals designed to kill bacteria. Many antibiotics (whose name literally means “against life”) do not discriminate in their activity but kill broad groups of diverse bacteria whenever they are used. The worldwide environmental dumping, over the past 65 years, of huge quantities of synthetic antibiotics has initiated the most pervasive impacts on the earth’s bacterial underpinnings since oxygen-generating bacteria supplanted methanogens 2.5 billion years ago. It has, according to medical researcher and physician Stuart Levy, “stimulated evolutionary changes that are unparalleled in recorded biologic history” (Levy 1992, 75). Bacteria had to evolve resistance. If not, due to their crucial role in the ecological functioning of this planet (and our own bodies), all life, including the human species, would already have been killed off by those very same antibiotics.

Ecological disruption has also played an extensive role. For example, the damage to wild landscapes, intrusions into forest ecosystems, the cutting of those same forests to make way for suburbs, and the damage to plant diversity and its crucial homeodynamic functions by suburban and agricultural intrusions have all had a place in stimulating the emergence of new disease groups. A study from the State University of New York is representative:

This study examined 11 years of surveillance data in New York State to measure the relationship between forest fragmentation and the incidence of human babesiosis. Adjusted Poisson models showed that increasing edges of contact between forested land and developed land, as measured by their shared parameters, was associated with a higher incidence of babesiosis cases, even after controlling for the total developed land area and forest density, and temperature and precipitation. Each 10-km increase in perimeter contact between forested land and developed land per county was associated with a 1.5% increase in babesiosis risk. Higher temperature was also strongly associated with increasing babesiosis risk, wherein each degree Celsius increase was associated with an 18% increase in babesiosis risk. (Walsh, 2013)

Human movement into previously unoccupied forest lands significantly increases the risk of infections, from both the ecological pressure put on the infectious organisms and the increasing numbers of people in that habitat. For example, studies of forest ticks in southern Poland have found that 77 percent carry Anaplasma, 60 percent Babesia, and only 3 percent Borrelia. Coinfection with Anaplasma and Babesia was found in 50 percent of the ticks. The more that such locations are inhabited by people, the more likely it is that they will get bitten and develop disease. Too, the unique grouping of the infectious organisms in that ecological zone determines the kinds of coinfection complex people will develop. Thus in that part of Poland there is a much higher chance of becoming infected with Babesia and Anaplasma than Lyme. This is something that physicians should understand: they live in a particular ecological habitat and the grouping of disease organisms in that habitat’s ticks is always going to be unique—as is the immune health of that region’s people.

Also crucial to the emergence of these coinfections is the reduction of wild predator populations (not only of mountain lions, for example, but of the bird species that eat insects and mice). This creates subsequent increases in the deer, mice, and insect populations that carry those bacterial pathogens, which in itself increases the movement of disease into human populations.

And finally, the reduction of large, wild mammal populations in undisturbed forest habitats plays its own important role. As fewer and fewer wild animal populations are available as hosts for the bacterial diseases that once were (mostly) limited to those populations, the bacteria have had no choice: they have had to jump species in order to find hosts in which to live. Because human beings now live in the habitat formerly occupied by those animals, many of the bacteria have moved into us. We are not inadvertent hosts. We are becoming primary reservoirs for many of these emerging diseases.

Unfortunately, bacterial resistance and ecological disruption can’t help but intersect—with, of course, terrible ramifications. Many of the primary coinfections of Lyme are closely related to some of the most potent resistant bacterial organisms known. They are all members of the Proteobacteria phylum, a large and closely related group of bacteria.

One branch of the Proteobacteria includes Bartonella spp., and another includes Ehrlichia spp., Anaplasma spp., Rocky Mountain spotted fever, and the other rickettsia—all of which are coinfections of Lyme. A different but closely related branch includes Klebsiella spp., E. coli, cholera organisms, Pseudomonas spp., Salmonella spp. (including Salmonella enterica, the cause of typhoid fever), and Shigella spp.—all now resistant to many antibiotics. It also includes Yersinia, the organism responsible for the plague, a bacteria transmitted by fleas much as Bartonella is. Still another branch includes the bacteria responsible for gonorrhea infections (also resistant), and another includes both Helicobacter and Campylobacter organisms.

There is strong evidence that both resistance and virulence factors are being shared among all members of this phylum. In other words, the various bacteria are teaching each other how to resist antibiotics and how to more easily infect people, thus making them sicker. They do this, usually, through sharing segments of DNA that have within them resistance and virulence information. Bartonella organisms, as an example, are often coinfective with many of the bacteria in this phylum and, in many instances, these kinds of multiple infections show a remarkable synergy during the disease process. In other words, the bacteria work together to reduce the effectiveness of the immune response and thus enable long-term infection.

In practical terms what all this means is that a great many more diseases are emerging out of the ecological matrix of the planet and infecting human beings. As well, many of them possess, or soon acquire, resistance to the majority of antibiotics that people use to treat bacterial diseases. And what they do together in the body is a great deal more complex than what any one of them does alone. The unique nature of the Lyme group of emerging infections, for example, is causing many researchers to refer to them not only as stealth pathogens but as second-generation pathogens. That is, they are very different than the bacteria (first-generation pathogens) for which antibiotics were created in the latter half of the twentieth century.

One of the most important understandings now facing us is accepting the limits of pharmaceuticals in the treatment of many of these emerging diseases. While antibiotics do still have a role, sometimes a very important one, they can no longer be relied on to provide the sole response to these kinds of infections as they spread through the human population. We have to approach treatment with a more sophisticated eye.

There are two important aspects to this. The first is realizing that single-treatment approaches, most of which were developed out of an inaccurate nineteenth- and early-twentieth-century bacterial paradigm and were based on identifying the bacterial pathogen involved and killing it (i.e., monotherapy), are going to have to be abandoned as the primary method of treating these kinds of diseases. (Something that newer generations of physicians, especially in countries other than the United States, are beginning to understand.) The second is coming to understand just what the bacteria do in the body and then designing a treatment protocol that is specific in counteracting what the organisms do. In essence this means designing treatment protocols that address bacterial cytokine cascades, the particular health or non-health of the person’s immune system, and the specific symptom picture that is reducing the quality of the person’s life. Combined with antibacterials, of whatever sort, this creates the most sophisticated basic approach to the treatment of bacterial diseases. (If you add to that approach sophisticated human-to-human interactions oriented around deep caring and personal presence, something most physicians do not understand, you have the core of the most elegant and potent paradigm of healing disease that can occur.)

Some additional sophistications can occur for those who wish to go even deeper. Among them are the synergy that occurs among the healing agents that are used and the synergy that exists between the different bacteria. The use of healing agents (pharmaceuticals or herbs) always involves synergy between the agents used—though this is rarely addressed in a positive light. It’s usually the side effects of a drug combination or drug/herb combination that are highlighted. However, herbs are synergistic with each other and can be synergistic with pharmaceuticals. For example, Chinese skullcap (Scutellaria baicalensis) root and licorice (Glycyrrhiza spp.) are synergists; they enhance the action of other herbs with which they are combined. They can, as well, enhance the action of pharmaceuticals. For example, Japanese knotweed (Polygonum cuspidatum) root, when used along with formerly ineffective antibiotics, can enhance the drugs’ actions enough to make them effective.

As well, the microbial pathogens are often synergistic with each other. That is, when an infection involves two or more Lyme-group organisms, the impacts on the body are often more severe. And this increase in severity is not additive, it is synergistic. This means that a simple linear approach will not give you an understanding of what the pathogens are doing in the body. As Telfer et al. (2010) comment:

Most hosts, including humans, are simultaneously or sequentially infected with several parasites. . . . Indeed, effects are typically of greater magnitude, and explain more variation in infection risk, than the effects associated with host and environmental factors more commonly considered in disease studies. We highlight the danger of mistaken inference when considering parasite species in isolation rather than parasite communities. . . . Single parasite studies may yield incorrect or incomplete conclusions. Nonetheless, most epidemiological studies, in animals and humans, still focus on single species.

COINFECTION DYNAMICS

To generate sophisticated, reliable inverventions with these second-generation bacteria, there are a number of important dynamics to understand. The primary ones are understandings of the specific cytokine cascades that occur, the immune health (and preexisting conditions) in the host, the synergy between the various microorganisms, and their synergy with the vector of transmission.

Cytokines

The past several decades have seen a shift in the way many researchers (but regrettably few physicians) are approaching disease, nowhere more so than with the stealth pathogens that, due to their nature, often cause a wide range of symptoms. Researchers Ian Clark et al., for example, have done some marvelous work on the dynamics of cytokines specific to various disease conditions, especially malaria and its close relative babesiosis. They note:

It is our view that focusing on malaria [and babesiosis and Lyme] in isolation will never provide the insights required to understand...