Healing Lyme Disease Coinfections

Complementary and Holistic Treatments for Bartonella and Mycoplasma

Stephen Harrod Buhner

• Publisher: Healing Arts Press
• Year: 2013
• ISBN:
  9781620551370
• Topic: Médecine
• Subtopic: Médecine alternative et complémentaire

A guide to the natural treatment of two of the most common and damaging coinfections of Lyme disease--Bartonella and Mycoplasma • Reveals how these conditions often go undiagnosed, complicate Lyme treatment, and cause a host of symptoms--from arthritis to severe brain dysfunction • Outlines natural treatments for both infections, with herbs and supplements for specific symptoms and to combat overreactions of the immune system • Reviews the latest scientific research on Bartonella and Mycoplasma coinfections and how treatment with antibiotics is often ineffective Each year Harvard researchers estimate there are nearly 250, 000 new Lyme disease infections--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. Two of the most common and damaging Lyme coinfections are Bartonella and Mycoplasma. Nearly 35 million people in the United States are asymptomatically infected with each of these pathogens, and at least 10 percent will become symptomatic every year--with symptoms ranging from arthritis to severe brain dysfunction. Distilling hundreds of peer-reviewed journal articles on the latest scientific research on Bartonella, Mycoplasma, and Lyme disease, Stephen Buhner examines the complex synergy between these infections and reveals how all three can go undiagnosed or resurface after antibiotic treatment. He explains how these coinfections create cytokine cascades in the body--essentially sending the immune system into an overblown, uncontrolled response in much the same way that rheumatoid arthritis or cancer can. Detailing effective natural holistic methods centered on herbs and supplements, such as the systemic antibacterial herb Sida acuta, which acts to protect blood cells from invading organisms, he reveals how to treat specific symptoms, interrupt the cytokine cascades, and bring the immune system back into balance as well as complement ongoing Lyme disease treatments.

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.

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.

ANDREA GRAHAM 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 have flowed from hospital settings into the general community, but also of diseases emerging in the human population due to overpopulation and the environmental disruption it causes. Lyme was among the emerging diseases that caught my attention and, as time went on, the coinfections that often accompany Lyme infection did 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 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 now 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 the end of all infectious disease was just around the corner. 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 the 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 David 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 extreme ecological disruption that increasing human population density 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. Increasing damage to wild landscapes, intrusions into forest ecosystems, the cutting of those same forests to make way for suburbs, damage to plant diversity and its crucial homeodynamic functions by suburban and agricultural intrusions, the reduction of wild predator populations, and the increases in deer, mice, and insect populations as a result, have also put tremendous pressure on bacterial populations. 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 no choice; they have to jump species—they have to find new hosts. Because human beings now live in the habitat formerly occupied by those animals, many of the bacteria are now learning to live in human beings.

Unfortunately, both 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 genomically close group of bacteria.

One branch of the Proteobacteria includes bartonella (Bartonella spp.), and another includes Ehrlichia spp., Anaplasma spp., Rocky Mountain spotted fever, and the other rickettsias—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 spp., 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 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. And many of them possess, or soon acquire, resistance to many or most of the 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. All this can make them very difficult to treat.

One of the most important understandings now facing us is accepting the limits of pharmaceuticals in the treatment of many of these 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 diseases. 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 are 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 U.S., 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—exactly. In essence this means designing treatment protocols that address bacterial cytokine cascades, the particular health or nonhealth 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, among them the synergy that occurs among the healing agents that are used and the synergy that exists between the different bacteria. That is, we must learn to look at what happens when there are multiple infectious bacteria, all coming into the body from, say, a tick bite. Studies on the complex interactions that occur between coinfectious bacteria are uncommon but, when combined with the experience of clinicians, they are revealing.

COINFECTION DYNAMICS

Coinfective bacteria interact both in the vector that spreads them (for example a flea or tick) and then in the host they are transferred to. One of the better articles on this is “Transmission consequences of coinfection: Cytokines writ large?” by Andrea Graham et al. (2007). The authors propose a unique approach to understanding the dynamics of coinfections. Instead of focusing on the organisms themselves, they suggest focusing on the cytokine cascades that the organisms produce in the body. They comment, “When the taxonomic identities of parasites are replaced with their cytokine signatures, for example, it becomes possible to predict the within-host consequences of coinfection for micro-parasite replication” as well as symptom picture, treatment approaches, and treatment outcomes.

Cytokines are small cell-signaling molecules released by the immune system, and the glial cells of the nervous system, that are important in intercellular communications in the body. In practical terms, when a bacteria touches a cell, the cell gives off a signal, a cytokine, that tells the immune system what is happening and what that cell needs. Each type of infectious bacteria initiates a particular kind of cytokine cascade, that is, an initial and very powerful cytokine is released into the body, that initial cytokine stimulates the production of others, and those still others—all of which have potent impacts on the body. It is these cytokines, in fact, that create most of the symptoms that people experience when they are ill. What I explore in the more technical material on what these coinfections do when someone is infected is their cytokine cascades. This determines many of the most effective approaches to treat the conditions they cause—which I go into in the protocol section. And, of course, the impact of the vector of transmission plays a crucial part in this as well.

Bacteria have learned to work synergistically together or, for instance, to take advantage of the biologically active components in tick saliva in order to facilitate avoidance of the immune system—tick saliva itself begins a cytokine cascade that Lyme bacteria take advantage of in order to more successfully infect a new host. Although little research has occurred on louse and flea feces, two main routes of infection for bartonella, researchers comment that a similar dynamic might be playing out here as well: “It is also quite likely that under natural conditions components of the flea feces other than B. henselae may enhance the development of Bartonella-induced lympoadenopathy and thus enable the onset of disease at a lower dose of infection in humans” (Kunz et al. 2008). Given the very long evolutionary relationship between ticks and Lyme or fleas and bartonella, it is not surprising that the bacteria have learned to utilize both to assist their infection of new hosts.

Bartonella species, like many infectious bacteria, utilize the immune system of whatever mammal they infect as part of their infection strategy. They essentially use our own body’s response to them to promote their agenda. As Graham et al. (2007) note: “The influence of cytokines on effector responses is so powerful that many parasites manipulate host-cytokine pathways for their own benefit,” as is indeed the case with bartonellas and mycoplasmas. Most crucially, the authors continue, “The magnitude and type of cytokine response influence host susceptibility and infectiousness. Susceptibility to a given parasite will be affected by cytokine responses that are ongoing at the time of exposure, including responses to pre-existing infections.” In other words, the bacteria use the inflammatory processes already occurring in the body (e.g., if you have preexisting arthritis) to facilitate successful infection. This is more pronounced if infection occurs by more than one organism. Graham’s research confirmed that, as the researchers put it, “Coinfection increases the reproductive number for the incoming parasite species and facilitates its transmission through the host population.” In other words, while the immune system is often compromised by the cytokine dynamics initiated by one type of bacteria, multiple, simultaneously initiated cascades are more potent in their impacts—infection is much more easily accomplished. In addition, you begin to get assaults on multiple body systems. If bartonella is a coinfection with Lyme, for example, what you then get is assault on and resultant degradation of the collagen systems of the body by the Lyme spirochetes while a simultaneous assault on red blood cells occurs with continual subversion and abnormalization of endothelial cells and their functions. So, the infected person is battling not only Lyme arthritis or neurological Lyme (both caused by collagen degradation) but a red blood cell infection (with potential anemia and lowered oxygen availability in the blood) and abnormal endothelial cell growth in the blood vessels themselves.

But the bartonella bacteria also use what the Lyme bacteria are doing for their own purposes. Once Lyme spirochetes damage collagen tissues, for instance in the joints of the knee, the body sends CD34+ cells to that site to help repair the damage. This is a normal part of the healing process when collagen is damaged. But bartonellas typically invade CD34+ cells, so some of those CD34+ cells will be infected and the bartonellas will take advantage of the local inflammation to establish a colony of their own in that location. The existing inflammation actually facilitates their growth. Once established, they will begin their own cytokine cascade, which will itself contribute to even more collagen degradation at that location.

Were the infected person already suffering a preexisting inflammation in that joint location (as is common in the aged), the process is even easier for the bacteria. The inflammation would, by itself, stimulate the movement of infectious bacteria to that location.

If you add other coinfectious bacteria to the mix, the picture becomes even more complicated. For example, if Babesia bacteria are present then, once bartonella bacteria enter the body, the red blood cells are going to have two organisms infecting them, thus increasing the negative impacts on red blood cells. This is, as Graham et al. (2007) comment, more common than otherwise: “Hosts that are coinfected by multiple parasite species seem to be the rule rather than the exception in natural systems and some of the most devastating human diseases are associated with coinfections that challenge immune response efficacy.”

The foundations of this phenomenon are ecological more than anything else. As Graham et al. (2007) observe, “Coinfections could, thus, increase vulnerability to the emergence of new parasites by facilitating species jumps if the coinfected portion of a population provides favorable conditions for an emerging parasite to adapt to a new host species.”

Another very fine paper on this subject, by S. Telfer et al. (2010), echoes Graham et al. when its authors note, “In natural populations ‘concomitant’ or ‘mixed’ infections by more than one parasite species or genotype are common. Consequently, interactions between different parasite genotypes or species frequently occur. These interactions may be synergistic or antagonistic with potential fitness implications for both the host (morbidity and/or mortality) and parasite (transmission potential).” In other words, if you want to successfully treat someone who is infected with a vector-borne infection you need to realize up front that it is usu...