Learning About Lyme Disease by Dr. Ola Buhr
Learning About Lyme Disease by Dr. Ola Buhr
In this newsletter I will be covering the topic of Lyme disease. An entire book can be written about the bacterium Borrelia burgdorferi, that is the cause of Lyme disease; however I will try to be as concise as possible and include the most pertinent and applicable information for the reader. Within this article, I will discuss the characteristics of this bacterium and its stealth abilities to invade the human host, briefly discuss co-infections that can exist alongside Lyme disease, laboratory testing for this microorganism, post-Lyme disease syndrome (PLDS), as well as the infamous Chronic Lyme disease. Some of this information may sound a little scary, however knowledge is empowering and there are ways we can protect ourselves from this highly adept pathogen. I also want to mention that there is hope out there for those who are affected by Chronic Lyme disease. 
Borrelia burgdorferi is an anaerobic (meaning it dislikes oxygen) gram-negative spirochete, which literally means, coiled hair. Under the microscope it looks like a very active little worm with many hairs (flagella) that support its rapid motility and chemotactic properties. This unusual bacterium was discovered in 1981 under the microscope of Willy Burgdorfer Ph.D. who isolated the spirochetes from the Ixodes tick. Spirochetes are ancient bacteria and have been around for billions of years. They were even found in “Otzi the iceman” who was discovered in 1991 in the Tyrolean Alps and lived 5,300 years ago. Borrelia burgdorferi cannot live without a host. It resides inside of arthropods such as ticks (aka. vectors). Vectors are typically biting insects that spread microbial pathogens from one animal (host) to another. In other words arthropods (such as ticks) are the transport vehicles for these little “parasite-like” bacteria. Here is a rather unsettling piece of information; Borrelia species (yes, there are several of them) have not only been found in ticks, but also in mosquitoes, biting flies, mites, fleas, and in arthropod feces. “Transmission to humans has been documented from biting flies (Connecticut and Germany), from mites (Russia), and to hamsters by mosquitoes.” (Buhner p. 32) More research still needs to be done regarding these other insect vectors and their ability to transmit the bacterium. It is known that the Ixodes genus of tick is the most common and most well studied arthropod to transmit Borrelia burgdorferi (among other Borrelia species).
Borrelia burgdorferi is capable of living in a multitude of environments and is known to use up to 300 different animal species as their hosts. (The white-footed mouse and deer are definitely not the only ones.) Birds are very involved in widely disseminating these microorganisms throughout the world (primarily via their migration routes). Not only do we see this play out internationally, but within North America as well when the birds migrate north to south and back north again. The ticks (which are infected with the spirochetes) drop off the birds just in time to find a new reservoir. These “reservoirs” include many ground-dwelling mammals, lizards, large animals such as bear and elk, as well as farm animals, and our beloved pets (cats and dogs). These spirochetes have been found in seabirds and penguins; they have been documented in the Subarctic and Arctic regions especially since ticks can adapt to very cold environments (-22 degrees Fahrenheit) all the while carrying the Borrelial bacteria. Therefore, “there is no land mass on this planet where Borrelial organisms do not exist nor act to infect people, their companion animals, or wild animal species.” (Buhner p. 97) Of course there are the notoriously endemic areas where Lyme disease is most prevalent and these include the Northeastern U.S., Northern California, Southeastern U.S., and the Wisconsin/Minnesota region. Just because one doesn’t live in a Lyme endemic area doesn’t mean he or she cannot get Lyme disease, every state is affected.
So what is Lyme disease? Lyme disease was first recognized in the mid 1970s when a group of children began experiencing arthritis in a small town of Lyme, Connecticut. Physicians initially misdiagnosed it as juvenile rheumatoid arthritis until a group of highly concerned mothers pushed for further investigation at Yale University. They found that the organism associated with Lyme disease was the bacteria Borrelia burgdorferi. Once Borrelia enters its host (via an arthropod vector – most commonly a tick) it can cause a wide range of symptoms that affect many different areas of the body. Most common initial symptoms are flu-like and tend to occur in late spring and summer. We have to remember that a bull’s-eye rash (also known as a target lesion or erythema migrans ‘EM’ rash) only occurs in 30 percent of cases in the initial stages of infection, (this is because only some genotypes of Borrelia burgdorferi can actually generate the rash). As I’ve already mentioned above there are other species of Borrelia and many of these species cause relapsing fever, and this is different from Lyme disease. The Tick-Borne Relapsing Fever (TBRF) occurs from species such as: Borrelia miyamotoi, Borrelia hermsii, Borrelia turicatae (just to name a few), which are also transmitted by ticks.
Various organ systems can be affected such as joints, the nervous system including the brain, spinal cord, and peripheral nerves, the heart, and even skin. How can so many areas of the body be involved? This is because the spirochetes have an affinity for collagenous tissues; these prime locations provide the best sustenance and growth conditions for the organisms to “divide and conquer.” Lyme disease can mimic many disease complexes such as arthritis, Alzheimer’s dementia, multiple sclerosis, schizophrenia, severe unremitting anxiety and depression, chronic fatigue syndrome, and fibromyalgia just to name a few. This is why Lyme disease is referred to as the “Great Imitator.” Unfortunately, relatively poor diagnostic tests exist, and this can make the condition very difficult to diagnose.
Why is Lyme disease so difficult to diagnose? There are several reasons. “During the first 2-4 weeks of infection only about half of infected people produce measurable antibodies to Lyme spirochetes. The spirochete numbers may be so low that they do not show on even the most sensitive tests; they often cannot be found even with biopsy. Additionally, antibiotic therapies can cause the motile spirochete levels, already low, to drop by a factor of one thousand in the body, making detection of any remaining spirochetes nearly impossible by any means. Antibody response can be weak or nonexistent at different stages of the disease in different people.” (Buhner p. 47) Lyme serology testing using the two-tiered testing process (ELISA and western blot) as recommended by the Centers for Disease Control (CDC) is sensitive only 50 to 75 percent of the time. Current studies reveal, “The tests are not reliable and, even at best, only show about a 60 percent positive infection rate even in groups clinically known to be infected.” (Buhner p. 50)
Rates of Lyme disease have been increasing steadily. In 2004 the CDC was publishing statements “that only 20,000 new Lyme infections were occurring yearly… [however] in response to tremendous pressure from researchers and Lyme support groups, in 2013 the CDC altered that figure, finally agreeing that, at least, 300,000 infections were occurring every year in the United States.” (Buhner p. 38) Why are we seeing a rise in Lyme disease incidence? Well, to be frank, there is a “human-generated ecological disruption” happening on our planet. As a human species we have heavily fragmented our environment through urban development and suburban sprawl. In essence we have encroached upon the habitats of many animals, insects, and microorganisms. Humans have significantly altered the ecological landscape and have dramatically risen in population. Secondly, climate change is becoming more a factor. Cities now form “urban heat islands” which ticks prefer and thrive in; therefore those arthropods can be found in abundance in our city parks, green belts, and cemeteries. A 2014 study by Buczek A. revealed, “microclimate conditions and pollution within urban heat islands can affect the abundance and activity of Ixodes ricinus nymphs and females which more frequently attack humans and medium-and large-size animals.”
Newer research has revealed that transmission times of Borrerial organisms occur much faster than previously thought. Most physicians have the understanding that removing an attached tick within 48 hours will prevent Lyme disease, (unfortunately this knowledge is outdated and was gathered from very early research on the topic). Recent work by scientist Michael Cook in the UK has revealed that Borrerial organisms can be transmitted via a tick in as little as 10 minutes and ranging up to 72 hours, also transmission times of under 16 hours were observed to be the most common. One more scary detail (I’m sorry)… ticks don’t always carry just one bacterium. Ticks are able to transmit a variety of coinfections to a host mammal. Coinfections can occur in roughly 20 percent of Lyme disease cases and the most common pathogens are: babesia, bartonella, chlamydia, ehrlichia, mycoplasma, rickettsia, and last but not least anaplasma. Symptoms tend to be more severe and with higher fevers (or even relapsing fevers) when one or more of these little guys happen to hitch a ride.
Another (maybe not so awesome fact) is that Borrelia burgdorferi has one of the largest genomes out of any bacterium. Therefore, the more DNA an organism has, the more it can be re-arranged and re-structured forming numerous different strains, genotypes, and subspecies. In other words, the Borrelia burgdorferi in Connecticut is different from the Borrelia burgdorferi in Wisconsin, which is different than the Borrelia burgdorferi in California and so on. This may also be the reason that one antibiotic (or herb) works for one person, but not for another, as well as offers an explanation for creating different symptom pictures among people. Buhner described this perfectly when he stated, “When you get Lyme disease, you don’t have just one bacterial species in your body making you sick but rather an infectious swarm of similar but not identical genetic variants.” (p. 29) This is one reason why Borrelia burgdorferi is such a stealth pathogen; through its various genetic manipulations it can evade, suppress, or even activate different branches of our immune system for its own means. It is also highly motile and a faster little swimmer than our own white blood cells. Not only is it hard to catch and be engulfed by our white blood cells, it has the ability to make biofilms and wall itself off from being captured. These little motile creatures are “designed for swimming through liquid environments such as blood, lymph, cerebral spinal fluid, and for squirming and tunneling through viscoelastic gel environments like the extracellular matrix and other connective tissues.” (Berndtson 2013) One more interesting piece of information: when Borrelial organisms feel threatened (when they are under attack with antibiotics for example) they can morph into little cysts and stay dormant within the human body for up to ten months. TEN months! It only takes about one minute for them to form into these little round bodies.
There is still a lot of controversy as to whether or not Chronic Lyme or post-Lyme disease syndromes even exist. Extensive national and international research literature describes numerous studies regarding people who suffer from Chronic Lyme and describes how certain people treated with conventional antibiotic regimens relapse into a chronic disease state when those drugs are discontinued. Symptoms tend to improve while people are on antibiotics; unfortunately people stay on antibiotics for many months to years to achieve symptom suppression. Certain groups of people also suffer from something called post-Lyme disease syndrome, which means that they’ve been “successfully treated with antibiotics but, due to bacterial damage to organ structures, still suffer a range of symptoms.” (Buhner p. 66) Therefore the spirochetes damage the collagen tissues within the body especially those in the central nervous system. Nerve cells take a long time to repair themselves (and they also need the proper building blocks to do that adequately). Unfortunately autoimmune processes can also occur in the background setting of Lyme disease. As the Lyme bacteria attack cells in our body those cells break down and release their inner contents. Our white blood cells recognize those contents as foreign (because they’re not supposed to belong outside of our cells) and mount an immune attack against our body’s own proteins.
What are some things we can do to prevent Lyme disease? Get into the habit of daily routine tick checks during the spring and summer season (remember, it doesn’t even need to be a hike in the woods for you to get exposed). Purchase a natural tick repellant and apply it when going outside. (You can make your own at home using a variety of essential oils and 95 percent grain alcohol.) The single most important thing we can do to minimize Lyme disease infection is to keep our immune systems as strong as possible. This means eating a nutrient-dense diet, getting a good amount of sleep, staying away from environmental toxins, and managing stress appropriately (i.e. not burning the candle at both ends).
Treatment regimens are different in acute versus Chronic Lyme disease situations and it is beyond the scope of this article to cover those details. If you are suffering from Chronic Lyme disease and feel as though you may not have had adequate treatment, it would be wise to seek out a ‘Lyme literate’ practitioner, one who is well versed in both antibiotic and herbal treatments for Borrelia burgdorferi and possible coinfections. You can visit the website www.ilads.org for more up-to-date information on the topic. I also strongly recommend the book “Healing Lyme” by Stephen Harrod Buhner to learn everything there is to know about Borrelia burgdorferi.
References
Berndston K. Review of evidence of immune evasion and persistent infection in Lyme disease. Int J Gen Med. 2013;6:291-06.
Buczek A. et al. Threat of attacks of Ixodes ricinus ticks and Lyme borreliosis within urban heat islands in South-Western Poland. Parasites Vectors. 2014;7:562.
Buhner, Stephen Harrod. Healing Lyme. Silver City: Raven Press, 2015. Print.
Horowitz, Richard. Why Can’t I Get Better? Solving the Mystery of Lyme and Chronic Disease. New York: St. Martin’s Press, 2013. Print.
