[vc_row rt_row_background_width=”default” rt_row_style=”light-style” rt_row_borders=”” rt_row_paddings=”true” rt_bg_image=”3874″ rt_bg_effect=”classic” rt_bg_image_repeat=”repeat” rt_bg_size=”cover” rt_bg_position=”right top” rt_bg_attachment=”scroll” rt_bg_video_format=”self-hosted” rt_bg_overlay_color=”rgba(255,255,255,0.6)”][vc_column rt_wrp_col_paddings=”false” rt_border_top=”” rt_border_bottom=”” rt_border_left=”” rt_border_right=”” rt_border_top_mobile=”” rt_border_bottom_mobile=”” rt_border_left_mobile=”” rt_border_right_mobile=”” rt_bg_image_repeat=”repeat” rt_bg_size=”auto auto” rt_bg_position=”right top” rt_bg_attachment=”scroll”][vc_custom_heading text=”Neurotoxic Disorders:” font_container=”tag:h2|text_align:left|line_height:150%25″ use_theme_fonts=”yes”][vc_custom_heading text=”Reactivity to Lyme, Coinfections, Molds, and Petrochemicals” font_container=”tag:h3|font_size:150%25|text_align:left” use_theme_fonts=”yes”][/vc_column][/vc_row][vc_row rt_row_background_width=”default” rt_row_style=”alt-style-1″ rt_row_borders=”” rt_row_paddings=”true” rt_bg_effect=”classic” rt_bg_image_repeat=”repeat” rt_bg_size=”cover” rt_bg_position=”right top” rt_bg_attachment=”scroll” rt_bg_video_format=”self-hosted” rt_bg_color=”#ffffff”][vc_column rt_wrp_col_paddings=”false” rt_border_top=”” rt_border_bottom=”” rt_border_left=”” rt_border_right=”” rt_border_top_mobile=”” rt_border_bottom_mobile=”” rt_border_left_mobile=”” rt_border_right_mobile=”” rt_bg_image_repeat=”repeat” rt_bg_size=”auto auto” rt_bg_position=”right top” rt_bg_attachment=”scroll” offset=”vc_hidden-sm vc_hidden-xs”][content_icon_box heading=”” heading_size=”h6″ icon_position=”left” icon_style=”style-3″ link_target=”_self” icon_name=”icon-attention”]
This information on this website is provided for educational purposes only, and is not intended to diagnose or treat an individual. Please understand that Dr. Anderson and Gordon Medical cannot prescribe or recommend treatment to patients they have not seen. If you are a Gordon Medical patient with questions, contact your Practitioner.
[/content_icon_box][/vc_column][/vc_row][vc_row rt_row_background_width=”default” rt_row_style=”alt-style-1″ rt_row_borders=”” rt_row_paddings=”true” rt_bg_effect=”classic” rt_bg_image_repeat=”repeat” rt_bg_size=”cover” rt_bg_position=”right top” rt_bg_attachment=”scroll” rt_bg_video_format=”self-hosted” rt_bg_color=”#ffffff”][vc_column rt_wrp_col_paddings=”false” rt_border_top=”” rt_border_bottom=”” rt_border_left=”” rt_border_right=”” rt_border_top_mobile=”” rt_border_bottom_mobile=”” rt_border_left_mobile=”” rt_border_right_mobile=”” rt_bg_image_repeat=”repeat” rt_bg_size=”auto auto” rt_bg_position=”right top” rt_bg_attachment=”scroll” rt_padding_left=”2%” rt_padding_right=”2%”][rt_heading style=”style-1″ size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Introduction[/rt_heading][vc_column_text]By Wayne Anderson ND – Originally published in the Townsend Letter – June 2012 – interview by Nancy Faass, MSW, MPH
We originally thought of Lyme disease as primarily an infection caused by the spirochete Borrelia burgdorferi. In the decades that followed, researchers began identifyingother tick-borne bacteria and toxins that frequently accompany Lyme infections. We have come to realize that the symptoms which we once described as “Lyme disease” frequently involve other bacteria, such as Babesia, Bartonella, Ehrlichia, or Mycoplasma, or rarer species such as the Rickettsia group or tularemia. Transmitted in the digestive tract of ticks or fleas, these pathogens may be carried by cats, rats, mice, deer, and other animals, depending on the microbe. These pathogenic bacteria are among the smallest known life-forms on earth. Unlike most bacteria, they are harbored within the cell as a virus would be or within the interstices between the cells, making it difficult for the immune system to dislodge them.
Certain types of toxigenic mold can also be a major factor in neurotoxic conditions. Petrol-based pesticides, insecticides, and solvents are a third major contributor to neurotoxic inflammation. The extensive neurotoxic effects of pesticides, for example, have been well documented. Heavy metals are sludge toxins with some of the same neurotoxic effects as petrol-based chemicals. Mercury, lead, cadmium, and arsenic involve similar neurotoxic mechanisms of action and can cause similar symptoms.
Microbes and toxins stored in fat tissue: Lyme, molds, and petrol-based chemicals all contain lipid molecules. The lipid molecules in the structure of the pathogens and toxins are attracted to the fat in our bodies (lipophilic) and can become embedded in that fat tissue and persist.[/vc_column_text][vc_empty_space][rt_heading style=”style-1″ size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Neurological inflammation[/rt_heading][vc_column_text]These neurotoxins are particularly attracted to the lipids in the myelin sheath, which surrounds all the nerves in the body. Once they are absorbed into the myelin sheath, although they do not destroy it, they accumulate and can serve as chronic irritants to the underlying nerve. Similarly, the brain contains high fat content – 50% fat and 50% nerve. When these toxins are absorbed into fatty tissue of the brain, they can irritate nerve cells within the brain and impair brain function.[/vc_column_text][vc_empty_space][rt_heading style=”style-1″ size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Intracellular Bacteria and Toxins[/rt_heading][vc_column_text]Many of these intracellular pathogens proliferate very slowly, over months, years, or even decades. They gain access to the body’s cells through a simple process and can remain for years.
Step 1. Toxic build-up: Following exposure, the toxin is absorbed through the cell membrane and penetrates the cell. Our own cell membranes consist of two layers of fat (bilipid), which normally provide very effective gatekeeper functions, allowing into the cell what should be allowed as a nutrient and repelling what should be rejected as a toxin. However, because the pathogens also contain lipid molecules, they confuse the gatekeeper mechanism of cell membranes, penetrating the cell wall, and essentially hijacking the cell.
Step 2. Immune reactions: The immune system is activated and tries to destroy or remove the toxins harbored within the cell, but frequently cannot do so. When the system cannot break up or destroy these microbes, inflammation results. As these efforts by the immune system become more and more intense, activity shifts from cellular immunity to antibody production. This frantic immune activity is often associated with the symptoms of autoimmune conditions.
Step 3. Attempts at detoxification: Neurotoxins are typically detoxified through the methylation pathway. This pathway involves numerous genetic strands that all coordinate to remove waste from within the cell, through the cell membrane, to move toxins back into the bloodstream.
If toxins build up within the cell, the cell’s function is diminished. These irritants can dysregulate the mitochondria, lowering energy production by the cell. No matter where the cell is located in the body, there will be reduced function or even lack of function. If the toxic cells are stored in muscle tissue, that may be experienced as weakness, pain, or an array of symptoms resembling fibromyalgia. If the toxins have accumulated within the brain, that will create symptoms related to functional neurological deficits such as impaired memory, cognitive processing, and brain fog, as well as mood instability resulting in depression or anxiety.
Initially these toxins do not damage the cells: they primarily compromise the function of cells. The function of entire systems may also be compromised, particularly systems that maintain homeostasis – the brain and nervous system, as well as the immune and endocrine systems and the gut. Ultimately, the neurotoxic disorders also result in inflammation. However, before inflammation is apparent, there will be a compromise in function. Clinically, we often note this in retrospect, because many patients are able to compensate for the lack of function for a time, without any evidence of inflammation.[/vc_column_text][vc_empty_space][rt_heading style=”style-1″ size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Progression of Neurotoxic Disorders[/rt_heading][vc_column_text]In the past, Lyme-literate clinicians thought in terms of a staged disease. However, I have come to believe that to think in terms of detailed stages can be a distraction. When an initial acute infection is not fully resolved, neurotoxic illness can progress with tremendously varied presentation. That said, there are two subsequent patterns of development that are noteworthy: rapid or gradual progression.
Rapid progression: Approximately 15% of the patients whom I see appear to have some form of genetic vulnerability to neurotoxins. In these patients, unresolved Borrelia or coinfections can evolve into a second stage with intense emergent symptoms, which can become extremely debilitating within a year or two.
Gradual progression: As many as 85% of my patients with unresolved Borrelia and neurotoxic infections tend to have conditions that develop slowly over years or even decades. For these patients, the infection is exacerbated much later in their lives, typically following some type of catastrophic event that reduces or suppresses immune function. Immune suppression could be emotional, resulting from a divorce or the death of a loved one or could be primarily physical, such as an accident, an injury, a major infection, menopause, or andropause.
The illness will take an individual course and presentation, influenced by the patient’s genetics, comorbidities, emotional stresses, and general level of health. As a result, more dysfunction is observed in some people and less in others.[/vc_column_text][vc_empty_space][rt_heading style=”style-1″ size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Systemic Effects[/rt_heading][vc_column_text]The typical features of neurotoxic illness bear much in common. We now realize that to speak of Lyme disease in isolation is in a sense simplistic, because these are shared mechanisms triggered by a number of similar toxins and pathways.
Load dependent: Neurotoxic disorders tend to wear down the immune system due to their chronic presence and persistent nature. If the patient’s exposures are minor and the tick bite contained a weak strain of bacteria, the load is not great, and the immune system can simply fight it off. However, if there is compromise in any of the immune mechanisms, additional opportunistic infections can develop. If one contracts Lyme first and then has a mold exposure, that mold is going to have a greater impact. When a patient has 3 parts Lyme and 3 parts mold, he or she is 6 parts sick.
Neurologic effects: One of the commonalities of the neurotoxic pathogens is that they all produce some form of toxin that affects the brain and nervous system. Due to the nerve to fat ratio, there is a disproportionately greater effect on nerve tissue and the inflammation that they cause tends to be more exacerbated in the nervous system.[/vc_column_text][vc_empty_space][rt_heading style=”style-1″ size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Autoimmune Reactions[/rt_heading][vc_column_text]The toxins trigger an inflammatory response, stimulating the release of both anti-inflammatory and pro-inflammatory cytokines, generated by the immune system in its attempts to restore balance and reduce inflammation. As the system becomes upregulated, that typically causes a greater predominance of pro-inflammatory cytokines and autoimmune symptoms. This is the immune system spinning out of control – what would normally be a protective process becomes unproductive as the system becomes overwhelmed.
The most successful bacteria shut down certain aspects of immune function to assure their own survival and proliferation. In the case of Borrelia, the microbe can also cloak itself and effectively hide from the immune system. When these mechanisms are in play, the immune system may fail in its attempts to rid the body of the pathogens.
Unfortunately, it is the efforts of the immune system that result in the patient’s symptoms, which may be diagnosed as an autoimmune condition. This is the misfiring of the immune system, in its attempts to deal with toxins or microbes, harbored within the body’s cells. In cases of Hashimoto’s, we believe that the immune system may be combating infection or toxins within the thyroid. In this excessive response, the immune system eventually targets normal tissue of the thyroid, creating an elevated antibody level. I also believe that rheumatoid arthritis and even gluten intolerance can be caused by this type of exacerbated immune reaction.
When autoimmune disease is present, there can be value in reframing our view of immune function. If we focus on the challenge of combating these elusive stealth bacteria, we recognize the immune system as our ally. The system becomes our partner and one of the goals of patient care is to support immune function.[/vc_column_text][vc_empty_space][rt_heading style=”style-1″ size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Laboratory Testing[/rt_heading][info_box style=”info”]Disclaimer: It is important to indicate that this is simply a report of my clinical experience and by no means reflects the broader picture. These observations are drawn from the patients seen in my practice. In addition, there can be regional differences in the symptoms triggered and also differences from one subspecies of microbe to another.
GMA note: This article was published in 2012, and testing has advanced since then. Please talk with your practitioner about what is best in your individual case. [/info_box][vc_column_text]In the medical system, physicians are trained to diagnose primarily using laboratory testing. In fact, without confirmative lab results, a doctor is on shaky ground to make a diagnosis. That has been a major problem with Lyme disease, since to date there have not been any laboratory tests that are completely conclusive. Currently we have testing for fewer than 5% of the neurotoxic pathogens that have been identified by researchers.
Today, antibody testing is the gold standard for Lyme and the coinfections. Since antibody levels vary based on the relative severity of the infection and the length of time that the patient has been infected, they can serve as a good marker. However, they are not a direct measure of the organism, but rather an indication of the body’s response to the organism. Antibodies have been identified for Babesia, Bartonella, Ehrlichia, and Mycoplasma, but there are a surprising number of subspecies, and more are identified every year.
State of the testing: In terms of Babesia, we have the ability to test for two Babesia organisms, but more than 100 strains have currently been identified. For Bartonella, there are tests for two strains, although at least 26 have been identified. For Mycoplasma, there is only one test at this time, although hundreds of strains of Mycoplasma have been identified. Note that it takes years to develop a single test for a pathogen, and the researchers are discovering these microbes so quickly that the lab assessments cannot keep up.
Literally hundreds of intracellular bacteria have been identified by the researchers, with many strains and tremendous species diversity within these pathogen groups. Currently in the literature, the most reliable source of information is the veterinarians, who are tracking the subspecies of Bartonella. Essentially, we are learning that these microtoxic pathogens are much vaster than we ever imagined.
Cultures: Lab cultures are considered the most reliable form of testing in the infectious disease community. However, culturing Borrelia bacteria has proven very difficult and very expensive. Consequently, there has not been a commercially available culture, and thus Lyme diagnosis and treatment have had minimal importance in the scientific community, because there is no confirmatory testing. In fact, a range of tests have been developed, but they have also fallen short because there are so many spirochetes in the body that are nonpathogenic. The tests have not been able to differentiate a nonpathogenic spirochete from the pathogenic Borrelia spirochete. In terms of testing for other sources of neurotoxic illness, much of the testing for molds, petrol-based chemicals, and heavy metals is also unreliable. The good news is that within the past five months, the Advanced Systems Lab has developed a culture test for Borrelia using serum. The new test, which costs less than $600, involves DNA sequencing.
Chemicals: Urinalysis is available for chemicals, but the clinician must have a strong suspicion of which chemical to test for, because each test is specific to a particular chemical. Otherwise we are looking for a needle in a haystack. There are many thousands of petrol-based chemicals in the environment, so although there are panels of tests available for chemicals, unless the clinician has a strong suspicion of the probable exposure, there is no way to identify it.
Heavy metals: We do have good laboratory testing for metals, in the form of challenge testing using oral or IV chelating agents, collecting urine over 6 hours. Hair analysis can be done, but is less specific.
Environmental Relative Moldiness Index (ERMI): In terms of mold, we do not have a good test to evaluate levels of mold within the body: we can measure mold antibodies, but these tend to be variable. However, there is an effective test to evaluate mold within the home: the ERMI test. This assay is an evaluation of dust in the home and has been found to be a very accurate measure of the level of mold in the home environment.
Western blot antibody testing: Antibodies have been identified for Borrelia, Bartonella, Babesia, Ehrlichia, and Mycoplasma. Although the antibodies are not a direct measure of the organism, they do reflect the body’s response to the organism.
Public health departments use the western blot antibody test to confirm that a patient is Lyme/Borrelia positive or negative. This test has been the gold standard, so it is important to point out that not all western blots are equal. Integrative practitioners have relied on IGeneX for highly accurate and comprehensive testing, including the western blot, which IGeneX has refined to be much more accurate. Commercial western blot testing provided by LabCorp, Quest, and other labs tends to be less accurate. However, the mainstream medical community seems to discount IGeneX because it has so many positive test results. If one goes to Kaiser with an IGeneX positive, it will not accept the test result. For the record, IGeneX has passed the most stringent laboratory evaluations by the most stringent regulatory agencies. These assessments always show a high level of statistical significance and accuracy, confirmed in double-blind evaluations.
Frylab antibody testing: The Frylab, directed by Stephen Fry, is doing very good work in developing antibody testing, which uses blood smears and looks for elements in the blood that can be suggestive of Bartonella and Mycoplasma. Fry’s work includes testing using several different staining techniques.
PCR testing: PCR testing is provided by IGeneX and other labs as well. PCR can be very accurate, providing an evaluation based on just a few pieces of the genetic material of pathogens such as Borrelia or the coinfections. We do have PCR profiles on these microbes. The challenge is that the DNA of the pathogen must be present in that specific blood sample for the test to be positive, so there are many false negative tests as a result of PCR. However, when a PCR is positive, that is a highly accurate result.
Evaluation of cytokine levels: Neuroscience Laboratories has a very interesting test that evaluates cytokine levels associated with Borrelia, so the test is only for Borrelia. The lab cross-references antibody activity with elevated cytokine levels. Again, this is not a direct measure of the bacteria, but it can serve as a fingerprint indicating that the bacteria are present because it identifies the specific cytokines that are elevated.
Immune fluorescent testing: IGeneX also has a useful immune fluorescence test that involves staining the blood. If there is even a minute piece of genetic material in that blood, it will stain with a fluorescent illumination. The lab is able to image that fluorescent illumination and identify the organism as present or not.
Fluorescent immune sensitivity: Fluorescent immune sensitivity is now available for Bartonella and Babesia. Although this is an interesting test, it has limitations. As an analogy, think of sitting on a lake in a boat with a bucket. If one dips the bucket into the water, and there are fish in the bucket, clearly there are fish in the lake. However, the key question is, if there are no fish in the bucket, does this mean that there are no fish in the lake?
CD-57: LabCorp is the one lab that does a good CD-57. It is worth mentioning that in the past clinicians have tracked Lyme using the CD-57 (natural killer cell receptors on the surface of the lymphocytes). There can be some usefulness in this test, but again, it is limited because it is an indirect marker. It can be correlated with symptoms as a marker of how well the innate immune system is functioning. However, we are realizing that there are other factors that can affect the CD-57, so it is not a definitive test for Lyme. Although this test apparently indicates Borrelia, it is possible that these markers also reflect the presence of certain viruses and perhaps even mold. Consequently, the CD-57 is not completely conclusive, but can provide another aspect of the picture.
Indirect measures of Borrelia: There are a number of tests which use markers in the blood that serve as general indicators of inflammation, based on the work of Ritchie Shoemaker, MD. These markers can be useful in determining whether the inflammation is being caused by a neurotoxin. The tests do not differentiate the source, but because neurotoxins have similar mechanisms of action, they also affect certain lab values in terms of inflammation or dysregulation of the body’s systems, particularly in relation to the immune, endocrine, and nervous systems. These tests include:
- evaluation for complement components 3a and 4a
- MSH (melanocyte-stimulating hormone)
- VEGF (vascular endothelial growth factor)
- MMP9 (matrix metallopeptidase)
Ultimately, testing depends on cost. It becomes very expensive to perform the lab work, so the choice of testing depends on the patient’s funds. Clinicians certainly welcome all the information that they can get.[/vc_column_text][vc_empty_space][rt_heading style=”style-1″ size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Symptom Patterns[/rt_heading][vc_column_text]Our goal as practitioners is to accumulate as much information as possible regarding the health of the individual patient who sits in front of us. Identification of symptom patterns associated with the presence of specific pathogens can be useful in developing a hypothesis. These patterns are also helpful in testing that hypothesis with a challenge protocol.
The series of symptom presentations provided here are general, because every patient will be a little different in relation to how he or she manifests symptoms. Each patient’s symptoms will reflect that individual’s genetic vulnerabilities and health history. In my own practice, I use the following process to develop and assess patients.
- Gather as much information as possible: take a detailed history, ask key questions, perform a physical exam, and evaluate all relevant lab work.
- Create a hypothesis regarding the presumed pathogen.
- Challenge the patient with a therapeutic intervention that is as specific as possible to the suspected pathogen, making note of aggravated symptoms if the hypothesis is correct.
- Evaluate the patient’s response to the therapeutic challenge.
- Moderate the challenge dosage to minimize discomfort to the patient.
[/vc_column_text][vc_empty_space][rt_heading style=”” align=”” mobile_align=”” size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Borrelia [/rt_heading][vc_column_text]Borrelia burgdorferi is the specific bacterial spirochete associated with Lyme disease. It is important to treat acute Borrelia infections aggressively with antibiotics before they deepen and compromise immune function, enabling other opportunistic infections.
- transmission: most common tick-borne disease in North America; various species worldwide
- major symptoms: fatigue, pain, immune suppression
- exhaustive fatigue, achiness, poor stamina
- insomnia, nonrestorative sleep
- moderate to severe joint pain or sore muscles
- frequent severe headaches, disabling memory problems, poor concentration, ADHD
- depression, anger, overwhelm, panic, or bipolar syndrome
- minor injuries that can take months to heal
- for 85%, varied symptoms that develop gradually over a period of years
- for 15%, neurologic symptoms resembling multiple sclerosis, Parkinson’s, dementia, or Alzheimer’s
[/vc_column_text][vc_empty_space][rt_heading style=”” align=”” mobile_align=”” size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Bartonella[/rt_heading][vc_column_text]
- In a patient with Bartonella, pain is almost always the primary symptom: predominant complains are joint pain and headaches. Bartonella settles in the joints with pain that tends to migrate, affecting different joints at various times. This pain is frequently mistaken for arthritis in its intensity. Headaches, which are often severe, range from sharp piercing pain to dull occipital pain. Typically other neurotoxic infections (Babesia, Ehrlichia, and Mycoplasma) tend to penetrate deep within the body. In contrast, Bartonella tends to linger on the surface and causes symptoms involving the skin and mucus membranes. When a patient presents with chronic pain, headaches, swollen lymph nodes, and sore throat, consider Bartonella.
- transmission: cats (cat scratch or a bite), tick bites
- clinical prevalence: the most frequently observed coinfection
- primary complaint: pain, particularly joint pain or headaches
- cognitive, memory, and mood problems, but not as extreme as Babesia
- hot and feverish, although actual temperature is often normal
- can cause swollen lymph nodes and congested lymphatic system; sore throat
- acne-like skin lesions, skin streaking, or stria
- neuropathy involving the feet, particularly the toes
- pain, burning sensations, or discomfort on the soles of the feet
- can involve the liver and spleen; may elevate liver enzymes slightly
[/vc_column_text][vc_empty_space][rt_heading style=”” align=”” mobile_align=”” size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Babesia[/rt_heading][vc_column_text]Babesia can cause emotional symptoms that resemble every diagnosis in the DSM-IV due to inflammation of the brain. Another classic symptom of Babesia is dysfunction of the autonomic nervous system with symptoms such heart palpitations (which are not a problem of the heart but due to autonomic regulation of the heart) or shortness of breath (which is not a problem of the lungs, but due to oxygen saturation levels). As a clinician, I do not rely on any one symptom. These are symptom patterns, so when a patient is diagnosed with carpel tunnel and also has severe brain fog, mood instability, and night sweats, then I begin thinking in terms of Babesia.
- anecdotal/clinical prevalence: the coinfection second to Bartonella; when caused by a tick bite, Babesia and Bartonella tend to occur together
- primary complaints: cognitive and memory problems; mood and emotional instability
- depression, anxiety, panic disorder, OCD, ADD
- racing irregular heart rate
- malaria-like symptoms: severe chills, fever, sweats, disoriented thinking
- drenching night sweats or even day sweats
- sudden symptoms of intense flu that can last weeks to months
- carpal tunnel in the wrists or neuropathy in the hands or feet
- hepatomegaly and/or splenomegaly
[/vc_column_text][vc_empty_space][rt_heading style=”” align=”” mobile_align=”” size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Ehrlichia[/rt_heading][vc_column_text]
- primary symptoms: any neurological sensation in the extremities
- sciatica, numbness, tingling paresthesia, burning
- less involvement in the brain
[/vc_column_text][vc_empty_space][rt_heading style=”” align=”” mobile_align=”” size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Mycoplasma[/rt_heading][vc_column_text]In cases of Mycoplasma, fatigue is pervasive, resulting in a sense of total exhaustion. All the neurotoxic conditions cause nonrestorative sleep, but debilitating fatigue is a hallmark of Mycoplasma. These disorders also frequently cause inflammation of the fascia (which wraps every muscle in the body), resulting in chronic muscular pain or aching. In sum, if the patient is utterly exhausted with symptoms of joint pain, tender fascia, or skin irritations, consider Mycoplasma.
- primary symptom: extreme, debilitating fatigue
- fibromyalgia-like pain or symptoms: muscular pain or aching throughout the body
- joint pain; tight shoulders or tight hips
- inflammation or involvement of the lungs
- symptoms involving the skin or mucus membranes
[/vc_column_text][vc_empty_space][rt_heading style=”style-1″ size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Challenge Testing[/rt_heading][vc_column_text]We have an increased index of suspicion of neurotoxic illness when the patient’s symptoms are predominantly neurologic, and have not responded to treatment, with symptoms that could include pain and involve multiple organ systems. If we have made the determination that this patient could have a neurotoxin condition, we need to hypothesize which of these pathogens is likely to be dominant (which has the immune system’s attention at the moment). The response of the immune system will be reflected in the patient’s symptomatic presentation. Developing a hypothesis involves pattern recognition, connecting the dots between signs and symptoms that would otherwise seem unrelated. Once we have developed a hypothesis, we test the theory with a challenge protocol. The challenge agent selected is an antibiotic, antimicrobial, botanical, or homeopathic remedy that has been shown to reduce symptoms associated with that particular pathogen. The therapeutic variable could include one of the following:
- prescription antibiotic or antimicrobial
- herbal product or formula that is sensitive and specific enough to elicit a predictable patient response
- a homeopathic nosode specific to the microbe
[/vc_column_text][vc_empty_space][rt_heading style=”style-1″ size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Theory of Challenge Testing[/rt_heading][vc_column_text]In this approach, the practitioner uses a single, specific therapeutic variable as a challenge and then evaluates the patient’s response. In the past I have used antibiotics for Borrelia and the coinfections. I now find that herbal protocols are also effective in challenge testing. In my experience the botanical extracts contained in the Byron White Formulas are gentle, yet strong enough to provoke a highly specific immune response: a Herxheimer reaction. The formulas are invaluable tools in challenge testing. I also use them extensively as a form of immune support. (Immune support protocols are included at the end of the article.)
Note: The botanical extracts can be powerful immune system modulators and restoratives, so they should only be provided under the supervision of a practitioner who is familiar with their use.[/vc_column_text][vc_empty_space][rt_heading style=”style-1″ size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Case study[/rt_heading][vc_column_text]Consider the case of a patient whose symptom pattern suggests an infection by a pathogen in the Babesia family. At this point we need to test that hypothesis. One way to confirm that this patient has Babesia is to challenge him with a Babesia-specific immune variable. In my practice, I use a botanical 1:1 extract, the Byron White Formula A-BAB. Dosage is highly individual, and I typically begin patients on one or two drops, supervising them carefully to assure their comfort level. If the therapeutic variable triggers an intensification of that symptom pattern, that is preliminary confirmation of the hypothesis.
Herxheimer response: In this example, if the patient does have a Babesia-like infection, the botanical extract will typically result in a die-off reaction or Herxheimer response. A Herx often indicates more die-off than the body can detoxify, which results in an activation of symptoms. In the past we thought that the greater the Herx response, the more we were helping the patient. We believed that it was desirable to have a significantly aggravated response. We now realize that an intense Herx is probably confusing to the immune system and may only be creating more havoc.
Dosage in challenge testing: In my experience, the progressive rate of increase in dosage is different for each patient. If the patient is highly sensitive, I initially begin with one or two drops and definitely go slower; if she is a hardy, healthy individual, I will probably increase the dosage somewhat faster. The process involves gradually increasing the dosage, and monitoring the patient’s symptoms for an aggravated response. If a Herx response is observed, I take that as a preliminary confirmation of the hypothesis.
I then move to an immune support protocol using the same herbal extract but at a lower dosage, which is increased more gradually. We give just enough of the botanical extract to have a mildly provoking effect and elicit a mild Herx. However, if that response becomes too intense, we stop, and allow those symptoms to subside. The ability to calibrate the dosage with a product such as the Byron White Formulas makes these extracts unique, because they can be adjusted in response to the patient’s reaction. The optimal dosage is the specific number of drops that support improvement in that individual patient, gradually reducing symptomatology without provoking a full-blown Herx.[/vc_column_text][vc_empty_space][rt_heading style=”style-1″ size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Case Study: Babesia Infection[/rt_heading][vc_column_text]This case demonstrates the use of the herbal protocols alone without the need for antibiotics. Note that as a provider, I typically find that I need to ask key questions to identify the patient’s complete symptom pattern. In this case, the information obtain through my inquiries is listed under Additional History.
Patient: 32-year-old female
Chief complaint: Irregular heart rate with shortness of breath and dizziness. Evaluated in ER and by two cardiologists, who found no cardiac pathology.
Patient report: Slow onset of fatigue over the course of one year. Symptoms of restless legs syndrome, resulting in delayed sleep onset. Restless sleep in last year with frequent waking. Unrefreshing sleep. Episodic, low-level headache that can last for days without a known trigger, seems to be worse with poor-quality sleep. Some minor joint pain, no redness or swelling, worse in ankles when walking.
Additional history: Overheated at night, alternating with chill, pulls covers up or throws covers off. Night sweats 3 out of 7 nights, occasionally needs to change nightshirt. More anxious at night. Anxiety states worse during headache episodes. Headaches can be severe if the episode coincides with menses. Episodes of irregular heart rate either at rest or during exercise, which can be worse in the days preceding menses. Shortness of breath experienced independently of irregular heart rate.
Assessment: Patient has a symptom picture that is consistent with that of other patients who respond to A-BAB administration.
Challenge testing: Started A-BAB challenge beginning at lowest dosage two times per day (b.i.d.). Instructed patient to stop if she experienced uncomfortable aggravation of her symptoms, or to quickly decrease the number of drops. Patient will follow up in 2 weeks.
Office visit at 2 weeks: There was a mild Herx response to A-BAB. Suggested that patient continue use with a slow increase in number of drops until she notices a mild increase in symptoms. The patient was advised to hold the dosage at that level for several days and then gradually continue to increase as tolerated.
Office visit at 6 weeks: The patient identified tolerable symptom dosage, and was instructed to continue until symptoms again plateaued and then increase by one drop as tolerated.
Office visit at 12 weeks: After 6 weeks more, patient was symptom free and was advised to maintain the dosage at that level for an additional 30 days. She remained symptom free and discontinued the formula after the additional 30 days.[/vc_column_text][vc_empty_space][rt_heading style=”style-1″ size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Case Study: Babesia, Borrelia, and Mold[/rt_heading][vc_column_text]In this case, we took an integrative approach to patient care, using botanical extracts for challenge testing and immune support and periodic treatment with targeted antibiotics and other medications.
Patient: 34-year-old female
Medical History: Previously healthy young woman with progressively worsening symptoms over the last 5 years. Known tick bite, which occurred in a region of the country where Lyme disease is endemic. No complicating comorbidities. No postexertion fatigue. No history of prescription medication use. As a child, chronic allergies with mild episodic asthma, dysthymic depression, and IBS.
Chief complaint: Unstable mood (both anxious and depressed), problems with cognition, memory processing, and fatigue, as well as difficulty falling asleep and staying asleep
Laboratory testing: Positive IGeneX Western blot IgM and IgG. LabCorp CD-57 level 68. Complement testing: C4a at 8000. HLA-DRB typing positive, indicating mold predisposition.
Patient report: Dizziness, shortness of breath, occipital head pain. Easily overwhelmed, increased problems at work due to difficulty multitasking
Additional review of symptoms: Head pressure, minor low back pain, and mild bilateral neuropathy in the hands. Night sweats, temperature intolerance, and periodic chills. Intermittent diarrhea with multiple food allergies, gas, and bloating. Energy 4/10. Shortness of breath, similar to air hunger.
Assessment: Symptom picture suggests probable coinfection with a Babesia-like organism accompanying a Borrelia infection (confirmed by western blot) and a possible mold component (known susceptibility per HLA typing).[/vc_column_text][rt_heading style=”” align=”” mobile_align=”” size=”h5″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Immune Support Protocol 1[/rt_heading][vc_column_text]Protocol: Challenge testing was done using A-BAB, followed by 10 weeks of A-BAB in progressively increased dosage as tolerated, followed by 6 weeks of Mepron and Zithromax.
Symptoms improved after 4 months: improvement in symptoms including memory and cognitive processing. Less dizziness, fewer night sweats, chills, or anxiety states. (Symptoms that improved are all typical of a Babesia symptom picture.)
Persisting symptoms: Mild headache, moderate depression (symptoms typically associated with Borrelia). Abdominal gas with bloating (persisting symptom typically of a fungal symptom picture).
Worsening symptoms: Back, neck and shoulder pain, moderate neuropathy hands L>R, moderate to severe bilateral leg muscle aching, and significant fatigue (energy 2/10). (A strong Borrelia-like symptom picture)
Assessment: Babesia symptom picture 70% improved in 4 months of immune support.
Borrelia symptom picture now more dominant; consider Borrelia protocol: Patient’s LabCorp CD-57 dropped from 68 to 31 (of 360). Low CD-57 levels associated with a Borrelia symptom picture; the lower the level, the greater the severity.[/vc_column_text][rt_heading style=”” align=”” mobile_align=”” size=”h5″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Immune Support Protocol 2[/rt_heading][vc_column_text]Protocol: Rocephin IV 2 gm b.i.d., 4 days on 3 off, with doxycycline 100 mg, 2 tablets 2× per day, and Actigall.
Response after 2 months: Resolved symptoms included reduced back, neck, and shoulder pain. No headache, pressure, or occipital head pain
Improved but persistent symptoms: Moderate neuropathy in hands improved to mild. Mild bilateral muscle aches. Sleep improved but still restless. Fatigue (energy 4/10) associated with a Borrelia symptom picture.
Worsening symptoms: Shortness of breath, asthma-like symptoms, severe abdominal bloating and gas. Dark mood with flat affect. Sinus congestion and mild sore throat (symptoms associated with a fungal symptom picture).
Assessment: Inflammation more superficial with much of the mucous membranes involved. Neurological symptoms much improved, with only remaining neuropathy in hands, now bilateral. Borrelia symptom picture improved; dominant mold presentation persisting.
Unresolved: Are the abdominal bloating and gas related to the mold symptom picture, or a result of the antibiotics, or both?[/vc_column_text][rt_heading style=”” align=”” mobile_align=”” size=”h5″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Immune Support Protocol 3[/rt_heading][vc_column_text]Protocol: With the probable dominant mold symptom picture, a recommendation of 3 months on Byron White Formula A-FNG for fungal conditions
Response: This patient was sensitive to a small dosages starting at 1 to 2 drops a day. Immune support was carefully guided to avoid aggravation of her symptoms, and gradually increased in response to patient tolerance. After 3 months she continued protocol with resolved depression, and less shortness of breath (common mold symptom picture).[/vc_column_text][rt_heading style=”” align=”” mobile_align=”” size=”h5″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Immune Support Protocol 4[/rt_heading][vc_column_text]Persisting symptoms: The patient continued to experience unresolved muscle aches and neuropathy, similar to a Lyme symptom picture.
Protocol: In the final immune support protocol, patient used A-Lyme Complex for one month with improvement. The goal was to continue unloading the Borrelia without additional adverse effect on the gut. A-L Complex was stopped after 30 days of additional use with no relapse in improved symptoms.[/vc_column_text][vc_empty_space][rt_heading style=”style-1″ size=”h3″ font_color_type=”” font=”” custom_font_size=”” link=”” link_open=”_self”]Interventions and Patient Care[/rt_heading][vc_column_text]The discussion of antibiotics and botanicals is relatively limited for a number of reasons, which include the potential severity of neurotoxic disorders and the tremendous sensitivity of many patients with Borrelia and/or coinfections. In patient care for these conditions, a particular antibiotic will heal one patient and worsen the symptoms of the next. A single drop of an herbal extract will hardly be noticed by most patients, yet in a highly sensitive patient can provoke symptoms. Ultimately, this reflects the tremendous variation in both patient health and biochemical individuality.[/vc_column_text][vc_empty_space height=”20px”][vc_column_text]Copyright 2012 Townsend Letter
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