My Story - Physical Illness

Discussion in 'Fitness & Nutrition' started by METALLlC BLUE, Apr 5, 2002.

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  1. Lyme Disease:


    Many people with various physiological and psychological complaints may in fact be infected with Lyme disease or other ticks spread infections, and yet continue to go untreated for a variety of reasons. The condition of tick spread illness (especially Lyme disease) is drastically underrated, and It is very likely that Lyme disease is mimicking many of the chronic (so called incurable) conditions in our communities. Many of the people who get Lyme disease often are misdiagnosed - they are told they have everything from: multiple sclerosis, Alzheimer's, asthma, food allergies, inflammatory bowel disease, eating disorders, and other abstract psychological ailments. Is it also true that many patients are told by their doctors that, "nothing is wrong - all your tests are negative" regardless of what the patient has reported first hand based on their symptoms. If the patient persists in complaining about the symptoms - it isn't uncommon that they are told they suffer from hypochondria and then end up being referred to a psychiatrist. This disease can disseminate through the entire body of a human being in only a months time from the date of the initial tick bite. Many students, parents, and even teachers are at risk if they live near or take part in activities around the woodland areas in the United States, and they must be made aware of just how serious this and other tick spread infections are. People who are active outdoors are most at risk. This disease is most likely present right in our own backyards.

    Much of what is discussed publicly about Lyme Disease is very inaccurate. That which is accurate in the media tends to severely minimize the disease drastically by only describing the illness vaguely - such as the bull's-eye rash, or feeling sickly after the initial tick bite. The media tends to focus on prevention and the tick itself primarily. Prevention isn't enough in my opinion. This is an intricate disease, with many faucets, and a complete picture is necessary. Prevention is important, but so is the impact the disease has on the individual, and so is the correct treatment protocol. If these areas are overlooked then many thousands of people fall through the cracks of the medical system and are not receiving the care they desperately need. Patients need to know what symptoms to look for if they do get sick. They also need to know how to pursue the right medication, as well as the correct duration of treatment. Leaving it up to the doctor is simply not enough with this illness. Under-treatment & complete relapse is common, and controversy among the medical community is incredibly high right now regarding what constitutes "curative" treatment for Lyme. By the media minimizing this condition it has led to misunderstanding by both the public as well as physicians treating the public for the disease. Many doctors locally simply don't have enough information on this illness even though the medical literature is loaded with thousands of articles regarding what works and what does not. Unfortunately because of the diseases complexity one would have to specialize in it to fully grasp it, and to fully grasp it they would have to have a firm understanding of everything from politics, ethics, microbiology up through psychiatry and infectious disease. If the general public can be made aware of this disease from the point of prevention all the way through the conclusion of appropriate treatment protocol - then it would drastically improve the publics ability to face this disease and ensure people get help before it destroys their lives.

    If you think my story might help someone - then feel free to pass it on. Due to the length of this document I have broken it down into 3 main groups for you convenience. The summary is basically a primer - it provides general information and facts about Lyme Disease. If people would like to read the entire document after reading the primer - that is fine. You have my permission to give any part of this material out as educational material or to alert anyone you feel may need it.

    • Past History & Symptoms.
    • Summary - General Information on Lyme Disease.
    • The Complexities of Lyme Disease. (Listed As the last post of this thread)

    Past History & Symptoms:

    I grew up in East Longmeadow Massachusetts, and visited the camp grounds and beach areas of southern RI, and southern CT as a young child. I was constantly active and extremely outgoing as a child, and I enjoyed exploring the woodland areas that I'd become so familiar with. I grew up in an alcoholic home, but with assistance from my mother I was entered into therapy through a counselor to gain coping skills around age 7. It was hard at this time to separate my problems from physiological or psychological originals, especially since I was so young. As I got older and symptoms increased, so did my search for answers. The wild goose chase was on. Today I am a 24 year old adult living in Enfield Connecticut, and I believe I've been sick for well over 16 years (Since age 9) with Lyme Disease. My story begins like so many others with this disease.

    I've had many food allergies as of age 20, and multiple chemical sensitivities as disease progression occurred in the later stages around age 19-22. It was quite obvious that my organs and gland were exhausted from fighting some form of chronic illness which had been plaguing me since I was a child. If I ate anything that contained sugar/refined simple carbohydrates, dairy (especially Milk) the symptoms would increase significantly and I would become extremely nauseated. I had become allergic to almost all foods, and eventually had to stop eating. Today I have no sensitivities that I know of or any problems with food after having steroid treatment, antibiotics as well as anti-inflammatory medications.

    The symptoms have been extremely complex and seemed to have progressed from joint, and muscle pain, as well as a sporadic chronic fatigue to depression around age 12-14, and then symptoms became far more severe as time went on. Vision problems, such as constantly seeing stars, floaters, and actually losing my vision a few times have occurred. I did a lot of work as a body builder from age 13 - 17 for sports, and self confidence. As I took part in these activities problems constantly cropped up while in the gym. Motor coordination became affected around age 16 and increasingly deteriorated. Then general (seemingly minor symptoms became noticeable such as acid reflux, drowsiness, and numbness/headaches), and finally full blown chronic fatigue, hair loss, chronic muscle/joint pain, and other symptoms including organ pain (kidneys, heart/chest, bowel). Most of the symptoms as a young child were centered on being tired, and having a lot of problems with memory and emotional processing.

    The symptoms listed below are recorded as happening sporadically for at least a period of 2 weeks or more over a 16 year span, and then reoccurring on and off in a chronic fashion. Many of the symptoms that are listed occur on a daily basis; causing debilitation, and complete disability. The earliest symptoms noted, included; low blood pressure, chronic fatigue, bowel disturbance, depression, neurological disturbance, arthritic pain, and general phantom pain throughout various tissues without known cause.

    • Tiredness,
    • Abdomen pain
    • Extreme weight loss (80lbs in 4 months)
    • Headaches,
    • Nausea
    • Acid Reflux
    • Drowsiness
    • Concentration problems
    • Irritability
    • Dizziness
    • Anxiety
    • Memory Loss
    • Bladder Pain
    • Pain Urinating
    • Visual disturbances (Seeing Stars, and Losing vision once or twice while conscious)
    • Depression
    • Fainting/blackouts
    • Nightmares
    • Digestive problems (spasmodic pain below navel and pain throughout the colon, and small bowel)
    • Rectal Bleeding
    • Constipation
    • Diarrhea
    • Anal Fistula's
    • Rectal infections
    • Constant Malaise
    • Appendectomy (misdiagnosed surgery)
    • Aching eye sockets
    • Lack of sex drive
    • Indecisiveness
    • Heart palpitations
    • Internal Trembling
    • Mental confusions
    • Undue Excessive Sweating (Night Sweats Saturating Bed)
    • Bad breath
    • Antisocial behavior (Isolation alone)
    • Hyperactive (Manic Episodes)
    • Unsociable behavior (Drastic Personality Changes)
    • Gasping for breath
    • Restlessness
    • Backache - Spinal Pain
    • Skin tags
    • Cold hands & Feet
    • Numbness - Hands & Feet
    • Sleep Paralysis (Including Waking up In Panic or Dread)
    • Nervousness
    • Exhaustion
    • Shortness of breath
    • Temper outbursts
    • Sensitivity to light
    • Sensitivity to noise
    • Allergies
    • Muscle Pain
    • Muscle Spasms
    • Phobias
    • Crying spells
    • Negative thoughts and attitudes
    • Feelings of going mad or insane
    • Suicidal thoughts or tendencies
    • Staggering
    • Sneezing Constantly & Coughing.
    • Craving for sweets
    • Unnecessary and excessive worrying
    • Mood swings (with or without people around)
    • Waking up tired and exhausted
    • Arms and legs or body hurts when first rising in morning badly
    • Feel best after 7 PM
    • Sighing or yawning often
    • Motor mouth (constant talking)
    • Kidney & Organ Pain
    • Abnormal Hair Loss
    • Joint Pain (knee's & hips mostly and sometimes shoulders)
    • Accident prone

    The Search For Answers:

    In the 16 years I went searching for answers I was misdiagnosed with everything from Anorexia, Manic Depression, ADHD, Crohn's Disease, Chronic Fatigue Syndrome, to finally Lyme Disease, this year. 12 times I was misdiagnosed.

    In 1999 I had actually begun losing a lot of weight. Every week that passed between Christmas 1999 - May of 2000 I noticed about 5-10lbs being lost. I was 205lbs in December and shrunk down to a meager 125lbs in 4 months. I remember waking up one afternoon to go to work, and seeing myself in the mirror as I passed it to get in the shower. I realized that the person I saw in the mirror wasn't recognizable. It was at this point that I became scared. I began researching online more compulsively and constantly, calling doctors, and searching for answers. Time was running out.

    The Emergency Room:

    Eventually I was no longer capable of walking. I became so weak that I would go into shock If I made an attempt to get out of bed. I decided that if the doctors would not allow me to come to them, then I would force them to see me. I would go to the emergency room. At the ER they ran general tests, (Blood pressure, checked eyes, ears, nose, mouth, and took a urine sample) and found... "get this!" *Nothing is wrong, your test was negative*. I had heard this phrase over 35 times and each time the novelty hadn't worn off. I asked if an Upper GI could be done or perhaps some general blood testing for anemia or an infectious disease. They "shrugged" and said they didn't have time, or someone available to run the tests. Can you imagine the nerve of someone telling me in the "Emergency Room" that they didn't have a person available to run an Upper GI or general blood test? I became infuriated, and more upset. As I was leaving the hospital via wheel chair I asked the nurse if she could get me a large trash bag. She then immediately asked, "Why do you need such a large bag?" I then responded saying, "I have to have something large enough to carry all my symptoms and suffering out through this door." She then gave me a disapproving look as if I was overreacting, and I became even more bitter. I was defeated again by a medical establishment which refused to acknowledge the truth, and an enemy without a face.

    You see, by February of 2000 - I had seen most of the doctors in my area, most of which had blackballed me from returning to their practice. When one doctor in an office blackballs you - you are then refused service by all other physicians indirectly, whether they know the truth of the matter or not. By this time I was either refused service by all in the area or I was refused treatment simply because the physicians didn't know what was wrong. Now logic dictates that if a physicians doesn't know what is going on - if they actually believe the complaint they are hearing is valid, they in turn will refer that patient on to someone more competent who may be able to help. Instead of referring me on to someone who may be able to help, I instead was left to my device and told "You're not sick, you have to stop doing this". I had asked numerous times to be referred on, but all I got were glazed eyes and excuses. My persistence was a threat, and quite annoying from their perspective I'm sure - . I had been abandoned by those who were supposed to be helping me - by those I was supposed to trust with my life. My employer continued to batter me with complaints. I was required to work even though I was debilitated, and yet the excuses with my employer were running thin as to why I was losing weight, and missing so many days of work. I had one last chance, and that was to go online, and just ask for help to anyone who would listen. One woman heard me, and her name was Bernie. She is an Anascopic nurse at the local hospital (Baystate Medical Center Springfield Massachusetts) right up the street from me. The very same hospital which I visited just days earlier in the ER. I explained my story to Bernie, and she immediately gave me her phone number. We talked, and the very next day I went to see a specialist who she setup an appointment with. The specialist was Dr. David Pleet, a gastroenterologist in the Springfield Massachusetts area.

    A Diagnosis & An End To The Suffering?

    After seeing Dr Pleet on May 1st, 2000, a diagnosis was made running an upper GI barium test. He began treatment with 40mgs of prednisone, 100mgs of Imuran (Azathioprine), 800mgs of Asacol daily, Flagyl at 1,500mgs, and Cipro at 1,000 mgs per day. I could not tolerate the Imuran at all as I was allergic to it. We tried to plow through the horrible side effects over 3 times in the period of 2 months. The Imuran caused chronic infection in my lungs (coughing up), and also brought on incredible joint pain in my knees, and hips I literally could not walk while on the Imuran, and had to use a wheel chair when going to the hospital, or doctors office.

    Within 2 months I gained back the weight I had lost while using Prednisone - a Cortico-Steroid. The side effects of the medication included; Joint pain, swelling, moon face, abnormal excessive weight gain, mood swings, depression, as well as acne on my back and chest. Initially when I used the medication I experienced mild psychosis (Feelings of going mad or insane). It was not an enjoyable experience

    The Asacol had no side effects, but also did very little to alleviate my symptoms. As the Dr. lowered my prednisone slowly it became increasingly difficult to function. I became exhausted, and the symptoms listed above slowly returned. Eventually when I got down to 15 mg's of prednisone the symptoms came back in full force, and I had a major flare up of serious, sharp pain, and bleeding.

    Back To Work Or A Hospital Stay?

    I have been out of work from May 1st - Present. I did attempt to go back to work on June 31st of 2000, and all was well for about a week. On July 7th I went to work at 6 PM as it was my normal schedule, but around 8 PM I began having uncomfortable pains coming from my lower right side. The pain began as a 2-3 on the 1 - 10 pain scale. Then within 10 minutes became an alarming 8 on the scale. I began clenching my side in agony, and called a supervisor over to assist me. I called my doctor who was "not" on call that night at 8:30PM. The doctor who spoke with me asked a number of questions, and decided to have me take some Tylenol, and hold off until 9 PM to see if the pain became manageable. Those 30 minutes seemed to last forever as I was in unspeakable pain. 9 PM came, and went, and I called the doctor back. It was off the Emergency Room once again. I was then diagnosed in the hospital as having a Crohn's flare up. The Cat Scan and X-rays showed severe amounts of inflammation from 6 inch's into the terminal Ileum, down through half the colon. I was hospitalized from July 7th until Saturday July 15th.

    While in the hospital I was then given:
    • 80mg's of Prednisone,
    • 3,600mgs of Asacol,
    • Calcium supplements,
    • Multi vitamins,
    • Morphine 15mg (Every 2 hours),
    • Methotrexate (Intermuscular Injection) 1ml,
    • Remicade (2 hour infusion), and a lot of fluid through IV to bring my blood testing numbers back into the normal range.

    My white cell count remained at 15,000 even after being released. While in the hospital there was one morning where the pain became so excruciating that I began convulsing in my bed. The pain had reached a 9, which is the most pain I've ever endured in my life. It felt as though acid was being poured on my waist and my genital area. The burning and sharp stabbing became so unbearable that I no longer could endure it on my own. I immediately pressed the "call nurse" button, which I had refused to do earlier since I'm a stubborn son of a bitch. The nurse came running, and could clearly see I was in agony. She gave me 15mg's of morphine, and eventually over 45 minutes the pain became manageable at a 5-6.

    Mycobacterium Avium Subspecies Paratuberculosis:

    This is just a fraction of my experiences throughout my adolescents. After being told there was no hope of a cure by Dr. Pleet - I felt it was in my hands to search for a solution. Dr. Pleet may have saved my life, but he did so arrogantly and ignorantly. He remained adamant that no cure existed for Crohn's Disease, regardless of what the newest medical literature presented. Every week he made tirades about my unwillingness to accept the condition. He must have tried every psychological technique he had to try to get me to see things he way - including manipulation, and threatening to cut off my treatment. He told me I would just have to accept my condition, and move on. I decided to no longer see him. You're either with me or against me became my motto. I spent about 3 years studying holistic medicine, and medical data to find a cure for Crohn's disease - during my studies I found what I believe to be the infectious pathogen responsible - a bacterium called "Mycobacterium Avium Subspecies Paratuberculosis". A select few in the medical community had been doing research on this pathogen over the last century. An upsurge of new research had come about in the 1980's when a microbiologist by the name of Roderick Chiodini cultured the pathogen from Crohn's Disease patients for the first time in the known literature.

    "Mycobacterium paratuberculosis (Mp) causes a debilitating intestinal disorder in cattle. Diarrhea, excessive weight loss, reduced milk production and ultimately death characterizes the disease in cows, identified more than a century ago by Heinrich Johne. Named after its identifier, Johne's disease (pronounced YO-neez) in cattle is similar to Crohn's disease in humans (pronounced kronz). This chronic inflammatory disease of the gastrointestinal tract also results in severe diarrhea, excessive weight loss and -- for humans, who live a lot longer than cows -- debilitating abdominal pain, rectal bleeding, bowel obstruction, fistulas and abscesses. Chronic Crohn's will likely lead to surgery for removal of inflamed intestine, as well as a lifetime of harsh drug therapy that often doesn't work." -Lisa Chamberlain, The Cleveland Times.

    The idea that a pathogen could be coming through dairy and beef products and still surviving pasteurization is not a new issue - however after multiple studies on this specific pathogen known as MAP it's likely that it could be a serious threat to human health. More research must be done before the general public receives treatment, but I personally had enough circumstantial evidence to begin calling every single medical researcher and doctor around the globe who would listen to me.

    The Exhausting Effort:

    Over a period of 24 months I had contacted thousands of people involved in medical research - I questioned them, asked about specific studies - I continued to read through medical journals, began studying immunology, and pathology in depth. I began studying nutrition, health, the effects of herbs, and natural foods on the body to an extreme. I had to force myself to remember everything else I risk overlooking seemingly minor information.

    I realized what many probably knew - that the human body is more then capable of cleansing itself if given the appropriate tools that it requires naturally.

    So I setout performing experiments and different tests on myself - of course all of which were anecdotal & unscientific, but as long as "I" recovered that's all I cared about at this point. People weren't listening, and I wasn't being heard, so I had to begin with myself. Many tests showed extremely positive results, but many mistakes were made - I did not recover, but I gained significant relief. I also gained a lot of knowledge through running the tests. Through "doing" these tests, I was able to remember a great deal of knowledge from the books that had I not performed them would have been forgotten. Some natural treatments that were monitored even sent me to the ER - I'd lay by the toilet vomiting, feeling as if I would die before I ever found a solution, but I had little choice. I couldn't quit. It wasn't an option. I had to find away to hold on a little longer.

    Dr. Walter Thayer - Specialist In MAP:

    In 2001 I managed to make enough contacts to reach the number one research scientist and medical doctor whom had pioneered a lot of the research on Mycobacterium Paratuberculosis. His name was Dr. Walter Thayer. He saw me a number of times between a 12 month period - from December 2000 - through December 2001 - he turned me down for the antibiotic therapy a number of times which I sought him for to cure my Crohn's disease - he said "the treatment is too controversial, and you simply are not a good candidate for the treatment."

    The treatment consisted of 4 Antimicrobial antibiotics used against conventional MAC infections - patients with AIDS often are given rounds of Rifabutin, Clarithromycin, Ethambutol, and Clofazamine to destroy Mycobacterium Avium Complex infections - a bacterium which is in the same grouping as MAP.

    It was infuriating to hear him decline me after all the work I had done - Here I stood in no shape to even be alive - I was barely able to walk, my bowels were bleeding constantly, and I was in such debilitating pain I could not perform any of my daily functions and he has the nerve to decline me?! Well it was another impasse and I wasn't quitting here.

    The fight with my insurance company over disability was a huge painful process as well - nobody believed me when I stated how sick I was. Even those doctors who dealt with Crohn's Disease dismissed my "exaggerated" claims of illness. I'd been locked away because of my resistance to admit that Crohn's Disease was solely responsible for my declining health. They felt I was unstable mentally, and they simply did not feel my symptoms or disease were as advanced as my persistent claims. I spent months in Psychiatric institutions where I was locked away strapped to beds. Daily they would make attempts to come in and force medication on me to treat my "mental disorder" as they called it. I'd struggle, strain, and even spit the medication in their face. I'd lie screaming for help while they injected medications to sedate me. It was hopeless. I was losing my grip of reality, all at the hands of the ignorant. As the years passed my doctors continued to constantly send my Insurance company - disability information suggesting I should return to work and that I was capable of doing activities even though I stated I could not. I walked around like a zombie, barely capable of feeling, or expressing myself. The anger was mounting and yet what was soon to come would be shocking to all those who tried to resist my information.

    Time To Give Up?

    At this time it was January 2002 - Over 16 years, 40 general doctors of all variations, and some 100 others - infectious disease, Psychologists, Psychiatrists, Gastroenterologists, Pathologists, Cardiologists - many physicals, blood tests, and yet no solution still. My health was slowly declining to the point around this time that I was beginning to believe death would soon be coming.

    In an appointment with Dr. Thayer in January he continued to push me telling me I needed to exercise and inferring I was not doing what I was capable. I interjected multiple times telling him he was not in my shoes - had he been in my shoes he'd understand I was incapable of exercise, working, or any activity. My blood pressure would drop to extremely low levels whenever I would attempt to initiate physical activity, even walking or standing. My blood sugar would drop as well - my hair was falling out. I could not perform a function which my body was incapable of doing, and yet even he did not understand this. He then stated that I probably had Chronic Fatigue Syndrome - another incurable illness with little knowledge to support its etiology and little hope of relief.

    A New Suspect:

    Dr. Thayer suggested I see an infectious disease specialist down the hall from him - I nodded with little hope since I'd already been to multiple infectious specialists, but he said she was very good, and her labs was excellent.

    To make this utterly incredibly long story short I saw her - she was excellent, and she found a small glimmer of hope in my multitude of blood testing. She found an antibody to a pathogen I had long ago come up against during my research - B. Burgdorfri a bacterium known to cause Lyme Disease and spread via the bite of deer ticks. In my search for answers it had come to my attention by one woman that this was possibly the culprit of my condition. However during this time nearly one year ago I was studying nearly every disease known to man. Everything from Lupus to Cancer - I tried to narrow down all possibilities. My main focus was on inflammatory diseases. It was amazing how close I had come to an answer. When I first met this new doctor/. It was Lyme diseases that I most sought for her to test - she agreed, and it was discovered.

    She told me however the antibodies in my blood were not above the ceiling where I could be "diagnosed" she stated that the levels must reach a specific level and mine did not, so it was unknown if I had the condition and she could not provide me medication or a diagnosis. She did not have high hopes from the way she was acting - in fact I had to pry information out of her by asking her what she would do if she were in my shoes? She immediately perked up as if she was worried about what she might say and said "If I was in your shoes I would pursue this avenue diligently - My opinion is the ceiling on these Lyme tests is too high and that you probably have Severe Lyme Disease". She gave me the number of two specialists who were known as the best infectious disease specialists in New England whom deal with Lyme Disease. Dr. Sam Donta and Dr. Stephen Philips. Philips did not take my insurance, so it was off to see Donta.

    Immediately that day upon arriving home I began to do research and to my surprise, I found while rummaging through search engines and medical journals a select percentage of patients who get Lyme Disease also developed Crohn's Disease - the debilitating inflammatory bowel condition. I jumped and was shocked, but yet upon reading the other research it was clear that Lyme Disease often could mimic almost any condition with an "Immune system dysfunction" such as Lupus, MS, ALS, you name it and Lyme could mimic it depending upon the individual person. Many patients with Lyme also complained about chronic fatigue, and hair loss - among all the other symptoms I had been suffering. My complaints were now about to be validated and rewarded.

    Lyme Disease, Is It Just Another Goose Chase?

    I finally saw Dr Sam Donta on February 16th of 2002. He diagnosed me with Lyme Disease. He was very thorough and very kind. His testing was simple, and he told me to keep in touch over E-mail and by Phone. The antibiotic prescribed is Tetracycline at 500mgs 3 times per day, and then Clarithromycin, which was quit ironic. I began to power the link between antibiotic use and Lyme, but have not come to any conclusions or sound theories to date. I continued eating correctly, juicing fruits and vegetables, as well as preparing alternative holistic therapies. I have yet to begin these therapies as my doctor wanted me to wait. When he gives the green light I will begin combining my herbal therapies. It should be quite effective now that I have a specific illness to aim at.

    It's quite possible, but not currently known if the Chronic Fatigue Syndrome and Crohn's Disease I was suffering with, and continue to suffer with are being triggered and caused by the Lyme Disease bacterium which has the ability to mimic these conditions, or if they are each separate conditions. I have begun taking specific antibiotics for Lyme Disease. I must be on treatment for 18 months in total. Within 4-5 months time most patients with Lyme Disease begin to recover - the longer the individual has had the disease, often the longer it takes to recover. I have found the fatigue to be decreasing significantly as time passes. It is also noted that the Crohn's Disease seems to become almost non-existent on days where the Lyme is being overwhelmed by the antibiotics. My hope of course is to be cured of all ailments in 18 months.

    If the Crohn's Disease and Chronic Fatigue Symptoms disappear it's quite likely Lyme Disease was causing these conditions. As of today whenever the Lyme flares up so too does the Crohn's Disease, but when the Lyme declines so too do the Crohn's Disease symptoms. In fact it all but disappears. It's not uncommon for Lyme Disease to cause Chronic Fatigue Syndrome and other conditions of the immune system, but it is not "always the case". It is a Neurological/Central Nervous System Disease for the most part due to the fact it causes severe inflammation in the brain, spinal column, and nerve tissues throughout the body. It is curable; however complications due to disease progression may be permanent depending on how much damage has been done to joints, nerve tissue and the brain. Although the infection may clear up some symptoms may linger, but with therapies, and exercise it's possible to solve many of these problems. My current Brain Scans show changes to the frontal lobe and temporal lobe. This is not surprising for severe Lyme Disease and long term disease progression. My current understanding is much of this will heal with rehabilitation and my functions mentally and physically should return with hard work.


    General Information on Lyme Disease - All Information below provided by Lyme Disease Foundation Inc.

    Lyme disease (LD) is a multi-system bacterial infection caused by a the spirochete Borrelia burgdoferi (Bb). The pathogen was named in honor of the discoverer and a founding board member of the Lyme Disease Foundation, Willy Burgdorfer, PhD, MD (hon).
    Research has proven that the bacterium that causes Lyme disease has been in the U.S. for over 100 years.

    These spirochetes are maintained in nature in the bodies of wild animals and is transmitted from one animal to another through the bite of an infective tick. Humans and pets are incidental hosts to ticks.

    The body does not maintain a natural immunity to the disease. Thus, a person can be reinfected with the disease on subsequent tick bites.

    How Is Lyme Disease Transmitted:

    Lyme disease is transmitted by the bite of an infective tick. Ticks go through four life stages: egg, larva, nymph, and adult. They evolve from one life stage to another by molting Each of the last three stages (the "active" life stages) requires a blood meal. If the tick feeds on an infected host animal, the tick becomes infected. Ticks that transmit Lyme disease can retain the infection throughout their life and are able to transmit the infection to subsequent hosts. This ability to pass the infection on to other hosts makes the tick "infective". Adult ticks generally do not pass the spirochete on to the next generation.

    Transmitters of the bacteria in North America include: the Western black-legged (Ixodes pacificus) tick in the West, and the black-legged tick (Ixodes scapularis) in the rest of the country. The black-legged tick was temporarily known as the "deer" tick (Ixodes "dammini"). Research is underway to determine if the lone star tick (Amblyomma americanum) may also transmit the infection.

    Other host-specific ticks may play a minor role in maintaining the infection in nature. This creates a type of "bi-cycle". One cycle being animal-tick-animal feeding and the other cycle being animal-tick-human feeding. The wood rat (Ixodes neotomae) and the rabbit tick (Haemaphysalis leporispalustris) are two examples of ticks that may maintain the infection in nature, but not transmit it to humans. These ticks feed almost exclusively on the hosts mentioned in their common name.

    In other parts of the world, other ticks are responsible for transmitting the disease to people, such as the sheep tick ( Ixodes ricinus) in Europe, and the Taiga tick ( Ixodes persulcatus) in Asia.

    These ticks can be anywhere - in the woods, by the seashore, or even in your backyard.

    While ticks can bite year-round, peak tick season in the northeast is April - September, and on the West coast is November - April. Ticks can survive under a variety of conditions as long as adequate moisture is available.

    An infective tick with local infection must be attached to the host for a day or more before transmission of Bb occurs. However, a systematically infected tick or improper tick removal may cause transmission of LD much sooner.

    Tick infection rates vary geographically and from one year to another.

    How Wide Spread Is Lyme Disease:

    LD accounts for 90% of vector-borne infections in the U.S. From 1980 to 1998 about 112,000 cases have been reported from 49 states. Montana is the only state having no federally reported cases of Lyme disease. Those patients who have acquired the infection in their state are not yet being reported past the state level.

    Due to underreporting, the disease case count is likely to be 13 - 15 times higher. However, those are the cases that fit the government narrow case reporting criteria. The true number of cases may be significantly higher. One study estimates that there may be close to 1.5 - 2 million cases of Lyme disease.

    Evidence of infection has been found on all continents - from positive cultures, to positive antibody tests with clinical signs, to infected ticks on birds.

    What Are The Symptoms Of Lyme Disease:

    LD symptoms can imitate other diseases and can be misdiagnosed.

    Early Localized Disease:

    Signs and symptoms of Early Local Lyme Disease often starts with flu-like feelings of headache, stiff neck, fever, muscle aches, and fatigue. About 60% of light-skinned patients notice a unique enlarging rash, referred to as erythema migrans (EM), days to weeks after the bite. On dark-skinned people, this rash resembles a bruise.

    The rash may appear within a day of the bite or as late as a month later. This rash may start as a small, reddish bump about one-half inch in diameter. It may be slightly raised or flat. It soon expands outward, often leaving a clearing (normal flesh color) in the center. It can enlarge to the size of a thumb-print or cover a persons back.

    To be considered local disease the rash must be at the tick bite site with no other major organ system involvement. A rash occurring at other than the bite site in an indication of Disseminated Lyme Disease.

    Don't confuse a local reaction to a tick bite, with signs of infection. A small inflamed skin bump or discoloration that develops within hours of a bite and over the next day or two is not likely to be due to infection - but rather a local reaction to the disruption of the skin.

    Disseminated Lyme Disease Infection:

    Some people do not notice these early indicators of infection. Early manifestations usually disappear, and disseminated (other organ system involvement) infection may occur. General symptoms alone do not indicate Lyme disease.

    General Symptoms: Profound fatigue, severe headache, fever(s), severe muscle aches/pain.

    Brain: Nerve conduction defects (weakness/paralysis of limbs, loss of reflexes, tingling sensations of the extremities - peripheral neuropathy), severe headaches, stiff neck, meningitis, cranial nerve involvement (e.g. change in smell/taste; difficulty chewing, swallowing, or speaking; hoarseness or vocal cord problems; facial paralysis - Bell's palsy; dizziness/fainting; drooping shoulders; inability to turn head; light or sound sensitivity; change in hearing; deviation of eyeball [wandering or lazy eye], drooping eyelid), stroke, abnormal brain waves or seizures, sleep disorders, cognitive changes (memory problems, difficulty in word finding, confusion, decreased concentration, problems with numbers) and, behavioral changes (depression, personality changes).

    Brain Notes: Other psychiatric manifestations that have been reported in the scientific literature include: panic attacks; disorientation; hallucinations; extreme agitation; impulsive violence, manic, or obsessive behavior; paranoia; schizophrenic-like states, dementia, and eating disorders. Many patients have committed suicide.

    Eyes: Vision changes, including blindness, retinal damage, optic atrophy, red eye, conjunctivitis, "spots" before eyes, inflammation of various parts of the eye, pain, double vision.

    Skin: Rash not at the bite site (EM) - This skin discoloration varies in size and shape; usually has rings of varying shades, but can be uniformly discolored; may be hot to the touch or itch; ranges in color from reddish to purple to bruised-looking; and can be necrotic (crusty/oozy). The rash may develop a bull's-eye rash or target look. The shape my be circular, oval, triangular, or a long-thin ragged line.

    Skin Notes: disseminated skin problems include: lymphocyte, which is a benign nodule or tumor, and acrodermatitis chronica atrophicans (ACA) which is discoloration/degeneration usually of the hands or feet.

    Heart & Blood Vessels: Irregular beats, heart block, myocarditis, chest pain, vasculitis.

    Joints: Pain - intermittent or chronic, usually not symmetrical; sometimes swelling; TMJ-like pain in jaw.

    Liver: Mild liver function abnormalities, Swelling.

    Lungs:[ Difficulty breathing, pneumonia, Asthma

    Muscle: Pain, inflammation, cramps, loss of tone.

    Stomach & Intestines: Nausea, vomiting, diarrhea, loss of appetite, anorexia, inflammation.

    Spleen: Tenderness, enlargement.

    Pregancy: Miscarriage, premature birth, stillbirth, and neonatal deaths (rare). Congenital LD has been described in medical literature.

    It is possible for the bacterium to pass from mother to fetus across the placenta, resulting in congenitally acquired LD. A link between LD and adverse outcomes in pregnancy is under investigation. However, most studies show that mothers who are promptly diagnosed and treated appear to have perfectly normal babies.

    Nursing women with LD often call to ask us whether they should continue nursing. There has been no proved cases of transmission through human milk. There is research that demonstrates that Bb can be found in the colostrum of infected cows and mice. Animals’ studies have demonstrated that ingestion of Bb can result in infection. Some physicians recommend nursing mothers discard breast milk during active infection. Breast feeding can resume after treatment is completed and the woman becomes symptom-free. The decision to do so should be discussed with your physician.

    There is no test that can determine if a patient is infected with the LD bacterium and then demonstrate that the patient has become bacterium-free. Therefore, LD is clinical diagnosis, based on signs and symptoms, with the patients travel history to endemic areas and test results being additional pieces of information in the complete picture. No test can "rule-out" Lyme disease.

    What Laboratory Tests Aid In The Diagnosis of Lyme Disease?

    Indirectly Tests (Antibody Tests)

    Antibodies are the immune system's response to "fight off" infection. Tests strive to be both sensitive (detecting any LD antibodies) and specific (detecting just LD antibodies).

    Test Interpretation:

    False Negative tests occur due to defects in test sensitivity; too low an antibody level to detect (e.g. they are bound to the bacteria, with too few free-floating; the patient taking antibiotics or other drugs; naturally low antibody production); the bacterium has changed, limiting recognition by the immune system; or bacterial strain variations.

    False positive tests occur due to test failure or cross-reacting antibodies (e.g. syphilis, periodontal disease, ANA or RF).
    Types of Tests

    Titer (ELISA, EIA, IFA) - These tests measure the level of Bb antibodies in fluid. Laboratories use different detection criteria, cut-off points, types of measurements, and reagents.

    Western blot - This test produces bands indicating the immune system's reactivity to Bb. Laboratories differ in their interpretation and reporting of these bands.

    Direct Detection Tests:

    Antigen detection - These tests detect a unique Bb protein in fluid (e.g. urine) of patients. This may be useful for detecting LD in patients taking antibiotics or during symptom flare-up.

    Polymerase chain reaction (PCR) - This test multiplies the number of Bb DNA to a detectable measurable level.

    Culturing - Growing the bacterium in culture is difficult and can take months.

    Staining - Staining of tissue is time consuming and has low yield. The problem is that in Lyme disease there are too few of the Lyme spirochete in the body, and could result in the biopsy having no bacteria.

    How Is Lyme Disease Treated:

    Treatment varies and depends on how early a diagnosis is made and the organ system(s) involved. No definitive treatment regimens have been determined, and failures occur with all protocols.

    Oral antibiotics may be sufficient for early stages of non-disseminated infection.

    Long-standing or Disseminated Lyme Disease responds best to one or several courses of either oral or intravenous antibiotics for 1-3 years. Tetracycline 500mgs 3 x per day and Biaxen/Plaquenil seem to be the therapy of choice among Lyme Disease specialists currently.

    Physicians and researchers agree that it is unethical not to treat people with demonstrated, persisting infection. Therefore, some people receive retreatment or longer treatment.

    About The Lyme Disease Bacterium:

    The causative agent, Borrelia burgdorferi, is a type of spirochete. Spirochetes are long, thin, spiral-shaped bacteria. Other spirochetes include the causative agents of syphilis, relapsing fever, and gum disease.

    The bacterium is thousands of times larger than a virus. However, it still requires a powerful microscope to see one. Roughly 1,500 Bb must be laid end to end to equal one inch. About 100,000 of Bb laid side to side would equal one inch.

    When Bb was first discovered in 1982 it was thought that there was just one strain. Since then, about 100 U.S. and 300 worldwide strains of the bacterium have been discovered.

    In the mid-1990's genospecies were formed to group the many variations into subcategories.

    " Borrelia burgdorferi sensu lato" is name given to the overall category. In North America there is just one genospecies variant - Bb sensu stricto. In Europe there are three categories Bb sensu stricto, B. garinii, and B. afzelii. Asia has B. garinii and B. afzelii. Japan has B. japonica and B. miyamoto. These groups are evolving as new research discoveries occur.

    A new pathogen causing Lyme or "Lyme-like" disease has been reported. While not culturable, it has been named B. lonestari sp.

    The bacterium is able to move around the body through the bloodstream and between tissue. It can also invade tissue, replicate, and leave the cell - destroying the cell as it emerges. Sometimes, as the bacterium emerges, the cell wall collapses around the bacterium, forming a "cloaking device". This action may aid the bacteria's ability to hide from the immune system response.

    It is a popular misconception that Lyme disease was discovered in the late 1970's in Lyme, Connecticut. However, medical literature is actually rich with more than a century of writing about the condition, although most of it has been published only in Europe.

    Where Did Lyme Disease Come From:

    The first record of a condition associated with Lyme disease dates back to 1883 in Breslau, Germany, where a physician named Alfred Buchwald described a degenerative skin disorder now known as acrodermatitis chronica atrophicans (ACA).

    In a 1909 meeting of the Swedish Society of Dermatology, where a physician named Arvid Afzelius presented research about an expanding, ring like lesion he had observed. Afzelius published his work 12 years later and speculated that the rash came from the bite of an Ixodes tick.

    Throughout the early twentieth century, associations were being made among many of the symptoms and signs that constitute Lyme disease. Some of these associations were: joint involvement in patients with late disease (1921), the link between the EM rash and neurological problems (1922), psychiatric symptoms in patients with the EM rash (1930), patients with benign lymphocytomas observed to also have either EM or ACA (1934), and the description of heart involvement that appeared in patients with both the EM rash and arthritic symptoms (1934). By mid-century, physicians were experimenting with still-novel antibiotics and reporting successful results.

    In 1970, for the first time, an incidence of EM known with certainty to have been acquired in the United States was reported by Rudolph Scrimenti, who diagnosed and treated a patient who had been bitten by a tick while hunting grouse in Wisconsin and acquired the disease.

    In 1976, the first US case of clustering of this disease was reported by researchers at the Naval Submarine Medical in Southwestern Connecticut.

    In 1977, physician Allen Steere et al described the first clustering of the disease misdiagnosed as juvenile rheumatoid arthritis. They named this condition 'Lyme arthritis'.

    In the early 1980's, an entomologist at the United States Rocky Mountain Laboratories of the National Institutes of Health by the name of Willy Burgdorfer, MD, Ph.D. was investigating outbreaks of Rocky Mountain spotted fever. Research scientists Jorge Benach and Edward Bosler, Ph.D. collaborated in the dogged and dangerous work of gathering and testing ticks for disease-causing pathogens. During the course of the research, attention shifted from dog to black-legged ticks and in the fall of 1981, one of the batches of ticks yielded something dramatically new. Burgdorfer noticed an embryonic form of parasite in the body fluid of two of the ticks. Guided by his extensive knowledge of the early scientific writings of European researchers, he undertook a very close inspection of the tick--and found poorly stained, sluggish spirochetes. Within a year, the spirochetes had been named Borrelia burgdorferi (Bb), in his honor, and definitely identified as the causative agent of Lyme disease. Dr. Burgdorfer was the partner in the successful effort to culture the spirochete, along with Alan Barbour, MD.

    Next came a period of consolidating and expanding of knowledge. After the discovery of Bb and the diseases associated with it, researchers began to learn more about how the infection lodges itself in the body. In 1985, Paul Duray, a Lyme disease researcher, declared that the Lyme disease bacterium disseminates itself through the body early in the course of infection. The prevailing wisdom at the time was that infection was slow to. Duray's findings are now the prevailing thought. Also in 1985, Burgdorfer was able to demonstrate that ticks infected with the Lyme spirochete could be found across the country.

    In 1988, the LDF was founded and started the major push to bring Lyme disease in the spotlight. It was the effective partnerships among patients, government officials, and researchers that enabled volunteers around the world to bring Lyme disease the attention that has helped make it a household term.

    For more information on Ticks & Tick Prevention CLICK HERE

    This post continues on post number 16.
    Last edited by a moderator: Dec 18, 2002
  2. Fatghost28

    Fatghost28 Guest


    That's rough man. Will the anti-biotics cure the lyme disease or is it only a treatment? Good luck with everything...but you're a stubborn bitch, you'll beat it!
  3. Pace

    Pace Guest

    Thanks for the post, full of very good information regarding chronic pain, medications, and dealing with hospitals and doctors. Good luck with your ongoing battle against and treatment for the Lyme Disease and it's complications. And remember, one of the best things you can do for yourself is to keep up the positive attitude you seem to have.
  4. lilox

    lilox Live fast, Die old

    Aug 29, 2001
    Likes Received:
    wow much respect for perservering and fighting a system which is in place to help you, the health system is only good for things it see regulary, my father was diagnosed with a hietus hernia but ended up 3 months later having a tumor the size of a can of coke removed from his heart and lungs,

    I read all of your post as I know someone with chromes desease, it really makes those "how do i get a six pack" posts seam really petty.

    Good luck on your recovery, I hope you go from strength to strength.
  5. trifle

    trifle Guest

    Wow...amazing...glad to see you had so much courage and determination during such a rough time.. :bigthumb:
  6. arch

    arch HELP!

    Jan 22, 2001
    Likes Received:
    Lost at work
    :bowdown: :bowdown:
    i don't think i would be able to put up with all that. Good job in puling thru. Good luck on future treatments and your recovery:bigthumb:
  7. totaly

    totaly Guest

    Geat googly fuckin moogly:eek:

    i can't believe you wrote that whole thing out...

    Must feel good to express it all doesn't it....

    Good luck to you best wishes
  8. Ripnero

    Ripnero Best Rider in the World

    Jul 16, 2001
    Likes Received:
    Atlanta, GA
    Been there i wont bore you with details but i had alot of the symptoms you had
    after 7 months of every doctor and test they sent to a mental institute for people who suffer from anxiety, which made me worse.
    anyway after a year of bullshit i was diagnosed with a low T3 count and my thyroid was being attacked by my own immune system, i had the radiation treatment and medication and i am fine today.

    I love the way doctors who dont know shit always blame stress and tell you to take it easy for a while......

    Well lets think i feel like shit i couldn't stand up without falling over and i also know what that feeling is when you think you may loose it and not recover, its like your mind is calculating too many things, of course i am fucking stressed.
    nearly a year to diagnose a thyroid problem.
  9. cASe SenSiTive

    cASe SenSiTive Tires spitting gravel, I commit my weekly crime

    Oct 24, 2001
    Likes Received:
    Dangerously close to Detroit
    Damn dude...

    At least you've nailed down what it is. Good luck with the recovery.
  10. Fatghost28

    Fatghost28 Guest

    Hey Metallic, you're very right about Chinese medicine not getting enough respect or attention here.
  11. Fatghost28

    Fatghost28 Guest

    My diabetes ward at the local hospital is like that though, they send patients to all sorts of classes for training on things like meditation, nutrition, exercise, as well as the usual prescriptions for medications. It;s pretty holistic and involves more than the usual barrage of heavy machinery/drug therapy.
  12. Sakino

    Sakino I Live In A Giant Bucket

    Mar 14, 2002
    Likes Received:
    Nice write up, I see you do your research when it coems to important topics. A lot of people look up to people like you, I know I couldn't go thru something like that. Lots of respect man, and best of luck in the future.
    Ohh and thanks a lot for all the help.
  13. tstrandh

    tstrandh New Member

    Feb 14, 2002
    Likes Received:
    I appreciate the good read, man. Just hope all will be well with you in the near future.
  14. Filmboy44

    Filmboy44 Guest

    wow, I am very impressed. Keep the fight in you as I know you will! I can't say enough for how you inspire me to never give up!

    Thank you!
  15. Diablo3305

    Diablo3305 Guest

    I agree...keep it up man..
  16. Continued From Post Number 1

    The Complexities of Lyme Disease:

    All Information provided by Thomas M. Grier, MS of Lyme Alliance:

    Lyme Disease is a multi-system disease which can affect virtually every tissue and every organ of the human body. It is a disease which can be mild to some, and devastating to others. It can cripple and disable, or fog your mind. It can affect men, women, and children, and even your family dog. (1-5, 7-19) You may test negative for the disease, and still have it, or test positive and be symptom free. Some will get symptoms within days of a tick bite, while others may have it for years before they are even diagnosed. Some Lyme patients are told they have fibromyalgia, chronic fatigue syndrome, MS, or some other disease of unknown origin. (See abstracts of the 1996 International Lyme Conference) There are some studies which strongly support that the infection can be transmitted from mother to the unborn fetus, and may even cause still birth and has been implicated in some SIDs deaths. (MacDonald 20, 45, 52, 53)

    Why is Lyme disease such a mystery? Why does it mimic so many other diseases? Why is it so difficult to detect? The reasons come from the microbiology of the bacteria that causes Lyme Disease.

    Lyme disease is caused by a spiral shaped bacterium known as a spirochete. Diseases that are caused by spirochetes are notorious for being relapsing in nature, difficult to detect, and great imitators of other diseases. Syphilis, Tick-Borne Relapsing Fever, and Leptospirosis are other examples of spirochetal diseases. Lyme disease is caused by a bacterium called Borrelia burgdorferi, named after the man who isolated it from a Deer Tick in 1981, Dr. Willy Burgdorfer. The following is a tutorial to help explain away the mysteries of this bacterium, and why it causes so much controversy between patients and the medical community. (1)

    The Structure of the Lyme Bacteria

    The structure of the Lyme spirochete is unlike any other bacteria that has ever been studied before. It is one of the largest of the spirochetes (0.25 microns x 50 microns) It is as long, as a fine human hair is thick. Borrelia burgdorferi is a highly motile bacteria, it can swim extremely efficiently through both blood and tissue because of internal propulsion. It is propelled by an internal arrangement of flagella, bundled together, that runs the length of the bacteria from tip to tip. Like other Borrelia bacteria Borrelia burgdorferi has a three layer cell wall which helps determine the spiral shape of the bacteria. What makes this bacteria different from other species, is that it also has a clear gel-like coat of glyco-proteins which surround the bacteria. This extra layer is sometimes called the Slime Layer or S-layer. (See diagram 1) (45, 46, 59)

    This means: This extra layer of glyco-proteins may act like a stealthy coat of armor that protects and hides the bacteria from the immune system. The human immune system uses proteins that are on the surface of the bacteria as markers, and sends attacking antibodies and killer T-cells to those markers, called outer surface protein antigens (OSP antigens). This nearly invisible layer is rarely seen in washed cultures, but can be seen regularly in tissue biopsies. (46)

    The Lyme bacteria is different from other bacteria in its arrangement of DNA. Most bacteria have distinct chromosomes that are found floating around inside the cytoplasm. When the bacteria starts to divide and split in two, the chromosomes divide and the new copies of the chromosomes enter the new cell. The arrangement of DNA within Borrelia burgdorferi is radically different. It is arranged along the inside of the inner membrane. It looks something like a net embedded just underneath the skin of the bacteria. (46)

    This means: We really don't understand the mechanisms of how Bb regulates its genetic material during its division.

    Another unique feature to Borrelia burgdorferi is Blebs. This bacteria replicates specific genes, and inserts them into its own cell wall, and then pinches off that part of its cell membrane, and sends the bleb into the host. Why it does this we don't know. But we do know that these blebs can irritate our immune system. Dr. Claude Garon of Rocky Mountain Laboratories has shown that there is a precise mechanism that regulates the ratio of the different types of blebs that are shed. (46) In other bacteria the appearance of blebs often means the bacteria can share genetic information between themselves. We don't know if this is possible with Borrelia species. There have been reports of a granular form of Borrelia, which can grow to full size spirochetes, and reproduce. These granules are so small that they can be filtered and separated from live adult spirochetes by means of a micro-pore filter. (Stealth Pathogens Lida Mattman Ph.D. 66)

    The division time of Borrelia burgdorferi is very long. Most other pathogens such as Streptococcus, or Staphylococcus, only take 20 minutes to double, the doubling time of Borrelia burgdorferi is usually estimated to be 12-24 hours. Since most antibiotics are cell wall agent inhibitors, they can only kill bacteria when the bacteria begins to divide and form new cell wall. (35, 59-62)

    This means: Since most antibiotics can only kill bacteria when they are dividing, a slow doubling time means less lethal exposure to antibiotics. Most bacteria are killed in 10-14 days of antibiotic. To get the same amount of lethal exposure during new cell wall formation of a Lyme spirochete, the antibiotic would have to be present 24 hours a day for 1 year and six months! Note: Antibiotics kill bacteria by binding to the bacteria's ribosomes, and interrupting the formation of cell wall proteins.

    Like other spirochetes, such as those that cause Syphilis, the Lyme spirochete can remain in the human body for years in a non-metabolic state. It is essentially in suspended animation, and since it does not metabolize in this state, antibiotics are not absorbed or effective. When the conditions are right, those bacteria that survive, can seed back into the blood stream and initiate a relapse. (59-62, 70)

    This means: Just because a person is symptom free for long lengths of time doesn't mean they aren't infected. It may be a matter of time. Whereas viral infections often impart a lifelong immunity, Lyme, like other bacterial infections, does not retain active immunity for long periods of time. People are often reinfected with Lyme. (96)

    How does the Lyme bacteria travel from the bloodstream to other tissues? While we have known for a long time that the Lyme spirochete can show up in the brain, eyes, joints, skin, spleen, liver, GI tract, bladder, and other organs, we didn't understand the mechanism by which it could travel through capillaries and cell membranes. (Abstract 644) Then Dr. Mark Klempner presented at the 1996 LDF International Lyme Conference an interesting paper that gave us part of the answer.

    Many researchers have observed that the Lyme spirochete attaches to the human cells' tip first. It then wiggles and squirms until it enters the cell. What Dr. Klempner showed was that when the spirochete attached to the human host cell, it caused that cell to release digestive enzymes that would dissolve the cell, and allow the spirochete to go wherever it pleases. This is very economical to the bacteria to use our own cell's enzymes against us, because it does not need to carry the genes and enzymes around when it travels. Dr. Klempner also showed that the spirochete could enter cells such as the human fibroblast cell (The skin cell that makes scar tissue.) and hide. Here the pathogen was protected from the immune system, and could thrive without assault. More importantly, when these Bb-fibroblast cultures were incubated with 10 x the MIC for IV Rocephin, two thirds of the cultures still yielded live spirochetes after two weeks, and in later experiments for more than 30 days. If we can't kill it in a test tube at these high concentrations in four weeks, how can we hope to kill it in the human body? (22, 48, 79, 80,)

    This means: The infection can enter the tissue that is optimal for its survival, and it may evade the immune system and antibiotics by hiding inside certain types of cells.

    Another interesting observation about this bacteria is how it interacts with our body's immune system; Dr. David Dorward of Rocky Mountain Labs made a video tape of how Borrelia burgdorferi acts when surrounded by B-cells. (The type of white blood cell that makes antibody.) The spirochete attached tip first, entered the B lymphocyte, multiplied and ruptured the cell. It repeated this process for three days until the B-cells were able to come to an equilibrium. A matter of concern was that some of the spirochetes were able to strip away part of the B-cell's membrane, and wear it like a cloak. (Dorward, Hulinska 1994 LDF Conference Vancouver BC)

    This means: If this spirochete is evolved enough to attack our B-lymphocytes, then it may also be evolved in other ways that we do not yet understand. It is for certain that its ability to kill B-lymphocytes evolved as part of a defense mechanism to evade its own destruction. The observation that it can use the B-cell's own membrane as camouflage indicates that it may be able to go undetected by our immune system. The way our immune system is supposed to work is that it recognizes foreign invaders as being different from self, and attacks the infection.

    Unfortunately, the immune system sometimes attacks our own cells. This is called autoimmune disease. If a foreign invader has a chemical structure similar to our own tissue antigens, our bodies sometimes make antibodies against our own tissues. In people with Lyme disease scientists have discovered auto-antibodies against our own tissues including nerve cells (axons), cardio lipid, myelin (also seen in MS), myelin basic protein (also seen in MS), and neurons (brain cells) (23,28,38-40,43,45,56,57,60,88)

    When the immune system finds a foreign invader, it tags that invader in a number of ways. A cell called the macrophage can engulf the bacteria, and then communicate to other immune cells the exact description of the bacteria. Another cell might mark the cell with antibody which attracts killer T-cells. Some types of T-cells communicate to other cells what to attack, and regulate the immune assault. But sometimes the body can produce a type of antibody that doesn't attack or help. A blocking antibody will attach and coat the intruder, but it won't fix compliment, and it shields the bacteria from further immune recognition. In Lyme we have seen quantities of IgG4 blocking antibody such as is seen in some parasitic infections. (Tom Schwann RML 92 LDF Conference) *Note: Compliment is a term used for a series of 18 + digestive proteins that are only activated by signals from our immune system, such as compliment fixing antibodies.

    In order for the immune system to make an attacking antibody, the immune system must first find an antigen which it can attack. Unfortunately, as seen by freeze fracture electron microscope, photographs of the Lyme bacteria show that most of the antigens are on the inside of the inner membrane, and not on the outside. (60) This makes the bacteria less visible to the immune system and more difficult to attack. The most intriguing fact about Borrelia spirochetes is their well documented ability to change the shape of their surface antigens when they are attacked by the human immune system. When this occurs, it takes several weeks for the immune system to produce new antibodies. During this time the infection continues to divide and hide. (1, 47, 63, 66)

    It appears that Borrelia are able to change their surface antigens many times, and can do it quickly. In one study by Dr. Andrew Pachner MD, he infected mice with a single strain of Borrelia burgdorferi. After several weeks, he was able to isolate two slightly different forms of the bacteria. The bacteria from the bloodstream was attacked and killed by the mouse's immune sera, but the bacteria isolated from the mouse's brain was unaffected by the immune sera. The bacteria isolated from the mouse's brain had a new set of surface antigens. It appears that contact with the CNS caused the bacteria to change its appearance. Since the brain is isolated from the immune system and is an immune privileged site, the bacteria became its own separate strain. (47, 97)

    This means: Infections of the bloodstream may be different from the infections that are sequestered in the brain. While we continue to have active immunity in the bloodstream, the brain has no immune defenses except for circulating antibodies. So, if those circulating antibodies are ineffective to attack the bacteria in the brain, then the brain is left without any defenses, and the infection goes unabated.

    Over 100 references, abstracts and diagrams are inserted into the text to support the statements in this chapter.

    Another peculiar observation of these bacteria is seen inside the bacteria. When the genetic control mechanisms of this bacteria are inhibited with antibiotics known as DNA Gyrase Inhibitors (ciprofloxin) the bacteria start to produce bacterio-phage. A phage is a virus that specifically attacks bacteria. In this case there are two distinct forms. This means the Lyme bacteria at one time were attacked by viruses. It was able to suppress them, but the DNA to make the phage is still incorporated within the DNA of the bacteria. Perhaps activation of this phage could one day be beneficial to treating chronic Lyme patients? (JTBD 94)

    What happens when the infection gets to the brain? In the case of Lyme disease, every animal model to date shows that the Lyme spirochete can go from the site of the bite to the brain in just a few days. (41, 60, abstract 644) While we know these bacteria can break down individual cell membranes and capillaries, its entrance into the brain is too pronounced for such a localized effect. When the Lyme bacteria enters the human body, we react by producing several immune regulatory substances known as cytokines and lymphokines. Several of these act in concert to break down the blood brain barrier. (E.g. Il-6, Tumor Necrosis Factor-alpha, Il-1, Transforming Growth Factor-beta etc.) In addition to affecting the blood brain barrier, these cytokines can make us feel ill, and give us fevers. (54, 60,) (JID 1996:173, Jan)

    Since the brain has no immune system, it prevents infection by limiting what can enter the brain. The capillary bed that surrounds the brain is so tight that not even white blood cells are allowed to enter. Many drugs can't enter either, making treatment of the brain especially hard. For the first ten days of a Lyme infection, the blood brain barrier is virtually nonexistent. This not only allows the Lyme bacteria to get in, but also immune cells that can cause inflammation of the brain. (41) *Note: The breakdown of Bb was shown to occur by tagging WBCs, albumin, and other substances known not to cross the BBB with radioactive Iodine. The CSF was tested, and then the animals were infected with Bb. Then the CSF was tested everyday for several weeks. The result: No cross over of Iodine in the control group, 100% crossover in the infected group for 10 days. The infection had the same result as injecting the radioactive iodine directly into the brain. (60)

    When the human brain becomes inflamed, cells called macrophages respond by releasing a neuro-toxin called quinolinic acid. This toxin is also elevated in Parkinson's Disease, MS, ALS, and is responsible for the dementia that occurs in AIDS patients. What quinolinic acid does is stimulate neurons to repeatedly depolarize. This eventually causes the neurons to demyelinate and die. People with elevated quinolinic acid have short-term memory problems. (27, 29-37, 40-42, 74, 75, 82-84, 87-90)

    This means: If we think of all of our brain cells like telephone lines, we can visualize the problem. If all of the lines coming in are busy, we can't learn anything. If all of the lines going out are busy, we can't recall any memories. Our thinking process becomes impaired.

    A second impairment to clear thinking that a patient's experience with Lyme is the restriction of proper circulation within the blood vessels inside the brain. Using an instrument called the Single Photon Emission Computer Tomography scanner (SPECT scans); we are able to visualize the blood flow throughout the human brain in 3-D detail. What was seen in the brains of chronic neurological Lyme patients was an abnormal "swiss-cheese" pattern of blood flow. The cortical, or thinking region of the brain, was being deprived of good circulation; the occipital (eyesight) regions had an increase flow. This could help explain why most Lyme patients complain of poor concentration and overly sensitive eyes. (91)

    Lyme Tests:

    There's a Lyme test, so what's the problem? There are several Lyme tests, but most of them are dependent on the body's ability to make antibody against this bacteria. As we have seen, this may be a problem. There is the S-layer protecting the bacteria; the surface antigens are not readily exposed; there may be a blocking antibody; the bacteria might be inside a human cell; the bacteria might be down regulating the immune system through cytokines; the bacteria might have altered its antigenic appearance to fool the immune system; the bacteria might be cloaked in B-cell membrane; the bacteria might be hiding in joints, tendons, white blood cells, skin cells or the brain. Remember, if even just one spirochete survives, it could cause a relapse. Then there is another problem - the tests that detect antibody can only detect free uncomplexed antibody. (23, 25, 55, 70)

    When an antibody is formed, it is meant to latch on to something and never let go until it is destroyed. Like a lock and key, antibodies fit their associated antigens. Once the antibody attaches to the antigen it is no longer is a detectable antibody, because it has now become an antibody-antigen complex. This complex is not measurable using today's commercially available tests. Also, as the amount of antigen increases, the amount of antibody can decrease, because the antigen will trap out the available antibody and sequester it. So, a person who has a bad infection but is making a limited amount of antibody can be overwhelmed by antigen, thus making antibody detectable only if you can detect the complex.

    This means: People who have the worst infections may have the lowest antibody titers, and test negative. Note: It takes four weeks from the tick bite to test positive.

    There are two main categories of Lyme tests. The most common and least specific is the Enzyme Linked Immune Sera Assay or ELISA, the other is an Immuno Blot or Western Blot. The Western Blot essentially makes a map of the different antibodies we make to the bacteria. The map separates the antibodies by size and weight, and is reported in units called kilo daltons or kDa. For example, a Western Blot may report bands at 22, 25, 31, 34, 39, and 41 kDa. Each of these bands represents an antibody response to a specific protein found on the spirochete. The 41 band indicates an antibody to the flagella protein, and is non-specific. The 31-kDa band represents the OSP-A protein and is specific for Borrelia, as is the 34 band OSP-B and 25 kDa OSP-C.

    In 1994, the NIH decided that there should be consistency between labs reporting Lyme Disease Western Blots, and that a specific reporting criteria should be established. This sounds good, but one could argue they made a bad situation worse. The consensus committee decided to set the standards for a positive test based on the number of bands that appear. Whereas every lab prior to the hearing had accepted bands 25, 31, and 34 as specific and significant, the NIH, without any clear reasoning, disqualified those bands from being reportable. The result was that what had been a fair good test had now become poor or even useless. (90)

    How badly did the NIH bootstrap this test? The following is an analysis of the new guidelines presented as an abstract and lecture at the 1995 Rheumatology Conference in Texas. (1995 Rheumatology Symposia Abstract # 1254 Dr. Paul Fawcett et al.)

    This was a study designed to test the recently proposed changes to Western Blot Interpretation. At the Second National Conference on Serological Testing for Lyme Disease, sponsored by the NIH, the committee proposed limiting the bands that could be reported in a Western Blot for diagnosis of Lyme Disease. An IgG Western Blot must have five or more of these bands: 18, 23, 28, 30, 39, 41, 45, 58, 66, and 93 kDa. An IgM Western Blot must have two or more bands of the following three bands: 23, 39, and 41. Conspicuously absent are the most important bands, 22, 25, 31 and 34, which include OSP-A, OSP-B and OSP-C antigens - the three most widely accepted and recognized antigens. These antigens are so immuno-reactive that they were the antigens chosen for human vaccine trials. Yet they are not considered important enough to include in the diagnostic criteria. Why?

    This abstract showed that, under the old criteria, all of 66 pediatric patients with a history of a tick bite and Bull's Eye rash who were symptomatic were accepted as positive under the old Western Blot interpretation. Under the newly proposed criteria, only 20 were now considered positive. That means 46 children who were all symptomatic would probably be denied treatment! That's a success rate of only 31 %. The number of false positives under both criteria was ZERO %. * Note: A misconception about Western Blots is that they have as many false positives as false negatives. This is not true. False positives are rare. The conclusion of the researchers was: "the proposed Western Blot Reporting Criteria are grossly inadequate, because it excluded 69% of the infected children."

    We are told by manufacturers, health departments, and clinics that the Lyme ELISA tests are good and that they are useful, but in two blinded studies that tested laboratories accuracy, they failed miserably. In the latest study, 516 labs were tested. The overall result: 55% inaccurate! You are actually better off to flip a coin! (98, 99)

    Repeatedly, there have been patients who are seronegative for antibodies, yet culture positive. Despite this, our medical community is dependent on these tests and relies upon them as though they were 100 % accurate. No matter how bad the tests are, as long as we have them doctors will use them. This is why doctor Samual Donta, M.D., called for a complete ban of the Lyme ELISA test at the 1996 LDF Lyme Conference. He found that, in some cases, Lyme ELISAs were more than 75 % inaccurate, yet it was relied upon as though it were the last word - and all too often it is.

    The worst problem for chronic Lyme patients is that, after they are treated with antibiotics, they are told they are cured even if they have a recurrence of symptoms. There is a persistent dogma in medicine that 28 days of IV antibiotics cures all Lyme Disease. In fact, the ongoing six-year-old Nantucket Island Lyme Treatment Study showed IV antibiotics to have the highest relapse rate in late Lyme disease! This was because doctors put too much faith in IV antibiotics as being so powerful, that they did not follow up IV's with oral antibiotics. The key to treating late Lyme appears to be the length of antibiotic treatment, not the method. If IV's are followed up by six months or more of oral antibiotics, the relapse rate dropped to 13%. (Dr. Leslie Fein MD, MPH, Magnarelli MD, MPH 96 LDF Conference)

    I have included in the references several published studies, case histories and abstracts that deal with culture positive patients who had been previously treated aggressively with antibiotics, often including intravenous antibiotics. Most of these cases are patients who are seronegative for any Lyme antibodies, yet are culture positive. If we are repeatedly culturing this bacteria out of patients who have been treated and who are negative by all other tests, we need to rethink our understanding of this disease! We need to treat symptoms, not tests; we need to recognize that, while Lyme is a treatable disease, in some cases it appears to be incurable. I would not like to be the doctor who under treats this disease, now knowing that relapses are potentially more dangerous than treating until the symptoms are gone. (4, 6, 42, 49, 67, 68, 70-96) (Lawrence C, Lipton RB, Lowy FD, and Coyle PK. Seronegative Chronic Relapsing Neuroborreliosis. European Neurology. 1995; 35(2): 113-117)

    Too often, I have seen the word cured used in Lyme Disease Studies, only to find that the researchers have redefined the word cure to mean seronegative. Seronegativity is not synonymous with cure. The numerous culture positive cases in recent years should have negated that kind of logic years ago, and yet, in 1997, researchers are still publishing studies that use antibodies and PCR as the end point for cure. It's time to ask the patients one simple question: How are you feeling?

    So, let's say hypothetically you are bitten by an infected tick, you get a rash, you get sick, and you have a positive test. So you get 2-4 weeks of antibiotics and you get better, but then you get sick again. No problem! You go back to your doctor, and he says, "Well, we'd better give you another Lyme test" - and it’s negative. Why? Even though you have an active infection, the antibiotics cleared that infection from your blood stream. That is where your immune system is. The rest of the pathogens are hiding from the immune system inside your joints, your tendons, and your brain. Only now you don't have antibiotics to fight the infection, or any antibodies!

    This post continues on post number 22.
    Last edited by a moderator: Dec 18, 2002
  17. gsxtasyd

    gsxtasyd Lift Big........Eat Big........Sleep Big........GE

    May 27, 2001
    Likes Received:
    San Diego-Back in Cali, Love it.
    :bowdown: :bowdown: :bowdown: amazing story
  18. taichi2

    taichi2 Guest

    Wow man, your post is truly inspirational. Sometimes when I think it's bad that I missed a deadline or screwed up a project, something 100000% worse could have happened to me.

    Like you said, without health you have got little to nothing.

    Keep up the good fight and never say die!
  19. Guest

    Guest Guest

    Who friggin cares dude. I got enough of this over at I cant believe you have the time to write that and I cant believe you think people wanted to know that. Let me sum up what you took 10 minutes of my life reading, You are fucked up.
  20. A number of people cared. Allow me to redirect you to the posts before your own and you'd notice that.

    It's true I posted some of my story at LS1 over 2 years ago before I or anyone else knew I had Lyme. By bringing the issue to other peoples attention I was able to get help and ideas that allowed me to finally find a cure. Had I kept it in the dark I'd still be sick. LS1 was my previous home online for anyone who is curious. I left LS1 because of individuals like Ramsey here. I felt it wasn't really an enjoyable place to hang out anymore like it once was. I had been a member there for 4 years. I now post here, and enjoy it quite a bit. I felt it was necessary for people to understand my situation so I posted it. Sharing with all of you allows you to get to know me, and by putting myself out there I may make friends and meet people who can offer me the same in return.

    I can't believe you had the time to complain about something which you claim you " don't care" about. And you think people aren't interested? Allow me to redirect you once more my insensitive friend. I must have been mistaken when I read some 15 posts before yours claiming the post was helpful, interesting, inspiring among other adjectives.

    Now if I may be so humble to sum up that you are a tard. Now let me state the facts since it's so blatantly obvious your to dense to take notice:

    1: You spent 10 minutes reading something that you'd previously read and .....didn't like.

    2: Now once more you took the time again to read it here expecting that somehow the second time around was going to instill a sense of pleasure over the first read but did not.

    May I ask you now .....who's fault is that? It's certainly not mine. I didn't force you to click the link. YOU clicked the link. You averted your eyes away from other posts and specifically selected this one to read. It was YOU who used your eyes and read carefully through each line of each sentence for a total of 10 long, boring..minutes. Am I making sense yet?

    I'll put you on ignore so we can get your little tantrum over with quickly. :rolleyes:
    Last edited by a moderator: Dec 14, 2002
  21. Guest

    Guest Guest

    You left LS1 because you are a liar. All your looooong posts were outed. You plagerized answers to questions and passed them off as your own. Please tell everyone that you did this.
  22. Continued From Post Number 16

    Conclusion -

    In a study by Dr. Musher, M.D., he looked at incompletely treated Tertiary Syphilis patients, and compared them to those Tertiary Syphilis patients who never got antibiotics. He found that the incompletely treated group went into dementia faster.

    Why? Because they had no natural immunity left. Their ability to make sufficient antibody was diminished, because the antibiotics eliminated the stimulus from the blood stream, but the infection was still hidden in the brain! (35, 61, 62, 65, 74, 83)

    Conclusion: Lyme is an extremely complex disease that can cause long term chronic infections. Patients can be seronegative, yet culture positive (even after aggressive antibiotic therapy). The infection enters the brain early in the infection (within days). The sequestered bacteria within the CNS can be so different from the initial infection that serum antibodies are ineffective. Incomplete antibiotic treatment of Lyme Encephalitis can harm the patient.

    Addendum 1:

    The Final Note: Recently, there have been some very large educational institutions that have maintained a strong position on Lyme disease being easily detected and treated, with a high degree of success. Let me site two such examples:

    First, several state health departments, including the Minnesota State Department of Health, have received mailings from Yale University pertaining to Lyme Disease. (Reference: The Yale Medicine Special Report by Marc Wortman, 1996 Yale Medicine Magazine pp.1-15, May 15th, 1996) This report was sent to several health departments throughout the United States who had received a CDC grant to initiate a patient education program on Lyme disease.

    In the table of contents, Yale describes themselves as being the "Lyme Dream Team". The "dream team" then goes on to recommend what to do, "If you are bitten by a Deer Tick....” (Excerpts from page 11, Yale Medicine, May 15th, 1996)

    If you suspect the tick was attached for at least 36 hours, observe the site of the bite for development of the characteristic skin rash, erythema chronic migraines, (sic) usually a circular red patch, or expanding "bull's eye", that appears between three days and one month after the bite. Not all rashes at the site of the bite are due to Lyme disease. Allergic reactions to tick saliva are common. Preventative antibiotic treatment is not necessary, is costly, and may cause side effects.

    If symptoms of later-stage Lyme disease develop - arthritic swelling of a joint, most often the knee, or facial nerve palsy - have a test done. If the test is positive, have a more precise test done. Only if this test proves positive should a course of antibiotic therapy begin. Expect some symptoms to linger up to three months. No further antibiotic treatment is necessary.

    Once the Minnesota State Health Department became aware of this passage, the reprint was pulled from their educational literature sent to Health Department Lyme Education Trainers. (A program developed from a CDC grant.) The advice in this excerpt is in direct conflict with the Minnesota Guidelines for the Treatment of Lyme Disease. More importantly, in my opinion, it is bad advice that is potentially dangerous to patients!

    The passage infers that, if you have a tick attached for 35 hours, you couldn't get Lyme. If you do have a tick bite and a rash, there is no need to seek treatment - don't go to the doctor unless you have late symptoms. The symptoms the Yale medical "Dream Team" deems as important enough to go to the doctor are a severely swollen knee, or Bell's Palsy. Even if you have these symptoms, but your ELISA Lyme test is negative, you can't have Lyme and should not seek treatment. If the ELISA is positive, you need to have a second confirmatory Western Blot Lyme test. If this test is negative, you can't have Lyme disease!

    Let's review this medical advice: You are bitten by a deer tick, it is attached for 35 hours, you get a rash at the site of the bite, you develop late stage symptoms, you have a positive ELISA Lyme test, but you shouldn't pursue treatment if a second test is negative!! Apparently, antibiotic therapy is more dangerous than having late stage disease!

    If your doctor wants to take on the medical/legal risk of not treating a positive tick-bite rash, symptoms, and a positive test, then he is a very brave soul. In my opinion he would be at risk of malpractice and could be held accountable for any irreparable harm that occurs due to refusal to treat late stage Lyme symptoms with antibiotics.

    This article by Yale is an example of two erroneous prevailing attitudes within the medical community about Lyme disease. First, don't treat seronegative Lyme disease (even apparently in presence of a rash, and late state symptoms, post tick bite), the test are accurate. Second, once you treat with antibiotics, even despite the persistence of symptoms, the patient is cured. The trouble with relying on these two absolutes in Lyme disease is that they are quickly dismissed by any case of seronegative Lyme, or a single patient that is culture positive post-antibiotic treatment.

    I would not want my reputation and credential dependent upon such a flimsy foundation. If one example of seronegative Lyme exists, or culture positive Lyme post treatment, it refutes everything these institutions have insisted is true. (See two such references, Lawrence & Masters.)

    Why do these erroneous beliefs persist? Let me cite my second example of large educational institutions disseminating information to doctors that supports these beliefs. The American College of Physicians and Surgeons offers a teaching seminar to doctors on how to diagnose and treat Lyme disease. Included is a VHS video tape that has several vignettes of doctors dealing with patients with potential Lyme disease. In every case, there is either a dependence on Lyme testing - or, once the patient has been treated, they are no longer capable of sustaining infection.

    In my opinion, the absence of information about the accuracy of Lyme testing, the incidence of sero-negative Lyme, and the possibility of relapse post treatment, indicated to me that the tape is designed to give doctors a method of dumping Lyme patients. In no case presented is sustained treatment advocated, suggested, or advised. If symptoms persist, the patient has either post-Lyme Syndrome, or needs further testing, including a psychological work up, to find some other cause for the patient's symptoms.

    In my opinion, the advice on the ACP video is based on two wrong conclusions: First, that serological Lyme tests are accurate. Second, that active infection cannot persist post-antibiotic treatment - therefore treating relapses with further antibiotics is unnecessary. (Unless supported by further serum antibody testing.) In every case that is presented, the doctor is given an opportunity to give up on his patient before considering sustained antibiotics to treat the persisting symptoms. It is a wonder that any of the patients are diagnosed at all, considering the apparent lack of recognition of even the most common Lyme disease symptoms.

    Nowhere on the tape do I hear doctors asking about common and frequent symptoms of Lyme disease, such as: stiff, crunchy neck, visual complaints, heart palpitations, muscle twitches (especially in the face), fatigue, depression, urinary frequency, and memory problems. The only symptoms the educators seemed concerned about was a history of a deer tick bite, a bull's eye rash, and swollen joints. How can you make a clinical diagnosis if you don't know the most basic of symptoms? The truth is, there is no effort made to make a clinical diagnosis, except by an erythema rash. What is distressing about using the rash as diagnosis is that, in the Vanderhoof study of over 1000 chronic Lyme patients, it took on average 5.3 doctors to diagnose Lyme even in the presence of a bull's eye rash. This same study showed that a delay in treatment of more than a few months led to a much higher incidence of relapse, or chronic symptoms.

    The key to dumping a Lyme patient is how to write the patient's chart to support a non-Lyme diagnosis. In no instance is the patient ever asked how they are feeling, nor is the patient's response to antibiotics ever to be considered as the end point of treatment. Once again, the clinical picture is ignored in favor of either serology, or a blind belief that all Lyme patients are cured with a few weeks of treatment. But I as you what brought the patient to the doctor? Symptoms! So, if the cure does not alleviate the symptoms, what good has the short course of antibiotics done? I can understand why treatment is discontinued in patients who feel cured, but when they are still sick it seems unconscionable. In fact, I find that the very same doctors who advocate short term treatment in Lyme disease, rarely seem to follow the same protocol when they or a family member gets sick.

    I once had a discussion with an Internal Medicine Specialist, whom I've known for ten years, about the length of treatment for his Lyme patients. He was very vocal about how most Lyme is really Ehrlichiosis, and that all Lyme patients get two weeks of doxycycline, period - no exceptions. Except one. When I met him at an airport that summer, I came to learn his son had been bitten by a tick that spring. As a precaution, he kept his son on amoxicillin for three months, even though he had no symptoms or rash! Yet his late stage Lyme patients still receive two weeks of doxycycline.

    Apparently the treatment for the proverbial goose is different than for the gander! It is always difficult to refute large educational institutions, and any individual doctor who tries may be jeopardizing his career. An equally difficult battle is getting doctors who have adopted these false tenets as absolutes to change their minds. It is a difficult thing for a doctor to admit that his or her paradigm of diagnosis and treatment is flawed and possibly harmful. The revelation that perhaps hundreds of patients should have received extended therapy could be an unsettling realization for many doctors.

    The first hurdle is having to go against large teaching institutions that have the full support of the NIH, CDC, or AMA.Then, there is the second issue of having to confront previous patients. What does a doctor say to a patient who really had a treatable illness instead of MS? Any new change in diagnosis and treatment is a scary proposition for most doctors if it means confronting failures. Few want to be the vanguard force in leading that crusade, but the ones who do support their patients are heroes.

    While large institutions continue to disseminate their opinions and view points to millions, it is a much smaller audience that the opposition can address. Right now, doctors have to win their battles one patient at a time, and in doing so they face persecution and criticism.

    Treating Lyme patient is not a profitable endeavor. Lyme patients take too much time, require lots of counseling and education, and often continue to return with symptoms despite aggressive treatment. The physician who treats Lyme disease aggressively enters into a controversial area of medicine. It is simply easier to avoid Lyme patients than treat them, because, in treating them, they have to go against all the major medical institutions who have declared only their treatment protocols are acceptable. But let's look at the real area of interest that large institutions have in not treating Lyme disease - profit!

    No profit in treating Lyme patients - treatment is a low yield return. Today's clinics thrive on high profit, low overhead procedures. It is much more profitable and less risky to do a fifteen minute $600 EMG test for carpal tunnel syndrome than it is to encourage Lyme patients to spend an hour in an exam. The net reward per time spent is too small. Low overhead, low risk, high dollar return is why hospitals focus on programs to combat smoking, weight loss, drug rehabilitation, repetitive strain disorders, depression, birthing centers, diabetes education, etc. How often do you see hospitals seeking out quadriplegics, MS patients, ALS, and other chronic disabling diseases? Many of these programs have to be government subsidized before they are profitable enough for institutions to take them on.

    Every major medical research facility in the last few years has been focused on two areas of research: vaccines and tests. While only 15,000 patients a year are reported as having Lyme disease (CDC figures), hundreds of thousands are tested. By one institution's own figures, they give 100 tests for every case they treat. Amazingly, Olmstead County in Minnesota has yet to report a single case of Lyme disease to the CDC. This means they have made their money by testing, not treating. (Most tests are unnecessary, because Lyme disease, according to the NIH, is a clinical diagnosis made on the basis of symptoms.) Perhaps millions of people will be vaccinated with the new vaccines. So, whoever owns that concession stands to make a fortune.

    Addendum 2:

    It used to be a dogma that you either publish or perish, but now it's applied for patents or perish. The last four major announcements of "new Lyme tests" were released as press releases before a single study was published in any peer review journal as to the real effectiveness of the tests. Institutions now compete with each other for patents on tests. The real money is to own the test that is going to be the new standard in medicine. This is why they publicize the slightest advancement even before they publish. They want the business before they are forced to compare their product to the competition. None of these institutions want to tell you how bad their test is they only want to tell you how much better it is than the competition's.

    Let me give you an example: the University of Minnesota tried to develop a new PCR test for early Lyme detection. The PCR test is only as good as the primers1 you use, and, if you won the patent with bad primers, you are stuck. You either buy the rights to use someone else's primers, or you use what you have. So, what do you do if you have lousy test results? You don't compare them to the competition, but rather with an easier standard. In this case, the University didn't compare their test to other PCR tests, but instead compared it to culturing. The abstract stated that patients with tick bite and bull's-eye rash were only successfully cultured 4% of the time, but the PCR was 18% positive therefore, the PCR test was four times more useful than culturing. The trouble with this comparison is that most labs can get 80% culture success, thus the researchers are setting arbitrary standards to make the test look good. This PCR test is actually four times less accurate than culturing, if the culturing is done by a competent lab.

    What nobody seems to question is that the bull's-eye rash indicates 100% of the test subjects were infected, and that this PCR test only detected 18 out of every 100 tested! But no one wanted to summarize the conclusion that their test was poor, and worse than the competition. The newspaper headline read "New Lyme Test More Accurate in Early Lyme." More accurate than what??? It's all in how you express your conclusion. This study, of course, was never published, because peer review journals would have rejected it. Instead, an abstract was presented at a rheumatology conference, and a press release issued on what the press called "…a new and better Lyme test."

    The trouble is that it's all hype, yet many doctors will read the headline and think that this is a better test just because it is new. The fact is that most new tests aren't better; they just represent new patents, and have better press. Recently, the Minneapolis Tribune published a press release from the U of MN on a new, FDA approved PCR test for Lyme that used synovial fluid from an enlarged knee. In the article, it gave the cost of the test, where to send it, and the labs telephone number for people to make arrangements for sending in samples. What the article implied was this was the best and newest Lyme test available. What the article failed to do was compare it to any other test, or to emphasize that most press releases of this type are less than altruistic. The patients have become secondary in the business of Lyme disease. The patients are tested, vaccinated, and sent out the door in a rush to maintain rapid turnover. Complicated patients that require treatment slows this process down, and decreases profits.

    The days of doctors going on house calls are a thing of the past. It's not the doctor's fault, though. Monthly administrative meetings within most large clinics look at profit and loss statements just as though medicine were any other business. Administrators address issues of income and expenses, just like any other corporation. If patents on tests are profitable, that's what you do. If house calls aren't, then that's what you stop. The formula is maximum amount of money per hour versus least expenses per hour, with the least possible risk. The net result is: tests are profitable, vaccines are profitable, and treating Lyme patients is not profitable.

    So, how do you justify not treating? You create treatment protocols that fit the needs of the clinic and not the patient. Then, you put the entire weight of the institution behind these protocols, and intimidate everyone who disagrees. Let's put these protocols to the test. If one sero-negative, culture-positive patient exits post-antibiotic treatment, their protocols crumble. It is interesting that, while most published studies supporting Lyme as a relapsing disease of active infection are either position papers, opinion/editorial pieces, or are based on that institution's own Lyme serology tests! When an institution uses its own serology tests as an endpoint for cure, the fox is definitely watching the hen house.

    Serology cannot determine cure. EVER! Yet it is still being done! The American College of Physicians and Surgeons has recently published a newsletter, "The ACP Initiative on Lyme Disease, Vol. 1, Issue 1". Which sites a recently published paper that uses serology as an end point for cure, and has a short period of a few months as a follow up. At no time were the patients symptoms assessed as the basis of successful treatment. Instead, serologies were used as the determinant (Reference: Cetriaxone (IV Rocephin) compared with doxycycline for the treatment of Lyme disease. Dattwyler RJ, Luft BJ, Kunkel MJ, Finkel MF, Wormser GP, Rush TJ, Grunwaldt, et al New England J. of Med. 3373(5):289:294 July 31 1997.) The conclusion of this paper was that a short course of doxycycline (the least expensive drug known for treating Lyme disease) is as effective as a short course of "costly" IV Rocephin.

    It is quite a bone to throw to the health insurance industry by saying all Lyme patient can now be treated a short period of time with the least expensive drug, but is it true? Let's examine this article and premise: At the 1993 LDF Conference, a study was presented by Dr. Daniel Cameron, MD. In his study of more than 40 nursing home patients, he found that the relapse rate for IV Rocephin for four weeks was 25%, but the relapse rate for doxycycline was 87%. The difference in this study was that the follow up was 13 months not three months.

    In a six year, ongoing study using the population of Nantucket Island, there was an interesting statistic that occurred involving the use of IV Rocephin. Since the entire population of 5000+ on the island went to only four doctors, it was easy to do long term follow-ups on patients who were treated for Lyme disease. What was found was IV Rocephin had the highest rate of relapse, unless followed up for several moths with oral antibiotics. This was because the short duration of four weeks of treatment was inadequate to prevent relapse. This was why 57% of these patients had documental relapses.

    So, any current study that compares short-term doxycycline success with IV Rocephin is comparing two inadequate treatments to each other. Yet, the conclusion does not talk about total effectiveness it simply states the two drugs are equally effective (or ineffective). By not doing long filially to determine overall relapse rate, the New England Journal study makes doxycycline look good.

    The key to the Nantucket Island study, spotting the high incidence of relapse, was in the length of the follow-up. The longer the follow-up, the higher the relapse rate. Some have said that this high relapse rate may be due to reinfection, but subsequent animal models have shown this to be otherwise.

    At the 1997 LDF conference, a study was presented using naïve beagles as subjects. In this study, three groups of six beagles were studied. One group of six was infected; using infected ticks, and treated with four weeks of amoxicillin. Another group was infected and treated with a double dose of doxycycline for four weeks.

    The third group was the control. In the doxycycline treated group, at three months post-treatment, it appeared that 100% were cured. But, at two years at autopsy, five of the six (5/6) beagles were shown to have active infection, or complete relapse. The key to uncovering the high incidence of relapse was a long, two-year follow-up period. The current study cited by the ACP totally ignored this experience showing the necessity of long follow-up periods, and the fallibility of antibody serologies used as end points to treatment, or as a measure of affecting a cure.

    A more basic study showing the inadequacy of doxycycline goes back to 1989, in an abstract from Austria. Here, the researcher incubated a live culture of Borrelia burgdorferi with doxycycline for two weeks. The culture appeared to be dead, as both motility and reproduction had ceased. The culture did not have the appearance, however, of the amoxicillin treated culture, which was filled with Lysed cells. So, using micropore filters, the researcher filtered doxycycline treated cultures, and separated the intact Borrelia from the supernatant. He then washed them, and placed the filtrate back into fresh culture media. Over two thirds of the cultures reactivated, becoming motile and beginning to reproduce. It appeared that doxycycline immobilized the bacteria by interrupting protein syntheses and metabolism. This pushed the cells into a non-metabolic state. Since the doubling rate is often used as a means of determining if the cells are alive, it was assumed that the cultures were dead, when they were in fact just dormant.

    The most recent New England Journal study is deeply flawed, yet it will have an immediate impact on the use of IV Rocephin. The design of this study has ignored previous studies that show a long-term follow-up is needed. It ignores the fact that the use of antibody serology cannot be used as the endpoint for treatment, or for determining cure. It does not use adequate methods to document the presence of live bacteria. The study does not use the patient's symptoms as a basis of cure. So, I ask, who has something to gain from this kind of study?

    It seems very coincidental that, in the past, paid medical advisors on Lyme disease for the insurance industry produce study after study showing that, in the short term, doxycycline is as effective as other more expensive drugs. Once again, the basis of this study is a dependence on serologies, and short-term treatments leading to total cure. There are dozens of studies, case histories and abstracts, which document sero-negative.

    Lyme, and culture positive Lyme post-treatment. Yet, these studies are being ignored. Today, major health institutions have backed themselves into a corner, and are using their influences, economic resources, and authority to make their view point the only viewpoint.

    But do these physicians that disseminate this anti-Lyme point of view really believe what they are promoting, or are they just defending a position they have taken because they don't what to admit they have taken a position which may prove to be wrong? The answer is in the fact that most of these researchers have chosen to completely ignore studies documenting active infection post-treatment, or sero-negative Lyme disease. Instead, they only accept their own studies, using their own antibody tests as endpoints for cure.
    Last edited by a moderator: Dec 18, 2002
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