Borrelioosidiagnoosin hän sai vuonna 1995. Antibioottihoidot "herättivät" hänet zombie-olotilasta. Hän ei kuitenkaan ole tullut hoidoilla kokonaan oireettomaksi. Oireet palaavat aika ajoin syklimäisesti. Nyt hänellä on, riippuen siitä kenen lääkärin mielipidettä hän kysyy, krooninen borrelioosi + lisäinfektioita + liian aktiivinen immuunijärjestelmä, krooninen fatiikki jonka syytä ei tiedetä, fibromyalgia jonka syytä ei tiedetä tai post-Lyme -syndrooma siihen liittyvine autoimmuunireaktioineen."
"I was raking leaves at a home near Lake Wequaquet on a Saturday in April 1986. On Monday, I felt very weak, and was at a doctor's by Thursday. I had three reddish oval rashes on my chest, but back then, physicians were looking for the now ''classic'' bulls eye rashes, so my Lyme Disease went undiagnosed.
I recovered some on my own, without treatment, but had numerous relapses over the next months. A year after the tick bite, I could barely get out of bed. For the next eight years, I was diagnosed, wrongly, with Chronic Fatigue Syndrome. In 1995, my Lyme was detected by an astute physician to whom I went to for another problem. In the next years I received substantial oral anti-biotic treatment. It lifted me out of the zombie category, but I never will be genuinely healthy. All the symptoms continue, less severe, and so does the characteristic cycling. Now, depending on who I ask, I have Chronic Lyme Disease with continuing infection and an up-regulated immune system, or Chronic Fatigue Syndrome, cause unknown , or Fibromyalga Syndrome, cause unknown, or Post Lyme Syndrome, with an auto-immune etiology.
I became curious about why medicine has so many different views of the same set of symptoms.
The dispute is over whether the causative agent of Lyme, the spirochete bacterium Borrellia Burgdorferi (Bb), eludes both the immune system and significant courses of antibiotic treatment, as some say, or if the host individual experiences some sort of post-infectious syndrome. The debate is heated, to say the least. Other spirochetes cause syphilis and Relapsing Fever.
These Bb little guys are only 20 microns, 20 millionths of a meter long. They move with the aid of flagella, like little worms with several sets of legs. They sequester in numerous tissues, preferring neural tissue. Bb's locomotive capacities allow it to move from through the skin and into the blood stream, then into other parts of the body including the brain.
Antigenic variation is another tactic of Bb survival, and is a very interesting phenomenon. Bacteria have Outer Surface Proteins (OSPs), or antigens, to which the humoral immune system develops antibodies which then attack and destroy the bacterium. Antigenic variation gives the bacterium the capacity to up-regulate (increase the number) or down regulate specific OSPs, presenting a complex and varying pattern to the immune system. A set of antibodies sufficient to control the bacteria's spread at one point becomes inadequate later.
Other cards up Bb's sleeve are that, in the host, it can exist in alternate forms, against which antibiotics are ineffective. It has a cyst form, an egg- like mode from which the full bacterium can later emerge.
Another variation is a cell wall deficient form, which protected it from antibiotics which attack cell walls. Bb also exchanges DNA with others of its kind. This is the mechanism which produces bacterial antibiotic resistance, which has become a very serious medical problem.
Bacteria have been shown to communicate bio-chemically with each other. Bb may be one of those with this capacity, and there is evidence that it produces neurotoxins."