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|part 3-A, LYME ON THE BRAIN by TOM GRIER, 8-25-10|
|Written by Bettyg|
|20 September 2010|
We have talked about how the Lyme spirochete attaches to the endothelial cells in blood vessels, and creates “LEAKY” blood vessels. Due to the spirochete’s exceptional motility, this allows the bacteria to enter virtually any tissue in the human body.
The big questions are: Where is it going? Why does it want to go to specific places? What happens when it gets to places where it can hide and survive?
Bacteria don’t have brains, but they do have millions of years of evolution that improved their overall survival through shear trial and error. The bacteria wants to survive.
For good or bad Borrelia bacteria have made their homes in ticks and mammals. How has evolution affected their genetics in order to enhance their own survival in ticks and mammals?
Let’s look at Borrelia bacteria from the bacterium’s point of view.
All known species of Borrelia bacteria that cause Relapsing Fever and Lyme Disease enter the blood of humans either by way of an insect bite such as from an infected tick, head-lice, or through infected blood contact.
Relapsing Fever caused by Borrelia recurrentis enters the blood stream through open bleeding capillaries on the head caused by the host scratching at lice and themselves until they are bloody, and then accidentally crushing the head-louse allowing the bacteria direct entry into the blood stream.
Dr. Joseph Dutton was infected with Borrelia duttonii when he was performing an autopsy on an African native who died very quickly of neuroborreliosis-encephalitis after contracting Relapsing Fever through the bite of the moubatta tick.
Unfortunately Dr. Dutton cut himself during this field autopsy, was also infected, and died of encephalitis within two weeks of initial infection.
Below is an excerpt from Dr. Willy Burgdorfer’s lecture on the history of spirochetes related to Lyme disease.
Take special note about the disappearance of classical formed spiral spirochetes in favor of granular-cysts, and also the ability of Borrelia to invade epithelial cells and appear to have disappeared.
This is a history and research that we cannot ignore and cannot afford to forget.
If we had looked at this evidence in 1982, we would have understood the paradoxes we were seeing and incorrectly dismissing as artifacts, in our diagnosis, treatment, and relapses of Lyme patients.
At the turn of the century, 1903 through 1905, the British physicians Dutton (Joseph Everett) and Todd (John Lancelot) working in the Congo, found that the disease referred to as "human tick disease" by David Livingston as early as 1857, was caused by a spirochete transmitted by the African soft-shelled or argasid tick, Orhithodoros moubata (Fig. 3).
Both Dutton and Todd contracted the disease.
Dutton, a pathologist, infected himself accidentally during a post mortem and died.
He is remembered by having had named the East African relapsing fever spirochete Borrelia duttonii.
Also playing an important role in relapsing fever research was the German microbiologist Robert Koch.
At the end of 1904, he was called to East Africa to investigate the widely distributed East Coast Fever in cattle.
He soon learned that most Europeans traveling into the interior regions had been suffering of recurrent fever first thought to be malaria.
Although Koch was not aware of the British findings in the Congo and Uganda, he confirmed the vector role of the Orhithodoros moubata.
He was the first to demonstrate that spirochetes were transmitted via eggs (transovarial transmission) to the progeny of infected female ticks.
Ever since it was demonstrated that the body louse (Pediculus humanus humanus) and the African O moubata were the vectors of the relapsing fever spirochetes known today as Borrelia recurrentis and B duttonii, respectively, intense studies have been carried out on the development of these microorganisms in their vectors, and on the mode of transmission to humans.
full part 3-A can be found here:
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