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SPIROCHETES | TRUTHCURES
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What are spirochetes?

Spirochetes are unique 

 

Remember Kingdom, Phylum, Class, Order, Family, Genus, Species? In basic taxonomy terms, spirochetes are their own phylum, "Spirochaetes" in the Eubacteria kingdom. That means they are quite different from other bacteria. The main distinction of Spirochaetes from other phyla is the unique structure and location of their mechanism of motility, their flagella. Syphilis is a well-known spirochete. Borrelia burgdorferi, the cause of Lyme disease, is another. 

Spirochetes are permanent

 

Spirochetes disseminate to immune-privileged tissues within days of a tick bite. They are not killed by antibiotics. The CDC, in 1964, explained that spirochetes that had been freeze-dried for a year could be rehydrated into viable form. And Jay P. Sanford, Uniformed Services University School of Medicine, wrote in The Biology of Parasitic Spirochetes, 1976 (p. 391):

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The ability of the borrelia, especially tick-borne strains to persist in the brain and in the eye after treatment with arsenic or with penicillin or even after apparent cure is well known (1).  The persistence of treponemes after treatment of syphilis is a major area which currently requires additional study.”

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Spirochetes are adaptable

 

Borreliae spirochetes are stealthy. They are able to adapt to different environmental conditions as a survival mechanism, by expressing different antigens on their surface. For example, they tend to express Outer Surface Protein A ("OspA") inside a tick's gut, but OspC when exposed to the warmer temperature of human blood. Barbara Johnson of the CDC published that they express OspA when exposed to zymosan, a yeast protein. They also are known to change to "cyst" form when exposed to antibiotics. Laboratories historically have found rat brains to be particularly effective storage media for Borreliae. 

 

A common misconception is that when Borreliae undergo environmental adaptation, somehow the outer surface antigens magically change from one to another, with the old ones simply disappearing as they are replaced by the new ones. In reality, the down-regulated surface antigens are sloughed off in a process called "blebbing", like a snake skin but in blobs that are covered in the "old" antigens. The organism then displays new antigens on its surface while the blebs are released into the host. A spirochete with blebs and outer surface proteins is illustrated above. 

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Spirochetes "stealth bomb" the immune system

 

The mechanism of immune evasion by spirochetes was explained by Alan Barbour and Stephen Barthold as "a bacterial Star Wars defense program" in The Scientist magazine's July 1996 issue. 

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Researchers Finding Rewarding Careers As Software Entrepreneurs, The Scientist, July 1996:

 

“Many researchers believe that the secret to B. burgdorferi‘s infectivity and inflammatory capacity lies in the interaction of its surface proteins with the host’s immunological system. Yale researcher Stephen Barthold, a veterinarian and professor of comparative medicine who developed the first mouse model of Lyme disease, studies the expression of B. burgdorferi surface proteins throughout various stages of the spirochete’s life cycle. He finds that during the early stages of infection, B. burgdorferi avoids immune detection by decreasing its expression of surface proteins or cloaking its expressed surface proteins under a layer of slime. “It’s using some sort of stealth-bomber-type mechanism,” he says. Or, using another diversionary tactic called blebbing, the spirochete can pinch off bits of its membrane in order to release its surface proteins. Explains Barbour: “It’s like a bacterial Star Wars defense program,” in which released surface proteins might intercept incoming host antibodies, keeping the spirochete safe from immunological attack."

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Why do blebs matter?

The spirochetal survival mechanism of antigenic variation can easily overwhelm the immune system because the blebs, covered in toxic lipoproteins, disseminate throughout the host. Alan Barbour explained this phenomenon in his patent for OspA, which was later marketed as a vaccine.

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