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I'VE READ & ACCEPTED YOUR TERMS & CONDITIONS

SPIROCHETES
/ THEY ARE THEIR OWN PHYLUM

 

In basic taxonomy terms, spirochetes are their own phylum, the phylum Spirochaetes. Remember learning taxonomy in fifth grade science class? All living things are organized by their similarities and differences. It goes like this: Domain, Kingdom, Phylum, Class, Order, Family, Genus, Species. Organisms from different domains are least like each other. At the Phylum level, organisms from different phyla are quite evolutionarily distinct. The main distinction of Spirochaetes from other phyla is the unique structure and location of their mechanism of motility, their flagella.

Some other characteristics of spirochetes, and specifically borrelia spirochetes:

Spirochetes are unkillable, from The Biology of Parasitic Spirochetes, 1976, by Jay P. Sanford, Uniformed Services University School of Medicine, Bethesda, Maryland, Page 391:

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.”

/ THEY ARE UNKILLABLE

 

The CDC, in 1964, explained that spirochetes (including borrelia) that had been freeze-dried for a year could be rehydrated into viable form, and isn't that convenient?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC277387/pdf/jbacter00438-0287.pdf

 

/ THEY ARE STEALTH PATHOGENS

 

Borrelia shed their outer surface, which is covered in lipoproteins, some of which are toxic, fungal-type antigens. This mechanism is demonstrated in Play-doh, below.

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. burgdorferiavoids 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."

For more on the mechanism of disease from borrelia, see OspA.

The shedding process is known as "blebbing." It's done as a way of changing the expression of surface antigens, or "antigenic variation." Stephen Barthold and Alan Barbour explained in a 1996 interview...

These blebs, covered in outer surface proteins (Osps) are far more abundant, and far more damaging than the spirochetes themselves.  This is by Alan Barbour in 1982, showing the relative abundance of blebs vs. spirochetes:

There  is more DNA (plasmid) packaged in released blebs – which have fungal osps all over them – than there are spirochetes.  Spirochetes are “stealth bombers.” That is how they cause chronic or immunosuppression disease.

J Infect Dis. 1994 Mar;169(3):668-72.

Target imbalance: disparity of Borrelia burgdorferi genetic material in synovial fluid from Lyme arthritis patients.

Persing DH1, Rutledge BJRys PNPodzorski DSMitchell PDReed KDLiu BFikrig EMalawista SE.

“Lyme arthritis is a late manifestation of Lyme disease that results in episodic synovial inflammation and swelling. Although this process is thought to be driven directly by the spirochetal etiologic agent, Borrelia burgdorferi, the organism itself has been recovered by culture only twice. In contrast, polymerase chain reaction (PCR) studies are usually positive. This apparent discrepancy in 19 culture-negative synovial fluid specimens from 18 patients with Lyme arthritis was investigated. In all 19, DNA sequences characteristic of plasmid-encoded genes OspA and OspB were easily detected. However, despite equivalent or even superior analytic sensitivity for detection of cultured organisms, the reactivity of two genomic DNA targets was often weak or absent altogether in the clinical specimens. This apparent overrepresentation of B. burgdorferi plasmid sequences was found exclusively in clinical specimens and not in cultured organisms. The physiologic imbalance of genomic and plasmid DNA reactivity in B. burgdorferi infection may signal an underlying pathogenetic mechanism."

Visit the OspA page for more on how OspA causes disease.