bacteria and disease cir group

8/2/2019 Bacteria and Disease Cir Group

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The Bacterial Etiology ofChronic Inflammation

or


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Bugs !

Inflammatory diseases are a chronicintracellular, polymicrobial infection, inwhich the DNA is horizontally mobile

between pathogen and host.


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Gee Elvira,

guess Ill be

seeing a lot

more of

you


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BugsI mean parasitic, stealth bacteria in your cells,are called by many names such as L-form (for ListerInstitute in England) or CWD (cell wall deficient).

Discovered decades ago, these microbes persist byevading your immune system.


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They are the smallest identified bacterialforms and are too small to be seen withnormal optical microscopes.


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There are many identified species of L-formbacteria. Many examples can be found inDr. Lida Mattman's slides in the textbook

Cell Wall Deficient Forms:Stealth Pathogens


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A few researchers are using dark field microscopy

Bacteria will not necessarily show up in labcultures

They will not show up in antibody testing

PCR tests may only showsmall quantities

Biopsy testing doesn't usuallywork

Its difficult to identify intracellular bacteria


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The inability of most research labs to be able to culture L-forms has been a big

obstacle, but this is not the prime reason for the stasis in research. It is asmuch political as anything else. It would be career destroying for a scientist tosay that the CDC and the Infectious Disease Society have been negligent in

ignoring the pleomorphic and persistent nature of bacteria

in compromised humans.

However, in a 2006 paper from the CDC titled Infectious Determinants ofChronic Diseasethe authors say than microbes can now be irrefutably linkedto pathology without meeting Kochs postulates..powerful tools of molecular

biology have exposed new causal links by detecting difficult-to-culture andnovel agents in chronic illness settings.

In the 19th century, Kochs Postulates caused physicians to rely almost totally

on a response to antibiotics in a Petri dish (in-vitro) rather than in-vivoto selectan appropriate antibiotic. But some pathogens have to be grown on special

substrates or do not show upin standard lab cultures.


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Science Friction


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Who are the stealth microbe hunters?


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1895 Richard PfeifferGerman bacteriologist described a form of the

bacteria Vibrio choleraethat is difficult to see witha light microscope. Others confirmed that thebacteria lacked rigid cell walls and were difficult to

grow using standard laboratory techniques.

1890s Ernst AlmquistSwedish bacteriologist and friend of

Louis Pasteur, cultured the L-form.


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1941 Emmy Klieneberger-NobelGerman microbiologist was exiled toEngland during the war and studied

the L-form. Grew colonies ofStreptobacillus moniliformis; confirmed

that several of the pathogens lackedproper cell walls. Named these variantsL-forms after the Lister Institute where

she worked.

1957 Ilia KuiumdzhievBulgarian scientist published Study on

pleuropneumonia-like organisms andL-formsof bacteria. Many Bulgarian

scientists continue this line of research,most notably Asen Toshkov.


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1960s US researcher Louis Dienes began work

with the L-form. Popularized the term Cell WallDeficient. Discovered that penicillin, and various other

factors, can make some of the bacteria

mutate into CWD variants of the same species.

1975 H M Butler and team described resistance ofL-forms to penicillin, and ability to change form.

Said such organisms may be clinically significant incases of chronic and recurrent infection.

1978 K A Bisset and R Bartlett identified L-formvariants of Bacillus licheniformiawithin red blood cells

apparently at different stages of its life cycle.


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1970s-80s

Thomas McPherson Brownexplores link between RheumatoidArthritis and CWD bacteria, devises

a treatment for RA using pulsedantibiotics, with encouragingresults.

1989 Emil Wirostko MDIn New York, he began to culture and photograph

L-forms found in white blood cells from the liquid inside

the eyes of patients with Sarcoidosis, JuvenileRheumatoid Arthritis and Crohns Disease. The L-formhave a membrane that keeps them from being digested

by the white blood cells.


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1982 Alan CantwellUS researcher applied a technique called acid-fast

staining to tissue sections of the skin and lymphnodes of Sarcoidosis patients and finds L-forms.

Convinced that L-forms are implicated

in many chronic diseases.


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1990s Lida Mattman US bacteriologist succeeded in growing L-forms using fluorescent antibodies and a

variety of staining techniques. Blood found to be saturated with a

variety of L-forms in patients with many diseases: Tuberculosis,Parkinsons, Lyme, Multiple Sclerosis, Sarcoidosis over 20incurable illnesses. Publishes numerous papers and in 2000, the

textbook Cell Wall Deficient Forms: Stealth Pathogens


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1997 Gerald Domingue

and team in New Orleans implicatedL-form bacteria in several kidney-

related diseases. Speculate about the

possibility of CWD bacteria in otherdiseases, including the so-called

autoimmune diseases.

1998 Kenneth NilssonIn Sweden he published photos of the

bacteria Rickettsia helveticaliving inside the whiteblood cells of patients with sarcoidosis.


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2002 A research team in the USinvestigated the connection between vitamin D,

L-form bacteria and sarcoidosis. They experiment

with an Angiotensin Receptor Blocker andlow-dose, pulsed antibiotics. Later came to believethat L-form bacteria are implicated in many other

chronic diseases. Inflammation Therapy isdeveloped and used experimentally for various

chronic inflammatory conditions.

Lida Mattman later calls it a miracle.


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2007 Bulgarian Academy of

Sciencesresearchers find L-forms are ableto internalize, replicate and persist

in the lungs of infected rats.Said cell wall deficient bacterial

forms may be involved in thepathogenesis of chronic and latent

lung infections.

"ResearchingL-forms is like trying

to catch a fish that appears on thesurface and quickly dives back

into the sea."

~ Dr Nadya Markova


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Research Continues.

Dr. Andy Wrightand his team in the UK are studying L-form in patients

with Chronic Fatigue Syndrome (CFS/ME)and have detected L-forms

in every CFS patient tested (600+).

Prof. Yoshinobu Eishi MD, DMSc, PhDin Tokyo has linked Sarcoidosis to L-forms.

P Woo & colleagues, Hong Kong: P B Fernandes,C Panos, E Calderon, A Albuerne, S Gonzalez,

L Winkler, T S J Elliott, P A Lambert


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Why cant my immune system kill

the stealth pathogens?

First, lets look at how yourimmune system should function toeliminate pathogens.


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AMPed Up immunity: how antimicrobial

peptides have multiple rolesin immune defense

Yuping Lai and Richard L. Gallo

http://www.ncbi.nlm.nih.gov/pmc/articles/PM

C2765035/


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As of 2009, scientists have found over 1200 proteinsmade by our DNA to make our own antimicrobials

(AMPs) to fight infection.

AMPs are called to action when the body is injured,whether through infection or injury

AMPs directly kill microbes

AMPs also boost specific innate immune responses

AMPs exert selective immunomodulatory effects on thehost

attenuate exacerbated inflammatory responses

stimulate certain beneficial aspects of inflammation potential to act as cytotoxic agents against certain type

of cancers

act as a bridge between innate and adaptive immunity


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Expression of AMPs relies on histone acetylation,

the action of the vitamin D receptor (VDRE) and themodulation of vitamin D action in specific tissues.

Histones are the protein packaging that spool your

DNA into condensed lengths. They are unwoundduring gene transcription by enzyme processescalled acetylation and deacetylation.

AMPs are transcribed because the vitamin Dreceptor (VDRE) has relayed a chemical message.

The chemical message was from active 1,25D which

is made from 25D using an iron-dependent enzymeCYP27 when the cell is in trouble. The active 1,25Dis then broken down by CYP24, a feedback loop for

homeostasis.


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Your DNA is inside the nucleus. The activated VDR gives chemical signals to

transcribe over 1000 genes and AMPs to keep you healthy. But stealth pathogens

have evolved strategies to block the action of the VDR.

If secosteroid hormone 1,25-vitamin D gets too high, it will also block the action

of the VDR. Giving vitamin D supplementation is not a good idea unless you

want to suppress the immune system further.


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The flipside of AMP regulation occurs whenexpression is turned off and is often

associated with increased susceptibility to

infection by pathogens.This happens because of chronicinflammation. If the call for help is chronic,

then the steroid concentrations are too highand can de-sensitize the receptor. The callfor help goes unanswered. Stress to the

cell causes inflammation. Can you think ofwhat the stressors might be?


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Is this why I cant kill thepathogens?

Yes.

Lets look at how these microbesare able to do this.


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Bacterial strategies for overcoming hostinnate and adaptive immune responses

Mathias W. Hornef, Mary Jo Wick,Mikael Rhen and Staffan Normark

https://chronicillnessrecovery.org/images/stories/Bacterial_Strategies__2002.pdf


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Microbial organisms have coevolved with their hoststo overcome protective host barriers and take

advantage of innate host responses. Secretion of bacterial toxins impairs protective

functions and facilitates colonization

Biofilms shield bacteria from the hostile environment Invading microbes successfully compete for nutritional

and spatial resources and displace commensal

organisms from their microbial niche

Microbes can modulate AMP receptor recognition

Bacterial proteases can degrade AMPs

Microbes can alter membrane structure to avoiddestruction

Direct penetration of the skin by vector-born microbialdiseases


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Microbes persist and proliferate in host phagocytes

Microbes can prevent oxygen radical production(bacterial killing) in macrophages

Microbes can reduce acidification which allowsintracellular survival and growth

Systemic spread of bacteria happens because theycan express proteases that degrade humoral defensesignalers

Some bacterial pathogens have evolved mechanismsfor modulating cytokine production by host cells, whichmodifies the hosts immune response

Bacterial pathogens can prevent stimulation of theadaptive immune response by interfering with antigenprocessingand much more yet to be discovered


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Do commensal or friendly bacteria

express factors that interfere withimmune defense?

Dont know.An important factor is the heterogeneity

of the host population: the geneticpolymorphisms of receptor or effectormolecules, and also the diversity of

environmental conditions including theconstitution of the resident microflora.


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How did I get these bacteria?

Inheritance Communicable Beta-lactams like penicillin promote transition of bacteria into

intracellular forms Beta-lactams are overused in meds and food supply (cook your meat

well done!) In the water In our food

Injectible meds such as vaccines Blood products In the air In the ground Sun bathing adds to vitamin D metabolism dysregulation vitamin D has been added to baby formula since the 1940s

L-form bacteria are everywhere. They are part of humanexistence. If they dont cause a disease when a person isyoung, they will ultimately cause diseases of aging. Acquiring

these pathogens is inevitable.


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*#@%!!

Get meout of

thismess!!


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Identification of specific pathogens isn't

necessary to begin Inflammation Therapy

L-form bacteria only move out of the infected cells when the cells die.They use biochemical mechanisms to delay apoptosis (cell death) and

make the cell stay intact as long as possible. When the cells die(apoptosis or phagocytosis) it might be possible to see them at that pointwith PCR (polymerase chain reaction) testing if the PCR probe sequenceis general enough. But PCR testing is expensive and only done in

specialty labs. Antibodies found in the blood are due to the pathogens which wereunsuccessful, the ones that were killed by the immune system. These arenot the pathogens that cause your illness. The intracellular bacteria donot appear in antibody assays.

Biopsy testing doesn't usually identify intracellular bacteria because thebacteria are destroyed when taken out of the body; their protectivehomeostasis is lost and the lysosomes in the immune system kill them.


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for more info

Chronicillnessrecovery.org

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