The Bacterial Etiology of Chronic Inflammation or

Bugs !
Inflammatory diseases are a chronic intracellular, polymicrobial infection, in which the DNA is horizontally mobile between pathogen and host.

Gee Elvira, guess Ill be seeing a lot more of you

BugsI mean parasitic, stealth bacteria in your cells, are called by many names such as L-form (for Lister Institute in England) or CWD (cell wall deficient). Discovered decades ago, these microbes persist by evading your immune system.

They are the smallest identified bacterial forms and are too small to be seen with normal optical microscopes.

There are many identified species of L-form bacteria. Many examples can be found in Dr. Lida Mattman's slides in the textbook Cell Wall Deficient Forms: Stealth Pathogens

Its difficult to identify intracellular bacteria

A few researchers are using dark field microscopy Bacteria will not necessarily show up in lab cultures They will not show up in antibody testing PCR tests may only show small quantities Biopsy testing doesn't usually work

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 as much political as anything else. It would be career destroying for a scientist to say 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 of Chronic Disease the authors say than microbes can now be irrefutably linked to pathology without meeting Kochs postulates..powerful tools of molecular biology have exposed new causal links by detecting difficult-to-culture and novel 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-vivo to select an appropriate antibiotic. But some pathogens have to be grown on special substrates or do not show up in standard lab cultures.

Science Friction

Who are the stealth microbe hunters?

1895 Richard Pfeiffer German bacteriologist described a form of the bacteria Vibrio cholerae that is difficult to see with a light microscope. Others confirmed that the bacteria lacked rigid cell walls and were difficult to grow using standard laboratory techniques. 1890s Ernst Almquist Swedish bacteriologist and friend of Louis Pasteur, cultured the L-form.

1941 Emmy Klieneberger-Nobel German microbiologist was exiled to England during the war and studied the L-form. Grew colonies of Streptobacillus moniliformis; confirmed that several of the pathogens lacked proper cell walls. Named these variants L-forms after the Lister Institute where she worked. 1957 Ilia Kuiumdzhiev Bulgarian scientist published Study on pleuropneumonia-like organisms and L-forms of bacteria. Many Bulgarian scientists continue this line of research, most notably Asen Toshkov.

1960s US researcher Louis Dienes began work with the L-form. Popularized the term Cell Wall Deficient. 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 of L-forms to penicillin, and ability to change form. Said such organisms may be clinically significant in cases of chronic and recurrent infection. 1978 K A Bisset and R Bartlett identified L-form variants of Bacillus licheniformia within red blood cells apparently at different stages of its life cycle.

1970s-80s Thomas McPherson Brown explores link between Rheumatoid Arthritis and CWD bacteria, devises a treatment for RA using pulsed antibiotics, with encouraging results. 1989 Emil Wirostko MD In 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, Juvenile Rheumatoid Arthritis and Crohns Disease. The L-form have a membrane that keeps them from being digested by the white blood cells.

1982 Alan Cantwell US researcher applied a technique called acid-fast staining to tissue sections of the skin and lymph nodes of Sarcoidosis patients and finds L-forms. Convinced that L-forms are implicated in many chronic diseases.

1990s Lida Mattman US bacteriologist succeeded in growing Lforms 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 20 incurable illnesses. Publishes numerous papers and in 2000, the textbook Cell Wall Deficient Forms: Stealth Pathogens

1997 Gerald Domingue and team in New Orleans implicated L-form bacteria in several kidneyrelated diseases. Speculate about the possibility of CWD bacteria in other diseases, including the so-called autoimmune diseases. 1998 Kenneth Nilsson In Sweden he published photos of the bacteria Rickettsia helvetica living inside the white blood cells of patients with sarcoidosis.

2002 A research team in the US investigated the connection between vitamin D, L-form bacteria and sarcoidosis. They experiment with an Angiotensin Receptor Blocker and low-dose, pulsed antibiotics. Later came to believe that L-form bacteria are implicated in many other chronic diseases. Inflammation Therapy is developed and used experimentally for various chronic inflammatory conditions. Lida Mattman later calls it a miracle.

2007 Bulgarian Academy of Sciences researchers find L-forms are able to internalize, replicate and persist in the lungs of infected rats. Said cell wall deficient bacterial forms may be involved in the pathogenesis of chronic and latent lung infections. "Researching L-forms is like trying to catch a fish that appears on the surface and quickly dives back into the sea." ~ Dr Nadya Markova

Research Continues. Dr. Andy Wright and 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, PhD in 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

Why cant my immune system kill the stealth pathogens? First, lets look at how your immune system should function to eliminate pathogens.

AMPed Up immunity: how antimicrobial peptides have multiple roles in immune defense Yuping Lai and Richard L. Gallo http://www.ncbi.nlm.nih.gov/pmc/articles/PM C2765035/

As of 2009, scientists have found over 1200 proteins made 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 the host 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

Expression of AMPs relies on histone acetylation, the action of the vitamin D receptor (VDRE) and the modulation of vitamin D action in specific tissues. Histones are the protein packaging that spool your DNA into condensed lengths. They are unwound during gene transcription by enzyme processes called acetylation and deacetylation. AMPs are transcribed because the vitamin D receptor (VDRE) has relayed a chemical message. The chemical message was from active 1,25D which is made from 25D using an iron-dependent enzyme CYP27 when the cell is in trouble. The active 1,25D is then broken down by CYP24, a feedback loop for homeostasis.

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.

The flipside of AMP regulation occurs when expression is turned off and is often associated with increased susceptibility to infection by pathogens. This happens because of chronic inflammation. If the call for help is chronic, then the steroid concentrations are too high and can de-sensitize the receptor. The call for help goes unanswered. Stress to the cell causes inflammation. Can you think of what the stressors might be?

Is this why I cant kill the pathogens? Yes. Lets look at how these microbes are able to do this.

Bacterial strategies for overcoming host innate and adaptive immune responses Mathias W. Hornef, Mary Jo Wick, Mikael Rhen and Staffan Normark https://chronicillnessrecovery.org/images/stori es/Bacterial_Strategies__2002.pdf

Microbial organisms have coevolved with their hosts to 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 avoid destruction Direct penetration of the skin by vector-born microbial diseases

 Microbes persist and proliferate in host phagocytes Microbes can prevent oxygen radical production (bacterial killing) in macrophages Microbes can reduce acidification which allows intracellular survival and growth Systemic spread of bacteria happens because they can express proteases that degrade humoral defense signalers Some bacterial pathogens have evolved mechanisms for modulating cytokine production by host cells, which modifies the hosts immune response Bacterial pathogens can prevent stimulation of the adaptive immune response by interfering with antigen processingand much more yet to be discovered

Do commensal or friendly bacteria express factors that interfere with immune defense? Dont know. An important factor is the heterogeneity of the host population: the genetic polymorphisms of receptor or effector molecules, and also the diversity of environmental conditions including the constitution of the resident microflora.

How did I get these bacteria?

L-form bacteria are everywhere. They are part of human existence. If they dont cause a disease when a person is young, they will ultimately cause diseases of aging. Acquiring these pathogens is inevitable.
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

*#@%!! Get me out of this mess!!

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 point with PCR (polymerase chain reaction) testing if the PCR probe sequence is general enough. But PCR testing is expensive and only done in specialty labs. Antibodies found in the blood are due to the pathogens which were unsuccessful, the ones that were killed by the immune system. These are not the pathogens that cause your illness. The intracellular bacteria do not appear in antibody assays. Biopsy testing doesn't usually identify intracellular bacteria because the bacteria are destroyed when taken out of the body; their protective homeostasis is lost and the lysosomes in the immune system kill them.

for more info Chronicillnessrecovery.org