Because it's not possible to test for the presence of intracellular CWD bacteria, medical practitioners must really on clinical evidence (inflammatory symptoms and lab markers) to identify patients who are candidates for Inflammation Therapy.

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We sincerely appreciate the time our survey respondents have given us in our efforts to provide hard evidence that Inflammation Therapy is an effective treatment for a variety of chronic inflammatory diseases.  After two and a half years we began a preliminary analysis and discovered there were many incomplete parts in the surveys. Unfortunately, this made the statistical analysis we were planning to do invalid, so we have decided to discontinue the survey at this point.  However, we will be writing a paper with data from the survey that will contain a series of case reports, which you will be able to view in the near future on the CIR website. Thank you very much to everyone who has taken part in our survey.   

HONcode

Keith Berndtson, MD, is a graduate of Rush Medical College, a board-certified family physician, and founder and medical director of Park Ridge MultiMed, an integrative medicine practice in Park Ridge, Illinois, where he focuses on the evaluation and treatment of chronic illness.

He is a member of the Institute of Functional Medicine. In 2012 he completed a Lyme disease training program sponsored by the Tick-Borne Disease Alliance. He now has a growing Lyme disease practice in the Midwest and is an advocate for patients with symptoms that persist despite usual medical care.

His essays, articles, reviews, and book chapters have appeared in the Journal of the American Medical Association, Current Review of Alternative Medicine, Chicago Medicine, Physician Executive, Ambulatory Outreach, and Healthcare Financial Management. He served as consulting editor for The Healing Power of Vitamins, Minerals and Herbs, and The Complete Guide to Herbal Medicines. He is also the coauthor of The Immune Advantage by Rodale Press. His latest book, Seek Wisdom: The Modern Quest for Health and Sustainability, is available through Amazon.com.

Dr. Berndtson will be presenting Lyme Disease: A Primer.

The existence of bacteria which are capable of invading human cells has been known about for over a century and a number of studies suggest disease associations. [1-5] These intracellular bacteria are identified by several names: nanobacteria, pleomorphic, stealth, coccoid bodies, mycoplasma and L-forms. L-forms are bacterial variants with defective cell walls and irregular growth and multiplication. They arise after the exoskeleton of the bacterial cell wall has been either degraded by bacteriolytic enzymes, or its biosynthesis has been disturbed by antibiotics and other inhibitors, or by defect mutations in essential genes for cell wall synthesis. L-forms were discovered in 1935 by Dr. Emmy Klieneberger-Nobel and subsequently described by many authors. [6,7] The cell wall deficient (CWD) bacteria are pleomorphic (i.e., they can change size and shape) and many are smaller than viruses (0.01 microns in diameter). [8] They're too small to be seen with normal optical microscopes [9] and they can survive under extreme conditions. [10] The lack of a cell wall enables them to enter human cells: and proliferate there if they remain undetected by the immune system. In particular, they enter the macrophages - the very immune cells deployed to kill invading pathogens.

Most microbes on the planet cannot be cultivated and are therefore difficult to study. CWD bacteria should be of interest for their putative pathogenic role but many microbiologists are unfamiliar with them or complain about the unusually labor-intensive and time-consuming process of L-form isolation and identification (they cannot be detected by standard laboratory tests that rely upon staining the cell wall). Diagnosing the presence of CWD bacteria is also problematic because they're very slow-growing and difficult to culture; conditions must be similar to those in the human body. However, this can be overcome by patient determination. [10-12] Some labs, such as Mattman's at Wayne State University, have been successful using blood agar at very specific pH and temperatures). [13] CWD bacteria aren't detected by antibody tests because they're able to persist for a long time inside cells (in the presence of inflammation, the life-span of a macrophage may be months) so very few antibodies are created in response to their presence. [14, 15]When the compromised phagocytes die (CWD bacteria use biochemical mechanisms to delay apoptosis [16]) it might be possible to identify them with PCR (polymerase chain reaction) testing if the probe sequence is general enough, but there are many limitations. For example, a particular sample may not be infected and the lab may look for a limited number of species (there are many strains of CWD bacteria). In addition, the application of PCR to clinical specimens has many potential pitfalls due to the susceptibility of PCR to inhibitors, contamination and experimental conditions. For instance, it's known that the sensitivity and specificity of a PCR assay is dependent on target genes, primer sequences, PCR techniques, DNA extraction procedures, and PCR product detection methods. [17] Biopsy testing doesn't usually look for CWD bacteria and they would be difficult to identify because they're destroyed when taken out of the body; their protective homeostasis is lost and lysosomes in the immune system destroy them. [18]

The inability of most research labs to culture CWD bacteria has been an obstacle to their acceptance, and reliance on Koch's postulates has made it difficult to correlate CWD bacteria to specific diseases. [18] But some researchers believe Koch's postulates may have to be redefined in terms of molecular data when dormant and non-culturable bacteria are implicated as causative agents of mysterious diseases. [8] In Emerging Infectious Determinants of Chronic Diseases, the authors report "microbes can now be irrefutably linked to pathology without meeting Koch's postulates".... and "...powerful tools of molecular biology have exposed new causal links by detecting difficult-to-culture and novel agents in chronic illness settings". [19]

CWD bacteria are ubiquitous and easily acquired throughout life. They're found in water, food, air, soil, and blood products. [20-24] They can pass the placental barrier (acquisition may begin in utero) and some may be small enough to pass through filters of injectable medications. [25] CWD bacteria grow very slowly but the process may be accelerated by exogenous immunosuppressants. [26] High levels of stress can also lower immunity by inhibiting lymphocyte populations, natural killer cell activity, and antibody production. [27] The authors of Emerging Infectious Determinants of Chronic Diseases state,  

A spectrum of diverse pathogens and chronic syndromes emerges, with a range of pathways from exposure to chronic illness or disability. Complex systems of changing human behavioral traits superimposed on human, microbial, and environmental factors often determine risk for exposure and chronic outcome. [19]

CWD bacteria are considered communicable but not contagious; protective immunity depends on an effective cell-mediated immune response. [28] It's now well appreciated that pathologic processes caused by infectious agents may only emerge clinically after an incubation of decades. [29] Among the speculated causes of the increase in chronic infections are overuse of beta-lactam antibiotics (which force bacteria into CWD form) and immunosuppression via medications or excess vitamin D. [30,31] Other factors (e.g., genetics, environmental, etc.) may also hinder the host response and contribute to bacterial pathogenicity; leading to pervasive microbial dysbiosis, endocrine/immune system imbalance and chronic inflammation. Almost 60 L-forms have been identified and research continues. [32, 33] Many microbiologists now believe at least some, if not all, of the inflammation which drives the chronic disease process is caused by the presence of stealthy pathogens. [34] In a book review John McDougal writes [35] "The editors of Infection and Autoimmunity boldly state that reading the chapters in this book brings one to the conclusion that all autoimmune diseases are infectious, until proven otherwise." A considerable body of experimental and clinical evidence supports the concept that difficult-to-culture and dormant bacteria are involved in latency of infection and that these persistent bacteria may be pathogenic. [8, 36-38] The Center for Disease Control and Prevention states, "Evidence now confirms that non-communicable chronic diseases can stem from infectious agents." [35]

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