Round Two

Round Two

This is the title page of what will become the second level to understanding Cpn and its treatment. A place where you can find out more about how Cpn operates in your body and what you can do to defeat it. There is more science and technical language in this module but you should by now have enough knowledge to get to grips with it. The content of this module will hopefully be an accessible and organised review of existing material from the handbook. Some material will be rewritten especially for it but there will be many links to the work done by members since the site's inception in August 2005.

Michèle Mon, 2008-05-19 12:45

CAP for MS: Q&A and Peer Reviewed Support

CAP for MS: Q&A and Peer Reviewed Support

A Beginners Guide to Combined Antibiotic Protocol for Multiple Sclerosis: Questions, Answers and Peer Reviewed Support One of the problems with learning about various Multiple Sclerosis theories is the perception that they are in conflict with what we already know about MS. Another problem is that we often get non-authoritative or somewhat questionable support for explanations we are offered. I have assembled the following questions and answers in an effort to help others who are interested in Multiple Sclerosis to understand the reasoning behind the Combined Antibiotic Protocol and how bacterial theory can be compatible with autoimmune theory. Each link (with few exceptions) should take you to a COMPLETE peer reviewed article from a medical journal that supports the answers provided. Please let me know about any new questions you think should be included, bad links or ideas to improve the post. It is notable that there are a LOT more articles that might even be better than those I have referenced, however, I have tried to only use resources that are free, complete and authoritative. YOUR CELLS TAKEN OVER AND CONTROLLED BY BACTERIA Q: Isn’t apoptosis supposed to protect my body from bacterial infection? A: Yes, but it doesn’t always work. Your cells are pre-programmed to self-destruct when they become infected through a process called apoptosis. When infected by Chlamydia Pneumoniae, many human cells, including immune system cells, become hosts for the bacteria instead of working to destroy the bacteria. To be absolutely clear, CPn bacteria cell - living within your body's cell. It has even been shown that CPn infected host cells can proliferate via mitosis, creating more infected host cells. Lancellotti, Marcelo et al. 2006 Bacteria-induced apoptosis: an approach to bacterial pathogenesis Geng, Yuemei et al. 2000 Chlamydia pneumoniae Inhibits Apoptosis in Human Peripheral Blood Mononuclear Cells Through Induction of IL-10 Rajalingam, Krishnaraj et al. 2001 Epithelial Cells Infected with Chlamydophila pneumoniae (Chlamydia pneumoniae) Are Resistant to Apoptosis Fischer, Silke et al. 2004 Protection against CD95-Induced Apoptosis by Chlamydial Infection at a Mitochondrial Step Fischer, Silke et al. 2004 Chlamydia Inhibit Host Cell Apoptosis by Degradation of Proapoptotic BH3-only Proteins Green, Whitney et al. 2004 Chlamydia-Infected Cells Continue To Undergo Mitosis and Resist Induction of Apoptosis Sasu, Sebastian et al. 2001 Chlamydia pneumoniae and Chlamydial Heat Shock Protein 60 Stimulate Proliferation of Human Vascular Smooth Muscle Cells via Toll-Like Receptor 4 and p44/p42 Mitogen-Activated Protein Kinase Activation Q: Do my cells function differently after they become hosts for Chlamydia Pneumoniae? A: Yes. Cellular expression can be dramatically altered. Genes related to apoptosis, the cell cycle and host metabolism are permanently differentially regulated by Chlamydia Pneumoniae. Chlamydia Pneumoniae has been shown to remain transcriptionally active while hosted by immune system cells. Infected human host cells have been found to significantly increase the release of interleukin (IL) 1b, IL-6, IL-8, IL-12, tumor necrosis factor alpha (TNF-a), intercellular cell adhesion molecule 1(ICAM-1/CD54) and gamma interferon (IFN-y). These cytokines stimulate the immune system. In addition CPn activates nuclear factor kappa B (NF-kB) and down regulates major histocompatibility complex class I molecules (MHC-1). Eickhoff, Meike et al. 2007 Host Cell Responses to Chlamydia pneumoniae in Gamma Interferon-Induced Persistence Overlap Those of Productive Infection and Are Linked to Genes Involved in Apoptosis, Cell Cycle, and Metabolism Krull, Matthias et al. 2004 Differences in Cell Activation by Chlamydophila pneumoniae and Chlamydia trachomatis Infection in Human Endothelial Cells Rupp, Jan et al. 2009 Chlamydia pneumoniae Hides inside Apoptotic Neutrophils to Silently Infect and Propagate in Macrophages Gencay, Mikael et al. 2003 Chlamydia pneumoniae Activates Epithelial Cell Proliferation via NF-κB and the Glucocorticoid Receptor Yang, Jun et al. 2003 Induction of Proinflammatory Cytokines in Human Lung Epithelial Cells during Chlamydia pneumoniae Infection Yamaguchi, Hiroyuki et al. 2002 Chlamydia pneumoniae Infection Induces Differentiation of Monocytes into Macrophages Rodel, Jurgen et al. 2000 Production of Basic Fibroblast Growth Factor and Interleukin 6 by Human Smooth Muscle Cells following Infection with Chlamydia pneumoniae Gaydos, Charlotte 2000 Growth in Vascular Cells and Cytokine Production by Chlamydia pneumoniae ANTIBIOTICS FOR MS Q&A Q: Has anyone actually demonstrated a relationship between CPn bacteria and MS? A: Yes, an excellent article was published in 1999 that effectively says that lots of folks with MS also have the CPn bacteria and the prevalence of the bacteria in folks with MS is significantly greater than average. Sriram, Subramaniam et al. 1999 Chlamydia pneumoniae Infection of the Central Nervous System in Multiple Sclerosis. Q: Has CPn bacteria been identified in the central nervous system? A: Yes, in fact CPn DNA has been identified in the brain and cerebrospinal fluid. Sriram, Subramaniam et al. 2005 Detection of chlamydial bodies and antigens in the central nervous system of patients with multiple sclerosis Contini, Carlo et al. 2008 Chlamydophila pneumoniae DNA and mRNA transcript levels in peripheral blood mononuclear cells and cerebrospinal fluid of patients with multiple sclerosis Itzhaki, Ruth et al. 2004 Infiltration of the brain by pathogens causes Alzheimer’s disease Tang, Yi-Wei et al. 2009 Qualitative and Quantitative Detection of Chlamydophila pneumoniae DNA in Cerebrospinal Fluid from Multiple Sclerosis Patients and Controls Q: Can Chlamydia pneumoniae infect cellular hosts within the CNS? A: Yes, it has been demonstrated that CPn can infect and reproduce in microglial cells. Furthermore, CPn can sustain a chronic infection in neuronal cells by interfering with apoptosis. Ikejima, Hideaki et al. 2006 Chlamydia pneumoniae infection of microglial cells in vitro: a model of microbial infection for neurological disease Appelt, Denah et al. 2008 Inhibition of apoptosis in neuronal cells infected with Chlamydophila (Chlamydia) pneumoniae Q: Have there been any studies that show how CPn infection can get out of the lungs? A: Yes. It has been shown that infected Alveolar Macrophages can transmigrate through the mucosal barrier, thus giving Chlamydia Pneumoniae access to the lymphatic and systemic circulatory systems. It is also notable that Neutrophil Granulocytes (one of the first immune system cells to encounter CPn in the lungs) can host and incubate Chlamydia Pneumoniae. Gieffers, Jens et al. 2004 Phagocytes transmit Chlamydia pneumoniae from the lungs to the vasculature Blasi, Francesco et al. 2004 Chlamydia pneumoniae: crossing the barriers? Van Zandbergen, Ger et al. 2004 Chlamydia pneumoniae Multiply in Neutrophil Granulocytes and Delay Their Spontaneous Apoptosis Rodriguez, Nuria et al. 2005 Polymorphonuclear Neutrophils Improve Replication of Chlamydia pneumoniae In Vivo upon MyD88-Dependent Attraction Q: Are there any studies that show the beneficial effect of antibiotics on MS? A: Yes, there have been several studies that link antibiotics to improvement in patients with MS. Brundula, Veronika et al. 2002 Targeting leukocyte MMPs and transmigration: Minocycline as a potential therapy for multiple sclerosis Minagar, Alireza et al. 2007 Combination Therapy With Interferon Beta-1a and Doxycycline in Multiple Sclerosis Q: A lot of folks are just taking Minocycline, why are multiple antibiotics required in the protocol? A: While Minocycline is a tetracycline that can work against CPn, it cannot kill CPn in all three phases of its life cycle: elementary body, reticulate body and cryptic form. Rifampin in combination with Azithromycin has been found to be more effective than single antibiotic therapy. Wolf, Katerina et al. 1999 Effect of Azithromycin plus Rifampin versus That of Azithromycin Alone on the Eradication of Chlamydia pneumoniae from Lung Tissue in Experimental Pneumonitis. However duel therapy does not eliminate CPn in its cryptic form, which is also referred to as persistent, nonreplicating, aberrant and refractory. The addition of a third antibiotic is needed to completely eliminate CPn bacteria from the body. Gieffers, Jens et al. 2001 Chlamydia pneumoniae Infection in Circulating Human Monocytes Is Refractory to Antibiotic Treatment Hogan, Richard et al. 2004 Chlamydial Persistence: beyond the Biphasic Paradigm Mukhopadhyay, Sanghamitra et al. 2006 Protein Expression Profiles of Chlamydia pneumoniae in Models of Persistence versus Those of Heat Shock Stress Response Q: When taking antibiotics, does dosage really matter? A: Yes, not following dosage frequency and amounts can induce persistence. Gieffers, Jens et al. 2004 First-Choice Antibiotics at Subinhibitory Concentrations Induce Persistence of Chlamydia pneumoniae. SOME COMPARISONS BETWEEN BACTERIAL AND AUTOIMMUNE PATHOLOGIES Q: Does the way MMP-9 has been implicated in MS correlate with CPn infection? A: Yes it does. Increased MMP-9 expression has been demonstrated in MS and MMP-9 has been shown to disrupt myelin and cause demyelination. Chlamydia Pneumoniae has been found to stimulate the production of MMP-9 in macrophages. Leppert, David et al. 1998 Matrix metalloproteinase-9 (gelatinase B) is selectively elevated in CSF during relapses and stable phases of multiple sclerosis Yong, V. Wee et al. 2001 Metalloproteinases in Biology and Pathology of the Nervous System Vehmaan-Kreula, Pirjo et al. 2001 Chlamydia pneumoniae Proteins Induce Secretion of the 92-kDa Gelatinase by Human Monocyte–Derived Macrophages Q: Does the way IL-6 has been implicated in MS correlate with CPn infection? A: Yes it does. CPn infection is known to upregulate IL-6 and IL-6 is known to be proinflammatory in MS. In an MS related illness, Transverse Myelitis, there is evidence that IL-6 causes demyelination and axonal injury. Dasgupta, Subhajit et al. 2003 Role of Very-late Antigen-4 (VLA-4) in Myelin Basic Protein-primed T Cell Contact-induced Expression of Proinflammatory Cytokines in Microglial Cells Kaplin, Adam et al. 2005 IL-6 induces regionally selective spinal cord injury in patients with the neuroinflammatory disorder transverse myelitis Johnston, S. Claiborne et al. 2005 Chlamydia pneumoniae Burden in Carotid Arteries Is Associated With Upregulation of Plaque Interleukin-6 and Elevated C-Reactive Protein in Serum Q: Does the way ICAM-1 has been implicated in MS correlate with CPn infection? A: Yes. ICAM-1 is barely detectable in the normal brain. However, increased expression of ICAM-1 has been shown on endothelial cells, microglia and astrocytes in active MS. More specifically, ICAM-1 has been shown to be crucial for leukocyte infiltration into the brain, and the process of migration across the brain endothelial layer can accelerate the breakdown of the blood brain barrier. Several lines of evidence indicate that ICAM-1 acts as a docking molecule for lymphocytes before migration. ICAM-1 further facilitates transmigration through the CNS endothelium by rearrangement of the endothelial actin cytoskeleton, meaning ICAM-1 stimulates the altering of the impermeable tight junctions of the blood brain barrier. Chlamydia Pneumoniae can infect human endothelial cells where it induces the expression of ICAM-1, which has also been linked to monocyte migration. Etienne-Manneville, Sandrine et al. 2000 ICAM-1-Coupled Cytoskeletal Rearrangements and Transendothelial Lymphocyte Migration Involve Intracellular Calcium Signaling in Brain Endothelial Cell Lines Bullard, Daniel et al. 2007 Intercellular Adhesion Molecule-1 Expression Is Required on Multiple Cell Types for the Development of Experimental Autoimmune Encephalomyelitis Dai, Jianfeng et al. 2008 ICAM-1 Participates in the Entry of West Nile Virus into the Central Nervous System Adamson, Peter et al. 1999 Lymphocyte Migration Through Brain Endothelial Cell Monolayers Involves Signaling Through Endothelial ICAM-1 Via a Rho-Dependent Pathway Buul, Jaap et al. 2004 Signaling in Leukocyte Transendothelial Migration Lawson, Charlotte et al. 2009 ICAM-1 signaling in endothelial cells Kol, Amir et al. 1999 Chlamydial and human heat shock protein 60s activate human vascular endothelium, smooth muscle cells, and macrophages Vielma, Silvana et al. 2003 Chlamydophila pneumoniae Induces ICAM-1 Expression in Human Aortic Endothelial Cells via Protein Kinase C–Dependent Activation of Nuclear Factor- B Q: Does the way Immunoglobulin G antibodies (IgG) have been implicated in MS correlate with CPn infection? A: Yes. The detection of elevated IgG in Cerebral Spinal Fluid (CSF) via oligoclonal bands has an extensive association with the diagnosis of MS by lumbar puncture. In fact, unique antibody patterns have been associated with the different types of MS and IgG from MS patients may provoke T-cell response. Likewise, anti-Chlamydia Pneumoniae antibodies (IgG) have been associated with MS. These have been identified in the CSF of MS patients and been shown to have greater gene transcription. Interestingly, it has also been shown that CPn infection can lead to an accumulation of IgG within an infected cell, which potentially correlates with increased IgG populations in patients with a longer history of MS. Ezio Paolino et al. 1996 A prospective study on the predictive value of CSF oligoclonal bands and MRI in acute isolated neurological syndromes for subsequent progression to multiple sclerosis Francisco Quintana et al. 2008 Antigen microarrays identify unique serum autoantibody signatures in clinical and pathologic subtypes of multiple sclerosis Holmoy, Trygve et al. 2003 T cells from multiple sclerosis patients recognize immunoglobulin G from cerebrospinal fluid (abstract only) Enrico, Fainardi et al. 2008 Under the microscope: focus on Chlamydia pneumoniae infection and multiple sclerosis (abstract only) Dong-Si, Tuan et al. 2004 Increased prevalence of and gene transcription by Chlamydia pneumoniae in cerebrospinal fluid of patients with relapsing-remitting multiple sclerosis Yao, Song-Yi et al. 2001 CSF oligoclonal bands in MS include antibodies against Chlamydophila antigens Pollack, David et al. 2008 Uptake and intra-inclusion accumulation of exogenous immunoglobulin by Chlamydia-infected cells Owens, Gregory et al. 2003 Single-cell repertoire analysis demonstrates that clonal expansion is a prominent feature of the B cell response in multiple sclerosis cerebrospinal fluid Q: Does the way IFN-y {gamma} has been implicated in MS correlate with CPn infection? A: Yes it does. IFN-y has been associated with exacerbations and oligodenrocyte death. It has been shown that IFN-y expression plays a central role in the bodys effort to control Chlamydia Pneumoniae infection. Panitch, Hillel et al. 1987 Treatment of multiple sclerosis with gamma interferon Mana, Paula et al. 2006 Deleterious Role of IFN in a Toxic Model of Central Nervous System Demyelination Rottenberg, Martin et al. 2000 Regulation and Role of IFN-y in the Innate Resistance to Infection with Chlamydia pneumoniae Q: Monocytes have been implicated in MS. How does this relate to CPn infection? A: Monocytes have been found to migrate across the blood brain barrier and contribute to inflammation. Some benefits associated with MS therapies have been linked to their targeting monocytes. Monocytes are easily infected with CPn and can disseminate CPn within systemic circulation. Bar-Or, Amit et al. 2003 Analyses of all matrix metalloproteinase members in leukocytes emphasize monocytes as major inflammatory mediators in multiple sclerosis Kopadze, Ted et al. 2006 Inhibition by Mitoxantrone of In Vitro Migration of Immunocompetent Cells: A Possible Mechanism for Therapeutic Efficacy in the Treatment of Multiple Sclerosis Minagar, Alireza et al. 2008 Combination Therapy With Interferon Beta-1a and Doxycycline in Multiple Sclerosis: An Open-Label Trial Burger, Danielle et al. 2009 Glatiramer acetate increases IL-1 receptor antagonist but decreases T cell-induced IL-1β in human monocytes and multiple sclerosis Hakki, Amal et al. 2007 Chlamydia pneumoniae infection modulates cytokine production by human T lymphocytes and monocytes Gieffers, Jens et al. 2001 Chlamydia pneumoniae Infection in Circulating Human Monocytes Is Refractory to Antibiotic Treatment Q: Besides monocytes, do other immune system cells have behavior that correlates between MS and CPn infection? A: Lymphocytes are also a major group of immune system cells that exhibit potentially corroborating behavior in MS and CPn infection. T-Lymphocyte and B-Lymphocyte migration through the brain endothelium/blood brain barrier has been associated with Multiple Sclerosis. Chlamydia Pneumoniae has been shown to infect and multiply in Lymphocytes. CPn infected Lymphocytes have been shown to be resistant to some antibiotic therapies. Alter, Andrea et al. 2003 Determinants of Human B Cell Migration Across Brain Endothelial Cells Prat, Alexandre et al. 2002 Migration of Multiple Sclerosis Lymphocytes Through Brain Endothelium Haranaga, Shusaku et al. 2001 Chlamydia pneumoniae Infects and Multiplies in Lymphocytes In Vitro Yamaguchi, Hiroyuki et al. 2003 Chlamydia pneumoniae Resists Antibiotics in Lymphocytes AUTOIMMUNE PATHOLOGY IS STILL A THEORY Q: Has it been proven that MS is an autoimmune illness? A: No. While science has pursued autoimmune theory for decades, it has yet to be proven that the underlying cause of MS is initiated or perpetuated through autoimmunity. Chaudhuri, Abhijit et al. 2005 Multiple sclerosis: looking beyond autoimmunity

notasperfectasyou Tue, 2009-06-09 12:53

Chlamydia Pneumoniae, Antibiotics and Reactions

Chlamydia Pneumoniae, Antibiotics and Reactions

  Chlamydia Pneumoniae, Antibiotics and Reactions Drawn from materials on www.cpnhelp.org Chlamydia pneumoniae (Cpn) is an intracellular bacterium, which means that it invades the body cells, and it is an obligate parasite, which means that it cannot supply its own energy source and so takes over the ATP of the body cells it invades for its own reproduction, depleting the host cells and leaving them less functional. One of the difficulties in eradicating Cpn is that it is a multiphase organism (see more detail on this below). This is not typically understood in standard medical management of Cpn infections, although it is well known that Cpn infections can be “persistent”. Standard medical treatment of Cpn infection utilizes a single antibiotic, typically for a couple of weeks or months. No matter how long a single antibiotic is used, nor how many courses, a single agent cannot kill the Cpn in all of its life phases. Dr. Charles Stratton’s lab demonstrated that monotherapy antibiotics (use of a single antibiotic such as azithromycin) that kill Cpn in one phase do not necessarily kill it in other phases. So unless a protocol uses agents that cover all three phases of the organism it simply converts to another phase to survive and then takes up reproduction and dissemination in the body once that antibiotic is withdrawn.

  • Standard serological tests for Cpn are often false-negative in the face of actual infection, rendering them unreliable indicators. Often treatment response to an empirical course of CAP treatment, when symptoms are suggestive for Cpn, is the best indicator of infection.
  • While it is transmitted as a respiratory infection, Cpn can be carried to other parts of the body and infect many other tissues, including nerve tissue, the brain, muscles, kidneys, liver, prostate, the lining of blood vessels and especially the immune cells (macrophages and monocytes). Thus, this single organism can cause a wide array of problems. (See “Cpn & Multiple Diseases” for more on this.)
  • Persistence and Resistance- The standard single antibiotic courses (monotherapy) typically used in medicine actually creates persistence of the organism by forcing it to convert into a different phase unaffected by the antibiotic. In addition, repeated courses of single antibiotic increases the risk of creating pools of Cpn resistant to that particular agent. Persistence being the re-emergence of an infection apparently knocked down by treatment; Resistance being the adaptation by a bacterium so that it is no longer susceptible to an antibiotic.
  • Combination Antibiotic Protocol- Using the highly sensitive measures they created at Vanderbilt, Dr. Stratton and his colleagues found that the only way to eradicate Cpn completely, avoiding both persistence and resistance, is to take a combination of antibiotics so as to kill it in all of its life phases so that nothing is left behind to re-infect. This is called a Combination Antibiotic Protocol or CAP. This can take a long time depending on the load of Cpn in your system, the organs infected and other variables. Typical courses of 1-3 years are not unusual. It also takes time in many cases because the progression onto full doses of the combined agents must be gradual to avoid precipitating debilitating toxic reactions to bacterial die-off and make the treatment tolerable.
  • Treatment reactions: There are three distinct and sometimes strong reactions to killing Cpn with a Combination Antibiotic Protocol that must be considered in its treatment. Calling these reactions collectively a “herx” (short for Herxheimer reactions) is both inaccurate and not useful to treatment, as only one of them is a classical Herxheimer reaction.
    • Endotoxin Reaction- Cpn contains at least two endotoxins (LPS and HSP60). Killing Cpn can release significant amounts of these endotoxins typified by drop or increase in body temperature (chills or fever), and cytokine (immune) cascade followed by widespread inflammation. Chronic immune activation and toxic load from long term and hidden Cpn infection also causes hidden tissue damage and disease.
    • Secondary Porphyria[i]- Cpn, as an obligate parasite, infects inside your cells and parasitically steals energy (ATP) from your body cells in order to replicate. Many of the cells it infects are responsible for producing heme an important constituent of our blood and used in many places in the body. Heme requires a huge amount of ATP to go from start to finish in its 6 step production process, and any of the intermediate compounds along the way (called porphyrins) are highly neurotoxic and oxidative. Cells parasitized by Cpn will not have enough ATP to carry through this process, and so accumulate these toxic porphyrins.

Killing the Cpn (which often kills the cells infected) releases porphyrins into the blood and other tissues causing symptoms of secondary porpyria: gastrointestinal disturbance, nausea, pain, light and sound sensitivity, anxiety, rapid heart rate, depression, brain fog, and other symptoms.

    • The parasitization of infected cells also renders those cells and the organs they are part of less functional over time as Cpn load increases in them. Cpn is well documented to infect the bone marrow, macrophages, monocytes thus rendering immune dysfunction, as well as the fatigue commonly seen in CFIDS.

Phases of the Cpn bacteria and antibiotic agents that effect those phases:  EB’s- Elementary Body What are they? EB’s are spore-like forms that are infectious and have minimal metabolism (aren’t using nutrients, replicating, exchanging with the environment, etc.). They are tough, tiny and reside in the intercellular tissues). EB’s attach to your body cells and invade them. Since there can be more EB’s than can get into cells, EB’s build up in local tissues where their endotoxins cause inflammation and immune response. They are killed by amoxicillin or NAC (N-acetyl cysteine) both destroy the cysteine bonds that hold the EB cell wall together. RB's- Reticulate Body Once an EB enters a host cell it transforms into a form that can replicate new EB’s that is called a Reticulate Body or RB. The RB has no energy source of it's own for this, so it must steal energy (ATP) from the host cell, leaving the host cell weakened and less functional. The RB also inhibits the natural cell death (apoptosis) of the host cell so that it can survive while it replicates. After the production of many new EB's the host cell bursts and dies, spreading the infectious new EB's into the surrounding tissue. RB's are inhibited in replicating by various antibiotics principally: doxycycline, azithromycin, roxythromycin, Isoniazid (INH), rifampin. Cryptic persistent form When RBs face an environment that threatens their survival (lack of food, antibiotics, etc) they can transform into a “Cryptic” form that stays inside the cell, but is in hibernation, so to speak. In this form Cpn is not vulnerable to regular antibiotics as it is not replicating or metabolizing, and can reside there until conditions change, then converting back to an RB again, replicating and reinfecting with EBs. As the Cryptic form is anaerobic, it is killed by Flagyl (metronidazole) or Tinactin (tinidazole). These drugs can be hard to tolerate for various reasons, and so are commonly “pulsed” by taking a course of them while continuing the regular antibiotics (protein synthase inhibitors), for 5 days every 3-4 weeks, rather than taken continuously. Some protocols may eventually have one of these drugs taken continuously for some period as the patient can tolerate. Patients may experience fatigue; nausea, bowel upset, deep joint achyness and muscle pain as the cryptic organisms are killed and the immune system engages in clean up. SUMMARY Amoxicillin and NAC kills the infectious spore-like EB forms which build up in the tissues. Rifamcin kills EB’s transforming to RB’s in a vulnerable enzyme transformation phase. Doxycycline and either Roxythromycin or Azithromycin, are used in combination to interfere with the RB’s ability to replicate. Two are usually used concurrently, as they work on different proteins and so together minimize chances of creating antibiotic resistance. Metronidazole or tinidazole will infiltrate the cells and kill the cryptic Cpn. Supplements are recommended to help counter the impact of Cpn on the body, and of the inflammatory effect of the die off during treatment.  The Combination Antibiotic Protocol (CAP) for Cpn therefore consists of building up gradually to:

  1. Two protein synthase inhibitors continuously (such as 200mg doxycycline daily plus 250mg azithromycin 3x per week)
  2. Alternately, daily Rifampin and/or Isoniazid
  3. 2400mg NAC daily or amoxicillin
  4. 5-day pulses of 1000-1500mg Flagyl or Tinidazole every 2-4 weeks.
  5. A regimen of supplements to enhance body function, detoxification, counter oxidation and inflammation, and enhance cell replacement.

Treatment can take months to years to completely eradicate Cpn from the body. What diseases has Chlamydia pneumoniae been implicated in? The following are just a few of the diseases associated with Cpn, more and more are being discovered all the time. Cpn is a vascular disease and therefore can affect all parts of the body. · Alzheimer's disease · Arthritis · Asthma · Cardiac disease · Chronic fatigue · Chronic refractory sinusitis · Crohn's disease · Fibromyalgia · Inflammatory bowel disease · Interstitial cystitis · Multiple sclerosis · Prostatitis [i] Secondary Porphyria- One of the significant discoveries made at Vanderbilt is that Cpn infection causes secondary porphyria, with significant effects on the nervous system, gut, and other tissues. Cpn interferes with heme production, a multiphase chemical process in the body that requires considerable ATP, by stealing the ATP from the host cell. Without adequate ATP, heme production is stopped at the point where unstable porphyrins, highly toxic, oxidizing and neurotoxic, build up. Highly simplified, heme synthesis looks like this: Heme precursors >> porphrinogens>> transformation to heme >> increased cellular transport including ATP production. Instead, Cpn interferes with this normal process, and this happens: Heme precursors >> porphrinogens >> inadequate ATP does not allow full transformation to heme >> build up of unstable heme precursors and porphyrins inside and outside cells >> free radical damage and further reduced ATP (energy) synthesis. When infected host cells already loaded with accumulated porphyrins are killed (apoptosis) by antibiotic treatment, these are dumped en masse into the bloodstream precipitating porphyric reactions such as nausea, intestinal disturbance and spasm, and neurological reactions including anxiety, neuropathy, profound fatigue, depression, “fogginess” and so on. Some of what has been mislabeled as a “herx” reaction to treatment is actually acute porphyria reaction and not a reaction to bacterial endotoxin– which is what a true Herxheimer reaction is about. Porphyrins are cleared only with difficulty from the body. Some are water-soluble and are excreted in urine. Others are fat-soluble and are processed by the liver and dumped into the bowel where they further aggravate bowel problems. Significant portions are actually reabsorbed from the bowel unless bound to a substance like activated charcoal or Questran. Re-absorbtion further burdens an already toxic overload.  

Michèle Tue, 2008-05-20 05:09

Dr. Charles Stratton on Cpn (Powerpoint presentation)

Dr. Charles Stratton on Cpn (Powerpoint presentation)

Here is a Powerpoint presentation by Dr Stratton, showing images of Cpn, diagrams explaining the life cycle and bullet point headings explaining the biochemical processes both of the bacterium and in vivo (in the body).

Michèle Sat, 2008-05-31 09:42

Supplements: Lists and Rationale

Supplements: Lists and Rationale

Nearly as important as the Antibiotics in the treatment of Cpn are the supplements. Different people will need different things but there is a rationale behind the list of recommended supplements and here you will find links that take you to previous discussions or articles that explain the reasons why we take them. List of Recommended SupplementsAntifungals and Probiotics Where to Buy Supplements Downloadable PDF of Supplements Monographs Links to articles on a number of the supplements we take. Vitamin D

Michèle Tue, 2008-05-20 05:45

Doing Some Research

Doing Some Research

Cypriane wrote this in 2006 to help people get more out of the Cpnhelp.org.   She tells her story and explains how she first got started with research on and off the site.  She also makes some useful observations about the history of research into Cpn.

Michèle Sat, 2008-05-31 09:57

Discussion on the Use of Longterm Antibitotics

Discussion on the Use of Longterm Antibitotics

The use of antibiotics has become a prickly issue for doctors, patients and the media.   There are several reasons for this:

  • Some bacteria have become resistent to antibiotics; this leads to 'superbugs' which are resitent to all but a handful of antibiotics.
  • Patients have been prone to asking for antibiotics when suffering from a viral infection.   Antibiotics have no action of viruses.
  • The practice of prescribing short courses of antibiotics means that a person suffering from a Cpn infection may appear to get better for a little while but will shortly feel ill again.   This may lead some doctors to think that either antibiotics are ineffective against Cpn or that the patient is suffering from a viral infection.

Here is an article that Jim wrote which answers some of the above concerns.

Michèle Sat, 2008-05-31 10:13