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Chlamydia is currently one of the most common sexually transmitted diseases — about 4 million cases of chlamydia occur in the USA each year. However, about half of all men and three-quarters of all women who have chlamydia have no symptoms and don't know that they have the disease. The disease is transmitted by the Chlamydia trachomatis bacterium. It can be serious but it is easily cured if detected in time. It is also, and possibly more importantly, the biggest preventable cause of blindness in the world. Blindness occurs as a complication of trachoma (chlamydia conjunctivitis). more...

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Almost half of all women who get chlamydia and aren't treated by a doctor will get pelvic inflammatory disease (PID), a generic term for infection of the uterus, fallopian tubes, and/or ovaries. PID can cause scarring inside the reproductive organs, which can later cause serious complications, including chronic pelvic pain, difficulty becoming pregnant, ectopic (tubal) pregnancy, and other dangerous complications of pregnancy. Chlamydia causes 250,000 to 500,000 cases of PID every year in the U.S.

In women, chlamydia may not cause any symptoms, but symptoms that may occur include: unusual vaginal bleeding or discharge, pain in the abdomen, painful sexual intercourse, fever, painful urination or the urge to urinate more frequently than usual.

In men, chlamydia may not cause any symptoms, but symptoms that may occur include: a painful or burning sensation when urinating, an unusual discharge from the penis, swollen or tender testicles, or fever.

Chlamydia in men can spread to the testicles, causing epididymitis, which can cause sterility. Chlamydia causes more than 250,000 cases of epididymitis in the USA each year.

Chlamydia may also cause Reiter's Syndrome, especially in young men. About 15,000 men get Reiter's Syndrome from chlamydia each year in the USA, and about 5,000 are permanently affected by it.

As many as half of all infants born to mothers with chlamydia will be born with the disease. Chlamydia can affect infants by causing spontaneous abortion (miscarriage), premature birth, blindness, and pneumonia.


Fortunately, chlamydia can be effectively cured with antibiotics once it is detected. Current Centers for Disease Control guidelines provide for the following treatments:

  • Azithromycin 1 gram by mouth once, or
  • Doxycycline 100 milligrams twice daily for seven days.


Because chlamydia is so common and because it often doesn't produce symptoms, it is especially important to take precautions against sexually transmitted disease by practicing safer sex.


Chlamydiae replicate intracellularly, within a membrane-bound structure termed an inclusion. It is inside this inclusion, which somehow avoids lysosomal fusion and subsequent degradation, that the metabolically inactive "elementary body" (EB) form of Chlamydia becomes the replicative "reticulate body" (RB). The multiplying RBs then become EBs again and burst out of the host cell to continue the infection cycle. Since Chlamydiae are obligate intracellular parasites, they cannot be cultured outside of host cells, leading to many difficulties in research.


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New discoveries in the successful treatment of Chlamydia, parasites and biofilms
From Townsend Letter for Doctors and Patients, 7/1/04 by Paul Yanick, Jr.

Drug-resistant micro-organisms continue to emerge and the number of patients susceptible to these infections is increasing dramatically. Consequently, any technologies and insights that utilize the innate powers of the immune system as a therapeutic agent will have the greatest benefit to sick patients. New scientific findings demonstrate that it is possible to employ molecular strategies that can strengthen the immune response to a given antigen or to direct it to combat an overlooked, hidden, or treatment-resistant foe. The complexity of the immune system with its abundance of compounds and molecular strategies can forge medical innovation and help practitioners to develop therapies that might combat maladies ranging from pneumonia that repeatedly afflicts people with cystic fibrosis to deep and silent infections that promote pain and inflammation in arthritic disorders. Improvement in pharmaceutical and nutraceutical delivery systems is of key importance now and in the future.


While the power and flexibility of the immune system against infection is remarkable, intracellular bacterial parasites, Chlamydia (Chlamydia trachomatis, Chlamydia psittaci and Chlamydia pneumonia) that proliferate within host cells and in the bone, gall bladder and sinus cavities are difficult for the immune system to conquer. In many cases, it seems to expend all its energy engaging in endless microbial warfare without ever completely winning the battle. The tremendous diversity and mutability of many infections and their ability to intelligently exploit the cells and interactions of the immune system to propagate themselves, is the main focus of this column. Why? Because infections of this nature are the most prevalent infections facing humans and are of serious concern in immunodeficient patients as they relentlessly produce endotoxins that activate prolonged inflammation and tissue damage in the organism. Unraveling the signals that cause these infections to proliferate will require that clinicians learn natural and safe ways to strengthen innate responses to invading microbes, mitigate the damage that immune cells do to the body, and correct or eliminate nutritional deficiencies that cause immunological unresponsiveness.

This column will focus primarily on biofilms, Chlamydia pasittaci and Chlamydia pneumonia as primary pathogens in the genesis of many high profile diseases. Chlamydia enters into cells via abnormalities of key cell membrane receptors, and settles down into anaerobic tissue sites as a mucous-like and sticky matrix where it aggregates, communicates, and constructs slimy edifices called biofilms. (1-7) Because biofilms resonate harmoniously and consist of a dense symbiotic aggregation of microbes embedded in a highly hydrated polymer, polysaccharide matrix of its own secretion, they often end up in the cornea, tonsils, wounds, nasopharynx, middle ear, prostate and urinary tract, teeth (under root canals, fillings, implants, or as chronic bacterial ostitis in extraction sites), dental plaque, oral soft tissues, gall bladder, GI epithelium, heart (endocarditis) and lungs, making them notoriously difficult to treat. Their anti-microbial resistance coupled with the inaccuracy of current lab tests to diagnose hidden biofilms and intracellular infections makes biofilms the greatest clinical challenge facing doctors today. (8-13)

Bacterial biofims are ubiquitous--dental plaque (which confront us daily) and the slime that grows inside a flower vase after two or three days are common examples. The biofilm concept of chronic infections explains a phenomenon that has troubled clinicians for some time: blood cultures from patients who show many signs of overt bacterial infection are often negative. According to Dr. J.W. Costerton, of the Center for Biofilm Engineering at Montana State University "biofilms are in all of the chronic infections examined in the 12 years during which this morphological series was pursued." He further states "When the model used to analyze a natural process is incorrect, our attempts to understand and manipulate the process will fail, many honest and conscientious people will be frustrated, and the reputations of whole research groups will be damaged. In the case of chronic bacterial diseases, diagnostic microbiology labs reported that cultures of Pseudomonas aeruginosa from Cystic Fibrosis (CF) patients were sensitive to antibiotics (e.g., cloxacillin), but pulmonary clinicians saw little improvement when these antibiotics were used. The sera of CF patients contained very large amounts of specific antibodies against Pseudomonas, but the disease persisted, and the use of anti-Pseudomonas vaccines resulted in the deaths of some patients. Middle ear specimens from children with chronic otitis media with effusion (COME) yielded negative bacterial cultures, so that a host-sustained inflammatory etiology was suspected, but the factors driving the inflammation could not be identified and serology did not confirm the persistent involvement of viruses. Patients with raging febrile prostate infections yielded expressed prostatic secretion (EPS) samples that produced cultures negative for bacteria, and material recovered from osteomyelitis debridations with frank pus yielded only a few colonies of skin and environmental organisms. All was shadows and fog, and the reputations of the microbiology units of many hospitals plummeted from the high levels they had attained earlier." (14)

Biofilms have material properties similar to those of a viscous fluid and micro-colonies are deformable as they oscillate in high-shear systems, breaking off and detaching as biofilm fragments that spread into different areas of the body. (15,16) Biofilm-related infections are involved in the deterioration of gums and jawbone that eventually leads to loss of teeth (periodontal disease); ear infections in the outer ear canal, middle and inner ear, stubborn sinus infections, and chronic gall bladder and cardiac infections. In addition, root canal teeth and dental implants often become colonized by Chlamydia creating a slow developing but persistent infection that often lingers for years. In most cases, we have found that the infection is extremely difficult to diagnose and eradicate.

Even in the healthy immune system, the unleashing of its magnificent and diverse arsenal of antimicrobial agents fails to conquer biofilms and intracellular Chlamydia. Likewise, even long-term treatment with one antibiotic after another, infections persist. Our research has begun to shed light on the mechanisms of biofilm resistance to antimicrobial agents. The primary problem is the inability of the antimicrobial agent to fully penetrate the biofilm leaving bacteria to exist in a protected state as they mutate and adopt a distinct and intrinsically resistant phenotype. Mutational aberrations may contribute to altered infectivity and changes in the amino acid signature patterns of Chlamydia, although additional studies will be required to address these issues.

Understanding Biofilm Resistance

A biofilm's exceptional resistance stems from several characteristics:

1. As they activate specialized resistance genes, bacteria in biofilms benefit from pooling their efforts. Colonies of bacteria can produce enzymes to inactivate the antiseptic hydrogen peroxide and allow other immune-fighting compounds (molecules and cells that the immune system unleashes) to be evaded. Microorganisms that attach to a surface turn on new genes, turn off others, and embark on a developmental path that is completely different from that taken by microbes growing in traditional suspended cultures. Moreover, the wide range of conditions present in a biofilm permit several bacterial species to live side by side and thrive as one species feeds off the metabolic wastes of another, aiding them both.

2. Dormant cells don't participate in the activity; they aren't usually vulnerable to drugs (although these bacteria don't actively contribute to the growing colony, they can weather the catastrophe of antibiotic treatment and quickly renew the biofilm afterward as competition from other microbes are decreased).

3. The interior of the biofilm offers a shelter from antibiotics (it harbors little oxygen, which some antibiotics need to work) and anti-microbial herbs (molecular structure is too large to penetrate or dissolve a biofilm). The diversity of bacteria in a biofilm can occupy a spectrum of physiological states, from rapidly growing to dormant.

4. Overburdening of the liver's detoxification mechanism with stressors (chemicals, dysbiotic bowels, mycotoxins, heavy metals, parasites, mycoplasma and herpetic infections, etc) causes biofilms to enter the gall bladder and damage the sphincter of oddi causing chronic duodenitis, the primary cause of maldigestion, malnourishment and inefficient liver detoxification, weakening the immune system even more. (17,18) To make matters worse, electron micrographs with laser scanning confocal microscopy document that biofims manufacture stones--"calculi" in the gall bladder and kidneys. (19,20)

5. Undiagnosed dental foci from old root canals, extraction sites, implants, cracked fillings, periodontal pockets allow bioflims to proliferate and spread into the sinus cavities, heart and gall bladder. Moreover, cells that detach from biofilms end up growing on native heart valves (resulting in endocarditis) and they usually circulate until they block or jam a capillary bed causing profound damage if they detach and find their way to critical loci in the lungs or in the brain. (17,18,42,43)

Understanding Effective Treatment Strategies

While the immune system can mop up free-floating bacteria in the blood, it has difficulty reaching bacteria in biofilms. In most cases, doctors resort to the overuse of antibiotics, but bacteria in biofilms clearly react differently than lone bacterial cells do to these assaults and all this treatment accomplishes is to allow the biofilm bacteria to flourish and gain resistance as the antibiotic eliminates susceptible cells and bacteria. Effective treatment should consist of strategies that:

1. Penetrate the biofilm. New biomolecular technologies developed by the author allow for the micronization (less than one hundredth of a millimeter) and concentration (100:1 to 600:1) of phytochemicals and anti-microbial herbs hold great promise for the eradication of biofilms. Understanding the diffusion methods of nutrients into biofilms and the mix of metabolic states at different layers of a biofilm, provide a methodology for the effective biomolecular penetration of anti-biofilm, antibacterial, antibiotic, antimycotic, antimicrobial, and antiviral phytochemical compounds deep into biofilms, thereby allowing them to dissolve and be eliminated. (21-26)

2. Remove all stressors. Stressors that overload and weaken the immune system must be eliminated. Most importantly, clinicians must remove interferences (dental foci, implants, etc) and define and weed out stressors (chemicals, overburdened detoxification functions, dysbiotic bowels, mycotoxins, heavy metals, mycoplasma and herpetic infections, etc). (27,28)

3. Disrupt the bacterial exchange of intercellular signals (analogous to hormones) that are important in mediating the formation of the complex architecture of natural biofilms. The recognition that biofilm formation is a biologically regulated process is an insight that carries profound medical significance because it envisions the use of phytomedicines as new therapeutic targets. Phytomedicines--concentrated from 100:1 to 600:1--break up biofilm infections. When micronized, phytomedicines can interfere with the biofilm developmental process so that the immune system can quickly conquer the infection. (4-7)

4. Optimize the immunological synapse to prevent Chlamydia entry into cells or attachment to biofilm sites. Without delving into the complexities of receptor dynamics and intracellular trafficking, cells communicate with their environment through membrane receptors, which recognize molecules and particles in the extracellular matrix, and gate them in or out of the cell. Our research has focused on the entry and intracellular traffic of Chlamydia due to specific biochemical imbalances. Receptors on lymphocytes (T lymphocyte antigen receptor and the receptors of a cytokine, the interleukin 2) are essential for the immune response. As an intracellular parasite, the entry of Chlamydia into the host cell, in particular by epithelial cells, determines its impact and resultant threat to human health. For an optimal immunological synapse, the cell membrane protein ezrin and the T cell antigen receptor should be polarized towards the antigen presenting cell contact site upon antigen recognition. In turn, polarized endocytic vesicles are transported to the cell-cell contact site and this transport facilitates the accumulation at the immunological synapse of membrane receptors that undergo cycles of endocytosis and recycling. However, when erzin has a negative charge due to an aspartic acid deficiency or is mutated, Protein Kinase C, a key signaling molecule for T cell activation that also translocates to the immunological synapse, is diminished, reducing T cell activation. Our preliminary findings indicate that correcting an aspartic acid deficiency while maintaining an adequate daily dose of the histamine-GLA-zinc complex to counter unwanted inflammation, (29,30) may help normalize the polarity of ezrin and thus provide a link between membrane and actin cytoskeleton components that helps proper molecular clustering at the immunological synapse and T cell activation. (6,32-42)

In summary, sophisticated tools of microbiology reveal that chronic diseases involve pathogenic mechanisms demonstrating unequivocally that bacterial biofilms are both present and metabolically active, even when bacteria cultures are negative. Biofilms force victims to submit to the abuse and overuse of antibiotics for the remainder of their lives. (45) The fact that chronic infections commonly grow in biofilms goes some distance toward explaining the perceived anomalies of many diseases, and offers a measure of hope that they can eventually be controlled.

Successful clinical treatment and reduction of tenacious biofilm stressors requires the development of new agents to control biofilm infections by interfering with the biofilm developmental process thereby allowing the immune response to naturally conquer the microbial threat of Chlamydia and other symbiotic infections. In some cases, an implant must be removed, a procedure that is often costly, dangerous, and traumatic for the patient.

A hallmark of all biofilm diseases is the chronic nature of the infections as infections linger for months, years, or even a lifetime as it compromises the quality of life and exhausts the immune system. With new exciting insights about biofilms and how Chlamydia enters cells, it becomes plausible that solutions to prolonged inflammation (commonly due to bacterial endotoxins) will be found. Since swollen and inflamed tissue allows biofilms to proliferate and block the immune system from fighting infection, it makes sense to find natural ways to diminish unwanted inflammation. (29-31)

In retrospect, it is astonishing that medicine has overlooked biofilms and has not used the elegant weapons of the plant kingdom in appropriate biomolecular concentrates to disrupt the microcolonies of bacteria that underlie biofilms.


1. Torres al. TCR dynamics in human mature T lymphocytes lacking CD3g. J. Immunol, 2003; 170, 5947-55.

2. Jutras I et al. Chlamydia entry into host cells involves cholesterol-rich membrane domains. Infect. Immun., 2003; 71, 260-266.

3. Weil R et al. Induction of the NF-kappaB cascade by recruitment of the scaffold molecule NEMO to the T cell receptor. Immunity, 2003; 18, 13-26.

4. Ragimbeau, J et al. The tyrosine kinase Tyk2 controls IFNAR1 cell surface expression. EMBO J. 2003; 22, 537-547.

5. Groysman M. et al Vav1 and Ly-GDI, two regulators of Rho GTPases function cooperatively as signal transducers in T cell antigen receptor induced pathways. J. Biol. Chem., 2002, 277, 50121-50130.

6. Das, V et al Membrane-cytoskeleton interactions during the formation of the immunological synapse and subsequent T cell activation. Immunol. Reviews, 2002; 189, 123-135.

7. Poupon V et al. Differential nucleocytoplasmic trafficking between the related endocytic proteins Eps15 and Eps15R. J. Biol. Chem. 2002; 277, 8941-8948.

8. Ellis M. Invasive fungal infections: evolving challenges for diagnosis and therapeutics. Mol Immunol 2002; 38:947-57.

9. O'Toole GA et al. Biofilm formation as microbial development. Annu Rev Microbiol 2000;54:49-79.

10. Ramage G et al. Biofilm formation by Candida dubliniensis. J Clin Microbiol 2001;39:3234-40.

11. Adam B et al Mixed species biofilms of Candida albicans and Staphylococcus epidermidis. J Med Microbiol 2002;51:344-9.

12. Chicurel, M. 2000. Slimebusters. Nature 408(Nov. 16):284.

13. Costerton, J.W et al. Bacterial biofilms: A common cause of persistent infections. Science 284 (May 1999):1318-1322.

14. Costerton et al J. Clin, Invest. 112:1466-1477 (2003)

15. Stoodley P et al. Biofilms as complex differentiated communities. Annu. Rev. Microbiol 2002; 56:187-209.

16. Stoodley, P et al. 2001. Growth and detachment of cell clusters from mature mixed species biofilms. Appl. Environ. Microbiol. 67:5608-5613.

17. Yanick P Disorders of the gall bladder and duodenum in overweight patients. June 1994. Townsend Letter for Doctors and Patients. 568-70.

18. Yanick P Detoxification Breakthroughs for Addictions and Chronic Toxicity. Townsend Letter for Doctors and Patients. 2001 (July) 93-95.

19. Sung, J.Y. et al. 1992. Ascending infection of the biliary tract after surgical sphincterotomy and biliary stenting. J. Gastroenterol. Hepatol. 7:240-245.

20. Sung, J.Y. et al. 1991. Bacterial invasion of the biliary system by way of the portalvenous system. Hepatology. 14:313-317.

21. Davies, D.G., et al. The involvement of cell-to-cell signals in the development of a bacterial biofilm. Science 1998; 280(April 10):295.

22. Givskov, M. 2001. The presence of AHL signals and the effects of signal inhibitors in Pseudomonas aeruginosa involved in cystic fibrosis infections infectious. Amer Soc for Microbio 101st General Meeting. Orlando.

23. Potera, C. 1999. Forging a link between biofilms and disease. Science 283(March 19):1837-1839.

24. Sauer, K. 2001. Biofilm phenotype and signaling mechanisms in Pseudomonas aeruginosa. American Society for Microbiology 101st General Meeting. May 23. Orlando.

25. Singh, P.K., et al. 2000. Quorum-sensing signals indicate that cystic fibrosis lungs are infected with bacterial biofilms. Nature 407(Oct. 12):762.

26. Stewart, P.S. 2001. Antibiotic resistance of biofilm bacteria. American Society for Microbiology 101st General Meeting. May 23. Orlando.

27. Yanick P Quantum Repatterning Technique Amer Chiropractic 2003; 50.

28. Yanick P The Quantum Repatterning Technique: Assessing Immunological Unresponsiveness in Prolonged Viral Illness. Townsend Letter for Doctors and Patients. 2003 (Jan) 128-130.

29. Yanick P Histadine-GLA-Zinc Complex to Block Unwanted Pain & Inflammation. Townsend Letter for Doctors and Patients. 2004 (Feb-March) 164-167.

30. Yanick P Nutrition/Flexoelectric Breakthroughs for the Relief of Prolonged Inflammation. Townsend Letter for Doctors and Patients. 2004 (in press).

31. Pant,DD et al Improved sensitivity of a modified polymerase chain reaction amplified DNA probe in comparison with serial tissue culture passage for detection of Chlamydia trachomatis in conjunctival specimens from nepal. Diagn Microbiol Infect Dis 1989: 12: 133-7.

32. Bebear DB et al Specific amplification of a DNA sequence common to all Chlamydia trachomatis using PCR. 1989. Res Microbiol 140: 7-16.

33. Storey CC et al Analysis of the complete nucleotide sequence of Chp1, a phage which infects avian Chlamydia psittaci. J Gen Virol 1989. 70 (Pt 12): 3381-90.

34. Storey CC et al Further characterization of a bacteriophage recovered from an avian strain of Chlamydia psittaci. J Gen Virol 1989. 70 (Pt 6): 1321-7.

35. Everett KD et al Sequence analysis, lipid modification of the cysteine-rich envelope proteins of Chlamydia. J Bacteriol 1991; 173: 3821-30.

36. Kaltenboeck B et al Detection and strain differentiation of Chlamydia psittaci mediated by a two-step polymerase chain reaction. J Clin Microbiol 1991; 29: 1969-75.

37. Kikuta A et al Antigenic analysis of avian Chlamydia psittaci using monoclonal antibodies to the major outer membrane protein. J Vet Med Sci 1991; 53: 385-9.

38. Kikuta LC et al Isolation and sequence analysis of the Chlamydia pneumoniae GroE operon. Infect Immun 1991; 59: 4665-9.

39. Zhong GM et al Antigenic determinants of the chlamydial major outer membrane protein resolved at a single amino acid level. Infect Immun 1991; 59: 1141-7.

40. Zhang L et al Characterization of a Chlamydia psittaci DNA binding protein (EUO) synthesized during the early and middle phases of the developmental cycle. Infect Immun 1998; 166: 1167-73.

41. Hornstein I et al. Vav proteins, masters of the world of cytoskeleton organization. Cell Signal 2004 (in press).

42. Nal B et al. Coronin-1 expression in T lymphocytes: insights into protein function during T cell development and activation. Int. Immunol, 2004.

43. Yanick P MCS: Understanding Causative Factors. Townsend Letter for Doctors and Patients. 2001 (Jan) 55-59.

44. Yanick P Oral Chelation of the Biliary Tract and Circulatory System in CV Disease. Townsend Letter for Doctors and Patients. 2002 (Nov) 52-55.

45. Kallings I Antibiotics against mycocardial infarction? The risk of resistance must be considered. Lakartidningen 1998; 95 2292-6.

Proof of Mycoplasma infection via vaccines?

Verkooyen RP; Sijmons M; Fries E; Van Belkum A; Verbrugh HA Widely used, commercially available Chlamydia pneumoniae antigen contaminated with mycoplasma. J Med Microbiol 46: 419-24 (1997)

by Paul Yanick, Jr., PhD [c]2004

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