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Rosacea Support Resource Pages
These pages hold in-progress web pages for the benefit of Rosacea Support Group members. Information provided herein is intended for informational purposes only and is not intended to replace medical advice offered by a physician or qualified healthcare provider. Feedback welcome to email@example.com
Studies have produced results that suggest that rosacea, and indeed many of the other chronic inflammatory (or autoimmune) diseases, are potentially caused by pathogen infection:
In particular, many studies suggest that Chlamydia pneumoniae (Cpn), currently being studied closely for its potential involvement in Heart Disease, Multiple Sclerosis, Asthma, Alzheimers and other inflammatory diseases, potentially could be a root cause for many of these diseases. And as a persistent gram-negative bacteria with both an intra-cellular and extra-cellular form, Cpn has also been shown to produce a chronic inflammatory response:
In fact, endotoxins, or rather lipopolysaccharides (LPS), portions of the outer membrane of gram-negative bacteria like Cpn, are widely known to induce a variety of inflammatory responses, ranging from mild to severe inflammation (and death) apparently based on the virulence of the bacteria endotoxins:
Interestingly, at least one study has linked Cpn with rosacea directly:
- "Chlamydia pneumoniae and Acne Rosacea
- Oral azithromycin has been used successfully to treat rosacea, a chronic skin disease that requires long-term therapy. A study was undertaken to determine if C. pneumoniae could play a causative role in acne rosacea. A series of 10 adults presenting with acne rosacea were selected to receive azithromycin alone for the treatment of acne rosacea. C. pneumoniae was detected in cheek biopsy specimens in 4 of 10 patients by immunoperoxidase stain (using monoclonal antibody to C. pneumoniae) and serum antibody against C. pneumoniae was detected in 8 of 10 patients. Fernandez-Obregon and Patton showed that all patients treated with azithromycin (250 mg three times a week) showed moderate to marked improvement of their rosacea without any undesirable side effect. These preliminary data imply a possible link between C. pneumoniae and acne rosacea as well as suggest a need for further investigation with clinical trials (22)."
Serum detection in 8 of 10 patients is high considering the number of false negatives current Cpn testing returns. This study can be found in the following link:
I believe the reference (22) is wrong in the above link, and that it actually belongs to the following:
- 21. Fernandez-Obregon A and Patton DL. The Role of Chlamydia pneumoniae in the Etiology of Acne Rosacea: Response to Oral Use of Azithromycin, Poster 9.07 at the 6th International Conference on the Macrolides, Azalides, Streptogramins, Ketolides & Oxazolidinones, Bologna, Italy, January 23-25, 2002.
Other studies suggest that infection with Cpn can lead to pustular rashes (acute generalized exanthematous pustulosis) and increased VEGF production as in the case with wet age-related macular degeneration. These of course are most likely caused as by-products of the chronic inflammation associated with this pathogen, but I point them out since papule and pustule rashes and increased VEGF production are also symptoms in rosacea:
In fact recent studies suggest that vascular endothelial growth factor (VEGF) itself is actually a "key biomarker" for sepsis, an infection of the bloodstream caused by toxin-producing bacteria:
Still other studies suggest that persistent Cpn infection of epithelial cells can produce a chronic inflammatory response resulting in production of a host of cytokines and growth factors:
- "Clinical persistence is probably a key concept in C. pneumoniae infection pathogenesis. Microbial persistence is a state of infection during which the host immune response does not eliminate the pathogen, thereby resulting in continuing damage to the host. Persistent infection may amplify airway inflammation in asthma and chronic obstructive pulmonary disease (COPD), but also in extrapulmonary diseases such as atherosclerosis, multiple sclerosis and Alzheimer's disease.
- Stephens 13 has recently revised the possible pathogenic mechanisms of C. pneumoniae infection. He underlines that C. pneumoniae can induce an inflammatory process elicited by infected host cells that is necessary and sufficient to account for chronic and intense inflammation and the promotion of cellular proliferation, tissue remodelling and scarring, the ultimate causes of disease sequelae.
- The cellular responses of epithelial cells, the primary home for C. pneumoniae, can be reliably induced upon acute, chronic and persistent infection. The cellular processes of the epithelial cells, elicited by chlamydial infection, cause the influx of inflammatory neutrophils, T-cells, B-cells and macrophages that are stimulated by the pro-inflammatory cytokine and chemokine environment. These cells become activated in both antigen-nonspecific and, for re-infection, antigen-specific responses to produce their own repertoire of cytokines and growth factors. The induction of host cell cytokines will promote foci of inflammatory responses in addition to promoting cellular proliferation, tissue remodelling and healing processes that, if persistent, result in scarring."
The full text of the study can be found in the following link:
Finally, studies suggest that chlamydiae have a unique development cycle that can lead to the type of persistent infection that could cause chronic inflammatory diseases:
- “The chlamydiae are an evolutionarily distinct group of eubacteria sharing an obligate intracellular lifestyle and a unique developmental cycle that has been well characterized under favorable cell culture conditions. This cycle begins when infectious, metabolically inert elementary bodies (EB) attach to and stimulate uptake by the host cell. The internalized EB remains within a host-derived vacuole, termed an inclusion, and differentiates to a larger, metabolically active reticulate body (RB). The RB multiplies by binary fission, and after 8 to 12 rounds of multiplication, the RB differentiate to EB asynchronously (78). At 30 to 84 h postinfection (PI), depending primarily on the infecting species, EB progeny are released from the host cell to initiate another cycle (78, 122).”
The full text of the study can be found in the following link:
Recent studies have also shown that the anti-microbial peptides, cathelicidins, when activated by kallikreins, seem to be involved in producing the bumps and pimples associated with rosacea as well as in promoting the angiogenesis associated with the disease:
While other studies have shown that Cpn seem to elicit unusually high levels of cathelicidin activity, and previous research suggests endotoxin activates the kallikrein-kinin system, yet cathelicidins seem to be ineffective in clearing Cpn infection (at least in in vitro studies):
Most interestingly, David Wheldon, Microbiologist and FRCPath in the U.K. has reported great results in halting and reversing progression of another chronic inflammatory disease, Multiple Sclerosis, through treating Cpn infection with long-term multiple antibiotic therapy:
Charles Stratton, MD at Vanderbilt University has reported similar results in treating patients for Cpn infection with long-term multiple antibiotic therapy:
Dr Stratton recently gave an interview related to his recent observations on Cpn infection to JimK, the founder of Cpnhelp.org. In it he summarizes some of the emerging research on Cpn, including summarizing how Cpn crosses from the lungs via infected macrophages and then sets up shop in other organs and small blood vessels throughout the body:
In summary, potentially rosacea is the result of chronic inflammation caused by the persistent infection with the gram-negative bacteria, Chlamydia pneumoniae. Potentially also Cpn is capable of inducing a chronic inflammatory response that can lead to co-infections with other pathogens (h. pylori, demodex mites, s. aureus, c. albicans, etc) that may only help exacerbate the symptoms of this disease.