Chlamydophila pneumoniae (Chlamydia pneumoniae)

Chlamydophila pneumoniae, also known as Chlamydia pneumoniae (CPn), is described as an obligate, intracellular bacterium that causes community-acquired atypical pneumonia, pharyngitis and bronchitis, and has also been linked to atherosclerosis and coronary artery disease. This organism is viewed as parasitic, infecting host cells in order to sequester nutrients and to reproduce, but it can exist outside a host for short period and is transmitted to others in an elementary body form in droplets produced in a sneeze or cough. This microbe exists in 3 life phases and, although it may begin as atypical pneumonia, confined to the lungs, if it is poorly treated it may disseminate via peripheral blood mononuclear cells and travel from the lungs to infect other body tissues, such as the blood vessels, brain and nervous system, kidneys, muscles, liver, prostate, and immune system cells (macrophages and monocytes). As CPn releases toxic substances, called endotoxins, this produces the tissue-damaging inflammation seen in these tissues, as well as the potential for triggering and perpetuating various autoimmune diseases, including rheumatoid arthritis.

Worthy of note is that a proportion of seronegative rheumatoid arthritis (RA) patients may in fact have some form of undiagnosed reactive arthritis (ReA), such as Reiter’s Syndrome, ankylosing spondylitis or psoriatic arthritis. Seronegativity in this context means there are no autoantibody markers to definitively diagnose RA, such as rheumatoid factor (RA) or anti-cyclic citrullinated peptides (anti-CCP). Although Dr. Brown was a “lumper” and believed in treating all rheumatic diseases in a similar way, there are variations in the antibiotic protocol (AP) approaches that are employed for CPn-induced autoimmunity due to the nature of this persistent infection in its various forms. Seronegative RA patients may therefore consider CPn testing to determine if this infection may be a component in their rheumatic disease.

For further information on CPn, please refer to the CPn Help website where specific antibiotic protocols are outlined for this infection, as well as expected reactions, remedies and helpful supplements.

Persistent Chlamydiae and chronic arthritis. Arthritis Research & Therapy 2001, 4:5; DOI: 10.1186/ar382

These authors provide a review of contemporary scientific literature of chlamydial infections and various inflammatory arthritides, including rheumatoid arthritis (RA). The call for a “realignment of thinking” in the hopes of eliciting discussion in the field of rheumatology regarding persistence of this organism and the mechanism by which it induces synovial pathogenesis and more targeted therapies.

Strong correlation in the serum levels of IgM rheumatoid factor and IgM anti-Chlamydia pneumoniae antibody. Lupus. 2009 Oct;18(12):1124.

This study abstract is unavailable to view for free online, but may be accessed with subscription to the journal. 

Chlamydial infection preceding the development of rheumatoid arthritis: a brief report. Clinical Rheumatology, , Volume 23, Issue 5, pp 453-455.

It is well-known that Chlamydia trachomatis is a causative infectious agent of reactive arthritis. Although joint fluid is typically sterile and the microbe difficult to isolate in culture studies, it’s DNA can be detected by polymerase chain reaction (PCR) testing. These case study authors present their success in isolating chlamydia in the synovial fluid of a young woman with rheumatoid arthritis (RA).

Chlamydia pneumoniae present in the human synovium are viable and metabolically active. Microbial Pathogenesis. Microbial Pathogenesis. Volume 29, Issue 1, July 2000, Pages 17-24.

In collaboration with the National Institute of Health (NIH), Arthritis and Rheumatism Branch, two major medical institutions in Michigan and Pennsylvania were able to isolate chromosomal DNA from Chlamydia pneumoniae (CPn) in patients with reactive arthritis/Reiter’s Syndrome and other forms of inflammatory arthritis. The results of this study demonstrated that CPn found in the synovium of patients infected by this organism were both viable and metabolically active and that their findings point to this infection playing a role in long-term joint disease and its pathogenesis.

Chlamydia pneumoniae serology: interlaboratory variation in microimmunofluorescence assay results. J Infect Dis. 2000 Jun;181 Suppl 3:S426-9.

In a Canadian study to determine the extent of Chlamydia pneumoniae (CPn) microimmunofluorescence test variation among 14 different laboratories in 8 countries, 22 identical sera panels were sent for IgM and IgG testing. Of note is that 4 laboratories failed to identify false positive IgM titers that were due to elevated rheumatoid factor (RF).

RBF Commentary: This research is based on the assumption that elevations in RF interfere with CPn IgM testing, producing false positives. However, it seems reasonable to question whether RF behaves as an acute phase reactant, appearing as a result of CPn infection (as has been shown by other infectious agents), or if a pre-existent elevation in RF in fact does produce false positive results in some cases. In light of this, it may be worthy of consideration that RF-seropositive RA patients who have a history of CPn, that a positive IgM may in fact be a true-positive result and that further testing is indicated. 

Age-related interference with Chlamydia pneumoniae microimmunofluorescence serology due to circulating rheumatoid factor. J Clin Microbiol. 1992 May;30(5):1287-90.

In a study conducted in The Netherlands, researchers ran microimmunofluorescence (MIF) serology IgM and IgG testing to look for Chlamydia pneumoniae (CPn) elementary bodies (EBs) in 286 patients with respiratory illnesses. Of these, 71% (n=205) were antibody-positive for CPn and 22% (n=64) were MIF-positive for recent (IgM) infection. Of the patients who were IgM-positive, 78% were also found to have circulating rheumatoid factor (RF) by rheumatoid arthritis latex-assay and RF frequency increased with age. When IgM sera was re-tested by absorption method with anti-human IgG, all samples became negative in the MIF assay. Active rheumatoid arthritis (RA) patients (n=25) in the study (with no apparent respiratory illness) were CPn-positive on both IgM and IgG testing. When re-testing after absorption of anti-human IgG, all IgM-positive sera reactivity disappeared on the MIF IgM assay. These authors conclude that recent infection with CPn becomes more prone to false-positive results with age unless sera testing is routinely absorbed with anti-human IgG prior to MIF testing.

RBF Commentary: Slight RF elevations are sometimes seen in otherwise healthy, non-rheumatic elderly patients. The RA patient cohort in this study bears significant relevance in that 14/25 samples – almost 50% – were also found to be positive for past (IgG) infection of CPn. Whether or not, IgM (indicating recent infection) results were proved to be false positives, a history of CPn infection, with the potential for systemic dissemination, may provide indication of chronic low-grade intracellular infection in these RA patients. For further RBF commentary, see above.


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