Author Topic: Have you been tested for dormant/cryptic Chlamydia?  (Read 104 times)


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Have you been tested for dormant/cryptic Chlamydia?
« on: October 19, 2022, 12:13:06 PM »
I'm wondering if anyone here has had their synovial fluid tested for CPN or other infections? I was positive for chlamydia years ago, treated with a single course of azithromycin which later showed negative in urinalysis. But, maybe I was infected long enough or it was able to switch to its dormant form without being completely killed off. I'm currently considering this as a thread to investigate for myself, not sure how to convince a specialist to pull fluid though. This might explain why some respond so well to ABX, only to have it come back. CPN treatment is usually a long combination antibiotic course.

What do you guys think?


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Re: Have you been tested for dormant/cryptic Chlamydia?
« Reply #1 on: November 09, 2022, 04:09:28 AM »
The testis is an immunologically privileged organ with myoid and Sertoli cells providing the morphological component of the blood-testis barrier such that the highly antigenic sperms do not come in contact with the immunocompetent cells present in the interstitial spaces between seminiferous tubules. On the other hand, the epididymis has intraductal lymphocytes and macrophages and is considered to be the most likely source of antibody secretion and cellular immunity and autoimmunity in the male reproductive tract. The impact of impaired epididymal integrity on autoimmune processes and infertility has been widely recognized. Antisperm antibodies (ASA) may result in the serum, seminal fluid or on sperm surface either as a result of transport of spermatozoal degradation products by the macrophages to the regional lymph nodes, breakdown of the blood-testis / blood-epididymis barrier due to trauma or infection with escape of sperm antigens directly into the microcirculation, or, by production of antibodies against infective agents like Chlamydia which cross react with spermatozoa. It is also possible that in obstructive infertility breach in the epithelium causes extravasation of sperms into the interstitium and brings them in contact with the immunocompetent cells in insufficient amounts to induce detectable ASA. However, repeated exposure to the antigenic sperms may induce a local cell mediated immune response which may be responsible for the histological changes reported in the epididymis.
The cause is probably the senescence of sexual organs and resultant inducible SASP, which also acts as a kind of non-diabetic metabolic syndrome.