Author: Admin (---.vnnyca.adelphia.net)
Date: 05-07-02 07:37
>> Please remember that this is an OLD discussion from early 2002, before we had proven that bacteria are the cause of Sarcodiosis. I am leaving it online as a snapshot of history, and because it shows the process by which the discovery was made. But the material is largely out-of-date and should not be relied upon.
..Trevor.. <<<
This message thread should be read in conjunction with the threads "Tick borne bacteria causes sarc in lungs" and the thread "Minocycline, Tetracyclines cure sarc skin lesions"
Mona,
Most sarcoid patients spend an overwhelming effort on trying to identify the cause of 'their sarcoid'. There are two issues here
1. The granulatomous reaction which caused shadowing on the X-ray and/or the granuloma in your organs was caused by a genetic pre-disposition which made your body over-react to immune challenge.
2. Everything that is visible on X-rays has taken place in the past, ongoing symptoms are being experienced because of ongoing inflammation which may, or may not, be related to any infection.
Many other things can trigger a sarcoid granulatomous reaction, including man made materials such as silica, titanium, et al. Some patiets have a proportion of man made granuloma (identified by patholological analysis of their biopsy slides) and also granuloma which seem to have nothing in them, nothing that is being encased by the body's granulatomous immune response. It is the mystery of these latter granuloma that is now being solved by the PCR DNA technology.
There is even an indication that the immune system may be capable of over-reacting to bacteria which are ubiquitous and relatively harmless, such as Propionibacterium acnes.
Ther can be no definitive "proof" that a violent granulatomous reaction in your body was triggered by the infection from the fleas until your biopsy material can be matched with DNA technology to the particular genus of R.Felis or whatever the infection was. This will not be possible for a few more years.
In the past your serum would have been cultured to try to grow bacteria (this is part of the due diligence before a sound sarcoid diagnosis) but many of these insect-borne diseases do not culture during periods of dormancy, because they thrive in the soft tissue. The PCR techniques allow us to look for species, one by one, and see if there is a match. The spectacular success of the researchers who found the Rickettsia Helvetica was because the exposure of their population was limited primarily to that single infection, and their PCR DNA test was tuned to look for it. Four of their patients did not have Rickettsia, however, and the "cause" of their granuloma still remains to be determined.
From the point of view of treatment, it seems obvious that any sarcoid patient showing symptoms which progress rapidly should be evaluated (and, if necessary, treated) for the possible presence of insect borne infections. This is not being done by any except the most enlightened pulmonology specialists. Yet the tetracycline antibiotics have relatively low risks compared with most drugs that sarcoid patients are prescribed. And the anti-microbial, Plaquenil (hydroxychloroquine) has been credited for some spectacular successes on some sarcoid patients. I just cannot condone the profession's intransigence on this issue.
Once active bacteria have been neutralized (and we know that they sometimes can hang around in a patient's body for years and years) then the focus must shift to the ongoing abnormally reactive inflammatory response of a sarcoid patient, and particularly the effects on the brain of the hormone 1,25 dihydroxyvitamin D3 and other granuloma/macrophage biochemicals, including ACE and Angiotensin II (and possibly Angiotensin IV).
We also need to re-evaluate (yet again) the use of Prednisone in sarcoidosis. Although prednisone can shut down a patient's inflammatory reactions and improve X-ray appearance, it leaves that patient vulnerable to infection, or to a relapse of a previous infection. Prednisone also does widespread systemic harm beyond its effects on the immune system.
So, IMO, it is not important whether the Typhus infection that you think you might have received is 'related to' Rickettsia or not. Any bacterial infection can produce 'foreign' DNA fragments after the active infection has been killed off. Some of this DNA has been found at the core of a violent granulatomous reaction in susceptible individuals. It is reasonable to expect that other, yet to be identified, infectious strains will also cause sarcoid granuloma to form. IMO it doesn't matter which specific bacteria is involved, what is important is that we now know why biopsy slides can show no cause for the granulatomous reaction under an optical microscope, whereas, under an Electron Microscope we can see bacterial fragments within those same granuloma. The fragments can then be localized to a specific bacteria by using DNA technology.
The full text of the Rickettsia paper contains some photographs of what they saw through their electron microscopy. I found it quite amazing. They even show a Rickettsia organism replicating by splitting into two. I strongly recommend that you go down to your local med library and grab a photocopy of this paper. I am giving a presentation in July to to the Southern California Sarcoidosis network on this topic, and will try to get some pictures to use during that presentation.
..Trevor..
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