Bowel diseases

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New kid on the block: Glad to find you!

Hello everyone-I'm so glad to find this site and others who understand what I'm going through!  I have suffered for at least 17 years with various illnesses that I now see may all be related to CPni.  My most recent addition to the plethora of illnesses I've experienced is severe tinnitus">i with 5-10% hearing loss. I recently had to purchase hearing devices, $3000 worth to drown out the ringing noise as it was driving me insane, literally! Finding out about CPn has made me feel like I have found a gold mine, thanks to my doc, (MD and toxicologist) that knows how to think outside the box. Sure has given me renewed hope. I actually found out I had it after my friend was diagnosed with it.  I had referred him to my doc as he had been experiencing CFSi and ADD symptoms.

What Is A Chronic Illness, Anyway?

             What Is A Chronic Illness, Anyway?

A chronic illness is a disease or disorder that a person has to cope with on a continuous basis. Many people become so ill, they are unable to work and are forced to give up activities they have always enjoyed. Often their  illness goes undiagnosed for years, leaving thousands of people frustrated, depressed and without answers to why their bodies will not cooperate with their desires.

Bacteroides: friends, foes, and what else?

If you ever ponder, while you're washing your hands, on which specific pathogens you are trying to protect yourself and others from, make a mental note about this group.  Bacteroides bacteria are the rabble masses of our gut flora.  They are indispensable to us for the work they do inside the gut, but when they leak out of the gut, they become our enemies.  To make matters worse, they "aid and abet" our other enemies (yes, I'm wondering if that includes Cpni).  That's pertinent to people with chronic inflammatory bowel conditions, but it also applies to all the rest of us.  When it comes to nasty infections, bacteroides are true "team players."  You'd be surprised at the places they can collaborate to cause

Digestive system improvements?

I'm feeling like being a little vague about this, but you guys should get it:

My digestive system tends to run... umm... "fast". Food moves through me too quickly and isn't digested all that well, especially fibrous stuff like raw veggies, etc.

Going on these antibiotics has not helped that.

Have any of you started with those sorts of symptoms, or maybe even developed them from the abxi, then got better?

I am taking some super-potent probiotics, but they have never really helped this.  Rather, I just want to protect against the abxi.


Diseases associated with Cpn: the exhaustive list

I have culled from Mitchell & Stratton patent #6,884,784 an exhaustive list of diseasesi where Cpni has been implicated as a possible cause or co-factor (reference: Mitchell & Stratton patent #6,884,784):

Diseases where an association has been discovered between chronic Chlamydia infection of body fluids and/or tissues with several disease syndromes of previously unknown etiology in humans which respond to unique antichlamydial regimens include:

Editorial comment: Strong findings from their research. If you have any of these it suggests to me that at least an empirical course of the combination antibiotic therapy is strongly indicated, with or without serologyi.

Multiple Sclerosis (MSi)
Rheumatoid Arthritis (RA)
Inflammatory Bowel Diseasei (IBD)
Interstitial Cystitisi (IC)
Fibromyalgiai (FM)
Autonomic nervous dysfunction (AND neural-mediated hypotension);
Pyoderma Gangrenosum (PG)
Chronic Fatigue (CF) and Chronic Fatigue Syndromei (CFSi).

Stratton/Mitchell & Siram Case Reports

Does it work?

It has been noted that most users of the combination antibiotic protocolsi commenting here have not been on the treatment long enough to give a big enough pool of reports to feel assured of the efficacy of this approach. I had asked Drs. Stratton, Wheldon, and Powell to perhaps tally up at least some basic numbers from their case experience to help us out with this problem, but this would involve problems of confidentiality and use of private data, etc.  

Then, I suddenly realized that we already have a good list of anecdotal reports of response to treatment reported data available to us... right in the Stratton/Mitchell patent materials! (Sheepish, embarrassed grin). So I took it as a project to summarize this data by disease treated. Occasionally I have used the exact wording from the patent materials as they were brief and descriptive. We have the full text referenced in our treatment and links if you want to see more detail.

All reported had with positive serologyi for Cpni using the highly sensitive tests developed by Stratton/Mitchell. I left out a few whose diagnosis was not clear to me, you can see them in the patent materials #6,884,784
All on some form of the combination antibiotic therapy protocol.

Beneficial role of melatonin on microcirculation in endotoxin-induced gastropathy... possible implication in nitrogen oxide

Beneficial role of melatonin on microcirculation in endotoxin-induced gastropathy in rats: possible implication in nitrogen oxide reduction.<

Liaw SJ, Chen JC, Ng CJ, Chiu DF, Chen MF, Chen HM.

Department of Emergency Medicine, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taipei, Taiwan.

BACKGROUND AND PURPOSE: Lipopolysaccharide (LPSi) induces hemodynamic changes and microcirculatory derangement in various organs. Melatonini may exert a beneficial effect on gastric tissue in LPS-induced gastropathy. However, the role of nitric oxide (NO) has not been clarified. MATERIALS AND METHODS: Adult male Sprague-Dawley rats were divided into three groups: control, n = 9; LPS (intraperitoneal LPS, 50 mg/kg), n = 9; and LPS + M (LPS, 50 mg/kg; intragastric melatonin 20 mg/kg), n = 9. Mean arterial blood pressure (MAP) was monitored throughout the experiment (8 h). In vivo microscopy was used to investigate gastric microcirculation, including flow velocity and leukocyte adhesion. Tissue malondialdehyde (MDA) and gastric aspirate parameters (protein content, glucose content, volume) were determined as the gastric damage index at the end of the experiment. Microdialysis was used to measure the sum of nitrite and nitrate concentrations. RESULTS: Compared with LPS alone, LPS with melatonin significantly improved gastric microcirculation but not systemic hemodynamics. LPS-induced gastropathy was quantified according to the increased adherent leukocyte count, decreased flow velocity in postcapillary venules, and increased tissue MDA production. Luminal glucose and protein content, the gastric mucosa injury index, were significantly increased. Intragastric melatonin improved microcirculatory and mucosa injury parameters. These effects of melatonin are directly associated with the tissue levels of NO products, which are increased with LPS only and much decreased with LPS and melatonin. CONCLUSIONS: This study demonstrated that melatonin contributes to the protective effects in LPS-induced gastropathy through a mechanism associated with regional production of NO.

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