Cpnhelp.org - Chlamydia Pneumoniae Treatment

Glad to hear this is being done. This has been in the works for a while re MSi (see below). JV Weinstock has also run trials in inflammatory bowel diseasei (see pubmed); I'm not sure whether that thing is still moving forward or what.

"[news article:] The scientists, who report their work in Annals of Neurology, studied 24 people with multiple sclerosis for more than four years, half of whom became infected with parasites after they were diagnosed with MS. Among the patients with parasites, there were only three clinical relapses, compared with 56 in the non-infected group. And only half of the infected patients incurred brain lesions from MS, compared with all of the non-infected patients."

Ann Neurol. 2007 Feb;61(2):97-108. Links Comment in: Ann Neurol. 2007 Feb;61(2):85-9. Association between parasite infection and immunei responses in multiple sclerosis. Correale J, Farez M. Department of Neurology, Raúl Carrea Institute for Neurological Research (FLENI), Buenos Aires, Argentina. jcorreale@fleni.org.ar OBJECTIVE: To assess whether parasite infection is correlated with a reduced number of exacerbations and altered immune reactivity in multiple sclerosis (MS). METHODS: A prospective, double-cohort study was performed to assess the clinical course and radiological findings in 12 MS patients presenting associated eosinophilia. All patients presented parasitic infectionsi with positive stool specimens. In all parasite-infected MS patients, the eosinophilia was not present during the 2 previous years. Eosinophil counts were monitored at 3- to 6-month intervals. When counts became elevated, patients were enrolled in the study. Interleukin (IL)-4, IL-10, IL-12, transforming growth factor (TGF)-beta, and interferon-gamma production by myelini basic protein-specific peripheral blood mononuclear cells were studied using enzyme-linked immunospot (ELISPOT). FoxP3 and Smad7 expression were studied by reverse-transcriptase polymerase chain reaction. RESULTS: During a 4.6-year follow-up period, parasite-infected MS patients showed a significantly lower number of exacerbations, minimal variation in disability scores, as well as fewer magnetic resonance imaging changes when compared with uninfected MS patients. Furthermore, myelin basic protein-specific responses in peripheral blood showed a significant increase in IL-10 and TGF-beta and a decrease in IL-12 and interferon-gamma-secreting cells in infected MS patients compared with noninfected patients. Myelin basic protein-specific T cells cloned from infected subjects were characterized by the absence of IL-2 and IL-4 production, but high IL-10 and/or TGF-beta secretion, showing a cytokinei profile similar to the T-cell subsets Tr1 and Th3. Moreover, cloning frequency of CD4+CD25+ FoxP3+ T cells was substantially increased in infected patients compared with uninfected MS subjects. Finally, Smad7 messenger RNA was not detected in T cells from infected MS patients secreting TGF-beta. INTERPRETATION: Increased production of IL-10 and TGF-beta, together with induction of CD25+CD4+ FoxP3+ T cells, suggests that regulatory T cells induced during parasite infections can alter the course of MS. PMID: 17230481 [PubMed - indexed for MEDLINE

You know what, I just realized that the stuff I just cited could have a big bias and might just be an illusion. This was not an interventional trial. The parasite-infected patients were selected because they presented with eosinophilia. I don't know whether presentation to medical care with eosinophilia happens in all parasite infectionsi, or not. In addition to their parasite infections, a genetic (or other pre-existing) Th2 bias may also be a factor in their presenting with eosinophilia - and could at the same contribute to a mild MSi course. Presumably, the non-parasite-infected MS subjects in the study's normal/comparison group were just average Argentine MS patients.

I haven't actually read the paper or the comments.

The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems.  Mohandas Gandhi

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The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi

hmmm, I just say eewwwwww

CFIDSi/ME 25yrs, FMSi, IBSi, EBVi, Cpni, (insomnia - melatonini, GABA, tarazadone, triazolam, novocycloprine, allergy formula, 3 gm tryptophan), Natural HRT peri-M, NACi 2.5 gm, 6-07 Doxy 200 mg day pm, Azith 375 mg M/W/Fday, Pulse8 750mg 4day,375X1 3-24-8

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CFIDSi/ME 32 yrs, FMSi, IBSi, EBVi, CMV, Cpni, chronic insomnia, Lymes, HME, Natural HRT peri-M, NACi 2.5 gm, 6-07 Doxy 200 mg day pm, Azith 375 mg M/W/Fday, Pulse#14 1000 mg X 5 days 9-19-08

Thanks to this ill-lumen-nation Eric. So what's the mechanism? Does it gear up innate immunei response in a way that might effect Cpni or other infection positively?  

CAPi for Cpn 11/04. Dx: 25yrs CFSi & FMSi. Protocol: 200mg Doxyi, 250mg MWF Azith, Tinii 1000mg/day pulses; Vit D1000 units, Iodoral 50mg, T4 & T3

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CAPi for Cpni 11/04. Dx: 25yrs CFSi & FMSi. Currently: 150mg BID Roxithromycin, Doxycycline 100mg BID, Tinii 1000mg/day pulses; Vit D2000 units, T4 & T3

These worms are felt to be Th2-directing, whereas MS and most comparable diseasesi are generally felt to be primarily Th1-mediated.

The Prineas and Barnett paradigm might suggest that T helper cells (Th) do not rule MS at all - at least not the plaques, that is; I believe David's page provides cites for diffuse brain inflammationi in MS, additional to the plaques.

I guess there is no consensus on a Th1 or Th2 dominance in CFSi, though I think N Klimas has supported Th2.

The whole worms thing is a big part of the hygeine hypothesis. The great apes seem to have a very big prevalence of worms, and I think the same may be true of humans who lack water free of fecal contamination. (A group which includes very many people today, as well as all of our ancestors over the millennia; only a few pre-modern civilizations, such as Rome, developed clean water - and I'm guessing that despite their low population density, hunter-gatherers faced at least some contamination during their day, which covered all of human history up to ~8000 BC). Asthmai seems to have a very low prevalence in the third world and there has been some research on this re worms.

Not all these worms are necessarily very harmful though there are some very bad worms out there (guinea worm, etc). The point is that evolution has no foresight. If these worms are virtually always around, the immunei system is going to accomodate their inputs into its computations of how it should behave overall - and when the inputs change suddenly, it will behave wrong. Evolution didn't know we were going to evolve into world-dominating ultra-generalist omnivores, so it relinquished the capacity to synethesize vitamin C back when our ultra-ancestors were hooting around in trees eating vitamin-C-rich fruit at every meal, and therefore didn't need to synthesize any. Almost all other mammals have the capacity to make their own vitamin C. Evolution only knows who's gonna live and who's gonna die today - it didn't know that apes would turn into British sailors who would get scurvy in the 1600s because they ate nothing but hardtack. It also didn't know (maybe) that molecules ABC and XYZ which figure in the overall regulation of the immune system actually come from worms, and that these might one day go away.

It's very important to ask whether the prevalence of worms in our lineage has generally closely approached 100% for a long time, which I have not studied. Even if the prevalence of worms is 99.7%, the human genome would still probably contain "plans" for how to function pretty well in their absence. ("Pretty well" might mean there is only, say, a 4-to-8-fold increase in the risks of a few serious pathologies, which isn't much.) However, if the prevalence of worms reaches 99.999% for a long time (hundreds or thousands of generations), then there will not be enough selective force to preserve these "plans" - and we might then expect that a hefty increase (40-fold, 100-fold) in the risks of certain serious pathologies (MS, Crohn's, whatever) might crop up in those who are deprived of worms. In essence, the human lineage would have become worm-addicted or worm-dependent, just as it is dependent on exogenous vitamin C, etc.

Asthma, I believe, is pretty clearly Th2-mediated, and the thought there is that the IgE & mast cell system may take up these deleterious activities out of, basically, boredom - the system is programmed to tend toward a certain activity level, and in the absence of a strong stimulus (worms) it has an increased tendency to respond to much lesser Th2 stimuli such as pollen.

So the interpretation of this that most people (maybe not Prineas and Barnett) would give for MS is, the reciprocal suppression between Th2 and Th1 is out of whack in the absence of worms because there is no Th2 activity, and the result is a novel and misbegotten (fitness-impairing) attack on brain tissue - or, if you like a role for infection, on something foreign in the brain that doesn't really need to be attacked with such vigor. That something could potentially be Cpni. Not every parasitic organism necessarily needs to be attacked. (Here I mean the breader, ecologist's sense of the word parasite, rather than the medical term which means worms and protozoans and such). If this scenario were true, then we might expect to find worm-infected people in Cameroon, or whatever, harboring Cpn in the brain with no measurable symptoms (or perhaps a subclinical syndrome of lowered energy and well-being, at worst). They would also have the same densities of Cpn as people with MS, and be the same in all other aspects of how the chlamydiae exist and behave; they just wouldn't be ill. (That's ideally; in practice, having MS or not having it could probably change some of the aspects of the infectionsi, and it would be hard to judge whether the altered aspects caused MS, or vice versa.) Of course this is all pure speculation.

 "worm-addicted"-- I never realized. So our difficulty is that we are in worm withdrawal, and manifesting all these diseasesi as our withdrawal symptoms.

Seriously, though, thanks for taking the time to parse through that line of thinking, Eric. It's perfectly plausible that we could have Cpni and be better immunomodulated by having our "proper quotient" of worms "balancing" our immunei system. After all, it's the inflammatory effect of Cpn that causes the tissue damage. The ATP parasitism only makes systems less functional. 

CAPi for Cpn 11/04. Dx: 25yrs CFSi & FMSi. Protocol: 200mg Doxyi, 250mg MWF Azith, Tinii 1000mg/day pulses; Vit D1000 units, Iodoral 50mg, T4 & T3

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CAPi for Cpni 11/04. Dx: 25yrs CFSi & FMSi. Currently: 150mg BID Roxithromycin, Doxycycline 100mg BID, Tinii 1000mg/day pulses; Vit D2000 units, T4 & T3

I realized while walking in the woods that even if the ancestral prevalence of worms is only 95% or some other rather low figure, worms might still have an effect on MS, and might decrease the risk*intensity product of serious (fitness-impairing) MS by something on the scale of 4- to 16-fold. The prevalence need not be 99.999% (thus producing "worm addiction") in order for worms to have some effect.

Most organisms face chronic undernourishment for Malthusian reasons: if there were excess food (mass and energy) available, they already would have assimilated it and converted it into progeny, because that's what organisms do. Ergo, hunger is the rule. (It doesn't look that way when horshoe crabs come up on Delaware Bay and lay 10 trillion eggs, or when 5,000 17-year cicadas come out in your yard, and birds gorge. However, these organisms are still playing "starvation games." They are collecting biomass from large expanses of space and time and concentrating it in a small piece of space-time in order to surfeit their predators, in order to make the most of their own starvation (their limited access to mass and energy). Many oaks produce a bumper crop every few years, with all oaks in the area behaving in synchrony - they are surfeiting the squirrels in the bumper years so that some acorns will survive, and starving the squirrels in the regular years, so that the squirrel population will decline.

So, even if certain worms do not cause disease per se, they might be worth attacking immunologically, because they steal host energy. (Of course our bodies don't know that most of us have access to unlimited food these days.) And of course, some worms do cause disease. Immunei functions also exact fitness costs by requiring energy, as well as causing (sometimes) fitness costs from impaired organ function. The widely accepted (haven't read much about it personally) reciprocal repression between Th1 and Th2 functions may be one way of balancing these costs (especially costs from symptoms which immune attacks themselves produce). The Th1 system may be telling the Th2 system, "hey, you need to reign in the anti-worm activity there, because we've got salmonella right now, and there is going to be a diminishing returns scenario if we spend too much energy on immunity and/or incur too much organ impairment." Whereas the Th2 system, when no worms are present, may tell the Th1 system, "hey, you can have all my energy and my symptomogenicity alotment (organ function impariment), so if there's anything on your agenda, you can go out there and basically go nuts."

So voila, Th1 turns it up, and maybe you get MS or crohn's. Now, in this scenario I am not accounting for what the deep cause of MS or crohn's is. The body did not turn up Th1 in order to give you MS and decrease your fitness; it did it in the expectation that your net fitness would increase because you would better resist pathogens for which a Th1 response is protective. MS is a by-product, the risk of which has a cost smaller (in a state of nature) than the benefits you realize from protection against infection when you crank up the Th1. In this scenario the deep cause of the MS diathesis might be an inability of the immune system to perfectly decide when it should attack. What is being attacked in MS could be a self-antigeni or a benign infection... but by definition it is something that ought not be attacked in this way because we are assuming that MS is deleterious to the inclusive fitness of the patient. Imperfect decision making by the immune system can persist forever, because pathogens continually evolve to be less identifiable.

Now, this too is speculation. And, again, I've entertained certain postulates (like MS being a Th1 disease) that I don't necessarily agree with... basically I've entertained any and all postulates that I think are needful for the "worm theory."

Here's an interesting looking paper. I don't have access right now, but the abstract was of interest to read:

http://www.blackwell-synergy.com/doi/abs/10.1034/j.1600-0706.2000.880110.x?cookieSet=1&journalCode=oik