Cpn Theory: Cpn Metabolism

Cpni Theory: Cpn Metabolism

Chlamydia Pneumonia is an obligate intracellulari pathogen that relies on the host cell for energy. It is able to obtain energy through multiple mechanisms. The primary mechanism is exchanging ATP for ADP with the host cell mitochondria. ATP and ADP are exchanged using a proton pump which may require a lower chlamydial pH than that of the host cell. Probably the use of protons to exchange ATP for ADP and the subsequent use of ATP lead to a homeostasis of Cpn pH so this should be able continue under normal circumstances. This pH level and reliance on ATP/ADP exchange probably represents the reticulate body phase in chlamydial development. At this pH level Cpn can probably make the proteins needed for replication.

When stressed Cpn may need to supplement ATP/ADP exchange with additional energy sources such as glycolysis (anaerobic fermentation to lactic acid) and amino acid catabolism (with an ammonia byproduct). The pathway that is chosen would be based upon host cell resource availability although presumably glycolysis dominates as that is the case in most cells and bacteria. If glucose or pyruvate is abundant it is probable that glycolysis is used for obtaining additional energy. This should efficiently reduce the pH within the Cpn membrane. If the Cpn pHi drops below some thresh hold, Cpn probably begin making proteins and enzymes needed to convert to the elementary body state. So "stressing" Cpn with adequate glucose or pyruvate should result in Cpn converting to an elementary body.

If glucose or pyruvate stores are limited, Cpn may obtain energy from amino acid catabolism which should increase pHi. Once the pH rises to the level of the host cell, Cpn would no longer be able to obtain energy from ATP/ADP exchange. And as the pH continues to rise it may no longer able to make many of the proteins that it normally does to replicate. However some protein synthesis such as production of HSPi-60 probably occur more readily. This higher pH level represents the cryptic state. The pH rise would be limited by a NhaD antiporter. Without the availability of ATP/ADP exchange, Cpn would necessarily have to obtain all of its energy from alternative sources and in cells with chronically low glucose levels, it is unlikely that Cpn would easily exit the cryptic state even if the initial stress is removed.

This may explain some observations surrounding Cpn infections. Cells with modest blood flow such as joints and skin should have lower availability of glucose and generally produce persistent infections. Cells with a very large number of mitochondria might also favor persistence as the mitochondria may compete with Cpn for glucose. Of course conditions in these persistently infected cells would sometimes change. A diet high in sugars, stimulants, or adrenaline release from stress might temporarily elevate the glucose levels in these cells and allow Cpn to return to reticulate body state and begin replicating. Also temporarily lowering the pH of the host cell should lower the pH of the Cpn as they have NhaD antiporters which should cause Cpn's pH to track down with the host cell. Corticosteroids would remove the stress caused by WBC's releasing interferon (and inducing iNOS) while also increasing glucose levels.

- Paul

 

very intersting, Paul - and not very easy for me to understand :) What should I do to rise the pH in the cpni and put them in a cryptic state, in which they can not replicate? I can not take any abxi now, because I had a lot of side-effects after three weeks doxyi. So I have to run some blood-tests now and wait that my jaundice goes away. My body needs some months to recover and I have to try to put some weight on, too. In this time I'd like to stop the cpn from replicating, I need them to give me a break to be able to get a little stronger and to be able, someday, to start with abxi again. To reach this goal should I be eating now a lot of meat, no sugar and no stimulants (coffee, cortison)?

best wishes,

raluca

 

Interesting; but, out of curiousity, is this your personal opinion or based on research?   I also read and I cited  a study here on the site that Corticosteroids potentiate CPNi?   http://cpnhelp.org/effect_hydrocortisone_suc< 

Also do you still advocate using pyruvate with the ABXi?

JeanneRoz 

JeanneRoz ~ DXi'd w/ CPNi 4/2007; 6/07 -"officially" dx'd w/CFIDSi/FM; also: HHV6, EBVi, IBSi-C, 100 Doxyi:BIDi<; 500 mg Biaxin BIDi; Tindamax Pulses, B12 shots, ERFA Dessicated Thyroid,Cortef, Iodoral 25 mg, Vit D-6,000 uni

Hi Jeanne,

It is based both on opinion and research. I still think pyruvate or caffeine (with antibiotics of course) are as good a way as any to eradicate the bulk of cryptic Cpni. We have shown both of them to induce Cpn into replication in vitro.

- Paul

Thanks for this, Paul, some of us are interested in keeping cpni from replicating, and keeping them in a cryptic state,  so if you have any ideas on diet to achieve help in this please advice. Keep away from sugar, glucose, tryptophan, red meat, dairy, Wheat, coffein ?
Treating PPMSi with Azithromycin 250 mg every other day, Doxyi 100 mg BiDi, Coconut oil 4 times daily,  five flagyli pulses. Been sick since June 2009. Having good success and very few symptoms.

My experience with coritcosteroids was hugely negative. I embarked on a short, sharp course many years ago for polyarthralgia and it took 4.5 years to be able to get off the drug. In the mean time, I experienced secondary adrenal insufficiency with Addisonian crises in that period. I was so so ill and despaired of every being able to wean off the drug.

I have seen a past paper written on corticosteriods and CFSi stating these drugs were not recommended for these patients. My adrenal glands finally kick started on lots and lots and lots of Vitamin C both IV and orally.

Please use caution

 

CFSi 32years/FM 14 years/ CRPS 5 years/.  Previously MPi 5 years. Off everything since 01/12/2012.

 

.

HI BeezNee,

I am not a big believer in corticosteroids as down regulating ones immune system can have negative consequences and is not necessary. Still they have been shown to work synergistically with antibiotics against C. Pneumonia so your experience is surprising. That is unless you were not taking antibiotics at the time in which case you should be clear about that.

Anyway I should also be clear that this post was not meant as a recommendation for any type of therapeutic approach. It is simply intended to explain some aspects of Cpni physiology.

- Paul

In defense of...........Cortef (not prednisone) is what literally got me out of bed.  I have been on it now for about 2.5 years (physiological dose).  I take 20mg of Cortef per day (which is the equivalent of 5 mg of Prednisone but not as taxing).  I also stress dose when needed.

 The protocol literally put me in bed the first year and a half and this was one script that enabled me to at least get vertical and out of bed.  I tried Isocort and other natural adrenal sup's but they were not enough. 

 I had severe orthostatic hypotension, hypoglocemia and several other issues pertaining to my adrenals gettting hit.  

I do believe it (Cortef) has made it more difficult for me in this treatment (i.e. potentiating and possibly creating resistance) because as recently as the last six months I still have severe breathing/respiratory issues having to use a nebulizer, inhalers, etc.  and I had a more difficult time recovering from pulsing.... but eventually recovery after pulsing got better after about year or so.

 I still have weak adrenals (orthostatic hypotension is much better, but still there) but I have a weak  HPA axis due to not having a thyroid -- ablated in '98 for Graves (which I now believe was CPNi)..  The protocol just really taxed it.    

There is an excellent medically-l oriented book written by Dr. William Jeffries, "Safe Uses of Cortisol".  Reading it definitely explains how beneficial corticosteroids can be and how our body needs them to heal.

Cortisol at physiological dosing is not like taking prednisone and many misunderstand the "benefits" of  corticosteroids at physiological dosing. 

I don't like having to take it, but without it (even with nutraceuticals for my adrenals) my body is not ready to wean from it.... 

JeanneRoz

JeanneRoz ~ DXi'd w/ CPNi 4/2007; 6/07 -"officially" dx'd w/CFIDSi/FM; also: HHV6, EBVi, IBSi-C, 100 Doxyi:BIDi<; 500 mg Biaxin BIDi; Tindamax Pulses, B12 shots, ERFA Dessicated Thyroid,Cortef, Iodoral 25 mg, Vit D-6,000 uni

Paul,

If caffeine and pyruvate increase ATP in the cells and cause the cryptic state to revert to RBs, should creatine and D-ribose have the same effect?

Started CAPi for Cpni on 11/14/10 - Per my doctor, paused Abxi 5/18/13 - NACi, T3, St Johns Wort, B-complex, Vit C, Vit D3 (8,000/day), Vit E, Astragalus, Chlorella, Chelation with Alpha Lipoic Acid">i. Started Buhner protocal (2nd edition) on 8/30/16.

Hi lleach,

Pyruvate could increase ATP but I think more importantly it enables cryptic Cpni to produce energy through fermentation which lowers its pH. Glucose does the same thing it just takes some more steps to convert it to pyruvate which is then converted to lactic acid. I do not think caffeine increases ATP (or energy) to cells. I think that it lowers the host cell pH by causing them to release calcium. I know that caffeine is considered to be a stimulant but that theory supposes that it acts on cells in the brain. In the lab we are able to induce Cpn into the RB state with caffeine in a cell culture which does not have these types of cells. Alternative theories are welcome of course but the pH one makes the most sense to me and the doctors working on this.

I am not sure about d-ribose or creatine. As far as I can see they would not lower Cpn's pH but they may be beneficial in some other way either therapeutically or symptomatically.

- Paul

Hi Paul!
 
Thanks for keeping us up to date with the newest research!
 
Im a bit comfused bc youre writing that caffeine induces cpni to rb state. in other statements you wrote you think  it would induce them to ebi state.
 
rb state doesnt sound like something i want cpn to convert into?
 
thanks in advance for explaining!
 
mikel
 
 
 

07/2010 Roxi 150 bidi, Doxyi 100 bidi,Metroi Pulses,Naci 1200 bid,Vit D3 + Suppl.

34Y,CF-IDS, IBSi-B (SBBO) >low weight,slight fibromyalgiai,chest pain,very cold limbs and sinusitis since 1999,chronic but slight Epididymitis/Prostatitis>2010

Hi Mikel,

I did state that but the experimental evidence suggests they are converting to RBs... Sigh. However the caffeine doses used in vitro were relatively modest and according to this theory if the pH drops further, Cpni would convert to the EBi state. Anyway while it is still possible that Cpn can be converted to the EB state with caffeine, there is no evidence to support this at this time. It may be possible to use larger doses or combinations of acidic promoting substances but the goal is to induce Cpn into the RB state and doing so directly as opposed to first converting to the EB state is perhaps preferable.

In the RB state Cpn produce the many proteins that can be inhibited to kill them. It could reasonably be argued that keeping them in the cryptic state is preferable as they cannot replicate but I am not so sure about that. In the CB state they produce inflammatory proteins which can cause all kinds of problems. Some of the more obvious problems are inflammation, fatigue, and interfering with the immune response. I would also speculate that plaque build ups are a result of the immune system attempting to repair damage that does not exist as a result of this inflammatory response.

I any event it is probably academic. I would expect than any Cpn that were in the RB state would be killed within a few days with antibiotics. So it is your choice when or if you induce them into the RB state. There are a number of ways to do this although I think they all relate to the underlying pH idea.

- Paul

Paul, looking at this comment from above "I did state that but the experimental evidence suggests they are converting to RBs... Sigh."

How do you see your encouraging folks to add the amount of caffeine to their programs as you did stand now?   Many people took their lead from you on that one.  Was it useless?  Is the addition of caffeine still to be encouraged in your opinion? 

I am glad that you added the word theory to this topic.  It might be well to continue to highlight as you post any deviations from the basic posted protocolsi here as such, distinctly separating your current theoretical persuite from the basic protocols that have helped so many as they stand be changed.  The basic protocols have one distinct advantage, they were designed to be the safest as part of their development.     I see this as particularly important for those that are self treating  and (there may be many more than we know, in my opinion, this is a globalwebsite) because there are not the availability of providers in their areas on the globe willing to take the responsibility of administering any for of combined abxi protocol, which is certainly beyond what is considered as generally acceptable treatment. 

So please consider how you form your suggestions for changes or adjuncts, I certainly do.     The thing about these discussions is they last and if they need editing in the future because of some realization, it is hard to get to all the out of date information out of the archives, literally impossible.   Desperate people with brainfog are not always able to make reasonable decisions or think through pros and cons of theory.  Many have no science or medically oriented background and each word is a challenge as they sift through the data here.  Many rely completely on the forum topics which is certainly not the way to get to the information that is why the tabbed information was redone several years ago to decrease the amount of questons on the basics of the protocols. 

So there you go, all the things that I have wanted to say to you in the past several years of your return to frequent posting here.  I know you have contacts, I have been told as such, and because of that many did not challenge you as they may have liked.  I am glad that you are talking more in theory now, less confusing for many and probably safer for them too.

The problem with CPni is of course, it is out there on the street corner, in the church pew, in the doctor's waiting room waiting to re-infect us even if we completely irradicate it from our bodies on this go round, same is true for all the tick carried infectionsi the cycle can be repeated even with proper treatment.    

  • CAPi(TiniOnly): 06/07-02/09 for CFSi<
  • MethylationProtocolSupplements: Started08/08
  • Intermtnt CAP: 02/09-02/10
  • Full MethylProtocol & LDNi 02/09
  • Off CAP: 02/10, cont LDN & MethlyProtocol support
  • <
thanks paul!
 
isnt it possible to use more caffeine in vitro and demonstrate the supposed EBi conversion as Dr, S did with lactic acid according to your ph effect thread?
 
why wouldnt we want it to convert to EB rather than RB? you wrote in your PH thread that cpni is most vulnerable to abxi wehn converting from EB to RB and may have to give up its resistance mechanism.(the pumps?)
 
please tell me if i understand the caffeine action correctly considering the resistance theory also:
 
in theory when we take abxi cpn pumps it out untill theres not enough energy to pump it out anymore and then converts to CB in order not to be killed. if we then take caffeine it may tend to convert to RB eventhough theres not enough energy to pump abx out properly and may die from this?
 
another question about the 3 day pump build up theory: wouldnt that suggest an intermittend treatment as cpn may build those pumps back when abx is removed for a certain period of time (?), and so for another 3 days be suspectible to abx again, wich would give us another chance to kill it in RB state?
 
THANKS!!!

07/2010 Roxi 150 bidi, Doxyi 100 bidi,Metroi Pulses,Naci 1200 bid,Vit D3 + Suppl.

34Y,CF-IDS, IBSi-B (SBBO) >low weight,slight fibromyalgiai,chest pain,very cold limbs and sinusitis since 1999,chronic but slight Epididymitis/Prostatitis>2010

Hi Louise,

The difference between converting to an EBi (and subsequently converting to an RB) and converting directly to an RB is relatively modest I think as the goal is/was to convert Cpni to an RB. Caffeine is still encouraged by both me and Dr. S, in fact perhaps more so as there is now more than just in vivo evidence of its activity. And I would never have recommended it if it had not been tested on numerous people. Because of its unique method of lowering pH, it will likely remain a part of a therapeutic approach down the road.

I will say that caffeine should be used with caution. Some people here did not follow the original recommendations and incorporated it with their CAPi. It may be that caffeine and metronidazolei work synergistically which is not necessarily a good thing in the early part of treatment. Anyway I think we are rapidly getting to an explanation of all of the agents that are used which should help keep people from inadvertently moving forward too quickly.

I am not sure exactly what you mean by contacts. I am pretty open about my involvement. I was the first one treated many years ago (I am not good with dates but over 15 years ago) and have funded the research since then. Also when I realized how long of a process this was going to be (for me anyway), I suggested this site be set up for patient support which Jim was kind enough to do.

Best regards,

- Paul

Hi Mikel,

It is possible to test higher doses and we will do that. And there is a some reason to believe that higher levels will lead to EBi conversion beyond just the in vivo results. There is a paper "Effects of Ascorbic Acid on Chlamydia trachomatis Infection..." that showed an increase in replication with lower doses of Vitamin C and a decrease with very high doses. And the lower results mirror our results using moderate doses of many acidic substances. Anyway that will have to wait as we are working on the mechanism of action of metronidazolei now. I am not going to post anything on that though as it has caused some bad feelings in the past.

Everything else you stated is correct. It might be better if Cpni would convert to an EB state. But OTOH even if Cpn do create pumps to antimicrobial agents that would not necessarily make them invulnerable. It just means the concentration of drug has to be greater and the MBC's of most agents used might be high enough.

I think it may be a bad idea to stop and start an antibiotic. Presumably this would allow Cpn to replicate and make more copies that share this type resistance as these pumps are spread around the Cpn membrane. A lot of experience was gathered with rifampin use when it was used in such a widespread and long term manner in eradicating TB. It was found that stopping and starting this drug could cause serious side effects in some people. Of course the time frame here would be important but 3 days would not be nearly long enough. I did try rotating antibiotics years ago and while I was pleased with the results in the short term, there are not enough different anti Cpn categories to do this effectively. And of course some pumps may be shared. My feeling at that time was that possibly rifamycins, quinolones, and macrolides use different mechanisms but that was only an observation by one person and was ultimately not successful anyway.

- Paul


I'm with Louise here. I had several objections to your Cpni pH theory when I saw it on another thread but I was short on time then. 

First of all, if you think that you can influence pH inside a Cpn cell, you may as well kill it. Such degree of control is unheard of. It's hard enough to adjust plasma pH, not to mention intracellulari pH, less so some nano-sized components of it. 

Second, IMOi you're lost in minute details of Cpn metabolism, much of which is based on speculation, at the cost of ignoring the grand picture. The key questions to a chronic disease caused by a common pathogen should not be how we can kill it, but what makes chronic patients different from the rest of the population and what allows this pathogen to persist in spite of body's natural defences.

Third, your dietary advice to use more glucose and pyruvate goes against what is known today as a healthy diet. I can see your rationale in promoting them when mitochondria generate so much ROSi that it makes you sick. Basically, you're saying screw the mitochondria, let's bypass it all together and get energy via glycolysis instead. I don't know, it may have place as a temporary fix... but it's hard not to be concerned, because glycolysis, being the most primitive form of glucose metabolism, is associated with metabolic disorders, infectionsi and the most dreaded of diseasesi: over 90% of all cancers rely exclusively on glycolysis and it is also the main way pathogens feed => whatever supports glycolysis will also support cancer and infections. 

I can also see how your advice to eschew protein in favor of simple carbs could have evolved from observation that low-protein diet was helpful to you, as it was to others, as reported here on the board. I can see how this observation may have served to support your current theory... But. 

There could be other interpretations to what is observed. One is the role of autophagy in immunity and health: it is well known that abundance of amino acids down-regulates autophagy, while their scarcity has the opposite effect.

There is plenty of info on autophagy, from wiki to pubmed, and I don't want to get into it in depth here. Suffice it to say that it is the body's primary defense against intracellular parasites, as well as its primary way of keeping mitochondria in top shape, which in turn determines the amount of destructive radicals present (produced largely by damaged mitochondria), which in turn has direct impact on degree of inflammationi, etc. In addition, autophagy is the way cells keep their cytosols clean of misfolded protein junk, accumulation of which is the hallmark of a long list of diseases headed by Alzheimer's.

So, a low-protein diet (better yet, low-protein periods, however long or brief) will upregulate autophagy, simply because the body will need to get those proteins somewhere, and what could be a better source than all that protein junk lying around? So it follows that not only a low-protein diet will cause the cells to start clearing the junk that clogs their cytosols and impedes their function, but will also counteract the dysregulation of autophagy by Cpn, for whom autophagy spells certain death.

Successful intracellular parasites disrupt autophagy, because that's how cells kill them. Disruption of autophagy not only allows intracellular pathogens to persists (usually in phagosomes that were meant to destroy them after merging with a lysosome), but also leads to accumulation of damaged mitochondria as well as misfolded protein junk, with all the dreaded consequences.


When asking what allows pathogens to persist, we should examine the body's natural defences against them. 

The first line of defense is the innate immunity and its main weapon, the anti-microbial peptides (AMPs) that kill pathogens directly. They are released immediately in reponse to bacterial proteins' activation of toll-like receptors on cell membranes. 

AMPs are small positively charged proteins with strong affinity to negatively charged bacterial membranes and work by clumping onto bacterial cells, disrupting the function and integrity of their membranes. So far so good, but... Mitochondria have very similar membranes (which led to speculation that they evolved from a bacterial symbiont). So, when AMPs are released in large numbers, depolarization of mitochondrial membranes becomes their collateral damage. The other aspect of AMPs' collateral damage is aggregation of spent peptides, both intra- and extracellulary, which is the hallmark of Alzheimer's and other diseases characterized by protein aggregates.

Depolarization of mitochondria is believed to be the first step in the long chain of events that may lead to cancer. Damaged mitochondria are supposed to be recycled via... guess what? yes, autophagy. When autophagy is disrupted by an intracellular parasite like Cpn, they accumulate, serving as the primary source of ROS that in turn damage DNA, which in turn can eventually lead to cancer..

Also, mitochondria are the initiators of apoptosisi, the orderly death that should be the fate of every defective beyond repair cell. When mitochondria are damaged, the apoptotic program fails, allowing a defective cell to persist. Interestingly, when mitochondria are severely damaged, glycolysis becomes the only way for that cell to obtain energy (use of glutamate being the second). On the other hand, when glucose is scarce, like during fasting or therapeutic ketogenic diet, defective cells starve to death..


The second line of defense against pathogens is the adaptive immunity. For it to work, the bugs have to be phagocytzed and lysed in lysosomes so that their proteins could be displayed by MHC on the surface of the cell. But.. phagocytosis in a lysosome is the integral part of autophagy. Again. See how important autophagy is for well-functioning immunei system?

So, disruption of autophagy is one of the main reasons pathogens manage to persist and whatever upregulates it will help the body rid of infection.


Another reason for persistent infections are biofilms (organized microbial communities). A variety of enzymes, from serrapeptase to cellulase, to various proteases and amylases, are used to break up the goo in which biofilm bugs protect themselves from the immune system and antibioticsi

Quorum sensing is how these complex microbial communities communicate and cooperate in their defense against the onslaught of the immune system (those who are not familiar with  this can look it up in wiki). There are substances called "quorum quenchers" that disrupt quorum sensing, transforming biofilm bacteria into planctonic forms, which, unlike biofilms, constitute easy pickings for both the immune system and antibiotics. Here you will be pleased to learn that caffeine is a well-known quorum quencher.


So, when I saw your advice on caffeine, low-protein diet and use of glucose/pyruvate, I wanted to bring this different viewpoint into the discussion, because what you observe can also be seen from another perspective and interpreted in a framework of another theory. I'm not saying that the one I offer is better than yours. Both are valid viewpoints. Of course, I prefer mine, because it comes from top-down approach and covers more ground.


Sorry for a long post. I better end it here, before again I'm accused of being a spammer or a troll. I got a lot of good info on your site and only wanted to share some of my insight in turn. Hope you find it useful.

Good luck to you in your speedy recovery!

PS
you can read more on protein cycling and autophagy here: http://knol.google.com/k/ron-mignery/protein-cycling-diet/2s3nmvrwklbxs/1#<

Hi FF,

Controlling the pH inside of a persistent intracellulari pathogen with acidic agents in order to make it susceptible to antimicrobial agents may sound a bit far out but we have been doing it for over 50 years with one of the most ubiquitous pathogens on the planet, TB. Pyrazinamide (PZA) is used to address "older" TB by lowering their intracellular pH. At least they think that is how it works although that debate may go one for another 50 years.

And while I would be the first to admit that things like lifestyle and diet play a big role in the development of a Cpni infection, why would you presume people can eradicate this infection without outside agents? Everybody dies and most people die from diseases in which Cpn may play a role.

I don't recall giving dietary advice. If I did it would just have been repeating what Dr. S. has suggested on the high carb stuff. I do not think he was advising a lifestyle change, simply recommending a diet that would help with symptoms during therapy.

Anyway thanks for your perspective and good luck as well.

- Paul

How long have you been on antibioticsi, Paul, if you are the first one treated 15 years ago and you are still taking them now? Could you please make it more clear for us, who do not know whole story?

Stratton/Wheldon protocol 02/2006 - 10/11 for CFSi and many problems 30 years

Hi Lala,

Much of what we tried early on did not work particularly well. And I ended up "curing" CFIDs twice now. The reason I had to do it twice is simply because of stupidity IMOi. But you learn a lot more from your mistakes than your successes so perhaps some good may come from it. Anyway I will write up something soon as I think there may some lessons from the experience.

- Paul

Hi Paul!
 
quote: ''There is a paper "Effects of Ascorbic Acid on Chlamydia trachomatis Infection..." that showed an increase in replication with lower doses of Vitamin C and a decrease with very high doses. And the lower results mirror our results using moderate doses of many acidic substances''
 
So one could assume that taking low doses like 200 mg of caffeine with abxi isnt such a great idea, leading cpni to replicate rather than help killing it?
or will it still help bc (as i think you agreed?) @least the ''awoken'' cpn, living in low ATP cicrumstances, may start metabolizing without being able to pump out abxi properly, wich should kill it in the long term?

 Thanks!!!

07/2010 Roxi 150 bidi, Doxyi 100 bidi,Metroi Pulses,Naci 1200 bid,Vit D3 + Suppl.

34Y,CF-IDS, IBSi-B (SBBO) >low weight,slight fibromyalgiai,chest pain,very cold limbs and sinusitis since 1999,chronic but slight Epididymitis/Prostatitis>2010

Hi Mikel,

I think that lower doses are OK. In the paper I referenced above they were not using antibiotics. So if they induced Cpni into the replicating state with moderate doses which seems to be the case, you would get more Cpn growth. However if you were taking a couple of antibiotics that inhibit protein synthesis while it is replicating, you would presumably kill it.

- Paul

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