Bacterial forms/stages

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The forms which Cpn can take on in it's life cycle.

Thinking outside the box-is there a future better way?

As one reads the entries on this site you learn of many challenges and hardships faced as one deals with the numerous reactions to the protocol. Many are due to the die off aspects.

It makes me wonder if somewhere in the future there could be another way that might be more tolerable and perhaps quicker. I'd like to toss out a few thoughts for different approaches that maybe someday might work(or not). Given the vast knowledge and experience of the members of this site, I invite and encourage other thoughts. Maybe there is an audience out there that might explore some of these ideas if they were captured here - you know - "plant the seed" or "put a bug in ones ear".

Here goes:

Help I am so confused

I am still trying to get a grasp on Chlamydia Pneumoniae, I just found out on 4-11-07.  But I have been sick for awhile  Cry.  I am just starting Antibioticsi again......eeeeek Foot in mouth.  My symptoms have been sinus infectionsi and uppper respitory infections , Phlaringitis, Broncotitis, Asthmai.  In and out of the Dr. office the month of April, and my throat swelled shut I could go on and on.  I ended up at an Infetious disease Dr.

Continuous Treatment

I haven't blogged my treatment for a while, as I've been waiting to see if I would stick with a shift in protocol. So far, still with it, so thought it might be time to report in and get other's thoughts. New folks, please read this as informational only. It does help clarify Dr. Stratton's use of the continuous rather than pulsed protocol, but the rest of the hypotheses here are presented as my own speculations, not scientific fact.

CHAIN GANGER -- DIAGNOSED NOV. 7, 2006

Hi CPNers,  My basic disorder is fibromyalgiai which many doctors think carries the autoimmune factor.  I've had sporadic bouts with it since 1989.  Fibro symptoms are heavy muscular pain, fatigue, brain fog and itchiness.  The present acute attack began in 10/06, brought on by mega stress factors in my life.  When I failed to respond to gamma globulin injections and home treatment, and instead worsened, my doctor ordered a CPN test which came back positive on 11/7/06.  The test further indicated that I'd had CPN for years, but I never felt CPN symptoms before this.  I've praised my doctor for being so knowledgeable on CPN.  He visits CPNHELP.ORG frequently.

This year I had a 5-month bout of severe exhaustion, undiagnosed; coulcn't do anything nor go anywhere.  In 2004 I had 7 weeks of even more severe exhaustion, undiagnosed.  I wonder if the strange exhaustion was caused by CPN.

could it be all cryptic? help with getting a diagnosis

Hi everyone!

I really hope you can help me, because I have yet to be diagnosed with much of anything.  I have a huge variety of symptoms including life-long asthmai and sinus/bronchial infection issues.  Throw on a healthy dose of mind-numbing fatigue, brain fog, joint pain, muscle weakness (relatively minor, not like the MS stories I have read), etc, etc... I've been getting worse and worse year after year.  It presents a pretty confusing picture to doctors.

Only only two things have helped me.  1) Flagyli, and 2) Secnidal (another drug in the same family as flagyl.)  I did a 5 day course of the first and a 10 day course of the second.  I felt nearly about 70% improved on the first, and nearly perfect after the second.  Both of these were shots in dark, and I went back to being ill 2 weeks after the antibioticsi were finished.

Essential Observations by Dr. Charles Stratton on Chlamydia Pneumoniae Infection and Disease

I am very excited to present the following article that summarizes Dr. Stratton's recent observations on Chlamydia pneumoniae infection. Putting it together has contributed greatly to my own understanding of Cpni as well as to my appreciation of Dr. Stratton's generosity with his time, and his great depth of knowledge of this area. Thanks to him for his contribution.

Jim K

Recent observations by Dr

Recent observations by Dr. Charles Strattoni on Chlamydia Pneumoniae (Cpn) Infection

Rickettsia

Is CPNi applicable to other intercellulari bacteria like rickettsia and if so do i follow the same antibiotic regime.

Many Thanks

Macrophage antioxidant enzymes regulate Chlamydia pneumoniae chronicity: Evidence of the effect of redox balance on host-pathoge

Immunobiology. 2006;211(5):325-39. Epub 2006 Apr 18. Related Articles, Links

Macrophage antioxidanti enzymes regulate Chlamydia pneumoniae chronicity: Evidence of the effect of redox balance on host-pathogen relationship.

Azenabor AA, Muili K, Akoachere JF, Chaudhry A.

Department of Health Sciences, University of Wisconsin, Enderis Hall, Room 469, 2400 E. Hartford Avenue, Milwaukee, WI 53211, USA.

Latency, chronicity and recurrent nature are the features of Chlamydia pneumoniae biology which play a central role in the course and outcome of C. pneumoniae-host interaction. Since redox status is directly an indicator of inflammatory response via molecular signaling mechanisms, we decided to study the regulatory role of macrophage cellular redox balance on the molecular indices of C. pneumoniae chronicity. We examined GSH-GSSG status, the activities of antioxidant enzymes (SOD, GPx and gamma-GCS), along with their protein and gene expression, the MOMP and cHSP-60 protein and gene expression, and the consequence of redox balance on the establishment of productive infection in macrophages. Results showed that C. pneumoniae caused changes in GSH-GSSG levels, antioxidant enzymes activity, mRNA gene and protein expression in macrophages. The relevance of this to the state and status of C. pneumoniae in macrophages was assessed by inhibitor induced attenuation of antioxidant enzymes and there was evidence that, while SOD attenuation did not significantly affect MOMP and cHSP-60 gene and protein expression, gamma-GCS attenuation increased cHSP-60 gene and protein expression. The increase in molecular evidence of chronic forms of C. pneumoniae (cHSP-60) was consistent with decrease in normal forms of C. pneumoniae. These findings reflect the importance of redox balance modulation on the outcome of C. pneumoniae infection in macrophages, a significant process in the pathogenesis of chlamydial diseases.

Chlamydia pneumoniae infection of brain cells

This pre-publication abstract is a remarkable piece of laboratory work. It strengthens the case for Cpni infection especially in MSi and Alzheimer's, and other brain diseasesi.

The two findings I've underlined which seem to have espeical importance is (1) the sensitivity of neuronal cells to infection, as big producers of EB'si, and their particular sensitivity to necrosisi (tissue death); and (2) the finding in microglial cells that they resist active replicating infection but appear to be potential reservoirs for persistant Cpn.

  Neurobiol Aging. 2006 Apr 16; [Epub ahead of print]

Chlamydia pneumoniae infection of brain cells: An in vitro study.

Boelen E, Steinbusch HW, van der Ven AJ, Grauls G, Bruggeman CA, Stassen FR.

Department of Medical Microbiology, CARIM (Cardiovascular Research Institute Maastricht), Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands; Department of Cellular Neuroscience, EURON (European Graduate School of Neurosciences), Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands.

Inspired by the suggested associations between neurological diseases and infectionsi, we determined the susceptibility of brain cells to Chlamydia pneumoniae (Cpn). Murine astrocytei (C8D1A), neuronal (NB41A3) and microglial (BV-2) cell lines were inoculated with Cpn. Infection was established by immunofluorescence and real-time PCRi at various time points. Productive infection was assessed by transferring medium of infected cells to a detection layer. Finally, apoptosisi and necrosis post-infection was determined. Our data demonstrate that the neuronal cell line is highly sensitive to Cpn, produces viable progeny and is prone to die after infection by necrosis. Cpn tropism was similar in an astrocyte cell line, apart from the higher production of extracellular Cpn and less pronounced necrosis. In contrast, the microglial cell line is highly resistant to Cpn as the immunohistochemical signs almost completely disappeared after 24h. Nevertheless, significant Cpn DNA amounts could be detected, suggesting Cpn persistencei. Low viable progeny and hardly any necrotic microglial cells were observed. Further research is warranted to determine whether these cell types show the same sensitivity to Cpn in an in vivo setting.

PMID: 16621171 [PubMed - as supplied by publisher]

Cross infection.

If CPni is at the root of my MSi is there a risk of me passing my infection onto my family or others? What is the rate of encounter of CPn in public places - and am I really a hazard to others? Should I be looking for or expect my children to have CPn infection? What do I do? R.

On DW protocol from Nov05 for MS.

Dr. Stratton Answers Some Questions:

In some recent correspondance with Dr. Stratton at Vanderbilt University, he kindly answered some of the questions which had formed as I've understood more about the combination antibiotic protocol and about Cpni. From the patient's perspective I wanted to correlate some observations about treatment reactions with his deeper understanding about the biology of the Cpn. I'll list the questions I put to him, and then his generous response below.

1.  In an earlier correspondance you had mentioned pulsing the INHi band metronidazolei together.
        * Why do that rather than take it continuously?
        * My understanding is that INH is one of the anti-replicatives, and the point is to use these continuously to drive the bug into the cryptic phase where it will be obliterated by the flagyl/tinii. Does INH act differently than the other antireplicatives?
        * I also understood that we use a dual abxi to prevent developing resistance. Why can we use INH alone without developing resistance?
 

Expression and localization of type III secretion-related proteins of Chlamydia pneumoniae.

What follows is a study sent to us by Dr Wheldon. Below I have pasted his comment about it...Marie
Med Microbiol Immunol (Berl). 2004 Nov;193(4):163-71. Epub 2003 Oct 31.

Expression and localization of type III secretion-related proteins of Chlamydia pneumoniae.

Lugert R, Kuhns M, Polch T, Gross U.

Department of Bacteriology, University of Gottingen, Kreuzbergring 57, 37075 Gottingen, Germany.

The entire developmental cycle of the obligate intracellulari bacteria Chlamydia pneumoniae takes place within the inclusion body. As many gram negative bacteria, Chlamydia possess a type III-secretion system (TTSS), which allows them to target effector molecules into the host cell. The expression and localization of several proteins constituting the TTSS apparatus and of proteins supposed to be secreted by the TTSS have been investigated. For the TTSS-constituting proteins, we selected representatives such as YscN (ATPase), LcrE (putative "lid" of the TTSS) and LcrH1 (postulated to be a chaperone). Furthermore, we focused on the putative effector proteins IncA, IncB, IncC, Cpn0809 and Cpn1020. Expression of these proteins was detected by reverse transcriptase-PCRi followed by immunoblot analysis using antisera that were generated against the corresponding recombinant proteins. Thereby, expression could be detected on the RNA and/or protein level. Intracellular localization of proteins under investigation was determined by immunofluorescence assays using the respective antisera. YscN was shown to be distributed equally throughout the inclusion body, whereas LcrE gave a more prominent staining of the inclusion membrane. IncA was detected mainly on the membrane of the inclusion body, whereas IncB and IncC were shown to be located within the inclusion. Immunofluorescence assays with antisera raised against Cpn0809 and Cpn1020 showed completely different labeling. Signals corresponding to Cpn0809 and Cpn1020 were distributed within the host cell rather than inside the inclusions. Taken together, the different localization patterns of the effector proteins indicate differences in function and interplay with the host cell.

senescence (aging) of immune cells

A recent entry on thisisms about researchers that discovered that in RAi and MSi people have prematurely aged immune cells so that the immune system appears to be that of an elderly person caught my eye. these researchers, in typical form showimg a bias towards the autoimmune model, wanted to know why the cells were aging prematurely and if this aged cell was incompetent thus provoking autoimmunity.HERE< is the article on thisisms.

Curious, I entered immunosenescence on google and discovered that cytomegalovirus induces this by turning off apoptosis in the cell invaded, thus preserving it's 'home'. Interesting, I thought, CPn turns off apoptosis also in order to preserve the cell ( it is, after all, it's home..). Clearly when a cell is stopped from apoptosis (programmed timed cell deathi) it lives beyond it's normal span and becomes an old cell. therefore CPn causes this also.

New Content

I added several interesting new articles sent by Jim on the research page under the heading for CPn bacterial research
Marie

Family Practice news article Persistence

And Persistent Chlamydia - Brief Article Family Pratice News, Nov 1, 2000 Found Here< Persistent chlamydia infection was identified in seven women with three or more recurrences over a 2- to 5-year time span, in a 10-year retrospective analysis of STDi clinic samples. Four of the women harbored the same genotype of Chlamydia trachomatis over the entire recurrence period, and the other three women had genotypes that mutated slightly, possibly due to drug therapy (J. Infect. Dis. 182[3]:909-16, 2000). Cultures taken between flare-ups tested negative, but C. trachomatis DNA was detected in 59% of samples in the seven women vs. 14% in reinfected patients. Class C serovars were more likely to be implicated in the persisting strains.
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