This dissertation by a brilliant researcher in Finland includes a wonderful overview of the CPnⁱ lifecycle and postulates the possibility of innoculating people against this ubiquitous pathogen. This is an extremely interesting paper uncovered by Jim the Curious whose indefatiguable interest in research related to CPn has filled these pages. The link to the paper is HERE

Journal of the American Geriatrics Society Volume 53 Page 583 - April 2005 doi:10.1111/j.1532-5415.2005.53204.x Volume 53 Issue 4 High Prevalence of Chlamydia Pneumoniae Antibodies and Increased High-Sensitive C-Reactive Protein in Patients with Vascular Dementiaⁱ Hideki Yamamoto, MD*, Takuya Watanabe, MD, PhD, Akira Miyazaki, MD, PhD, Takashi Katagiri, MD, PhD, Tsunenori Idei, MD, PhD§, Takashi Iguchi, MD, PhD§, Masaru Mimura, MD, PhD*, and Kunitoshi Kamijima, MD, PhD* Objectives: To determine the relationships between Chlamydia pneumoniae infection, carotid atherosclerosis, and dyslipidemia in patients with vascular dementia (VaD) and Alzheimer's disease (AD). Design: Case control study. Setting: Showa University Karasuyama Hospital, Tokyo, Japan. Participants: One hundred twenty-four elderly subjects: 31 with VaD, 61 with AD, and 32 age-matched controls without dementia.

Biochimie. 2003 Aug;85(8):763-9.

Cell death and inflammation during infection with the obligate intracellularⁱ pathogen, Chlamydia.

Perfettini JL, Hospital V, Stahl L, Jungas T, Verbeke P, Ojcius DM.

Laboratoire Apoptose, Cancer et Immunite, CNRS UMR 1599, Institut Gustave Roussy, 39, rue Camille-Desmoulins, 94805 Villejuif cedex, France.

Infect Immun. 2001 Dec;69(12):7880-8. Epithelial cells infected with Chlamydophila pneumoniae (Chlamydia pneumoniae) are resistant to apoptosisⁱ. Rajalingam K, Al-Younes H, Muller A, Meyer TF, Szczepek AJ, Rudel T. Department of Molecular Biology, Max Planck Institute for Infection Biology, D-10117 Berlin, Germany. The obligate intracellularⁱ pathogen Chlamydophila pneumoniae (Chlamydia pneumoniae) initiates infectionsⁱ in humans via the mucosal epithelia of the respiratory tract. Here, we report that epithelial cells infected with C. pneumoniae are resistant to apoptosis induced by treatment with drugs or by death receptor ligation. The induction of protection from apoptosis depended on the infection conditions since only cells containing large inclusions were protected. The underlying mechanism of infection-induced apoptosis resistance probably involves mitochondria, the major integrators of apoptotic signaling. In the infected cells, mitochondria did not respond to apoptotic stimuli by the release of apoptogenic factors required for the activation of caspases. Consequently, active caspase-3 was absent in infected cells. Our data suggest a direct modulation of apoptotic pathways in epithelial cells by C. pneumoniae.

Brian Balin has done a remarkable job of pursuing a consistent line of research looking at Chlamydia Pneumoniae as a causal source or co-factor in Alzheimer's diseaseⁱ.

Information about Dr. Balin can be found at this link.

Comments he has made about his research can be found at this link. Included is a comment he made which is very reminiscent of Dr. Sriram's answer's to negative studies by other researchers, noting that he, like Sriram, used frozen brain sections and found Cpnⁱ DNA, whereas the other researchers used formalin preserved sections and did not find Cpn evidence.

Hello! I have been blogging my progress as I have been on the Wheldon/VU protocol but the time has come for a patient story. I am now 6 months into treatment. If you would like to read my story of getting MSⁱ please see my blogs.

Dr David Wheldonⁱ has been treating and following some people using the Wheldon/VU regimen we have adopted here. This has generated a data set which while not public is interesting as an anecdotal tally.
7 were SPMSⁱ
1 was PPMSⁱ
2 were organic brain syndrome considered possible pre MS.

These numbers do not include people Dr Wheldon advises without seeing personally, or who are being followed by others with him consulting. These are people for whom he has done the assessments himself and therefore has a complete data set.

The results were improvements of some kind for all but three patients. Two of those who did not respond also did not renew prescriptions as expected (ie going through one month of meds in two months)and thus are not likely to have taken the medicines as required. It is very clear from the research here that suboptimal levels of medicines otherwise effective for CPn results in persistence. Only one patient appeared to be compliant but did not respond in spite of treatment.

Russell Farris and Per Marin MD PhD

The potbelly syndrome: how common germs cause obesity, diabetes and heart diseaseⁱ.

Basic Health Publications Inc, Laguna Beach, CA

Pp 246 ~ Paperback $17.95 (US) $23.95 (Canada)

Reviewed by David Wheldonⁱ MB FRCPath

This book explains how common, non-resolving intracellularⁱ infectionsⁱ can, over long periods of time, subvert the body's defences by causing chronic elevation of cortisol while provoking chronic activation of pro-inflammatory cytokinesⁱ; this has serious repercussions, including type II diabetes, atheroma and heart disease. Much of what we put down to ageing is caused by chronic infection.

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 metronidazole 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?