Infectious, spore-like, nonreplicating form of Cpn which accumulates in intracellular spaces, attaches itself to body cells, and invades them.

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

Jim K
Submitted by Jim K on Tue, 2006-09-12 16:57

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 Cpn 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 Stratton on Chlamydia Pneumoniae (Cpn) Infection

Dr. Stratton Answers Some Questions:

Jim K
Submitted by Jim K on Mon, 2006-01-30 22:13

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 Cpn. 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 INH 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/tini. Does INH act differently than the other antireplicatives?        * I also understood that we use a dual abx to prevent developing resistance. Why can we use INH alone without developing resistance? 

Comments by David Wheldon in response to questions about choice of antibiotics in his protocal versus the Vanderbilt protocal:

Jim K
Submitted by Jim K on Tue, 2005-08-23 22:21

I believe that Stratton and co-workers used a beta-lactam (penicillin, amoxycillin or similar) to attack the infectious stage
(elementary body) of the organism. They did some in vitro work to support this, which they should publish, because it's
fundamental. I reasoned that, as culture was so rare in persistent human infections, the numbers of elementary bodies would
be small. Also, any elementary body entering a phagosome in a cell containing bacterial protein-synthesis inhibitors would be
doomed, as the organism needs to fabricate proteins immediately to survive. Coupled with this was a native gut-reaction that
people would buy into the idea more readily if there were fewer antibiotics. And, further, that one is taught at med school
never to combine cidal and static agents. In the higher levels of microbiology that's not always true, but basically you just
want people to believe you and treat, as early as possible, and the more complications you put in their way the more difficult
that is.

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