Re: Nelly & Penny re: C. Pneumonia

[Guest guest]

"(...) and go into anon-replicating phase where they are aerobic and noteffected by the abx.

(...)The idazole killsthem in this intracellular form."

Jim,

Did you mean anaerobic? Imidazoles kill anaerobic bacteria. Or am I missing something (possible).

It's interesting that in the "Lyme world" people use imidazoles to drive the crypic (supposedly) non-replicating structures (lyme cysts) back to motile spiros in order to be able to get at them with conventional abx. Wheldon and Stratton seem to look at it from the opposite end ie using the cycline/macrolide combo to drive the EB (elemental body) into the RB (reticulate body) which will then be killed by the imidazole

Nelly

http://www.davidwheldon.co.uk/ms-treatment.html

Why are later short courses of metronidazole to be taken together with these antimicrobials?

Chlamydiae have a biphasic life-cycle. A small, infectious, non-replicating extracellular particle (the elementary body, or EB) spreads the infection both between persons and between host cells. On gaining entry to a host cell, the EB is able to transmute into a larger, diffuse form (the reticulate body, or RB) which utilises the host cell’s energy-generating organelles for its own use. It is an energy-parasite. By this means it is able to replicate rapidly, releasing multitudes of EBs into the extracellular milieu. Agents which block protein synthesis, such as doxycycline and roxithromycin, stall this replicating phase, but do not eliminate the intracellular organism.

Chlamydiae are complex organisms. Long ago their ancestors must once have been free-living. They must have possessed their own energy-generating pathways. The transformation from EB to RB is an active change, and an active change implies the retention of at least some of these pathways. The ones with the most utility for this purpose would be anaerobic, and thus susceptible to metronidazole. Metronidazole should kill the organism while it transformed itself from the EB to the RB.

Doxycycline and roxithromycin block the replicating phase and may be expected to force the organism to maintain itself by using its own primitive anaerobic respiratory mechanisms. In this suspended state it would be susceptible to anti-anaerobic agents such as metronidazole.

This is borne out by clinical evidence. The administration of metronidazole after doxycycline in a patient with likely high-load Chl pneumoniae infection causes a bacteriolytic reaction as severe as that following the original administration of doxycycline.

However, there is a difference: in this leg of treatment there is no risk of the emergence of resistance, for the organism is unable to replicate. Metronidazole need thus be given in courses only as long as can be tolerated. It will be seen that this cyclical treatment regime allows host cells to be used as a trap; extracellular EBs will enter cells, to be curtailed at the residual form, where they will be destroyed when metronidazole is next given.

In this way the total body EB load will gradually be depleted.

[infections] Nelly & Penny re: C. Pneumonia

Nelly and Penny-I'm just catching up on emails and wanted to chime inon the Cpn and Wheldon/Stratton protocol comments froma few days back.I'm also having gradual and real improvements withthis. I had quite a bit of herx, both with initialtetracycline (3 months), then again when I started thedoxy/zithro part. I had initial immediate return ofenergy starting the metronidazole, but could onlytolerate a few days and then got very sick, toxic andnauseous. I am finally trying tinidazole, whichWheldon told me some patients tolerate better, andseem to be managing it better. If this doesn't workI'll try Macrobid, an old urinary tract abx whichStratton reports has also has previously unreportedbactericidal effect on the cryptic form of Cpn.The reason you might have had herx when adding thetinidazole after doing the cycline/lactim combo, isthat the latter prevent replication by the organism,and drive it into the non-replicating "cryptic"intracellular form, ie under the "stringent" responseto the abx, the organism defensively (those thataren't killed by the abx) invade cells (particularlyimmune cells and endothelial tissues) and go into anon-replicating phase where they are aerobic and noteffected by the abx. They are, however, using up theresources of your cells energy-- especially ATP-- andproducing toxic byproducts. Wheldon notes that Cpn hasa protein which inhibits/prevents cell death of thehost cell which would usually occur. The idazole killsthem in this intracellular form. The herx from this(which I find is distinct from the herx from theregular abx) is in part from host cell death alongwith the sudden load of dead Cpn to be cleared.I was really interested to learn about theEnteraKlenz, since the other things I have triedhaven't been adequate to help with endotoxinabsorption. I'll try it once my credit card comes downa bit from all the IV treatments I've been gettinglately!Jim

[Guest guest]

Jim,

PS:

I think Wheldon when dealing with people with MS is probably not dealing with people with such HEAVY bacterial loads as the loads we, people infected with TBDs (as well as God knows what else but pbbly incl Cpn) are dealing with. So the problems with bacterial die-offs are more easily dealt with, maybe, just my gut feeling

Nelly