A TREATMENT RESISTANT EXTREMOPHILE

 

        Given their small size and growth rate, Nanobacteria should not flourish within the host environment.  First of all, the immune system should make short work of this tiny critter, but it can’t - N. sanguineum kills immune defense cells.  Second, more rapidly growing bacteria should hog all the available nutrients and crowd Nanobacteria out, but that doesn’t happen – Nanobacteria just slow down their growth rate or slowly kill the other bacteria. They even invade our RBCs and are easily transported elsewhere. Nanobacteria have developed means of shielding themselves and going “semi-dormant”, avoiding the immune system (biofilm and calcification). 

        Nanobacteria can survive extremes of temperature.  You can cook them, freeze them, and freeze-thaw them, but this won’t kill them.  Boiling Nanobacteria for 30 minutes will prevent their growth in tissue culture, but heavily calcified forms are resistant to one hour at 100°C.  Temperatures of 195F for 1 hour are required to kill them. Ultraviolet irradiation and autoclaving inactivates non-calcified Nanobacteria; but calcified Nanobacteria are not affected.  Drying at room temperature has no effect, while drying Nanobacteria at 100ºC will kill serum Nanobacteria (we could create huge chambers to dry out our patients at 100ºC – well, maybe there’s a better way).   

        Nanobacteria laugh at radiation.  0.05 megarads of radiation will kill mycoplasmas and other bacteria, but 1 megarad won’t touch Nanobacteria. 150 megarads is required to kill nanobacteria.  In the microbial world, radiation resistance typically involves sophisticated DNA repair systems.  N. sanguineum is too small for sophisticated enzyme systems.  The radiation resistance of N. sanguineum seems to be related to its slow growth rate, unique cell membrane, and the unique structure of its DNA.  When arteries restenose following PTCA, we can stent them.  When the stents stenose, we can restent the region (stent sandwich).  When this doesn’t work, the region can be dilated and irradiated (brachytherapy).  This seems to work better - Hmm.

        HCL and EDTA will decalcify Nanobacteria, but the unroofed organisms remain viable and virulent - and “pissed off”, in their rapid growth and biofilm production mode. Denuded from their calcific shell, the Nanobacteria feel vulnerable.  Their growth rate doubles and they elaborate biofilm, aiming either to establish a new protective shelter or to kill something.  Decalcification alone is not enough to kill Nanobacteria. Our immune system is easy prey as well. Some other agent must step in.

        Pressure equivalent to that of the ocean’s floor will not kill Nanobacteria, nor will fluctuations in pH or salinity.  Formaldehyde, hypochlorite, NaOH, glutaraldehyde, formalin and 11% H2O2 have no effect on Nanobacterial growth or replication.  Antiseptics have no effect; the one exception here is 1% Virkon® (potassium persulfate and sulfaminoic acid), which will kill Nanobacteria within thirty minutes (humans too).

        If you starve Nanobacteria, they simple slow down their growth rate and go dormant.  Over billions of years, Nanobacterium sanguineum has learned to comfortably and patiently live where no other bacteria can survive, such as in kidney stones or the walls of our blood vessels. 

        

        Commonly  employed antibiotics have no effect on Nanobacteria.  Toxic doses of aminoglycosides will slow down their growth rate, but for only a while.  In response to aminoglycosides Nanobacteria changes its morphology and ignores the irritation. 

        Cytoplasmic extensions will spring out from one organism and merge with the cell membrane of another (fig. 1), almost as if the Nanobacteria are exchanging information.  Then the Nanobacteria begin to grow again, and now the aminoglycoside has no effect. 

 

        Ciftcioglu and Kajander (confirmed later in clinical research by Mezo) found Tetracycline Hydrochloride to be the only antibiotic effective against Nanobacteria. Not even the close sisters of Tetracycline, Doxycycline and Terramycin, will work (Mezo). The larger studies have not shown Azithromycin to be effective in preventing coronary disease or in affecting it’s outcome; Azithromycin does not prevent restenosis.   Tetracycline, because of its chemical structure, is able to specifically kill nanobacteria.

        Cytosine arabinoside and 5-FU will kill N. sanguineum, but at levels that would kill the human host first. Given its benign track record, Tetracycline is certainly the preferred (and actually the only) antibiotic to be incorporated into anti-Nanobacterial therapy.

         If you are tempted to stop reading here, thinking that maybe EDTA and Tetracycline will be effective in killing Nanobacteria and eradicating heart disease, then please keep reading, because EDTA and Tetracycline alone will not get the job done.  EDTA and Tetracycline may work In Vitro, but to kill Nanobacteria In Vivo we need more.  We need a means of achieving a persistent, therapeutic EDTA level, and we need concomitant therapy to get at the soft plaque – more on this later on.

         We’ve completed the basic science section of this presentation.  Now on to part two - How Nanobacterium sanguineum affects humans, how we can measure disease burden in the coronaries, and how we can kill this organism and help our patients.

 

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