DIFFICULT TO DETECT – DIFFICULT TO KEEP OUT

 

            N. sanguineum is difficult to detect, difficult to exclude, and thus difficult to keep out of biological products.  N. sanguineum is present in fetal bovine sera, human and animal blood, vaccines, and diseased human tissues.  N. sanguineum is thus within us and within our field of vision, but we haven’t noticed it until now.  Why?

        First of all, N. sanguineum is essentially too small to see.  Apatite bearing Nanobacteria can be seen under microscopy using polarized light, but they don’t pick of standard stains, and are thus invisible under standard microscopy.  With their small diameter, electron microscopy is absolutely required.  Nanobacteria are coccoid to coccobacilar in shape, with a cell wall that varies between 20 to 200 nm in thickness.  Divisional septa may occur in the central part of the cell, indicating binary fission (fig. 1), or at the end of the cell, suggesting a budding process (fig. 2, cell division by budding).  Budding seems to start by formation of a capsule for a new cell, followed by transfer of cytoplasmic contents into this sheltered compartment. 

N. sanguineum does not grow in standard bacteriologic media; it grows only in cell culture media, and then only under the right conditions.  N. sanguineum grows only slowly, doubling once every three to six days, so patience is required.  Kajander and Ciftcioglu worked long and hard to learn how to culture this organism.  An American group tried to culture N. sanguineum out of kidney stones and they weren’t successful, but they didn’t follow Kajander and Ciftcioglu’s stringent protocol to isolate Nanobacteria.  Another NIH funded American group, specifically after being trained by Ciftcioglu & Kajander, worked for many months trying to develop a pure Nanobacterial culture, only to find it contaminated with regular bacteria. This NIH research group ran out of grant money and was unable to restart so his particular study was unsuccessful. The Mayo Clinic Infectious Disease, Microbiology & Nephrology Departments, after being taught by Ciftcioglu & Kajander, have been intensively studying Nanobacteria for 6+ years. Mayo has repeated and validated independently all of the work done by Ciftcioglu & Kajander; publication is expected in mid-2002.  

While Nanobacterial culture is difficult and time consuming, antigen and antibody testing is rapid and readily available.  TheNanobacTEST® was developed by Kajander and Ciftcioglu’s group, and is available in the US through their US collaborators, NanobacLabs.  The Antigen component of the NanobacTEST® will be positive if non-calcified, extracellular N. sanguineum is present in the blood; thus the antigen study picks up acute Nanobacteremia.  The IgG Antibody component of the NanobacTEST® will be positive in response to the presence of Nanobacterial biofilm and/or the presence of non-calcified Nanobacteria in the blood within the preceding four months.  Now, if one’s Nanobacterial infection is “contained” or semi-dormant, (calcified shelters in the vascular wall or within internal organs) and no Nanobacteria or Nanobacterial biofilm have leaked out into the circulation within the prior four months, then both antigen and antibody testing will return negative, even though the infection is still present, but dormant. It is not possible to think traditionally when thinking about these stealth bacteria that hide. When dealing with regular bacteria, we have traditionally just assumed that if antibody and antigen studies are negative, that the organism is gone and probably has been gone for at least 4 months. Not true with, as called by one journalist, Conan the Bacterium.

            In Finland, Nanobacteremia can be detected in 5% of medical students, 15% of blood donors, 80% of dialysis patients, and in a significant but not yet quantified percentage of individuals with coronary artery disease.  In the United States, from what  NanobacLabs research has shown thus far, 95% of heart disease patients are positive for Nanobacterial Antigen, Nanobacterial Antibody, or both.  My impression is that some degree of Nanobacteremia is part and parcel of modern human existence (just as transient bacteremia may occur with tooth brushing).   If we didn’t get it from our mothers, then we were injected with Nanobacteria when we got the polio vaccine (more on this later) or other vaccines made in fetal bovine serum! 

My thinking is that a healthy immune system can try to wall off areas of limited Nanobacterial insult, but that if the blood borne Nanobacteria encounter a region of weakness or impaired local defense, they invade it and begin the process of colony growth; ie: areas of ischemia (ex: brain, cardiac or muscle), injury (ex: joint, infection or tumors) or if trapped (ex: kidney, prostate, cataract or gall bladder). Given that calcified Nanobacteria double only once every six days, calcific clinical disease will not show itself for decades.  Consider the athlete who sustains knee damage.  The joint heals up, normal function returns, and he returns to the playing field.  At age 45, however, the joint is a little stiff.  At age 50, he can tell when the weather is going to change (of interest, Nanobacteria grow more rapidly at decreased atmosphere and secrete more biofilm, causing increased inflammatory reaction).  Some calcification can be seen on his X-Ray; this progresses (the growth rate of Nanobacterial calcific mass In Vitro is 44% per year, similar to the progression rate of coronary and kidney stone calcification), as do symptoms and functional impairment, leading to joint replacement at age 60.  Something caused this joint to calcify over the years, and my hunch is (and NanobacLabs research supports this hunch) that it was Nanobacteria, that settled into the joint when it was damaged on the gridiron.  Autopsy studies have demonstrated that early atherosclerosis is not uncommon in 20 year olds.  The disease progresses ever so slowly, manifesting itself as clinical coronary disease at middle age, but then its clinical expression speeds up, with artery after artery plugging up.  My hunch is that endothelial irritation or damage (e.g. smoking, local flow dynamics, vitamin C deficiency, elevated BP) at a young age allows transiently circulating Nanobacteria to gain a foothold within the artery wall.  The bugs are ever so small and grow ever so slowly, so at first little macroscopic disease is seen within the vascular wall, or in the myocardium as ”heart sand”. 

However, with constant doubling, the Nanobacterial mass, now calcium generating, and the inflammation and fibrosis that represent the immune system’s frustrated attempt to contain it and wall it of, reaches size to become a visible plaque.  Geometric growth continues; the 50% narrowing at age 45 becomes a 75% lesion at age 50, and you know what happens next.  We know that unstable angina is a pan-vascular phenomenon.  While the patient’s symptoms are typically related to the destabilization of one lesion in one artery, angioscopic study has demonstrated that plaques in other arteries are anatomically altered and activated (Nanobacterial biofilm stimulating the immune system cascade).  In the circulation, inflammatory markers such as CPR will rise.  Could it be that unstable angina is really acute Nanobacteremia?  Unroofed Nanobacteria release biofilm, leading to an aggressive immediate and long-term immune response and inflammation.  Inflammatory organ system dysfunction not infrequently accompanies CABG or major vascular surgery.  Free radical stress related to ischemia/reperfusion injury certainly plays a role here, but just as likely it is that when the surgeon incises the diseased artery, he is releasing previously calcified Nanobacteria out into the circulation, precipitating aggressive Nanobacterial growth, biofilm elaboration, and endotoxin production