The possibility of mandatory vaccinations for infectious diseases is a cause for concern by
those who understand the toxic mechanism of vaccines.
This simplified explanation of the underlying cause, method of action and remedial measures to
reduce the damage resulting from vaccinations is in contrast to medical journal reviews and
websites that belittle ‘anti-vaccination’ sites as emotional and anecdotal.
1. Introducing any bacteria or bacterial filtrate (alive or dead) results in a physical reaction
producing a blood clot resulting from intense microbial action and a reduction of Zeta Potential.
These clots may be small adhesions that attach to the blood vessels or organs, impairing their
function, or complete obstructions resulting in organ death, particularly in lung, kidney, liver and
brain.
Intravascular coagulation in the blood vessels in the sclera (whites) of the eyes is readily
apparent following vaccines or other infections.
Microorganisms take days to weeks to demonstrate their full effect on the system. This is known
as the Sanarelli/Schwartzman Phenomena. There are several hundred references to this
Phenomena in the National Library of Medicine.
2. Intense microbial action (infection) or microbial agents cause a reduction in Zeta Potential
which changes blood to ‘sludge’.
3. The administration of more than one vaccine at a time multiplies the effect, increasing the
amount of intravascular coagulation and resulting blood clots.
4. The use of aluminum salts to stabilize vaccines exacerbates the clotting effect by a multiple of
6000 times.
5. In summation, infection, whether by vaccine or other disease agents, lowers Zeta Potential,
resulting in clots. A person with high blood Zeta Potential may experience only local reduction
and aggravation. In other cases, infection can result in micro capillary clotting or death from
impaired organ function. (See Reference 1 - Control of Colloid Stability Through Zeta Potential by
Thomas M. Riddick Published for Zeta-Meter, Inc. by Livingston Publishing Company,
Wynnewood, PA)
This explains the wide range of mental/emotional disorders and physical reactions traced to
vaccines, since the site and degree of the clot is unpredictable. The effect may begin as only an
adhesion, but through further reduction of Zeta Potential, may change to a clot or hemorrhage.
Simple changes would greatly reduce risks of vaccinations.
These include:
a) administering a single vaccine later in life rather than at birth
b) eliminating aluminum salts
c) monitoring the blood vessels of the eyes for intravascular coagulation.
can occur immediately and continue for seven or eight years, or may not appear until one to six
years can occur immediately and continue for seven or eight years, or may not appear until one
to six years later. The reason for the delayed effect is beyond the scope of this paper, but is a
function of Zeta Potential.
The Sanarelli Phenomenon is induced by two properly spaced intravenous injections of
microbes or their products.
The Schwartzman Phenomenon is induced by a ‘preparatory’ intracutaneous injection of
bacterial filtrates followed after a proper time interval by intravenous ‘provocation’ with the same
or some similar material.
INTRACUTANEOUS (within the skin)
The Bordet Phenomenon is the production of hemorrhages and necroses by killed E. coli
cultures in tuberculous (but not in normal) guinea pigs.
More than a century ago, the Russian investigator Botkin (1858) discovered that following
application of irritating fluids to the frog mesentery, the capillaries become maximally dilated and
packed with agglutinated erythrocytes so that circulation stops.
These observations were confirmed, and greatly extended, by Hueter (1874), who claimed that
erythrocyte agglutination is caused by toxic substances, many of which make the surface of the
red blood corpuscles irregular and adhesive.
Klebs (1876) first observed multiple hyaline thrombi in the smallest blood vessels in patients with
extensive burns. Then Flexner (1902) noted that both bacterial and non bacterial pathogens can
produce so-called ‘agglutinative thrombi’, which appear to consist almost exclusively of
conglutinated erythrocytes. Subsequently, micro thromboses were seen in intravenous
administration of foreign blood, snake venom, placental extracts and many other substances,
including placebos.
Finally, Siegmund (1925) observed the development of minute fibrin nodules, attached to the
walls of the small veins or the endocardium in guinea pigs repeatedly infected with various
microorganisms.
In the course of their classic studies on Diptheria, Roux and Yersin (1888) found that single
intravenous injections of Diptheria toxin can produce multiple hemorrhages, particularly in the
lung, kidney, adrenal and heart of various experimental animals.
Moreover, it became evident that even killed microbes or microbial filtrates are active in this
respect, and that the predominant localization of the thrombohemmorragic lesions varies,
depending upon the type of pathogenic material used. The kidney, lung, heart and adrenals are
most commonly affected, but, under certain circumstances, lesions may also be found in the
gastrointestinal tract or on the hairless parts of the animal.
In 1894, Sanarelli noticed that, in the monkey, a first injection of typhoid toxin causes only
transient manifestations of disease, but, if a second injection of the same product is
administered two days later, the animal dies with a generalized purpuric eruption.
In 1928, Schwartzman discovered that if a rabbit is given a B.typhus filtrate intracutaneous,
followed by the intravenous injection of the same material 24 hours later, a hemorrhagic
necrosis results at the prepared skin site. (Note: Necrosis is defined as the death of one or more
cells, or a portion of the tissue or orga, or the complete organ.)
Paul Bordet (1931) observed that a suspension of killed E. coli microorganisms, normally well
tolerated by guinea pigs, kills them with hemorrhages in the peritoneal lymph nodes if they have
received BCG vaccine intraperitonealy 2-3 weeks earlier. E.Coli injected subcutaneously into
prepared guinea pigs produced topical hemorrhages with necroses.
Melvin Knisley injected monkeys with Knowles malaria, and discovered that blood coagulated
into a thick sludge at a level of only 5 - 30% invasion of red cells. Death occurred in as little as
three hours. There were no survivors in twelve hours. He identified 65 cases of severe
intravascular coagulation in patients on his ward stemming from 12 different diseases.
Live microbes and microbial products (filtrates and extracts) occupy a particularly important
place among the agents capable of eliciting the thrombohemmorragic phenomenon.
Thrombohemmorragic phenomena can be produced by spontaneous or experimental
infections, as well as by treatment with bacterial filtrates and extracts. The endotoxins of gram
negative bacteria proved to be especially effective in this respect. Both local
thrombohemmorragic reactions at the injection site, and generalized manifestations of the
thrombohemmorragic phenomenon can be produced in this manner, either by single or variably
spaced, repeated injections of suitable microbial products.
Selye’s thesis is that a microbial culture of dead or alive filtrates of such cultures result in
thrombosis (or hemorrhage) when they are suitably and in proper sequence injected into test
animals.
Perhaps it is appropriate to now consider the Sanarelli and Schwartzman phenomena as simple,
straightforward manifestations of a natural law. This law is delineated by the fundamental
principles of Zeta Potential. This physiochemical sequence is encountered so often and in so
many different forms that it is virtually a rule: the end result of vigorous and sustained microbial
activity on any aqueous colloid system is a lowering of Zeta Potential, leading to agglomeration
resulting in sedimentation.
Applying this to Sanarelli and Schwartzman, this rule would read: appropriate injections into a
test animal of the end product of vigorous and sustained microbial activity leads to a lowering of
Zeta Potential which leads to agglomeration and thrombus formation, then thrombosis and
disseminated intravascular coagulation that results in death.
This physiological sequence is of great biological importance.
It is irresponsible and shortsighted that thus far this facet of nature is not properly understood,
accepted and employed in the evaluation and alleviation of disease.
REFERENCES
(1) Control of Colloidal Stability Through Zeta Potential
By Thomas Riddick, pp 126-137
(2) Human Blood Coagulation
Biggs and McFarlane – F. A. Davis Co., Philadelphia 1962
(3) The Chemical Prevention of Cardiac Necroses
Hans Selye – Ronald Press, New York, N.Y. 1958
(4) Thrombohemmorragic Phenomena
Hans Selye, Charles C. Thomas 1966
(5) The Stress of Life
Hans Selye – McGraw Hill 1956
Selected Papers
Melvin Knisley and Associates on Intravascular Coagulation
The Settling of Sludge During Life
Acta Anatomica, Supplement 41-1 and Vol 44-S
S. Karger – New York 1961
Ante Mortem Settling
Angiology, Vol 9, No. 6, Part 2
December 1960
Sludged Blood Transactions of the American Therapeutic Society
Volumes XLVIII and XLIX – 1950
Settling of Blood in Human Patients
Angiology, Volume 9, No. 6
December 1958
Enforced Postponement of Selective Phagocytosis
Southern Medical Journal, Vol. 56, No. 10
October 1963, pp 1115-1127
Birmingham, AL
Experimental Separation of Quite Different Types of Circulatory Shock
Shock and Hypertension – Grune and Stratton, 1965
Intravascular Coagulation of Flowing Blood Following the Injection of Radiopaque Contrast
Media
Neurology, Vol. 8, August 1962
Minneapolis
Knowles Malaria in Monkeys II
Angiology, Vol. 15, No. 9, September 1964
Intravascular Erythrocyte Aggregation (blood sludge)
Handbook of Physiology, Section 2: Circulation Vol. 3
1965
Author Note:
This material may be freely reproduced and distributed in its entirety with proper credit to the
contributors.