by Viera Scheibner, Ph.D.
extracted from Nexus
Dec 2000 (Vol 8, No1) & Feb 2001 (Vol 8, Number 2)
PRESERVATIVES AND TISSUE FIXATIVES IN VACCINES
Vaccines contain a number of substances which can be divided into
the following groups:
Micro-organisms, either bacteria or viruses, thought to be
causing certain infectious diseases and which the vaccine is
supposed to prevent. These are whole-cell proteins or just the
broken-cell protein envelopes, and are called antigens.
Chemical substances which are supposed to enhance the immune
response to the vaccine, called adjuvants.
Chemical substances which act as preservatives and tissue
fixatives, which are supposed to halt any further chemical reactions
and putrefaction (decomposition or multiplication) of the live or
attenuated (or killed) biological constituents of the vaccine.
All these constituents of vaccines are toxic, and their toxicity may
vary, as a rule, from one batch of vaccine to another.
In this article, the first of a two-part series, we shall deal with
adjuvants, their expects role and the reactions (side effects).
The desired immune response to vaccines is the production of
antibodies, and this is enhanced by adding certain substances to the
vaccines. These are called adjuvants (from the Latin adjuvare,
meaning "to help").
The chemical nature of adjuvants, their mode of action and their
reactions (side effect) are highly variable. According to Gupta et
al. (1993), some of the side effects can be ascribed to an
unintentional stimulation of different mechanisms of the immune
system whereas others may reflect general adverse pharmacological
reactions which are more less expected.
There are several types of adjuvants. Today the most common
adjuvants for human use are aluminium hydroxide, aluminium phosphate
and calcium phosphate. However, there are a number of other
adjuvants based on oil emulsions, products from bacteria (their
synthetic derivatives as well as liposomes) or gram-negative
bacteria, endotoxins, cholesterol, fatty acids, aliphatic amines,
paraffinic and vegetable oils.
Recently, monophosphoryl lipid A,
ISCOMs with Quil-A, and Syntex adjuvant formulations (SAFs)
containing the threonyl derivative or muramyl dipeptide have been
under consideration for use in human vaccines.
Chemically, the adjuvants are a highly heterogenous group of
compounds with only one thing in common: their ability to enhance
the immune response - their adjuvanticity. They are highly variable in
terms of how they affect the immune system and how serious their
adverse effects are due to the resultant hyperactivation of the
The mode of action of adjuvants was described by Chedid (1985) as:
the formation of a depot of antigen at the site of inoculation, with
slow release; the presentation of antigen immuno-competent cells; and
the production of various and different lymphokines (interleukins
and tumor necrosis factor).
The choice of any of these adjuvants reflects a compromise between a
requirement for adjuvanticity and an acceptable low level of adverse
The discovery of adjuvants dates back to 1925 and 1926, when Ramon
(quoted by Gupta et al., 1993) showed that the antitoxin response to
tetanus and diphtheria was increased by injection of these vaccines,
together with other compounds such as agar, tapioca, lecithin,
starch oil, saponin or even breadcrumbs.
The term adjuvant has been used for any material that can increase
the humoral or cellular immune response. to an antigen. In the
conventional vaccines, adjuvants are used to elicit an early, high
and long-lasting immune response. The newly developed purified
subunit or synthetic vaccines using biosynthetic, recombinant and
other modern technology are poor immunogens and require adjuvants to
evoke the immune response.
The use of adjuvants enables the use of less antigen to achieve the
desired immune response, and this reduces vaccine production costs.
With a few exceptions, adjuvants are foreign to the body and cause
Part 1 deals with the following types of adjuvants (after Gupta et
emulsified oil adjuvants (complete and incomplete)
peanut oil adjuvant (adjuvant 65)
granulosumderived P40 component
and its components
Immunostimulating complexes (ISCOMs)
In the 1960s, emulsified water-in-oil and water-in-vegetable-oil
adjuvant preparations used experimentally showed special promise in
providing exalted "immunity" of long duration (Hilleman, 1966).
development of Freund’s adjuvants emerged from studies of
tuberculosis. Several researchers noticed that immunological
responses in animals to various antigens were enhanced by
introduction into the animal of living Mycobacterium tuberculosis.
In the presence of Mycobacterium, the reaction obtained was of the
delayed type, transferable with leukocytes.
Freund measured the
effect of mineral oil in causing delayed-type hypersensitivity to
killed mycobacteria. There was a remarkable increase in
complement-fixing antibody response as well as in delayed
Freund’s adjuvant consists of a water-in-oil emulsion of aqueous
antigen in paraffin (mineral) oil of low specific gravity and low
viscosity. Drakeol 6VR and Arlacel A (mannide monooleate) are
commonly used as emulsifiers.
There are two Freund’s adjuvants: incomplete and complete. The
incomplete Freund’s adjuvant consists of water-in-oil emulsion
without added mycobacteria; the complete Freund’s adjuvant consists
of the same components but with 5 mg of dried, heat-killed
Mycobacterium tuberculosis or butyricum added.
The mechanism of action of Freund’s adjuvants is associated with the
following three phenomena:
establishment of a portion of the antigen in a
persistent form at the injection site, enabling a
gradual and continuous release of antigen for
stimulating the antibody
provision of a vehicle for transport of emulsified
antigen throughout the lymphatic system to distant
places, such as lymph nodes and spleen, where new foci
of antibody formation can be established
Formation and accumulation of cells of the mononuclear series
which are appropriate to the production of antibody at the local and
The pathologic reaction to the Freund’s adjuvants starts at the
injection site with mild erythema and swelling followed by tissue
necrosis, intense inflammation and the usual progression to the
formation of a granulomatous lesion. Scar and abscess formation may
The reactions observed following the administration of the
complete adjuvant are generally far more extensive than with the
The earliest cellular response is polymorphonuclear, then it changes into mononuclear and later
includes plasmocytes. The adjuvant emulsion may be widely
disseminated in varrious organs, depending on the route of
inoculation, with the development of focal granulomatous lesions at
distal places. Various gram-negative organisms may show a
potentiating effect of the adjuvant, similar to that displayed by
The earliest use of oil emulsion adjuvants was made with the
influenza, vaccine by Friedwald (1944) and by Henle and Henle
(1945). Following their promising results on animals, Salk (1951)
experimented with such adjuvants on soldiers under the auspices of
the US Armed Forces Epidemiological Board. He used a highly refined
mineral oil, and developed a purified Arlacel A emulsifier which was
free of toxic substances, such as oleic acid which had caused
sterile abscesses at the injection site, and he administered the
vaccine by intramuscular route.
Subsequently, Miller et al. (1965) reported their, failure to
enhance the antibody and protective response to types 3, 4 and 7
adenovirus vaccines in mineral oil adjuvant compared with aqueous
vaccine. Unpublished studies have revealed the need for an adequate
minimal amount of antigen to trigger an antibody response to the
Salk et al. (1953) applied Freund’s adjuvant to poliomyelitis
vaccine, and later followed with extensive testing of killed crude
as well as purified polio virus vaccine in animals and humans, where
the reactions in humans were considered inconsequential.
Grayston et al. (1964) reported highly promising results with the
trachoma vaccine using an oil adjuvant. However, the trachoma
vaccine lost its relevance because, as demonstrated by Dolin et al.
(1997) in their 37 years of research in a sub-Saharan village, the
dramatic fall in the disease occurrence was closely connected with
improvements in sanitation, water supply, education and access to
health care. According to Dolin et al. (1997), the decline in
trachoma occurred without any trachoma-specific intervention.
Allergens in Freund’s adjuvant deserve special attention because
they can be dangerous. These dangers include an overdose, i.e., the
immediate release of more than the tolerated amount of properly
emulsified vaccine in sensitive persons, or the breaking of the
emulsion with the release of all or part of the full content of the
allergen within a brief period of time.
Long-term delayed reactions
include the development of nodules, cysts or sterile abscesses
requiring surgical incision. It is also likely that some allergens
used, such as house dust or mould, might have acted like mycobacteria to potentiate the inflammatory response. Such reactions
have been reduced with the use of properly tested and standardized
One must also consider that the first application of Freund’s
adjuvants was made at a time when modern concepts of safety were
non-existent Indeed, mineral oil adjuvants have not been approved
for human use in some countries, including the USA.
Aluminium phosphate or aluminium hydroxide (alum) are the mineral
compounds most commonly used as adjuvants in human vaccines. Calcium
phosphate is another adjuvant that is used in many vaccines. Mineral
salts of metals such as cerium nitrate, zinc sulphate, colloidal
iron hydroxide and calcium chloride were observed to increase the
antigenicity of’ the toxoids, but alum gave the best results.
The use of alum was applied more than 70 years ago by Glenny et al.
(1926), who discovered that a suspension of alum-precipitated
diphtheria toxoid had a much higher immunogenicity than the fluid
Even though a number of reports stated that alum-adjuvanted
vaccines were no better than plain vaccines (Aprile and Wardlaw,
1966), the use of alum as an adjuvant is now well established. The
most widely used is the antigen solution mixed with pre-formed
aluminium hydroxide or aluminium phosohate under controlled
Such vaccines are now called aluminium-adsorbed or
aluminium-adjuvanted. However, they are difficult to manufacture in
a physico-chemically reproducible way, which results in a
batch-to-batch variation of the same vaccine. Also, the degree of
antigen absorption to the gels of aluminium phosphate and aluminium
To minimize the variation and avoid the
non-reproducibility, a specific preparation of aluminium hydroxide (Alhydrogel)
was chosen as the standard in 1988 (Gupta et al., 1993).
The aluminium adjuvants allow the slow release of antigen,
prolonging the time for interaction between antigen and
antigen-presenting cells and lymphocytes. However, in some studies,
the potency of adjuvanted pertussis vaccines was more than that of
the plain pertussis vaccines, while in others no effect was noted.
The serum agglutinin titres, after vaccination with adjuvanted
pertussis vaccines, were higher than those of the plain vaccines,
with no difference in regard to protection against the disease
(Butler et al., 1962).
Despite these conflicting results, aluminium
compounds are universally used as adjuvants for the DPT (diphtheriapertussis-tetanus)
vaccine. Hypersensitivity reactions following their administration
have been reported which could be attributed to a number of factors,
one of which is the production of IgE along with IgG antibodies.
It was suggested that polymerased toxoids, such as the so-called
glutaraldehyde-detoxifled purified tetanus and diphtheria toxins,
should be used instead of aluminium compounds. They are used
combined with glutaraldehyde-inactivated pertussis vaccine.
Calcium phosphate adjuvant has been used for simultaneous
vaccination with diphtheria, pertussis, tetanus, polio, BCG, yellow
fever, measles and hepatitis B vaccines and with allergen (Coursaget
et al., 1986). The advantage of this adjuvant has been seen to be
that it is a normal constituent of the body and is better tolerated
and absorbed than other adjuvants. It entraps antigens very
efficiently and allows slow release of the antigen.
elicits high amounts of IgG-type antibodies an much less of IgE-type
Micro-organisms in bacterial infections and the administration of
vaccines containing whole killed bacteria and some metabolic
products and components of various micro-organisms have been known
to elicit antibody response and act as immuno-stimulants.
addition of such micro-organisms and substances into vaccines
augments the immune response to other antigens in such vaccines.
The most commonly used micro-organisms, whole or their parts, are
Bordetella pertussis components, Corenybacterium derived P40
component, cholera toxin and mycobacteria.
B. pertussis components
The killed Bordetella pertussis has a strong adjuvant effect on the
diptheria and tetanus toxoids in the DPT vaccines. However, there
are a number of admitted and well-describe reactions to it, such as
convulsion, infantile spasms, epilepsy, sudden infant death syndrome
(SIDS), Reye syndrome, Guilain-Barre syndrome, transverse myelitis
and cerebral ataxia.
Needless to say, the causal link to it is often
(even though not always) vehemently disputed and generally
Paradoxically, in one case of shaken baby syndrome in which the baby
developed subdural and retinal hemorrhages from the disease
whooping cough, doctors accused the father of causing these injuries
and strenuously denied that the disease pertussis can and does cause
such haemorrhages - forgetting that this is the very reason why
pertussis vaccine was developed against such potentially devastating
disease in the first place.
Such devastating effects are caused by
pertussis toxin, the causative agent of the disease (pertussis
is a toxin-mediated disease), employed as the active ingredient in
all pertussis vaccines whether whole-cell or acellular (Pittman,
Gupta et al. (1993) concluded that PT is too toxic to be
administered to humans, but chemically detoxified or genetically
inactivated PT may not exhibit the adjuvant effects comparable to
the native PT.
P40 is a particulate fraction isolated from Corynebacterium
granulosum, composed of the cell wall peptidoglycan associate with a
glycoprotein. In animals, it displays a number of activities such as
stimulation of the reticulo-endothelial system, enhancement of
phagocytosis and activation of macrophages.
P40 abolishes drug-induced immuno-suppression and increase
non-specific resistance to bacterial, viral, fungal and parasitic
infections. It induces the formation of IL-2, tumor necrosis
factor, and interferon alpha and gamma (Bizzini et al., 1992). In
clinical trials, P40 was claimed to be efficacious in the treatment
of recurrent infections of the respiratory and genito-urinary
Allergens coupled to P40 have been said to be instrumental
in desensitizing allergic patients without any side effects.
LPS is an adjuvant for both humoral and cell-mediated immunity. It
augments the immune response to both protein and polysaccharide
antigens. It is too toxic and pyrogenic, even in minute doses, to be
used as an adjuvant in humans.
Mycobacterium and its components
Interestingly, Mycobacterium and its components, as originally
formulated, were too toxic to be used as adjuvants in humans.
However, the efforts to detoxify them resulted in the development of
N-acetyl muramyl-L-alanyl-D-isoglutamine, or muramyl dipeptide (MDP).
When given without antigen, it increased nonspecific resistance
against infections with bacteria, fungi, parasites, viruses, and
even against certain tumours (McLaughlin et al., 1980).
However, MDPs are potent pyrogens (maybe that’s why they may be effective
against certain tumours - my comment) and their action is not
completely understood; hence they are not acceptable for use in
A major drawback with cholera toxin as a mucosal adjuvant is its
Liposomes are particles made up of concentric lipid membranes
containing phospholipids and other lipids in a bilayer configuration
separated by aqueous compartments.
They have been used parenterally
in people as carriers of biologically active substances (Gregoriadis,
1976) and considered safe.
Immunostimulating complexes (ISCOMs)
ISCOMs (DeVries et al., 1988; Morein et al., 199&, Lovgren : al.,
1991) represent an interesting approach to stimulation of the
humoral and cell-mediated immune response towards amphipathic
antigens. It is a relatively stable but non-covalently-bound complex
of saponin adjuvant Quil-A, cholesterol and amphipathic antigen in a
molar ratio of approximately 1:1:1.
The spectrum of viral capsid
antigens and non-viral amphipathic antigens of relevance for human
vaccination, incorporated into ISCOMs, comprises influenza, measles,
rabies, gp340 from EB-virus, gp120 from HIV, Plasmodium falciparum
and Trypanosoma cruzi.
ISCOMs have been shown to induce cytotoxic T-lymphocyte (CTL).
Following oral administration, some types of CTLs were found in
mesenteric lymph nodes and in the spleen, and specific IgA response
could be induced.
ISCOMs have only been used in veterinary vaccines, partly due to
their haemolytic activity and some local reactions all reflecting
the detergent activity of the Quil-A molecule.
Other Adjuvants - Squalene
Squalene is an organic polymer with some antigenic epitopes which
might be shared with other organic polymers acting as
immuno-stimulators. It has been used in experimental vaccines since
1987 (Asa et aL, 2000) and it was used in the experiments vaccines
given to a great number of the participants in the Gulf War.
included those who were not deployed but received the same vaccines
as those who were deployed.
The adjuvant activity of non-ionic block copolymer surfactants was
demonstrated when given with 2% squalene-in-water emulsion. However,
this adjuvant contributed to the cascade of reactions called "Gulf
War syndrome", documented in the soldiers involved in the Gulf War.
The symptoms they developed included:
abnormal body hair loss
elevated ESR (erythrocyte
systemic lupus erythematosus
(amyotrophic lateral sclerosis)
This long list of reactions shows just how much damage is done by
vaccines, particularly when potentiated by powerful "immuno-enhancers"
such as squalene and other adjuvants. Interestingly, vaccinators as
a rule consider such problems as mysterious and/or coincidental with
Since the administration of a multitude of vaccines to the
participants (and prospective participants) in the Gulf War is
well-documented (in fact, veterans claim they were given many more
than were even recorded), this list of observed reactions further
incriminates the vaccines as causing such problems.
- ANTIBODY RESPONSE
To explain the action of adjuvants, we should look into immunology.
The theory of vaccine efficacy is based on the ability of vaccines
to evoke the formation of antibodies. This is of varying efficacy,
depending on the nature of the antigen(s) and the amount of
antigenic substance administered.
However, the mechanisms for the diversity of immune reactions are
complex, and to this day are not quite known and understood. There
are numerous theories, the favored one being antibody response as
the sign of immunization (acquiring immunity).
Specific immunity to a particular disease is generally considered to
be the result of two kinds of activity: the humoral antibody and the
The ability to form antibodies develops partly in utero and partly
after birth in the neonatal period. In either case, immunological
competence - the ability to respond immunologically to an antigenic
stimulus - appears to originate with the thymic activity.
The thymus initially consists largely of primitive cellular elements
which become peripheralised to the lymph nodes and spleen. These
cells give rise to lymphoid cells, resulting in the development of
immunological competence. The thymus may also exert a second
activity in producing a hormqne-lilce substance which is essential
for the maturation of immunological competence in lymphoid cells.
Such maturation also takes place by contact with thymus cells in the
Stimulation of the organism by antigen results in proliferation of
cells of the lymphoid series accompanied by the formation of
immunocytes, and this leads to the antibody production. Certain
lymphocytes and possibly reticulum cells may be transformed into
immunoblasts, which develop into immunologically active ("sensitised")
lymphocytes and plasmocytes (plasma cells). Antibody formation is
connected with plasma cells, while cellular immunity reactions are
None of the theories for antibody formation comprehends all the
biological and chemical data now available. However, several
principal theories have been considered at length.
The so-called instructive theory holds that the antigen is brought
to the locus of antibody synthesis and there imposes in some way the
synthesis of the specific antibody with reactive sites which are
complementary to the antigen.
The clonal selection theory, evolved by Burnett (1960), presupposes
that the information requisite to the synthesis of the antibody is
part of the genetics. While the body develops a wide range of clones
of cells necessary to cover all antigenic determinants by random
mutation during early embryonic life, those clones which are capable
of reacting with antigens of the body ("self’) are destroyed,
leaving only those cells which are not oriented to self
Upon stimulation by a foreign antigen, the clones of
the cells corresponding to the particular foreign antigen are
stimulated to proliferate and to produce the antibody.
Other researchers demonstrated that there are at least four
different antigens formed by descendants of a single cloned cell. By
this mechanism, the information for antibody synthesis is contained
in the genetic material of each cell (DNA) but is normally
repressed. The antigen then assumes the role of a de-repressor and
initiates (provokes) the RNA synthesis for a particular messenger,
resulting in the corresponding antibody production.
would instruct the genetically predisposed capability of multipotential cells as to which antibody to produce and might also
command the cells to proliferate, resulting in clones of properly
There are two possible mechanisms for the elimination of antibodies
against self: immunological non-responsiveness and immunological
paralysis. There are several states of immunological
non-responsiveness; one is illustrated by the exposure of a fetus or
newborn to an antigen prior to the development of its ability to
recognize the antigen as non-self (immunological incompetence).
Immunological paralysis results from the injection of a very large
amount of antigen into immunologically competent individuals.
Nonspecific immunological suppression by cortisone, ACTH, nitrogen
mustards and irradiation is also well known.
Cellular sensitivity, also known as delayed or cellular
hypersensitivity, depends on the development of immunologically
reactive or "sensitive" lymphocytes and possibly other cells which
react with the corresponding antigen to give a typical delayed-type
reaction after a period of several hours, days or even weeks.
Cellular hypersensitivity depends on the original antigenic
stimulation and a latent period, and is specific in its response.
Delayed-type hypersensitivity is characteristic of the body’s
response to various infectious agents such as viruses, bacteria,
fungi, spirochetes and parasites. It is also characteristic of the
body’s response to various chemicals, such as mercury, endotoxins,
antibiotics, various drugs and many other substances foreign to the
The induction of a hypersensitivity reaction requires the presence
in the tissues of the whole organism or certain derivatives of it,
in addition to the specific antigen such as a lipid in addition to
tubercle bacillus protein.
Sensitization to a non-infectious
substance must be mediated through the skin or mucous membranes
which probably provide further necessary co-factors.
A delayed hypersensitivity reaction may be enhanced experimentally
by the employment of the antigen in a mineral oil adjuvant with
added Mycobacterium tuberculosis or by injection of the antigen
directly into the lymphatics. The delayed hypersensitivity response
is accompanied by mild to severe inflammation which may cause cell
injury and necrosis.
The inflammatory response which occurs in
delayed-type hypersensitivity may not be protective, and in many
instances may even be harmful (e.g., rejection of grafts is directly
linked to delayed hypersensitivity).
IMMUNO-PATHOLOGY OF HYPERSENSITIVITY REACTIONS
This is the antibody-type reaction that is a secondary consequence
to the beneficial effect of the combination of an antibody with its
This reaction results from the precipitative union of a large amount
of antigen with a highly reactive antibody in the blood vessels, and
leads to vascular damage. The cascade of events includes spastic
contraction of the arterioles, endothelial damage, formation of
leukocyte thrombi, exudation of fluid and blood cells into the
tissues, and sometimes ischemic necrosis.
results from a similar antigen-antibody reaction and is
characterized by inflammation of the smaller arteries and
periarterial structures. it is accompanied by proliferation of the
intima and two types of occlusion:
by proliferation or
by the formation of nodules containing neutrophils and eosinophils
Injection of antigen and its combination with antibody may cause
release from the cells (especially mast-cell fixed basophils) of
physiologically active substances such as histamine, serotonin,
acetyicholine, slow-reacting substances (SRS) and heparin.
on smooth muscle and blood vessels and cause anaphylactic
(hypersensitivity) shock, asthma attack, allergic oedema, rhinitis
or hay fever, and accumulation of fluid in the joints.
Atopy is caused by the union of antigen
- usually pollens, dust, milk,
wheat and animal danders - with a peculiar type of antibody (reagin).
This reaction is relatively heat-labile and cannot be demonstrated
by in vitro procedure. It has a special affinity for the skin and
for familial predisposition to the disease.
The reaction is
nevertheless similar to other immediate-type sensitivities, with the
release of histamine and its manifestation principally as asthma
(breathing paralysis), hay fever, urticaria, angioedema and
The typical pathology of delayed hypersensitivity due to infectious
agents involves perivascular infiltration of lymphocytes and
histiocytes with the destruction of the antigen-containing
parenchyma in the infiltrated area.
The visual manifestations may
vary from slight erythema and oedema to a violent reaction with
progressive tissue destruction and necrosis. Local reactions include
papular rose spots of typhoid fever, meningitis and a variety of
infectious diseases, and contact sensitivities to plant and chemical
substances manifesting as erythema, followed by papule and vesicle
formation with resultant tissue damage and desquamation. Systemic
reactions may accompany severe local reactions or may result from
inhalation of the allergenic substances.
Humoral antibodies do not seem to play a role in delayed
hypersensitivity reaction. The reactivity is transferred only by
cells, presumably sensitised lymphocytes, and it is unlikely that
histamine or other physiologically active substances play a role in
The reaction extends to any or all tissues where the
offending antigen may occur.
This is the result of an immunological reaction of a member of the
same species to the tissue of another member of the same species. A
blood transfusion reaction in a person given an incompatible blood
type is a typical example.
Another example is erythroblastosis
fetalis, which results from the transfer of antibodies against the
red blood cells of the fetus to the fetal circulation.
rejection of tissues or organs between nonisologous members of a
species is also immunologically based.
Immunological Disease Resulting from Adsorption of Foreign
Under certain circumstances, foreign substances such as medications
may combine with cells to render them antigenic.
to such a foreign substance results in lytic, agglutinative or other
types of cell-destructive activity. Such a reaction may involve red
blood cells (drug-induced anaemias), platelets (drug-induced
thrombocytopemc purpura), and leukocytosis (drug-induced
Bacteria or viruses may also alter cell surfaces by coating or by
unmasking antigens through enzymatic activity which may render them
vulnerable to immunological destruction.
Under certain circumstances, the body may respond immunologically to
its own components or to intrinsic substances which are related
antigenically to the host’s own tissues.
The circulating antibody or
sensitized cells which are produced are then active in causing
cellular injury to the tissues or organs of the body which bear the
Waksman (1962) proposed several mechanisms of
Vaccination with organ-specific antigens which are isolated from
the lymphatic channels and bloodstream and are not recognized as
self when brought into contact with the immunologic process. They
are represented in the central and peripheral nervous systems, lens,
uvea, testes, thyroid (thyroglobulin), kidneys and other organs.
Vaccination against constituents of tissues which have been
altered antigenetically by various factors. These include myocardial
infarction, X-irradiation, enzymatic or other chemical alteration,
and changes induced by infectious disease agents or by drugs.
Erythrocytes, platelets and leucocytes are the most affected cells.
Various organs may also be affected.
Vaccination with heterologous antigens which are sufficiently
different to permit an immunological response but sufficiently alike
to react with autologous antigens.
Alteration of the immunological apparatus so as to result in the
failure of recognition of self. This occurs in neoplasia of the
lymphatic system and in experimental grafting of immunologically
competent heterologous lymphatic tissues under conditions which
suppress the host’s response to the graft and give rise to the
wasting "runt disease" or "homologous disease".
Possible hereditary or other immunological abnormality. This is
represented by a hyper-reactivity to antigens or other aberrations
without apparent antigenic stimulation. Such mechanisms might be
related to certain forms of the "collagen diseases", such as
systemic lupus erythematosus in which there is an antibody against a
diversity of antigens.
Experimentally, Freund’s mineral oil adjuvant (usually with added mycobacteria) and certain bacteria or bacterial toxins may so alter
the host as to bring about a ready response to unaltered normal
homologous tissue. These "experimental autoallergies" include a wide
variety of organs and tissues, and are now being employed as model
systems for investigation of autoimmune phenomena.
Both humoral antibody and
sensitized cells may function in
Auto-antibodies seem to be involved in reactions
with cells which are easily accessible, such as the formed elements
of the blood (in haemolytic anaemia, leucopeni thrombocytopenia),
vascular endothelium, vascular basement membrane including the
glomerulus (in acute glomerulonephritis and ascites cells (neoplastic
Production of lesions in the solid vascularised tissues appears to
depend on delayed hypersensitivity reactions with sensitised
lymphoid cells (such as in allergic encephalomyeitis, thyroiditis,
subacute and chronic glomerulonephritis, orchitis, adrenalitis and
many other diseases).
It is quite obvious now that the same autoimmune mechanisms are
responsible for the same diseases in human beings and that the
extent of such damage is enormous and keeps increasing with more and
more vaccines added to to "recommended" schedule.
Indeed, vaccines such as the pertussis vaccine are actually used to
induce autoimmune diseases in laboratory animals, the best and most publicised example being the so-called
When, as expected, these unfortunate
animals develop EAE from the
pertussis vaccine, the causal link is
never disputed; yet when babies after vaccination with the same
vaccines develop the same symptoms of EAE as the laboratory animals,
the causal link to the administered vaccine is always disputed and
usually considered "coincidental". Lately, innocent parents and
other carers have been accused of causing the symptoms of vaccine
darn age by allegedly shaking their babies.
Systemic lupus erythematosus is one of the innumerable recognized
side effects of a number of vaccinations. One of the best papers (if
not the best on this is by Ayvazian and Badger (1948), and it has
not lost any of its punch and relevance since it was published. They
describe three cases of nurses who were literally vaccinated to
The authors surveyed a group of 750 nurses who trained at a
large municipal hospital between 1932 and 1946, and detailed the
cases of three nurses who were vaccinated with a multitude of
vaccines over a period of time and developed and succumbed to
disseminated lupus erythematosus.
Typically, these nurses were given the following tests and vaccines
in short succession:
three days later, the
seven days later,
later, another typhoid-paratyphoid vaccine (a double dose)
days later, the third typhoid-paratyphoid vaccine
later, the fourth typhoid-paratyphoid vaccine
Every time, the
recipient developed local erythema and/or fever and malaise, but it
did not deter the doctor from administering yet another series of
vaccines, starting only 14 days after the first lot of tests and
This time, after all these injections, one of the trainee nurses was
given her first injection of scarlet fever streptococcus toxin with
"no ill results". One week later, she was given the second injection
of streptococcus toxin, after which she developed joint pains and
fever. She did not report these reactions to the health office. Nine
days later, she returned and received the third injection of a
fourfold dose of streptococcus, after which she developed severe
arthralgia in the fingers and knees and a sore throat.
She was hospitalized for five days and discharged with the diagnosis
"Dick-toxin reaction". Only five days later her inoculations were
continued, first in lower and then in gradually increasing doses so
that the series included a total of 10 instead of the usual seven
Epinephrine was administered with each of these
injections of streptococcus toxin and toxin-antitoxin.
Two months after the last lot, the trainee nurse was re-admitted to
the hospital with swelling and pain of the ankles and toes and
tenderness of the joints of both hands, which had been constant
since the first Dick test five months earlier. The diagnosis was
"rheumatic arthritis". She was given aspirin, but two weeks later
the pain came back and she developed chills and fever, sore throat
One month later, the trainee nurse was re-admitted to
hospital for two weeks, and during this admission a streptococcus
vaccine was started in small doses, but because of her severe
reaction "further vaccines were refused". The diagnosis after this
admission was "rheumatoid arthritis and infectious mononucleosis".
Four months later, the trainee nurse noticed skin eruptions over her
nose and both cheeks, and her saliva became foul. The skin and
cheeks, upper lips and the bridge of the nose were covered with
purplish red, mottled and indurated rash eruptions.
later, the eruptions spread over much of the body. A year later, the
trainee nurse died, but not before developing severe symptoms of
high fever, tachycardia, diarrhea and showing abnormal blood tests.
It was not enough that this unfortunate trainee nurse died; there
were another two cases reported, almost identical to the first case.
We shall never know bow many of the remaining 747 trainee nurses
developed less lethal, but still health-incapacitating reactions.
If someone said that this type of "medical treatment’ had been given
to the inmates of the Nazi concentration camps, I would not be
surprised. However, this type of "medical treatment" was and is
being given with impunity to millions of babies, children, teenagers
and adults in so-called free and democratic countries as well as in
the Third World.
Meanwhile, the health authorities refuse to accept
that vaccines cause such reactions and even deaths.
A SAFETY WARNING
The conclusions which follow the study of relevant medical and
literature dealing with vaccines and the adjuvants
used in vaccines is that the absolute safety of these substances can
never be guaranteed.
According to Gupta et al. (1993), the toxicity
of adjuvants can be ascribed in part to the unintended stimulation
of various mechanisms of the immune response. That’s why the safety
and adjuvancy must be balanced to get the maximum immune stimulation
with minimum side effects.
My conclusion is that such balance is impossible to achieve, even if
we fully understood the immune system and the full spectrum of
deleterious effects of foreign antigens and other toxic substances
such as vaccine and drug adjuvants and medications on the immune
system of humans, and particularly on the immature immune system of
babies and small children. Injecting any foreign substance straight
into the bloodstream will only cause anaphylactic (sensitization)
Nature, over thousands and thousands of years, has
developed effective immune responses; yet man, without respect for
nature, demonstrably causes more harm than good.
Vaccination procedures are a highly politically motivated
non-science, whose practitioners are only interested in injecting
multitudes of vaccines without much interest or care as to their
effects. Data collection on reactions to vaccines is only paid lip
service, and the obvious ineffectiveness of vaccines to prevent
diseases is glossed over.
The fact that natural infectious diseases have beneficial effect on
the maturation and development of the immune system is ignored or
Consequently, parents of small children and any potential recipients
of vaccines and any orthodox medications should be wary of any
member of the medical establishment (which is little more than a
highly politicized business system) extolling the non-existent
virtues of vaccination.
Even though Australian law requires doctors
to warn patients about all side-effects of all medications and
procedures of a material nature, whether the patient asks or not,
doctors as a rule do not uphold this important law.
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