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ADVERSE
EFFECTS OF ADJUVANTS IN VACCINES ADJUVANTS,
PRESERVATIVES AND TISSUE FIXATIVES IN VACCINES ADJUVANTS 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 immune system. 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 immunocompetent cells; and the production
of various and different lymphokines (interleukins and tumour necrosis
factor). 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 adverse reactions. 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: 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 occur. The reactions observed
following the administration of the complete adjuvant are generally
far more extensive than with the incomplete adjuvant. 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 mycobacteria. 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 emulsified preparations. 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 standardised reagins. 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 toxoid. 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 conditions. 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 hydroxide varies. To minimise 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. Additionally, it elicits high amounts of IgG-type antibodies
an much less of IgE-type (reaginic) antibodies. The most commonly
used micro-organisms, whole or their parts, are Bordetella pertussis
components, Corenybacterium derived P40 component, cholera toxin
and mycobacteria.
Other Adjuvants:
Squalene 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 arthritis, fibromyalgia, lymphadenopathy,
rashes, photosensitive rashes, malar rashes, chronic fatigue, chronic
headaches, abnormal body hair loss, non-healing skin lesions, aphthous
ulcers, dizziness, weakness, memory loss, seizures, mood changes,
neuropsychiatric problems, anti-thyroid effects, anaemia, elevated
ESR (erythrocyte sedimentation rate), systemic lupus erythematosus,
multiple sclerosis, ALS (amyotrophic lateral sclerosis), Raynaud's
phenomenon, Sjorgren's syndrome, chronic diarrhoea, night sweats
and low-grade fevers. This long list
of reactions shows just how much damage is done by vaccines, particularly
when potentiated by powerful "immunoenhancers" such as
squalene and other adjuvants. Interestingly, vaccinators as a rule
consider such problems as mysterious and/or coincidental with vaccines.
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. Specific immunity
to a particular disease is generally considered to be the result
of two kinds of activity: the humoral antibody and the cellular
sensitivity. 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 thymus. 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 mainly
lymphocytic. 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 ("non-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. The antigen 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 instructed cells. There are two
possible mechanisms for the elimination of antibodies against self:
immunological nonresponsiveness and immunological paralysis. There
are several states of immunological nonresponsiveness; one is illustrated
by the exposure of a foetus or newborn to an antigen prior to the
development of its ability to recognise 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 body. 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. Sensitisation to a non-infectious substance must
be mediated through the skin or mucuous 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). IMMUNOPATHOLOGY
OF HYPERSENSITIVITY REACTIONS: Immediate
Hypersensitivity Arthus-type
Reaction Anaphylaxis Atopy Delayed Hypersensitivity 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. The reaction extends
to any or all tissues where the offending antigen may occur. Isoimmunological
Disease Immunological
Disease Resulting from Adsorption of Foreign Substances 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. Autoimmune
Disease Waksman (1962)
proposed several mecnamsms of autoimmunisation, such as: Both humoral
antibody and sensitised cells may function in autoimmune disease.
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 immunity). 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). 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 experimental allergic encephalomyelitis (EAE).
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 recognised 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 death. 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:
the Schick test; three days later, the Dick test; seven days later,
typhoid-paratyphoid vaccine; seven days later, another typhoid-paratyphoid
vaccine (a double dose); seven days later, the third typhoid-paratyphoid
vaccine; and seven days 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 typhoid-paratyphoid vaccines. 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. 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 and
cough. 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. Two months 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, diarrhoea 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-incanacitating. 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. VACCINATION:
A SAFETY WARNING 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 deliberately
suppressed. 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 politicised
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. References (in alphabetical order)
More
on vaccines: Adverse
effects of adjuvants in vaccines Click here
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