ADVERSE EFFECTS OF ADJUVANTS IN VACCINES by Viera Scheibner (Part 2)

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ADVERSE EFFECTS OF ADJUVANTS IN
                                VACCINES (part 2)
                                       Viera Scheibner Ph.D.

Nexus Feb 2001 (Vol 8, Number 2)

IMMUNOLOGY PRINCIPLES: 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 favoured one being antibody
response as the sign of immunisation (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 cellular sensitivity.

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 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.

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 ("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
This is the antibody-type reaction that is a secondary consequence to the
beneficial effect of the combination of an antibody
with its antigen.

Arthus-type Reaction
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. Periarteritis
nodosa results from a similar antigen-antibody reaction and is
characterised by inflammation of the smaller arteries and
periarterial structures. it is accompanied by proliferation of the intima
and two types of occlusion: (a) by proliferation or
thrombosis; or (b) by the formation of nodules containing neutrophils and
eosinophils.

Anaphylaxis
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. They
act 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
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 infantile eczema.

Delayed Hypersensitivity
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. The reaction extends to any or all tissues where the offending
antigen may occur.

Isoimmunological Disease
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 foetus to the foetal
circulation.  Homograft rejection of tissues or organs between nonisologous
members of a species is also immunologically
based.

Immunological Disease Resulting from Adsorption of Foreign Substances
Under certain circumstances, foreign substances such as medications may
combine with cells to render them antigenic.
Subsequent exposure 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 agranulocytosis).

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
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 sensitised cells which are produced are then
active in causing cellular injury to the tissues or organs of the body
which bear the corresponding antigen.

Waksman (1962) proposed several mecnamsms of autoimmunisation, such as:

1.Vaccination with organ-specific antigens which are isolated from the
lymphatic channels and bloodstream and are not
recognised 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.

2.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.

3.Vaccination with heterologous antigens which are sufficiently different
to permit an immunological response but sufficiently
alike to react with autologous antigens.

4.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".

5.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.

6.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 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).

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 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.

She was hospitalised 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 injections. 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 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
The conclusions which follow the study of relevant medical and
immunological 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 (sensitisation) reactions. 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 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.

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ADVERSE EFFECTS OF ADJUVANTS IN VACCINES by Viera Scheibner (Part 1)

[ALL INFORMATION, DATA, AND MATERIAL CONTAINED, PRESENTED, OR PROVIDED HERE IS FOR GENERAL INFORMATION PURPOSES ONLY AND IS NOT TO BE CONSTRUED AS REFLECTING THE KNOWLEDGE OR OPINIONS OF THE PUBLISHER, AND IS NOT TO BE CONSTRUED OR INTENDED AS PROVIDING MEDICAL OR LEGAL ADVICE.  THE DECISION WHETHER OR NOT TO VACCINATE IS AN IMPORTANT AND COMPLEX ISSUE AND SHOULD BE MADE BY YOU, AND YOU ALONE, IN CONSULTATION WITH YOUR HEALTH CARE PROVIDER.