Reflections On Immunity, Vaccinations and Smallpox
granted to PROVE to post to our site by author
Philip Incao, M.D. © December 11, 2001
One: The Phenomenon of Immunity
Part Two: How Do Vaccinations Work?
Part Three: Smallpox And Its
One: The Phenomenon of Immunity
Illness is a process that everyone experiences
repeatedly in one's lifetime. Until our modern era,
illnesses were classified according to their recognizable signs and symptoms. Today, in addition to the outward appearance of an illness, we also classify it according
to its unique features detectable with the microscope and with biochemical tests. Thus many illnesses of similar or identical appearance which were lumped together in the
past can now be distinguished from one another based on their microscopic or biochemical features. For example, what for hundreds of years was called influenza is now described as a group of
"influenza-like illnesses", each one associated with a different virus.
On the other hand, many diseases known for centuries
and recognizable by
their typical signs and symptoms have been confirmed by modern science to
distinct entities, i.e. to be associated each with its
own particular virus or bacterium
and with no other. Measles,
chicken pox and scarlet fever are examples of these.
It has long been known that in some illnesses such as
these, one experience of
the illness usually confers lifelong immunity. A second experience with measles or scarlet fever is extremely rare.
These observations by physicians and patients
throughout history, as well as
careful observations of the stages in a patient's recovery
from an acute
inflammatory illness like measles or scarlet fever, have led to certain basic concepts in
One of these concepts was formulated as "Hering's
Law" in the 19th century, although it was well-recognized and mentioned by the
ancient Greek physician Hippocrates. This law states
that as an illness resolves, its manifest signs and symptoms travel from the inner vital organs
and blood circulation to the outer surface of the body, often visible as a rash or as a discharge
of blood, mucus or pus. In this way we "throw
off" an illness.
Another basic concept arising from the phenomenology
of illness, i.e. from
observations of the directly perceptible behavior of human illness, is
the concept of immunity to or protection from an illness that one has had before.
This immunity to second episodes of certain illnesses
like measles or scarlet fever reveals a knowing function
of the human being in relation to illness. This inner
knowing allows us, without any conscious knowledge or effort, to recognize an illness we've had
before and to thereby resist it or quickly repulse it.
Hering's law on the other hand is evidence of an
innate doing function of the human being in healing,
i.e. we actively clear the illness from our body, we get it
out of our system as we heal. These inner activities of doing and knowing work more strongly during illness than in the
healthy state, and they were clearly recognized by the ancient physicians. Hippocrates said illness consisted of the active element pónos (labor) as well as the passive element pathos (suffering). Illness is intense inner
work. Hippocrates perceived this labor as a cooking
and digesting (pepsis) of our inner poisons during an inflammatory illness. Today we regard our inner work as a battle against a hostile virus or bacterium. The all-too-often overlooked point however, is that it is we ourselves who inwardly,
unconsciously determine whether or not to engage in the battle. The great medical pioneer Hans Selye, M.D., who introduced and elucidated the
role of stress in health and illness explained, "Disease is not mere surrender.but also fight
for health; unless there is fight there is no disease
The symptoms of an acute inflammatory-infectious
illness begin not when we are infected by a virus or bacterium, but when we respond. The magnitude of our response is influenced not only by the magnitude of the infection, but
also by the inherent strength of what is responding in us. For
the ancient physicians the responder in us was an aspect of our human spirit and our inner
vitality; our inner healing force. Today the physical
basis of our inner responder is what we call our immune system. The phenomenon of immunity hasn't changed, but our thinking about it has.
The severity of the early symptoms of a particular
illness is directly proportional to the vigor of our immune response and indirectly to the burden
and noxiousness of the infection to which we are responding. The surprising fact is that most of the symptoms of an infectious disease are caused not by
the germs themselves but by our own activity of the immune system in fighting the germs. The germ "invasion" of our body is often silent, and can take place gradually over a
long period of time without disturbing us. It is only
when our immune system decides to do battle with the encroaching germs that we start to feel sick.
The metaphor of battle is a convenient, but not fully
accurate description of the relationship between our immune system and the proliferating viruses
or bacteria during an acute inflammatory/infectious illness. Pasteur's germ theory assumes that disease germs have a predatory nature: that they prey on our flesh for their own survival, while contributing nothing to us in
return. The germ theory further assumes that the
harmful or lethal effects of infectious/inflammatory diseases are a direct result of this
predation of the human body by germs.
In early microscopic studies of host tissues in acute
inflammatory/infectious diseases, Pasteur, Koch and their colleagues repeatedly observed that
germs were proliferating while many host cells were dying. They
made the critical assumption, upon which all further thinking has been based, that the germs
attack and destroy otherwise healthy cells, thus causing direct harm to the human body.
It would have been equally justified by the observable
facts to assume that the cells were dying for inapparent biochemical reasons and that the
proliferating germs were attracted to the site of increased cell death and decay just as flies,
crows and vultures are attracted to death in outer nature. A
choice was available early on between regarding germs as predators and regarding them as
scavengers. The nineteenth-century thinking of the
time was captivated by the Darwinian images of "Nature red in tooth and claw" and the
relentless struggle for survival. The decision to see
germs as predators was perhaps inevitable, and that has made all the difference in our current
thinking about illness and health. That early
decision by Pasteur and his followers led to medicine's present nearly-exclusive focus on
combating germs, while neglecting all the subtle but far-reaching ways to strengthen the host
against lasting harm from inflammatory/infectious illness.
Just as flies, crows and vultures were regarded by the
Native Americans as playing a necessary and helpful role in the great chain of Being, so too with
germs which scavenge death and decay within our bodies. The
true causes of inflammatory/infectious illnesses will ultimately be found to reside not in the
germs, but in the various human frailties which allow the forces of death and decay to predominate
in us. The scavenging germs are the markers of our
waxing and waning states of physiologic imbalance when cell death and decay temporarily exceed
their normal limits.
The metaphor of battle between immune system and germs
is justified provided we remember that our real
enemies are the forces of death and decay. The germs
themselves become sacrificial victims marked for destruction by our immune system because their
role is to absorb the products of death and decay. Germs
become poisonous to us through embodying the poisons we create. In "battling" germs, the real battle is to overcome ourselves and to refine our nature. This concept is implicit in the following discussion of how our immune system does battle
Using battle as our metaphor, we can imagine three
possible scenarios. In the first, the attacking army
is not strong, but the defenders are, and the attackers are routed from the field in a bloody but
one-sided and brief battle in which the defenders suffer no casualties. This describes a typical case of a benign but acute inflammatory-infectious illness like
roseola which usually expresses itself in a very high fever of 105° or 106°F and an extensive
rash despite being no threat whatsoever to the host.
A second scenario would be when the opposing armies
are evenly matched and there is a fierce battle with many casualties on both sides. This could describe an acute life-threatening inflammatory illness like septicemia or an
overwhelming pneumonia, in which recovery or death is equally likely.
In the third scenario, the war reporter arrives late
at the battlefield and finds no carnage, in fact little or no evidence of any previous battle. The defending army is quiet and no attackers can be seen. The reporter at first concludes that it was a very quick and easy victory for the defenders
and the attackers have fled. On closer investigation,
however, he finds that no battle took place because the defenders were unable or unwilling to
fight. What our reporter at first thought was the
defending army in reality consists of non-combatant defenders who have been quietly and massively
infiltrated by the attackers. The attackers blend in,
occupying the defenders' homeland, and any defenders who would fight them have gone underground
where they intermittently harass and provoke the occupying enemy.
The point of this elaborate metaphor is to demonstrate
by analogy that the absence of fevers and other symptoms and signs of inflammatory illness (the
absence of a battle) does not always mean that our immune system (the defending army) has been
Today it is more often the case that when we don't
fight our battles vigorously and often enough, i.e. when our fevers and discharging inflammations
are very seldom and mild, then we are liable to be infiltrated by the enemy in disguise and suffer
from chronic allergic or autoimmune disorders. This concept today is called the hygiene hypothesis. In the 1920's Rudolf Steiner expounded essentially the same concept as a mutual interplay
between opposing forces of inflammation and of sclerosis, in which the healthy state is a dynamic
balance between the two.
Returning to our third scenario, there are of course
times when the absence of a battle, i.e. absence of obvious disease symptoms, indeed does mean
that the defending army has easily routed the enemy and is truly immune from further attack. Thus we see that two entirely opposite outcomes, 1. immunity from attack and 2. quiet
infiltration by the attackers into the defenders' homeland (the host body) can have the
exact same appearance superficially. This analogy
applies precisely to another pair of similar-appearing but inwardly opposite states, i.e. the true
immunity conferred by overcoming illness as opposed to the apparent immunity conferred by
vaccination. In both cases the host appears to be
healthy due to the absence of illness, but true health is much more than the absence of overt
illness. We will illustrate this point further when
we discuss smallpox in part 3.
To complete our phenomenological description of
immunity, we must note that in addition to the functions of clearing illnesses from the body and
of recognizing the illnesses it has previously encountered, the immune system has another
cognitive or knowing capacity. This is the
discrimination of self from non-self and the ability to "tolerate", i.e. to not treat as
foreign and to not react to, any elements of self. This
remarkable knowing of the immune system also extends to its ability to tolerate, in pregnancy, a
massive foreign presence in the body, the fetus, without reacting to it at all.
Thus we see the incredible skill and apparent
purposefulness of doing and the discriminating capacity of knowing possessed by the immune system. Although modern science rarely uses the words "knowing" and "doing" in its
descriptions of the immune system, nevertheless distinct knowing and doing functions are very
clearly and unavoidably implied in all scientific writing on immunology. Science prefers to focus on the molecular level, hoping to find in molecular events the
elusive key to understanding, if not why, at least how the immune system does what it does.
Today the immune system is most often described in
articles and textbooks as comprising those bodily organs, cells and functions which discriminate
between self and non-self. The molecules of self or
non-self which the immune system can recognize are called antigens. One branch of the immune system, called the humoral immune system, consists
primarily of antibodies which are protein molecules made by the body to specifically interact with
foreign antigens. Antibodies attach themselves to any
foreign antigens like bacteria or parasites which may exist in blood or body fluids outside of the
body's cells. Antibodies are attracted to such
extracellular antigens and usually coat these antigens as one step in the complex process of the
destruction, digestion and elimination of foreign matter in us by our immune system.
We come now to a beginner's question, one seldom or
never asked in the science of immunology. It is, why
does our immune system work in such an inconsistent way, providing for permanent immunity from
recurrence only after certain illnesses and not after others? A "why" question such as this is usually considered irrelevant in modern science, while
the equivalent "how" question is actively pursued. In
the case of immunity to illness, it is the "how" questions that have led science to the idea
and the practice of vaccination.
For science the pertinent question is, how can we
imitate nature and bring about lifelong immunity to an infectious-inflammatory illness, but
without having to experience the illness first? The
first task would be to learn exactly how nature itself manages to maintain permanent immunity in
us after a first experience of illness. What is
this process of lifelong maintenance of resistance to a particular illness? Can science duplicate it?
Two: How Do Vaccinations Work?
It is an interesting fact that sometimes
a practical scientific breakthrough happens out of an intuition, a hunch, long before the
discoverer or anyone else is able to explain just how and why this particular breakthrough works. This is true of the work of Jenner and Pasteur, the great initiators of the practice of
Astoundingly, in our modern era when
vaccinations are so widely acclaimed and practiced, science still cannot explain how they work.
In the New Scientist magazine of May 27, 2000, an
article on AIDS vaccine research quotes the following from two scientists: "I'm amazed by the amount of basic science we don't know," and "the assumption
that successful vaccines work by simply producing antibodies is almost certainly wrong." The article then describes how one vaccine researcher found that in a certain viral disease
of horses, vaccination was successful in inducing antibodies against the virus, nevertheless the
vaccinated horses died faster than the unvaccinated ones! Referring
to our present ignorance as to just why these vaccinated horses would succumb, he stated,
"It's an issue people haven't wanted to think about, but we might have to."
Vaccine science and practice have always been based on
certain assumptions, which we are only now beginning to examine. One of these is that antibodies in the blood (humoral immunity) confer protection against
an illness, and that the level of antibodies correlates with the degree of protection. This relationship between measurable antibodies in the blood and apparent protection from
illness has been observed for decades in many types of infectious diseases. It is not known however whether the antibodies persisting in the blood for months
or years after an infectious disease are themselves responsible for protecting us from recurrences
of that disease or whether they are merely markers of a protection that is accomplished by another
part of the immune system. It is also not known
whether the apparent protection associated with vaccination-induced antibodies is a benefit pure and simple or whether a hidden cost to the immune system is involved. The idea of a hidden cost is considered unthinkable by vaccine researchers for obvious
practical reasons, yet it continues to be a nagging doubt among an ever-widening circle of
parents, consumer advocates, chiropractors, holistic physicians and other discerning people.
The AIDS research quoted at the beginning of this
article suggests that it's not the antibodies which protect us, but rather it's the cellular
immune system. Also called the cell-mediated immune
system, it comprises the white blood cells, all the lymph nodes and lymphatic tissue throughout
the body and is concentrated in the thymus, tonsils, adenoids, spleen and bone marrow. It is generally agreed that the primary function of the cellular immune system is to
destroy foreign intracellular antigens like viruses and some bacteria as well as the cells that
harbor them. This is accomplished by the various
white blood cells which are able to move inside, outside and through the walls of our blood
vessels and to access every part of the body.
In the past I have been tempted to assign the immune
system's doing function to the cell-mediated branch and its knowing function to the humoral
antibody-mediated branch. This neat division of
function is not borne out by the facts. Research
shows us that each branch participates in functions of both knowing and doing, although most of
the immune system's muscle to destroy, digest and drive out intruders is flexed by its
cell-mediated branch. Thus, while immune system
functions of knowing and doing may be conceptually distinct, in the physical reality they are
overlapping in an exceedingly complex orchestration of organs, cells, molecules, hormones and
There are also other aspects of the immune system
which are beyond the scope of this article. Reading a
modern textbook of immunology can be frustrating as one finds a bewildering array of cellular,
molecular and antibody-mediated processes which science has discovered without knowing how they
all fit together and manage to cooperate in health and in illness in the human being. It's something like hoping to find an understanding of how an automobile performs by
studying its disassembled parts in an auto parts shop.
At the present time, it is thought that the encounter
between self and non-self, that is, between the immune system and a foreign "invader" like a
virus or bacterium begins in the domain of the cellular immune system with a cell called the
antigen-presenting cell. If the foreign guests are
not great in number or in their noxiousness, the cellular immune system is able to dispatch them,
digest them and clear them from the body without ever calling into action its coworker the humoral
or antibody-mediated immune system. This explains the
very important fact that without our awareness we are continually infected with many small numbers
of different germs in our body, some of them nasty, and the cells of our immune system continually
shepherd them and keep them in check without the assistance of antibodies.
Like dust and other unseen debris, these
microorganisms enter our bodies as we breathe, eat and drink. Only when the number or rate of growth of germs exceeds a certain threshold are they then
recognized by the humoral immune system, resulting in the formation of antibodies specific to the
particular provocative bug. At this stage we may have
only mild fleeting symptoms or none whatsoever. This
explains how we may be found to have antibodies against illnesses we don't remember ever having
had! This is called "subclinical infection", i.e.
infection without symptoms, and it happens commonly.
Thus science has discerned three levels of infection. The lowest level is our steady-state equilibrium of everyday life in which we peacefully
co-exist with our inner menagerie of germs without needing to form detectable antibodies against
them. At this lowest level our cellular immune system
is quietly busy keeping our bugs in line and when necessary pruning the flock. Thus, although small numbers of disease agents are within us, out cellular immune system
sees to it that we remain well and free of disease symptoms, and that our germs are under control.
At the second level of infection, we temporarily relax
our vigilance and allow a certain group of germs to begin rapidly multiplying to the point where
the humoral immune system is alerted and begins to produce antibodies against the offending bugs. This sets off a cascade of immune system functions which succeed in fairly quickly quelling
our rebelling germs, so quickly that the person hosting all these inner happenings is unaware of
having just gone through a subclinical illness. The
identity of the wayward germ can afterwards be diagnosed by the presence in the blood serum of the
specific antibodies produced against it by the humoral immune system.
At the third level of infection things get seriously
out of control and all our inner alarm bells go off as a tribe of germs proliferates wildly and
provokes the full defensive reaction of our immune system. This
is called the "acute inflammatory response", which usually includes fever, release of stress
hormones by the adrenal glands, increased flow of blood, lymph, mucus, and a streaming of white
blood cells to the inflamed area. The human host of these wisdom-filled events now feels sick and may experience
pain, nausea, vomiting, diarrhea, weakness, chills and fever.
have now emerged from the realm of the subclinical to a full-blown clinical illness, with all of
its intense and often frightening symptoms. It is
critical to a healthy understanding of these things to realize that we never merely suffer through
an illness in a passive, one-dimensional way. In an
acute illness, parts of us that in health are most active, like our mind and our muscles, are
subdued, while other parts like our blood, glands and immune system are much more
active than normal. Thus every illness rouses us
to become more inwardly active than usual, and this inner activity of ours is the cooking through,
the sweating out and the throwing off of the illness. This
is hard work, and every illness calls upon and exercises capacities in us which otherwise would
have remained dormant. Adults often notice these new
capacities as a change in attitude or outlook after an illness. Children
often manifest positive changes in their behavior or development after overcoming an acute
inflammation or fever.
Having successfully passed the challenge of a
particular illness, we may not need to experience it again. Something about the illness and our
response to it has made us immune to its recurrence. If
we knew what that something was, perhaps we could learn how to use it to create health and prevent
illness. Of course, this is the basic concept of
vaccination, but the all-important question is, does vaccination accomplish what we think it does?
We've already suggested that it's probably the
cellular immune system, and not antibodies, which protect us against illness. Surely antibodies can have no role in either preventing or overcoming first bouts of
infectious-inflammatory illness, because they are formed only after the illness has peaked. It must be the cellular immune system which confers the resistance to, as well as the
capacity to overcome, both first episodes and
subsequent episodes of infectious disease. To
understand how this might happen, it is helpful to examine more closely the very illness and its
vaccination which started the whole debate: smallpox.
Three: Smallpox And Its Vaccination
That vaccines can confer a degree of protection from
certain infectious-inflammatory illnesses is clear. What
is not clear, as mentioned earlier, is exactly what vaccinations do to the immune system to bring
about their protective effect. Researchers generally
agree that vaccines do not prevent the particular virus or bacterium from entering the body nor
from beginning to multiply within it. It is thought
instead that the vaccines stimulate or "prime" the immune system to quickly eradicate the
offending germ soon after it begins to infect the host.
Let us consider how this process might work in the
case of smallpox. Our knowledge about smallpox and
its vaccination is based on over 200 years of study of this dramatic and much-feared illness by
physicians in many countries.
The natural course of the illness begins when one
"catches" smallpox from someone with a smallpox rash or from the mucus or pus of smallpox on a
patient's bedclothes or dressings. For the next
twelve days there are no signs or symptoms at all and the new patient is not contagious even
though the smallpox virus is multiplying within the body. On
or about the twelfth day large numbers of smallpox virus enter the blood (viremia) and the
"toxemic" phase of the illness begins, meaning a poisoning or contamination of the blood
circulation. This blood poisoning of smallpox is the beginning of the overt illness, with
symptoms of fever, prostration, severe headache, backache, limb pains and sometimes vomiting.
After three or four days of these symptoms the typical smallpox rash begins to erupt and in
the next one to two days the fever falls to almost normal and the patient feels much better.
The skin eruption begins as red spots which over the
next few days evolve into raised pimples, which then change to blisters which then become
pus-filled (pustules). On the 11th to 13th day of the illness the pustules begin
to dry up and form crusts or scabs which then fall off by the end of the third week of the
illness. The fever usually returns, less severely,
after the pustules appear and then becomes normal as the crusts and scabs form. If one dies from smallpox, it may be in the first week of the illness if the
toxemia is very severe, but most smallpox deaths have occurred toward the end of the second week
after the pustules appear.
The majority of smallpox patients survive, and the
falling away of the dried-up scabs from the skin signifies the final stage of healing,
approximately 33 days after catching the infection. The
dramatic course of smallpox illustrates very well some of the concepts discussed earlier in this
article. The twelve-day incubation period during
which the smallpox virus actively multiplies in the body without provoking the slightest symptom
confirms the point that it is our response to infection, not the infection itself, which causes
the typical disease symptoms of fever, aches and pains and extreme weakness.
The fact that the fever drops and the patient feels
much better after the rash breaks out illustrates Hering's Law. The poisons circulating in the blood during the toxemic phase cause the most severe
symptoms of smallpox. These symptoms improve
considerably once the blood clears out its poisons by discharging them through the skin, producing
the typical pus-filled blisters of smallpox. The
chief danger of smallpox consists in the degree of blood poisoning and in the huge and exhausting
effort required for the immune system to push the poisons out of the blood and through the skin. When the toxemia, the poisons, are overwhelming and the patient lacks the
strength to discharge them out of the body, then the patient may die in the effort, either before
the eruption ever appears or else, utterly spent, afterwards.
The patients who survive smallpox will have lifelong
neutralizing antibodies to smallpox virus in their blood and permanent immunity to a second
episode of the illness. What does this mean?
Using the battle metaphor from part one, we could say
that the victorious defending army has acquired much valuable skill, know-how, and confidence
through its combat experience as well as certain medals awarded to acknowledge their participation
in combat. The first three attributes are comparable
to the inner strengthening of the cellular immune system which is attained through overcoming an
illness like smallpox. The medals as visible tokens
of achievement are roughly comparable to the antibodies visible on simple blood tests indicating
that the host has already won that battle and is likely to be immune to future attacks of the same
If a foolish general were under the illusion that
merely wearing a combat medal actually conferred the know-how, skill and confidence gained in
battle, then he might propose pinning medals on soldiers with no combat experience to make them
immune to dangerous future battles. That would bestow
the same outward appearance to the seasoned and unseasoned soldiers alike, belying their
In the same way, science bestows antibodies through
vaccination and mistakenly assumes that it is bestowing the immune strength that can only be
developed through the experience of illness. In
equating the significance of vaccine-induced antibodies with that of illness-induced antibodies,
science confuses the outer sign of the battle experience with the experience itself. Antibodies arising through illness are markers of
immunity and (unlike the medals in our battle metaphor) also contribute to immunity, but
antibodies alone are not sufficient to confer lasting immunity to a particular illness. There are several diseases which may recur repeatedly, such as herpes outbreaks, despite
high antibody levels. The evidence suggests that it
is our cellular immune system which confers lasting immunity, with antibodies playing a secondary
role in the process.
Immunity is really the result of our experience, of
having gone through, along with our cellular immune system, an active
process (the combat in the metaphor) of learning and strengthening. The immune system is a limb of us, and it learns from experience just as we do. Antibodies signify that we've had experience of illness, often repeatedly, but not
necessarily that we've gained anything from the experience. When on some level we respond with
greater initiative to our experience of illness, actively processing, digesting and ultimately
learning from such experience, then we are usually immune from having to repeat it. In such cases our cellular immune system has strengthened itself through its active
encounter with, and overcoming of, the illness. In
this view, immunity is the result of having successfully met the challenge of a particular illness
and having gained mastery over it. It is like
learning a particular skill, such as riding a horse, which is then usually retained for life. On the physiologic level, the skill and mastery we gain in overcoming illness accrue to our
cellular immune system.
This active process of acquiring mastery cannot be
replaced by a vaccination unless the host's immune response to the vaccination is essentially
identical to its response to the illness itself, even though reduced in intensity. This would mean that in order to produce genuine cellular immunity, a vaccination would
have to reproduce the experience of the illness, causing some of the same signs and symptoms,
though milder, that are caused by the illness. To see
if this is true, let us look at smallpox vaccination.
The vaccination consists of introducing live cowpox
(vaccinia) virus into the skin by multiple superficial punctures in a small area about 1/8 inch
diameter on the upper arm. The vaccination site is
then inspected twice after 3 and 9 days to determine if the vaccination "takes" or not. A primary reaction or "take" evolves as follows:
for three days after the vaccination there is no reaction whatsoever. On
the fourth day a small red pimple appears which gradually grows into a blister which becomes
pus-filled, surrounded by a zone of redness and often with tender, swollen glands in the armpit
and mild fever. This reaction peaks on the 8th to 10th day, after which the
pustule gradually dries up and forms a scab which eventually falls off leaving a scar.
Clearly the primary "take" reproduces the
experience of smallpox itself described earlier, but of course in a very limited way so as to
generate only one pock rather than many dozens of them. The
cellular immunity produced by smallpox vaccination is also limited, lasting from six months to
three years. This immunity probably coincides with
the length of time that the exercised "muscle" of the cellular immune system remains
strengthened from its labor of discharging the single cow pock resulting from the vaccination. The antibodies appearing in the blood after primary smallpox vaccination may remain for
over ten years, but these antibodies cannot be taken as a trustworthy sign of immunity. The official description of the currently available smallpox vaccine in the U.S., which was
manufactured by Wyeth Laboratories, states vaguely ".the
level of antibody that protects against smallpox infection is unknown."2 If we can state blandly that the protective level of antibody is still unknown after having
assumed for several decades that protection is directly correlated with antibody level, then
surely it is time to rethink that assumption.
In practice antibody levels were seldom used in the
smallpox era as a measure of immunity. Anyone not
vaccinated in the previous three years was considered to be susceptible to smallpox, regardless of
their antibody level.
The all-important question is how to interpret the
meaning of reactions to smallpox vaccination which are milder and briefer than the primary
"take" which peaks in ten days, and which does result in a genuine though short-lived immunity
of the cell-mediated system.
Since the early 1970's only two types of reactions
to smallpox vaccination have been officially recognized, as recommended by the World Health
Organization (WHO). For purposes of greater clarity, in this discussion I will be referring to the
older classification which recognized three types of normal reactions to smallpox vaccination.
The second type of normal skin reaction to smallpox
vaccination was called the accelerated or vaccinoid reaction, usually in people who had some
immunity to smallpox at the time of vaccination, either from a previous experience of the disease
or from a previous smallpox vaccination. In the
accelerated reaction, the skin blister which forms is smaller and reaches its maximum size and
intensity between the 3rd and 7th day after the vaccination. This reaction works in exactly the same way as the primary reaction but to a lesser degree,
boosting the cell-mediated immunity that is already present, but waning, from the previous
It is the third type of reaction to smallpox
vaccination that in my opinion has created all the problems, that has been at the root of a 200
year old controversy over the usefulness of smallpox vaccination. This stems from the fact that this reaction for years was interpreted as indicating
immunity to smallpox, when it often meant exactly the opposite. In many cases the bearers of this reaction may have had a suppressed cellular
immunity, making them on repeated revaccination more susceptible to smallpox than an unvaccinated
This third type of reaction to smallpox vaccination
was originally called an immune reaction, then later renamed an early or immediate reaction. A small pimple forms at the vaccination site which may evolve into a tiny blister, peaking
on the second or third day and diminishing thereafter. An
earlier textbook of viral diseases from the smallpox era states the following: "The early or immediate reaction is an indication of sensitivity to the virus and may be
given by persons who are either susceptible or immune to smallpox..[It] cannot be regarded as a
successful result and cannot be guaranteed to induce or increase the person's resistance to
smallpox."3 This is a typical scientific understatement that glosses over years of devastating results
of smallpox vaccination in which thousands of vaccinated people who were thought to be immune
based on their so-called "immune reaction" to vaccination later caught smallpox and died.
Ian Sinclair, writing on the history of smallpox,
"After an intensive four-year effort to vaccinate
the entire population between the ages of 2 and 50, the Chief Medical Officer of England
announced in May 1871 that 97.5% had been vaccinated. In
the following year, 1872, England experienced its worst ever smallpox epidemic which claimed
44,840 lives..In the Philippines, prior to U.S. takeover in 1905, case mortality [death rate]
from smallpox was about 10%..In 1918-1919, with over 95% of the population vaccinated, the
worst epidemic in the Philippines' history
occurred resulting in a case mortality of 65%..The 1920
Report of the Philippines Health Service [stated] . 'hundreds of thousands of people were
yearly vaccinated with the most unfortunate result that the 1918 epidemic looks prima
facie as a flagrant failure of the classic immunization toward future
How can this be? How can these historical facts be reconciled with my earlier statement that a primary take
in response to a first smallpox vaccination results in genuine cellular immunity for up to three
years? The usual explanation offered is that the
vaccine used was inactive due to loss of potency in storage, but this clearly cannot be the whole
answer to the many documented instances of failure of smallpox vaccination to protect from
The answer is an open secret which has been very well
known for years, but never fully understood: that
many first recipients of smallpox vaccine fail to produce a
take (primary reaction) and continue to fail to do so even when revaccinated many times. The textbook states,
"Easton (1945) records of one man who died of
smallpox that vaccination had been attempted at birth,
again in 1941 and ten times in 1943 without a take, thus emphasizing the danger of accepting
even repeated unsuccessful vaccination as evidence of insusceptibility to smallpox.."5
This is an excellent example of a vitally important
observation leading to an irrelevant, though not incorrect, conclusion. This example begs the question: how many
repeated failures to react does it take to justify the concern that continuing to revaccinate may
be doing more harm than good?
The relevant conclusion, in my opinion, is that due to
differences in immune response capability among individual human beings at the time of first
vaccination, in some individuals the cellular immune system lacks the muscle to push out the
single pock eruption that is the primary take. The
scratching of the virus into the skin of the arm is a strong challenge to the immune system. A successful take depends on the ability of the cellular immune system to respond to that
challenge in an equally vigorous way, to push the intruding virus right back out of the body. It is a simple matter of action and reaction, of challenge and response. If Charles Atlas challenges a 97-pound weakling to arm wrestling and his
opponent's arm immediately collapses, we would not think that the challenge ought to be repeated
indefinitely if the weak condition of the responder had no means of improving! Yet in thousands of individuals in the last 200 years who may have been weakened through
stress, poor nutrition and poverty, whose cellular immune systems were not vigorous enough to
respond to smallpox vaccination with a take, the effect of repeated revaccination, which was
commonly practiced, was to weaken these individuals' immune systems still further, making them
no doubt more vulnerable to smallpox than they had been before vaccination! This would explain the disastrous results of the above-mentioned smallpox vaccination
campaigns in England, the Philippines and in many other countries as well.
The ambivalent nature of the early reaction to
smallpox vaccination is analogous to the third battle scenario mentioned in part one of this
article. When little or no signs of battle (reaction)
are visible, it may mean that the defenders were easily victorious (the host is immune) or
contrariwise it may mean that the defenders lacked the strength to fight and their homeland was
subsequently quietly infiltrated by the attackers. When
a smallpox vaccine recipient lacks the immune muscle to respond to the viral intrusion of his or
her body with a vigorous pock-forming discharge, then we might expect that most of the intruding
virus has remained in the body. With each
revaccination the burden of vaccinia virus in the body increases, and the suppressive effect of
this viral burden on the cellular immune system also increases, eventually resulting in a
dangerous state of immunosuppresion. This may
also explain the occasional catastrophic effects that were observed resulting from a brief medical
fad in the 1970's: treating recurrent herpes
infections with repeated smallpox vaccinations.
The disease smallpox and its vaccination are fruitful
subjects to study in order to understand how the immune system works, because we can observe what
happens on the skin as vital clues to what might be happening inside the body. The main lesson from this study is the exceedingly important fact that a lack of a vaccine
reaction, and by extension a lack of illness symptoms, can by no means be taken as a sign of
immunity or of health.
The other critical fact confirmed by our historical
experience with smallpox vaccination is that individual differences in response to vaccination are
extremely important. One size most definitely does
not fit all. It is clear that although the smallpox
vaccine was effective in conferring a temporary immunity in some individuals, an unknown number of
other individuals were probably harmed by the vaccine. With
the smallpox vaccination the adverse effects were fairly obvious, they often appeared on the skin. With other vaccines in use today the adverse effects may not be so obvious. We've seen with smallpox that the same vaccination procedure which temporarily
strengthened the cellular immune system in some individuals probably weakened it in others,
especially upon repeated revaccination.
The possibility, that the up to 39 doses of 12
different vaccines which children today receive by school entry may be impacting the cellular
immune systems of many individual children in a negative way, suggests itself to the open mind. Science has most of the knowledge and the tools it needs to investigate and to find answers
to these unanswered questions. All it needs now is the will. May it
come soon, for our children's sake.
Selye, Hans. The Stress of Life. New York: McGraw-Hill, 1978, p.12
Rivers, T.M., and Horsfall, F.L., Jr. Viral and
Rickettsial Infections of Man.
Philadelphia: Lippincott, 1959, p.686.
Rivers, T.M., and Horsfall, F.L., Jr.
and Rickettsial Infections of Man. Philadelphia: Lippincott, 1959, p.687.