TETANUS SHOT: HOW DO WE
KNOW THAT IT WORKS? ~ By Tetyana Obukhanych, PhD
The cure for tetanus, a life-threatening and often deadly
disease, has been sought from the very inception of the modern
field of Immunology. The original horse anti-serum treatment
of tetanus was developed in the late 19th century and
introduced into clinical practice at the time when a
bio-statistical concept of a randomized placebo-controlled
trial (RCT) did not yet exist. The therapy was infamous for
generating a serious adverse reaction called
serum
sickness attributed to the intolerance of humans to
horse-derived serum. To make this tetanus therapy usable, it
was imperative to substitute the animal origin of anti-serum
with the human origin. But injecting a lethal toxin into human
volunteers as substitutes for horses would have been
unthinkable.
A practical solution was found in 1924: pre-treating the
tetanus toxin with formaldehyde (a fixative chemical) made the
toxin lose its ability to cause clinical tetanus symptoms. The
formaldehyde-treated tetanus toxin is called the
toxoid.
The tetanus toxoid can be injected into human volunteers to
produce a commercial human therapeutic product from their sera
called
tetanus immunoglobulin (TIG), a modern
substitute of the original horse anti-serum. The tetanus
toxoid has also become the vaccine against clinical tetanus.
The tetanus toxin, called
tetanospasmin, is
produced by numerous
C. tetani bacterial strains.
C.
tetani normally live in animal intestines, notably in
horses, without causing tetanus to their intestinal carriers.
These bacteria require anaerobic (no oxygen) conditions to be
active, whereas in the presence of oxygen they turn into
resilient but inactive spores, which do not produce the toxin.
It has been recognized that inactive tetanus spores are
ubiquitous in the soil. Tetanus can result from the exposure
to
C. tetani via poorly managed tetanus-prone wounds
or cuts, but not from oral ingestion of tetanus spores. Quite
to the contrary, oral exposure to
C. tetani has been
found to build resistance to tetanus without carrying the risk
of disease, as described in the section on
Natural
Resistance to Tetanus.
Once secreted by
C. tetani germinating in a
contaminated wound, tetanospasmin diffuses through the
tissue’s interstitial fluids or bloodstream. Upon reaching
nerve endings, it is adsorbed by the cell membrane of neurons
and transported through nerve trunks into the central nervous
system, where it inhibits the release of a neurotransmitter
gamma-aminobutyric
acid (GABA). This inhibition can result in various
degrees of clinical tetanus symptoms: rigid muscular spasms,
such as lockjaw, sardonic smile, and severe convulsions that
frequently lead to bone fractures and death due to respiratory
compromise.
Curative effects of the anti-serum therapy as well as the
preventative effects of the tetanus vaccination are deemed to
rely upon an antibody molecule called antitoxin. But the
assumption that such antitoxin was the sole “active”
ingredient in the original horse anti-serum has not been borne
out experimentally. Since horses are natural carriers of
tetanus spores, their bloodstream could have contained other
unrecognized components, which got harnessed in the
therapeutic anti-serum.
Natural Resistance to Tetanus
discusses other serum entities detected in research animals
carrying
C. tetani, which better correlated with
their protection from clinical tetanus than did serum
antitoxin levels. Nevertheless, the main research effort in
the tetanus field remained narrowly focused on antitoxin.
Antitoxin molecules are thought to inactivate the
corresponding toxin molecules by virtue of their toxin-binding
capacity. This implies that to accomplish its protective
effect, antitoxin must come into close physical proximity with
the toxin and combine with it in a way that would prevent or
preempt the toxin from binding to nerve endings. Early
research on the properties of a newly discovered antitoxin was
done in small-sized research animals, such as guinea pigs. The
tetanus toxin was pre-incubated in a test tube with the
animal’s serum containing antitoxin before being injected into
another (antitoxin-free) animal, susceptible to tetanus. Such
pre-incubation made the toxin lose its ability to cause
tetanus in otherwise susceptible animals—i.e., the toxin was
neutralized.
Nevertheless, researchers in the late 19th and early 20th
centuries were baffled by a peculiar observation. Research
animals, whose serum contained enough antitoxin to inactivate
a certain amount of the toxin in a test tube, would succumb to
tetanus when they were injected with the same amount of the
toxin. Furthermore, it was noted that the mode of the toxin
injection had a different effect on the ability of serum
antitoxin to protect the animal. The presence of antitoxin in
the serum of animals afforded some degree of protection
against the toxin injected directly into the bloodstream
(intravenously). However, when the toxin was injected into the
skin it would be as lethal to animals containing substantial
levels of serum antitoxin as to animals virtually free of
serum antitoxin.[1]
The observed difference in serum antitoxin’s protective
“behavior” was attributed to the toxin’s propensity to bind
faster to nerve cells than to serum antitoxin. The
pre-incubation of the toxin with antitoxin in a test tube, or
the injection of the toxin directly into the bloodstream,
where serum antitoxin is found, gives antitoxin a head start
in combining with and neutralizing the toxin. However, a skin
or muscle injection of the toxin does not give serum antitoxin
such a head start.
Researchers in the 21st century have developed an advanced
fluorescent labeling technique to track the uptake of the
injected tetanus toxin into neurons. Using this technique,
researchers examined the effect of serum antitoxin, which was
induced by vaccinating mice with the tetanus toxoid vaccine
ahead of time (the same one currently used in humans), on
blocking the neuronal uptake and transport of the tetanus
toxin fragment C (TTC) to the brain from the site of
intramuscular injection. Vaccinated and non-vaccinated animals
showed similar levels of TTC uptake into the brain. The
authors of the study concluded that the
“uptake of TTC by
nerve terminals from an intramuscular depot is an avid and
rapid process and is not blocked by vaccination.”[2]
They have further commented that their results appear to be
surprising in view of protective effects of immunization with
the tetanus toxoid. Indeed, the medical establishment holds a
view that a tetanus shot prevents tetanus, but how do we know
this view is correct?
Neonatal tetanus
Neonatal tetanus is common in tropical under-developed
countries but is extremely rare in developed countries. This
form of tetanus results from unhygienic obstetric practices,
when cutting the umbilical cord is performed with unsterilized
devices, potentially contaminating it with tetanus spores.
Adhering to proper obstetric practices removes the risk of
neonatal tetanus, but this has not been the standard of birth
practices for some indigenous and rural people in the past or
even present.
The authors of a neonatal tetanus study performed in the
1960s in New Guinea describe the typical conditions of
childbirth among the locals:
The mother cuts the cord 1 inch (2.5 cm) or less from the
abdominal wall; it is never tied. In the past she would
always use a sliver of sago bark, but now she uses a steel
trade-knife or an old razor blade. These are not cleaned or
sterilized in any way and no dressing is put of the cord.
The child lies after birth on a dirty piece of soft bark,
and the cut cord can easily become contaminated by dust from
the floor of the hut or my mother’s feces expressed during
childbirth, as well as by the knife and her finger. [3]
Not surprisingly, New Guinea had a high rate of neonatal
tetanus. Because improving birth practices seemed to be
unachievable in places like New Guinea, subjecting pregnant
women to tetanus vaccination was contemplated by public health
authorities as a possible solution to neonatal tetanus.
A randomized controlled trial (RCT) assessing the
effectiveness of the tetanus vaccine in preventing neonatal
tetanus via maternal vaccination was conducted in the 1960s in
rural Colombia in a community with high rates of neonatal
tetanus.[4] The design of this trial has been recently
reviewed by the Cochrane Collaboration for potential biases
and limitations and, with minor comments, has been considered
of good quality for the purposes of vaccine effectiveness (but
not safety) determination.[5] The trial established that a
single dose of the tetanus vaccine given before or during
pregnancy had a partial effect on preventing neonatal tetanus
in the offspring: 43% reduction was observed in the tetanus
vaccine group compared to the control group, which instead of
the tetanus shot received a flu shot. A series of two or three
tetanus booster shots, given six or more weeks apart before or
during pregnancy, reduced neonatal tetanus by 98% in the
tetanus vaccine group compared to the flu shot control group.
The duration of the follow up in this trial was less than five
years.
In addition to testing the effects of vaccination, this study
has also documented a clear relationship between the incidence
of neonatal tetanus and the manner in which childbirth was
conducted. No babies delivered in a hospital, by a doctor or a
nurse, contracted neonatal tetanus regardless of the mother’s
vaccination status. On the other hand, babies delivered at
home by amateur midwives had the highest rate of neonatal
tetanus.
Hygienic childbirth appears to be highly effective in
preventing neonatal tetanus and makes tetanus vaccination
regimen during pregnancy unnecessary for women who give birth
under hygienic conditions. Furthermore, it was estimated in
1989 in Tanzania that 40% of neonatal tetanus cases still
occurred in infants born to mothers who were vaccinated during
pregnancy,[6] stressing the importance of hygienic birth
practices regardless of maternal vaccination status.
Tetanus in adults
Based on the protective effect of maternal vaccination in
neonatal tetanus, demonstrated by an RCT and discussed above,
we might be tempted to infer that the same vaccine also
protects from tetanus acquired by stepping on rusty nails or
incurring other tetanus-prone injuries, when administered to
children or adults, either routinely or as an emergency
measure. However, due to potential biologic differences in how
tetanus is acquired by newborns versus by older children or
adults, we should be cautious about reaching such conclusions
without first having direct evidence for the vaccine
effectiveness in preventing non-neonatal tetanus.
It is generally assumed that the tetanus toxin must first
leach into the blood (where it would be intercepted by
antitoxin, if it is already there due to timely vaccination)
before it reaches nerve endings. This scenario is plausible in
neonatal tetanus, as it appears that the umbilical cord does
not have its own nerves.[7] On the other hand, the secretion
of the toxin by
C. tetani germinating in untended
skin cuts or in muscle injuries is more relevant to how
children or adults might succumb to tetanus. In such cases,
there could be nerve endings near germinating
C. tetani,
and the toxin could potentially reach such nerve endings
without first going through the blood to be intercepted by
vaccine-induced serum antitoxin. This scenario is consistent
with the outcomes of the early experiments in mice, discussed
in the beginning.
Although a major disease in tropical under-developed
countries, tetanus in the USA has been very rare. In the past,
tetanus occurred primarily in poor segments of the population
in southern states and in Mexican migrants in California. It
was swiftly diminishing with each decade prior to the 1950s
(in the pre-vaccination era), as inferred from tetanus
mortality records and similar case-fatality ratios (about
67-70%) in the early 20th century[8] versus the mid-20th
century).[9] The tetanus vaccine was introduced in the USA in
1947 without performing any placebo-controlled clinical trials
in the segment of the population (children or adults), where
it is now routinely used.
The rationale for introducing the tetanus
vaccine into the U.S. population, at low overall risk for
tetanus anyway, was simply based on its use in the U.S.
military personnel during World War II. According to a
post-war report[10]:
a) the U.S. military personnel received a series of three
injections of the tetanus toxoid, routine stimulating
injection was administered one year after the initial
series, and an emergency stimulating dose was given on the
incurrence of wounds, severe burns, or other injuries that
might result in tetanus;b) throughout the entire WWII period, 12 cases of tetanus
have been documented in the U.S. Army;
c) in World War I there were 70 cases of tetanus among
approximately half a million admissions for wounds and
injuries, an incidence of 13.4 per 100,000 wounds. In World
War II there were almost three million admissions for wounds
and injuries, with a tetanus case rate of 0.44 per 100,000
wounds.
The report leads us to conclude that vaccination has played a
role in tetanus reduction in wounded U.S. soldiers during WWII
compared to WWI, and that this reduction vouches for the
tetanus vaccine effectiveness. However, there are other
factors (e.g. differences in wound care protocols, including
the use of antibiotics, higher likelihood of wound
contamination with horse manure rich in already active
C.
tetani in earlier wars, when horses were used by the
cavalry, etc.), which should preclude us from uncritically
assigning tetanus reduction during WWII to the effects of
vaccination.
Severe and even deadly tetanus is known to occur in recently
vaccinated people with high levels of serum antitoxin.[11]
Although the skeptic might say that no vaccine is effective
100% of the time, the situation with the tetanus vaccine is
quite different. In these cases of vaccine-unpreventable
tetanus, vaccination was actually very effective in inducing
serum antitoxin, but serum antitoxin did not appear to have
helped preventing tetanus in these unfortunate individuals.
The occurrence of tetanus despite the presence of antitoxin
in the serum should have raised a red flag regarding the
rationale of the tetanus vaccination program. But such reports
were invariably interpreted as an indication that higher
than
previously thought levels of serum antitoxin must be
maintained to protect from tetanus, hence the need for more
frequent, if not incessant, boosters. Then how much higher
“than previously thought” do serum levels of antitoxin need to
be to ensure protection from tetanus?
Crone & Reder (1992) have documented a curious case of
severe tetanus in a 29-year old man with no pre-existing
conditions and no history of drug abuse, typical among
modern-day tetanus victims in the USA. In addition to the
regular series of tetanus immunization and boosters ten years
earlier during his military service, this patient had been
hyper-immunized (immunized with the tetanus toxoid to have
extremely high serum antitoxin) as a volunteer for the
purposes of the commercial TIG production. He was monitored
for the levels of antitoxin in his serum and, as expected,
developed extremely high levels of antitoxin after the
hyper-immunization procedure. Nevertheless, he incurred severe
tetanus 51 days after the procedure despite clearly documented
presence of serum antitoxin
prior to the disease. In
fact, upon hospital admission for tetanus treatment his serum
antitoxin levels measured about 2,500 times higher than the
level deemed protective. His tetanus was severe and required
more than five weeks of hospitalization with life-saving
measures. This case demonstrated that serum antitoxin has
failed to prevent severe tetanus even in the amounts 2,500
times higher than what is considered sufficient for tetanus
prevention in adults.
The medical establishment chooses to turn a blind eye to the
lack of solid scientific evidence to substantiate our faith in
the tetanus shot. It also chooses to ignore the available
experimental and clinical evidence that contradicts the
assumed but unproven ability of vaccine-induced serum
antitoxin to reduce the risk of tetanus in anyone other than
maternally-vaccinated neonates, who do not even need this
vaccination measure when their umbilical cords are dealt with
using sterile techniques.
Ascorbic acid in tetanus treatment
Anti-serum is not the only therapeutic measure tried in
tetanus treatment. Ascorbic acid (Vitamin C) has also been
tried. Early research on ascorbic acid has demonstrated that
it too could neutralize the tetanus toxin.[12]
In a clinical study of tetanus treatment conducted in
Bangladesh in 1984, the administration of conventional
procedures, including the anti-tetanus serum, to patients who
contracted tetanus left 74% of them dead in the 1-12 age group
and 68% dead in the 13-30 age group. In contrast, daily
co-administration of one gram of ascorbic acid intravenously
had cut down this high mortality to 0% in the 1-12 age group,
and to 37% in the 13-30 age group.[13] The older patients were
treated with the same amount of ascorbic acid without
adjustments for their body weight.
Although this was a controlled clinical trial, it is not
clear from the description of the trial in the publication by
Jahan
et al. whether or not the assignment of
patients into the ascorbic acid treatment group versus the
placebo-control group was randomized and blinded, which are
crucial bio-statistical requirements for avoiding various
biases. A more definitive study is deemed necessary before
intravenous ascorbic acid can be recommended as the standard
of care in tetanus treatment.[14] It is odd that no properly
documented RCT on ascorbic acid in tetanus treatment has been
attempted since 1984 for the benefit of developing countries,
where tetanus has been one of the major deadly diseases. This
is in stark contrast to the millions of philanthropic dollars
being poured into sponsoring the tetanus vaccine
implementation in the Third world.
Natural resistance to tetanus
In the early 20th century, investigators Drs. Carl Tenbroeck
and Johannes Bauer pursued a line of laboratory research,
which was much closer to addressing natural resistance to
tetanus than the typical laboratory research on antitoxin in
their days. Omitted from immunologic textbooks and the history
of immunologic research, their tetanus protection experiments
in guinea pigs, together with relevant serological and
bacteriological data in humans, nevertheless provide a good
explanation for tetanus being a rather rare disease in many
countries around the world, except under the conditions of
past wars.
In the experience of these tetanus researchers, the injection
of dormant tetanus spores could never by itself induce tetanus
in research animals. To induce tetanus experimentally by means
of tetanus spores (as opposed to by injecting a ready-made
toxin, which never happens under natural circumstances
anyway), spores had to be premixed with irritating substances
that could prevent rapid healing of the site of spore
injection, thereby creating conditions conducive to spore
germination. In the past, researchers used wood splinters,
saponin, calcium chloride, or aleuronat (flour made with
aleurone) to accomplish this task.
In 1926, already being aware that oral exposure to tetanus
spores does not lead to clinical tetanus, Drs. Tenbroeck and
Bauer set out to determine whether feeding research animals
with tetanus spores could provide protection from tetanus
induced by an appropriate laboratory method of spore
injection. In their experiment, several groups of guinea pigs
were given food containing distinct strains of
C. tetani.
A separate group of animals were used as controls—their diet
was free of any
C. tetani. After six months, all
groups were injected under the skin with spores premixed with
aleuronat. The groups that were previously exposed to spores
orally did not develop any symptoms of tetanus upon such
tetanus-prone spore injection, whereas the control group did.
The observed protection was strain-specific, as animals still
got tetanus if injected with spores from a mismatched strain—a
strain they were not fed with. But when fed multiple strains,
they developed protection from all of them.
Quite striking, the protection from tetanus established via
spore feeding did not have anything to do with the levels of
antitoxin in the serum of these animals. Instead, the
protection correlated with the presence of another type of
antibody called
agglutinin—so named due to its
ability to agglutinate (clump together)
C. tetani
spores in a test tube. Just like the observed protection was
strain-specific, agglutinins were also strain-specific. These
data are consistent with the role of strain-specific
agglutinins, not of antitoxin, in natural protection from
tetanus. The mechanism thereby strain-specific agglutinins
have caused, or correlated with, tetanus protection in these
animals has remained unexplored.
In the spore-feeding experiment, it was still possible to
induce tetanus by overwhelming this natural protection in
research animals. But to accomplish this task, a rather brute
force procedure was required. A large number of purified
C.
tetani spores were sealed in a glass capsule; the
capsule was injected under the skin of research animals and
then crushed. Broken glass pieces were purposefully left under
the skin of the poor creatures so that the gory mess was
prevented from healing for a long time. Researchers could
succeed in overwhelming natural tetanus defenses with this
excessively harsh method, perhaps mimicking a scenario of
untended war-inflicted wounds.
How do these experimental data in research animals relate to
humans? In the early 20th century, not only animals but also
humans were found to be intestinal carriers of
C. tetani
without developing tetanus. About 33% of tested human subjects
living around Beijing, China were found to be
C. tetani
carriers without any prior or current history of tetanus
disease.[15] Bauer & Meyer (1926) cite other studies,
which have reported around 25% of tested humans being healthy
C. tetani carriers in other regions of China, 40% in
Germany, 16% in England, and on average 25% in the USA,
highest in central California and lowest on the southern
coast. Based on the California study, age, gender, or
occupation denoting the proximity to horses did not appear to
play a role in the distribution of human
C. tetani
carriers.
Another study was performed back in the 1920s in San
Francisco, CA.[16] About 80% of the examined subjects had
various levels of agglutinins to as many as five
C.
tetani strains at a time, although no antitoxin could
be detected in the serum of these subjects.
C. tetani
organisms could not be identified in the stool of these
subjects either. It is likely that tetanus spores were in
their gut transiently in the past, leaving serological
evidence of oral exposure, without germinating into
toxin-producing organisms. It would be important to know the
extent of naturally acquired
C. tetani spore
agglutinins in humans in various parts of the world now,
instead of relying on the old data, but similar studies are
not likely to be performed anymore.
Regrettably, further research on naturally acquired
agglutinins and on exactly how they are involved in the
protection from clinical tetanus appears to have been
abandoned in favor of more lucrative research on antitoxin and
vaccines. If such research continued, it would have given us
clear understanding of natural tetanus defenses we may already
have by virtue of our oral exposure to ubiquitous inactive
C.
tetani spores.
Since the extent of our natural resistance to clinical
tetanus is unknown due to the lack of modern studies, all we
can be certain of is that preventing dormant tetanus spores
from germinating into toxin-producing microorganisms is an
extremely important measure in the management of potentially
contaminated skin cuts and wounds. If this crucial stage of
control—at the level of preventing spore germination—is missed
and the toxin production ensues, the toxin must be neutralized
before it manages to reach nerve endings.
Both antitoxin and ascorbic acid exhibit toxin-neutralizing
properties in a test tube. In the body, however,
vaccine-induced antitoxin is located in the blood, whereas the
toxin might be focally produced in the skin or muscle injury.
This creates an obvious physical impediment for toxin
neutralization to happen effectively, if at all, by means of
vaccine-induced serum antitoxin. Furthermore, no
placebo-controlled trials have ever been performed to rule out
the concern about such an impediment by providing clear
empirical evidence for the effectiveness of tetanus shots in
children and adults. Nevertheless, the medical establishment
relies upon induction of serum antitoxin and withholds
ascorbic acid in tetanus prevention and treatment.
When an old medical procedure of unknown effectiveness, such
as the tetanus shot, has been the standard of medical care for
a long time, finalizing its effectiveness via a modern
rigorous placebo-controlled trial is deemed unethical in human
research. Therefore, our only hope for the advancement of
tetanus care is that further investigation of the ascorbic
acid therapy is performed and that this therapy becomes
available to tetanus patients around the world, if confirmed
effective by rigorous bio-statistical standards.
Until then, may the blind faith in the tetanus shot help us!
References
1. Tenbroeck, C. & Bauer, J.H. The immunity produced by
the growth of tetanus bacilli in the digestive tract. J Exp
Med 43, 361-377 (1926).
2. Fishman, P.S., Matthews, C.C., Parks, D.A., Box, M. &
Fairweather, N.F. Immunization does not interfere with uptake
and transport by motor neurons of the binding fragment of
tetanus toxin. J Neurosci Res 83, 1540-1543 (2006).
3. Schofield, F.D., Tucker, V.M. & Westbrook, G.R.
Neonatal tetanus in New Guinea. Effect of active immunization
in pregnancy. Br Med J 2, 785-789 (1961).
4. Newell, K.W., Dueñas Lehmann, A., LeBlanc, D.R. &
Garces Osorio, N. The use of toxoid for the prevention of
tetanus neonatorum. Final report of a double-blind controlled
field trial. Bull World Health Organ 35, 863-871 (1966).
5. Demicheli, V., Barale, A. & Rivetti, A. Vaccines for
women to prevent neonatal tetanus. Cochrane Database Syst Rev
5:CD002959 (2013).
6. Maselle, S.Y., Matre, R., Mbise, R. & Hofstad, T.
Neonatal tetanus despite protective serum antitoxin
concentration. FEMS Microbiol Immunol 3, 171-175 (1991).
7. Fox, S.B. & Khong, T.Y. Lack of innervation of human
umbilical cord. An immunohistological and histochemical study.
Placenta 11, 59-62 (1990).
8. Bauer, J.H. & Meyer, K.F. Human intestinal carriers of
tetanus spores in California J Infect Dis 38, 295-305 (1926).
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the United States (1965-1966): epidemiologic and clinical
features. N Engl J Med 280, 569-574 (1969).
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II. N Engl J Med 237, 411-413 (1947).
11. Abrahamian, F.M., Pollack, C.V., Jr., LoVecchio, F.,
Nanda, R. & Carlson, R.W. Fatal tetanus in a drug abuser
with “protective” antitetanus antibodies. J Emerg Med 18,
189-193 (2000).
Beltran, A. et al. A case of clinical tetanus in a patient
with protective antitetanus antibody level. South Med J 100,
83 (2007).
Berger, S.A., Cherubin, C.E., Nelson, S. & Levine, L.
Tetanus despite preexisting antitetanus antibody. JAMA 240,
769-770 (1978).
Crone, N.E. & Reder, A.T. Severe tetanus in immunized
patients with high anti-tetanus titers. Neurology 42, 761-764
(1992).
Passen, E.L. & Andersen, B.R. Clinical tetanus despite a
protective level of toxin-neutralizing antibody. JAMA 255,
1171-1173 (1986).
Pryor, T., Onarecker, C. & Coniglione, T. Elevated
antitoxin titers in a man with generalized tetanus. J Fam
Pract 44, 299-303 (1997).
12. Jungeblut, C.W. Inactivation of tetanus toxin by
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332-336 (1926).
About the author
Tetyana Obukhanych earned her Ph.D. in Immunology at the
Rockefeller University in New York, NY with her research
dissertation focused on understanding immunologic memory,
perceived by the mainstream biomedical establishment to be key
to vaccination and immunity. She was subsequently involved in
laboratory research as a postdoctoral research fellow within
leading biomedical institutions, such as Harvard Medical
School and Stanford University School of Medicine.
Having had several childhood diseases despite being properly
vaccinated against them, Dr. Obukhanych has undertaken a
thorough investigation of scientific findings regarding
vaccination and immunity. Based on her analysis, Dr.
Obukhanych has articulated a view that challenges mainstream
assumptions and theories on vaccination in her e-book
Vaccine
Illusion.
Dr. Obukhanych continues her independent in-depth analysis of
peer-reviewed scientific findings related to vaccination and
natural requirements of the immune system function. Her goal
is to bring a scientifically-substantiated and dogma-free
perspective on vaccination and natural immunity to parents and
health care practitioners.
Her e-book can be purchased on
AMAZON
Source:
http://www.vaccinationcouncil.org/2014/07/10/tetanus-shot-how-do-we-know-that-it-works-by-tetyana-obukhanych-phd
