Tetanus Shot: How Do We Know That It
Thursday, October 16th 2014
Do we know how tetanus shots work? The medical establishment holds
a view that a tetanus shot prevents tetanus, but how do we know this view
The cure for
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
A practical solution was found in 1924: pre-treating the tetanus toxin
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
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
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:
muscular spasms, such as lockjaw, sardonic smile, and severe
convulsions that frequently lead to bone fractures and death due to
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 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
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." 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 TetanusNeonatal 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
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.
- "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
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. 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. 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, stressing the
importance of hygienic birth practices regardless of maternal vaccination
Tetanus In AdultsBased 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. 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 versus the
mid-20th century). 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:
- 1) 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;
- 2) throughout the entire WWII period, 12 cases of tetanus have been
documented in the U.S. Army;
- 3) 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
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.
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
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
Ascorbic Acid In Tetanus TreatmentAnti-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
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. 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. 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 TetanusIn 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
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 controlstheir
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
straina 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 agglutininso 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
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. 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.
Another study was performed back in the 1920s in San Francisco,
CA. 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
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
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 controlat the level of preventing spore germinationis 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!
Learn more by reading Tetyana's groundbreaking and lucid book Vaccine
About The AuthorTetyana 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
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.
www.naturalimmunityfundamentals.com for more
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M. & Fairweather, N.F.
not interfere with uptake and transport by motor neurons of the binding
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Vaccines for women
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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 crucial to vaccination and immunity. During her
subsequent involvement in laboratory research as a postdoctoral fellow
within leading biomedical institutions, such as Harvard Medical School
and Stanford University School of Medicine, Dr. Obukhanych realized the
flaws and limitations of current immunologic paradigms. Learn more about
her work on her
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