Tetanus Shot: How Do We Know That It Works?

<>Tetyana Obukhanych, PhD
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 is correct?

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 unthinkable.

A practical solution was found in 1924: 
pre-treating the tetanus toxin with 
(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: 
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 
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]
    * 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 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 
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 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 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!

more by reading Tetyana's groundbreaking and lucid book Vaccine Illusion.


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.  Visit 
for more information.


[1] Tenbroeck, C. & Bauer, J.H. 
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. 
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. 
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. 
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. 
for women to prevent neonatal tetanus. Cochrane 
Database Syst Rev 5:CD002959 (2013).

[6] Maselle, S.Y., Matre, R., Mbise, R. & 
Hofstad, T. 
tetanus despite protective serum antitoxin 
concentration. FEMS Microbiol Immunol 3, 171-175 (1991).

[7] Fox, S.B. & Khong, T.Y. 
of innervation of human umbilical cord. An 
immunohistological and histochemical study. Placenta 11, 59-62 (1990).

[8] Bauer, J.H. & Meyer, K.F. 
intestinal carriers of tetanus spores in 
California. J Infect Dis 38, 295-305 (1926).

[9] LaForce, F.M., Young, L.S. & Bennett, J.V. 
in the United States (1965-1966): epidemiologic 
and clinical features. N Engl J Med 280, 569-574 (1969).

[10] Editorial: Tetanus in the United States Army 
in World War II. N Engl J Med 237, 411-413 (1947).

[11] Abrahamian, F.M., Pollack, C.V., Jr., 
LoVecchio, F., Nanda, R. & Carlson, R.W. 
tetanus in a drug abuser with "protective" 
antitetanus antibodies. J Emerg Med 18, 189-193 (2000).

Beltran, A. et al. 
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. 
despite preexisting antitetanus antibody. JAMA 240, 769-770 (1978).

Crone, N.E. & Reder, A.T. 
tetanus in immunized patients with high 
anti-tetanus titers. Neurology 42, 761-764 (1992).

Passen, E.L. & Andersen, B.R. 
tetanus despite a protective level of 
toxin-neutralizing antibody. JAMA 255, 1171-1173 (1986).

Pryor, T., Onarecker, C. & Coniglione, T. 
antitoxin titers in a man with generalized 
tetanus. J Fam Pract 44, 299-303 (1997).

[12] Jungeblut, C.W. 
of tetanus toxin by crystalline vitamin C 
(L-ascorbic acid). J Immunol 33, 203-214 (1937).

[13] Jahan, K., Ahmad, K. & Ali, M.A. 
of ascorbic acid in the treatment of tetanus. 
Bangladesh Med Res Counc Bull 10, 24-28 (1984).

[14] Hemilä, H. & Koivula, T. 
C for preventing and treating tetanus. Cochrane 
Database Syst Rev 2:CD006665 (2008).

[15] Tenbroeck, C. & Bauer, J.H. 
tetanus bacillus as an intestinal saprophyte in 
man. J Exp Med 36, 261-271 (1922).

[16] Coleman, G.E. & Meyer, K.F. 
of tetanus agglutinins and antitoxin in human 
serums. J Infect Dis 39, 332-336 (1926).


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 website.

Disclaimer: This article is not intended to 
provide medical advice, diagnosis or treatment. 
Views expressed here do not necessarily reflect 
those of GreenMedInfo or its staff.

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