TETANUS SHOT: HOW DO WE KNOW THAT IT WORKS?

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).
9. LaForce, F.M., Young, L.S. & Bennett, J.V. Tetanus 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. 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 crystalline vitamin C (L-ascorbic acid). J Immunol 33, 203-214 (1937).
13. Jahan, K., Ahmad, K. & Ali, M.A. Effect of ascorbic acid in the treatment of tetanus. Bangladesh Med Res Counc Bull 10, 24-28 (1984).
14. Hemilä, H. & Koivula, T. Vitamin C for preventing and treating tetanus. Cochrane Database Syst Rev 2:CD006665 (2008).
15. Tenbroeck, C. & Bauer, J.H. The tetanus bacillus as an intestinal saprophyte in man. J Exp Med 36, 261-271 (1922).
16. Coleman, G.E. & Meyer, K.F. Study of tetanus agglutinins and antitoxin in human serums. J Infect Dis 39, 332-336 (1926).

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

FOLLOW-UP ARTICLE:

A Dose of Reality: Tetanus Vaccines Fail To Protect…

by MommyPotamus.com

“If you don’t do the DTaP (diptheria, tetanus and acellullar pertussis vaccine), what do you do if your child steps on a rusty nail? Do you choose to wait until that happens and go get a tetanus shot at that time instead of doing it as prevention?”

~ Comment from Lisa K. on this post

Great question, Lisa! Let’s jump right in, shall we?

Antibodies Do Not Equal Immunity

According to the CDC, “Because of the extreme potency of the toxin, tetanus disease does not result in tetanus immunity.”

How is it, then, that can you vaccinate successfully against tetanus? If the purpose of vaccination is to simulate normal immune responses with weakened or dead pathogens, why would vaccination yield immunity when the actual disease can’t?

According to experts, it’s because the bacteria that causes tetanus – Clostridium tetani – produces a neurotoxin which inhibits our ability to create the antibodies that fight infection. By introducing a dead form of the toxin (which cannot block antibody production) doctors hope that patients will build up immunity to the toxin. It seems like a plausible idea, but is that possible?

According to some experts, the answer is yes . . . and no. While it is is possible that the body will create antibodies to the toxin, antibody response to a vaccine does not equal immunity or protection. (Source 1, Source 2). The presence of antibodies after a vaccination indicates exposure to a pathogen, but it alone does not confer immunity.

Here’s what I mean: Say you send your first grader to school with the answers to her second period quiz in her back pocket. When test time arrives she has to go through the hassle of digging through her folders to find the answer sheet, read your chicken scratch handwriting (or maybe that’s just mine!), and write down the answers. She had to go through **some** effort to earn that A+, but having the right answers on that test does NOT mean she learned anything, or that she will be prepared to handle real-life events based on her “success” with the test.

In the case of the tetanus vaccine, injecting the body with dead toxins is essentially like handing it the answers to a quiz. Unless the whole immune system fully engages a live version of the pathogen it does not really learn anything. This is evidenced by the fact that according to this statement from the University of Chicago’s Neurology department, individuals with extremely high levels of titers (antibodies) can still contract severe – even fatal – tetanus. The idea that antibodies equal immunity is magical thinking not supported by the many documented cases of disease outbreaks among fully vaccinated populations. In fact, in one investigation into why a Corpus Christi middle school had an outbreak, researchers said that:

We conclude that outbreaks of measles can occur in secondary schools, even when more than 99 percent of the students have been vaccinated and more than 95 percent are immune.”

Okay, you may be thinking, the tetanus vaccine probably won’t work. But what harm can a little magical thinking do, really? Why not just get the vaccine in case? Well, according to a letter published by the The New England Journal of Medicine, the tetanus booster shot can actually cause T cells (vital to immune system function) to drop below normal, with the greatest decrease up to 2 weeks later. In some cases, the researchers observed that the T-cell count fell to levels found in active AIDS patients. Scary, yes? And that’s before we consider the generous dose of aluminum potassium sulfate, bovine extract, formaldehyde or formalin and Thimerosal (for adult doses) contained in each syringe!

Sadly, magical thinking is just the beginning. Much of the information we’ve been given regarding tetanus vaccination is either incomplete, misleading or flat out wrong.

Let’s Explore That, Shall We?

What I wish my dust bunnies looked like!

By now you’ve probably heard that tetanus exposure can come from rusty nails, but I’ll bet no one’s mentioned that it can also come from those dust bunnies under your bed, that toy your baby just dropped in the dirt and put in her mouth, and in that cow patty you scraped off your boot after the barn dance.

Yep, Clostridium tetani is actually found in common household dust, animal droppings and about 1/3 of the soil sampled around the world – it’s everywhere! (Source) In fact, the only reason rusty nails are ever a concern is that they come into contact with things like soil and have the ability to puncture skin – they don’t inherently contain Clostridium tetani.

So why are we not seeing rampant epidemics? Good question!

Natural Immunity Vs. Artificial Immunity

Normally when we encounter Clostridium tetani it enters our body through our mouth or nose – by breathing dust particles that contain it or eating food that has retained some from the soil it was grown in. However, unlike with puncture wounds, ingested Clostridium tetani is unable to produce large amounts tetanospasmin, the potent neurotoxin that causes the muscle spasms and fatalities associated with tetanus infection.

In fact – and I’ll bet this is something else you won’t hear at your local pedi’s – it appears that gradual exposure to tetanus in this way may create natural immunity.

Unvaccinated Populations With Proven Natural Immunity To Tetanus

In this study, “410 Indians not artificially immunised against tetanus showed that 80% had measurable antitoxin” levels against tetanospasmin. Researchers concluded this was due to ingestion of Clostridium tetani over time.

And according to these researchers,, when “adequate conditions appear, tetanus toxin is known to stimulate the immune system and produce detectable humoral antibodies [antitoxin]. . . The existence of natural immunization was unquestionably demonstrated by presence of protective levels of tetanus antitoxin in the blood of the majority of 59 surveyed subjects considering that none of them had ever received any tetanus toxoid and most of them never received a single shot of any drug.” (emphasis mine)

When researchers tested the blood of 200 individuals in an isolated community it was found that 197 had measurable levels of antitoxin and about 30% had “protective levels” according to Western standards. The researchers pointed out that immunity seemed to be age related, with the youngest being the most lacking in antitoxin. It is thought that this is because the immune response occurs over a period of time.

In Mali, samples from 48 adults found 20 individuals with protective tetanus antibody titers, 23 with measurable levels of antitoxin, and 5 devoid of tetanus antitoxin. Ninety-nine unvaccinated children ages 3 and under were also tested and then retested 7 months later. When the first serum sample was taken 12.1% were found to have tetanus antitoxin. Seven months later 16.2% had antitoxins and 4 children were found to have “protective levels.” According to the researchers, “The data suggest a silent oral immunization by tetanus bacilli thus boosting under unhygienic conditions the tetanus immunity with advancing age.”

Here we have our answer to how the body is designed to develop immunity to tetanus – through gradual ingestion rather than direct introduction into the bloodstream. Now, I’m NOT suggesting that you go out and try to find some tetanus-laden dirt to consume – we’ll be discussing far more effective ways to prevent your risk of tetanus soon!

What I want to draw attention to here is how different this scenario is from the conditions that lead to tetanus infection. Clostridium tetani needs an anaerobic environment (like a puncture wound) to replicate. Cuts and scrapes which have been exposed to oxygen are not a concern. Though the digestive tract is a low-oxygen environment it also somehow manages to disable reproduction. Researchers have not indicated why they think this is, but I believe it’s because the beneficial bacteria in our digestive tracts neutralize them before they ever get established.

On the other hand, Clostridium tetani introduced through a puncture wound bypasses our natural immune defenses and flows directly into the bloodstream. In that way a tetanus vaccine is actually very similar to the most dangerous way a person can encounter tetanus – through a puncture wound! When we inject tetanus into an individual we are simulating the wrong process – the “sneak attack” on the bloodstream which overwhelms the body instead of the slow exposure through ingestion that yields immunity.

But! But!

According to the CDC, tetanus rates continue to drop despite the fact that about 40% of the population is not vaccinated against the disease.

What about the dramatic drop in tetanus cases since the introduction of the vaccine? Even if it makes no logical sense we can see that it’s effective, right?

Um, no.

As it turns out ‘[d]uring the mid-1800′s there were 205 cases of tetanus per 100,000 wounds. By the early 1900′s (before a tetanus vaccine became available), this rate had declined to 16 cases per 100,000 wounds – a 92% reduction. Some researchers attribute this decline to an increased attention to wound hygiene.”(source, emphasis mine)

Here’s another statistic you may find interesting:

During the Second World War, there were 12 recorded cases of tetanus. Four of them occurred in military personnel vaccinated against the disease . . . The majority of those cases were over 50. During that time, no deaths occurred among any tetanus cases under 30 years of age. Tetanus vaccines are not responsible for the success, since they only immunize for 12 years or less, and most of the vaccines are given to children. Yet, in contrast, the tetanus vaccine itself results in a variety of serious complications, including recurrent abscesses, high fever, inner ear nerve damage, anaphylactic shock, loss of consciousness, and demyelinating neuropathy (progressive nerve degeneration). (See U.S. Morbidity and Mortality Weekly Reports for additional information on these statistics.)

The Vaccination Crisis

Why do most cases of tetanus occur in people over 50? According to my friend and chiro, Dr. Haggerton, it’s because some older adults have decreased circulation in their limbs due to conditions like diabetes. If they step on a sharp reed/nail/whatever and there is not enough circulation to make the wound bleed it will not properly aerate. This, of course, makes the wound an anaerobic environment where the multiplication of Clostridium tetani becomes possible. Because some diabetics experience a condition called neuropathy – decreased sensation in the feet – they may not even know they stepped on something and therefore do not clean and aerate the wound properly.

How To Prevent Tetanus

Despite what we’ve been told, there is evidence out there that plain old oxygen-rich hydrogen peroxide is more effective at preventing tetanus than the vaccine. Experts say deep puncture wounds and other at-risk injuries should be thoroughly cleaned and not allowed to close until the inner tissues have begun to heal. Make sure the wound bleeds as much as possible because the oxygen in the blood will help to aerate the wound alongside a hydrogen peroxide solution.

What To Do If You Suspect Tetanus

There is no blood test to confirm tetanus. However, if you suspect you or someone you love has it you should immediately go to the emergency room so that a doctor can assess you. If he/she believes you have tetanus request the Tetanus Immunoglobulin (TiG) shot. The TiG is an anti-toxin serum, not a vaccine. PLEASE MAKE SURE you actually see the packaging that the anti-toxin comes in, because in many hospitals standard procedure calls for suspected tetanus patients to be given the vaccine rather than the more expensive (and honestly, painful) anti-toxin. Obviously, this makes no sense because it takes weeks for the vaccine to stimulate “protective” levels of antibodies, but that is what it currently recommended in many clinical settings.

Tetanus Toxoid = Vaccine

Tetanus Immunoglobulin = Anti-Toxin

Got it? GREAT!!! Thanks for sticking with me through this uber long post!