Can You Actually Get Tetanus From Stepping on a Rusty Nail?

In his Aphorisms, written around 380 B.C.E, Ancient Greek physician Hippocrates describes a truly horrifying case of disease:

“The master of a large ship mashed the index finger of his right hand with the anchor. Seven days later a somewhat foul discharge appeared; then trouble with his tongue – he complained he could not speak properly. His jaws became pressed together, his teeth were locked, then symptoms appeared in his neck; on the third day opisthotonos appeared with sweating. Six days after the diagnosis was made he died.”

The ship’s master was suffering from tetanus – better known as lockjaw – a disease that still infects 209,000 people and kills 59,000 worldwide every year. If you have ever heard of tetanus, it is probably through being vaccinated against it before attending school. Or perhaps you have heard that you can contract the disease from stepping on or scratching yourself on a rusty nail. But is this really true? Can such a seemingly minor injury really lead to such dramatic symptoms? Well…yes – but not for the reasons you might think.

Tetanus has been humanity’s constant companion since the dawn of known history. The first description of the disease appears in the Ebers Papyrus, an Ancient Egyptian medical treatise written around 1500 B.C.E – though this is thought to have been copied from an earlier source dating back as far back as 3,000 B.C.E. The disease gets its name from the Ancient Greek word tetanos, meaning ‘taut’ or ‘to stretch’ – a reference to the stiffness and violent muscle spasms characteristic of the affliction. In severe cases these spasms can be so violent as to cause the sufferer to fully arch their back and neck – what Hippocrates refers to in his description as opisthotonos – or even tear muscles and break bones. While for thousands of years the cause of tetanus remained a mystery, as with most diseases there was no shortage of attempts to develop a cure. The Ancient Chinese, for instance, used acupuncture above the patient’s ears, while the Ancient Greeks and Romans, working from the Four Humours model of medicine, attempted to induce sweating by placing patients near fires, wrapping them in oil-soaked cloths, or making them drink copious amounts of wine – and for more on the Four Humours theory and its massive impact on the history of medicine, please check out our previous video What’s Up with the Increasingly Popular Practice of Modern Medical Leeches?

Later Medieval and Renaissance doctors recommended even more unpleasant treatments, such as covering the patient in manure – which, as we shall see, likely made the situation even more shitty beyond the obvious ways. Still, even in ancient times it was well-understood that tetanus had something to do with open wounds and that symptoms typically appeared within a week or so of the inciting injury, with Greek physician Aretaeus of Cappadocia writing in the First Century C.E.:

“The causes of these complaints are many; for some are apt to supervene on the wound of a membrane, or of muscles…and women also suffer from this spasm after abortion; and in this case they seldom recover.” 

While Hippocrates concludes his description of the disease with:

“Such persons as are seized with tetanus either die within four days, or if they pass these they recover.”

With the advent of modern weaponry such as explosive artillery shells capable of inflicting large numbers of deep, soil-contaminated wounds, tetanus became a leading cause of deaths for soldiers on the battlefield. During the American Civil War, for example, one in 500 men died of tetanus from infected wounds. The disease was also a common and feared post-operative complication even after the adoption of antiseptic surgical techniques, and even became associated with – of all things – American Fourth of July celebrations. Indeed, in the years before the widespread availability of vaccines, the holiday was commonly known as “the Bloody Fourth” due to the high number of tetanus deaths resulting from accidents involving fireworks and firecrackers.

However, it was not until the late 19th Century and the development of the Germ Theory of Disease that the true cause of tetanus was at last discovered. The first breakthrough came in 1884 when Antonio Carle and Giorgo Rattone, pathologists at the University of Turin, injected pus from human tetanus victims into rabbits. The animals proceeded to contract tetanus, demonstrating that the disease was transmissible and likely caused by a microorganism. That same year, German researcher Arthur Nicolaier discovered that certain bacteria commonly found in the soil produced powerful neurotoxins which, when injected into lab animals, produced the same symptoms as tetanus. This link was confirmed by Japanese researcher Kitasato Shibasaburo, who in 1891 isolated the causative pathogen from a human tetanus victim: the anaerobic soil bacterium Clostridium tetani.

Shibasaburo’s breakthrough, however, went far beyond discovering the cause of tetanus. While working at the University of Berlin, Shibasaburo and German researcher Emil von Behring discovered that when rats and other lab animals were injected with tetanus toxin, their bodies produced a substance capable of neutralizing said toxin as well as the tetanus bacterium. When this substance, which Shibasaburo and von Behring called antitoxin, was extracted from one animal’s blood serum and injected into another, it both cured existing tetanus infections and provided protection against future infections. This technique, known as serum therapy or antitoxin therapy, was among the most important breakthroughs in the history of medicine. Indeed, such was the impact of tetanus antitoxin that during the First World War, the Entente powers suffered only one case of tetanus per 5,000 wounded soldiers. Antitoxins were later developed for more dangerous and infectious diseases such as diphtheria and scarlet fever, saving millions of lives and winning Emil von Behring the 1901 Nobel Prize in Physiology and Medicine.

In the early years, antitoxin was produced commercially by injecting horses with bacteria, extracting their blood, and purifying the serum. While effective at producing large quantities of serum, this technique did suffer from a number of drawbacks. One of these was serum sickness, a cluster of symptoms such as rashes, joint pain, fever, and swollen lymph glands that arose 5-10 days after being injected with antitoxin. This effect was first noted in 1906 by Austrian paediatrician Clemens von Pirquet and Hungarian-American paediatrician Béla Schick, who determined that it was caused by the victim’s immune system reacting to foreign horse proteins in the serum. To describe this effect, von Pirquet and Schick combined the Greek words allos, meaning “other” and ergon, meaning “work”, to coin a now-familiar word: allergy. The discovery of serum sickness and other allergic reactions allowed Béla Schick to develop a simple and effective test to determine if someone was immune to diphtheria, which became known as the Schick Test. In this procedure, a small dose of diphtheria toxin was injected into one arm and heat-inactivated toxin into the other arm as a control. If the skin around the first injection became red and swollen, then the person did not have sufficient antitoxins – better known today as antibodies –  to fight off a diphtheria infection. If little or no swelling occurred, then the person was immune. French physician Charles Mantoux later adapted the Schick Test to the bacterial protein tuberculin, creating the eponymous Mantoux test – still the standard diagnostic test for tuberculosis infection in many parts of the world.

Another major downside of horse-produced antitoxin was the risk of contamination. On October 2, 1901, an American horse named Jim, who had produced nearly 30 litres of diphtheria serum over his lifetime, was found to have contracted tetanus and had to the euthanized. 17 days later, four young children in St. Louis, Missouri – Veronica Keenan and Bessie, Viola, and Frankie Baker – were given diphtheria antitoxin manufactured from Jim’s serum. Within four days, Veronica, Bessie, and Viola were dead of tetanus. This incident and others spurred research into safer alternatives to traditional antitoxin. In 1924, French biologist Gaston Ramon came up with a solution: toxoid or anatoxin, a version of the tetanus or diphtheria toxin treated with heat and formaldehyde such that it was no longer toxic to humans but still retained its immunologic properties. A perfected version of tetanus toxoid was used to protect U.S. troops during WWII, and in 1948 was combined with the vaccines for diphtheria and pertussis – AKA whooping cough – to create the DPT vaccine still given to schoolchildren around the world today. Yet traditional tetanus antitoxin never really went away, and survives to this day in the form of tetanus immunoglobulin or TIG. Unlike the first antitoxins, however, TIG is manufactured not from the blood of horses but volunteer human donors, who are injected with a small dose of bacterial toxin prior to donating blood.

Moving away from that diversion into the fascinating world of immunology, let’s get back to tetanus, about which much has been learned since the late 19th Century. As previously mentioned, tetanus is caused by Clostridium Tetani, a rod-shaped bacterium around 2.5 microns in length. An anaerobic bacterium that thrives in oxygen-free environments,  C. tetani commonly found in the soil as well as in the intestinal tracts and faeces of many animals including cats, dogs, cattle, sheep, chickens, horses, mice, and rats. While the bacterium itself is heat-sensitive and cannot survive in the presence of oxygen for long, outside the body of an animal C. tetani transforms itself into a dormant spore, which is a different beast altogether. Tetanus spores are extremely resilient, impervious to most antiseptics and capable of surviving typical sterilization temperatures of 120º Celsius for up to 10-15 minutes. This makes tetanus extremely difficult to eradicate, even in an otherwise sterile hospital environment.

 C. tetani typically enters the body via a puncture wound, and once in the anaerobic environment beneath the skin begins to multiply. As it does so, it produces two toxins as waste products: tetanolysin and tetanospasmin, which slowly spread throughout the victim’s nervous system. Tetanospasmin, more generally known as tetanus toxin, is one of the most potent poisons known to science. With an LD50 – that is, the dose that kills 50% of a test sample of lab animals – of 2.5 nanograms per kilogram of body weight, it is second only to botulinum toxin, produced by C. tetani’s cousin Clostridium Botulinum, the bacterium that causes botulism food poisoning. Tetanospasmin inhibits the function of inhibitory neurons, which prevent motor neurons from firing and allow muscles to relax after contraction. This inhibition causes the uncontrollable muscle spasms or tetany characteristic of tetanus. The incubation period of tetanus – that is, the time between initial infection and the onset of symptoms – can be up to several weeks or even months, but is usually on the order of around 10 days. Typically, the farther away the injury site from the central nervous system, the longer the incubation period. Initial symptoms include stiffness and pain in the muscles of the shoulders, back, neck, and jaw. Speaking and swallowing become increasingly difficult, until the jaw muscles tighten so much that it becomes difficult or impossible to open the mouth – the symptom known as trismus which gives tetanus its more common name of “lockjaw.” This is followed by fever, sweating, high blood pressure, rapid heart rate, and increasingly severe muscle spasms throughout the body. Without treatment these symptoms can last up to three or four weeks, with around 25% of untreated patients dying, and even with proper treatment around 10% of cases are fatal. In the absence of vaccines, the only treatment is supportive care, such as the use of muscle relaxants to relieve muscle spasms and ventilators to support breathing. Worse still, due to the extreme potency of tetanospasmin, a dose large enough to cause symptoms is typically insufficient to trigger an immune response, meaning that being infected with tetanus typically does not confer lasting immunity to the disease.

Thankfully, however, in much of the developed world tetanus toxoid or immunoglobulin is readily available, and can be administered either preventatively as a vaccine or reactively within 48 hours of initial infection for those who are unvaccinated or whose vaccines are out of date. In the form of the DTP vaccine, tetanus toxoid is typically administered in six doses throughout childhood and adolescence, with booster shots being required every 10 years in order to maintain immunity. Rare among vaccines, tetanus toxoid is considered to be nearly 100%  effectives, and thanks to widespread vaccination efforts, annual tetanus deaths worldwide have fallen from 333,000 in 1990 to around 39,000 today. In North America and Europe the death toll is only around 70 people per year – nearly all among unvaccinated individuals – with the vast majority of tetanus deaths occurring in the developing world.

All this brings us back to our initial question: can you actually get tetanus from stepping on a rusty nail? As with many old wives’ tales, there is a small grain of truth to this myth – albeit one that neatly demonstrates the classic error of conflating correlation with causation. For while you can indeed catch tetanus from a rusty nail, you can just as easily catch it from a seemingly clean nail, for the causative agent is not the rust itself but the Clostridium tetani spores that might be lurking on the nail’s surface. The supposed causal link between tetanus and rust stems merely from the fact that a nail or other metal object left outside to rust is likely also to have been exposed to soil, animal faeces, and other sources of tetanus spores, while the rough rusty surface of the nail provides an ideal hiding place for bacteria – and the perfect vehicle to enter the body if stepped on. Thus the better advice would be to avoid sharp metal objects embedded in – or even located close to – the soil. But even then, you may not be 100% safe. Due to their extreme resilience, tetanus spores can lurk on all manner of seemingly clean objects – including your own skin – and can easily cause infection unless special precautions are taken. For example, a handful of people every year are infected with tetanus through contaminated surgical and dental instruments, compound bone fractures, and bites from infected animals. Users of heroin and other intravenous drugs are also at high risk of contracting the disease. In the past, a major killer of newborn babies was neonatal tetanus, usually transmitted through the cutting of the umbilical cord with a non-sterile instrument. If the mother has been vaccinated against tetanus, then passive immunity is transferred to her child, meaning that today neonatal tetanus is encountered mainly in developing countries where vaccination rates are low. Thankfully, as with other forms of tetanus, thanks to concerted vaccination efforts this disease has been largely eradicated in all but 25 countries.

So in conclusion: while thanks to the wonders of modern immunology you are unlikely to contract tetanus from a rusty nail, it’s probably still a good idea to avoid stepping on rusty nails and other sharp metal objects. Unless you’re into that sort of thing; who are we to judge?

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