Tetanus

Tetanus often begins with mild spasms in the jaw muscles—also known as lockjaw. Similar spasms can also be a feature of trismus. The spasms can also affect the facial muscles, resulting in an appearance called risus sardonicus. Chest, neck, back, abdominal muscles, and buttocks may be affected. Back muscle spasms often cause arching, called opisthotonus. Sometimes, the spasms affect muscles utilized during inhalation and exhalation, which can lead to breathing problems. Prolonged muscular action causes sudden, powerful, and painful contractions of muscle groups, called tetany. These episodes can cause fractures and muscle tears. Other symptoms include fever, headache, restlessness, irritability, feeding difficulties, breathing problems, burning sensation during urination, urinary retention, and loss of stool control. Even with treatment, about 10% of people who contract tetanus die. In general, the farther the injury site is from the central nervous system, the longer the incubation period. Shorter incubation periods will have more severe symptoms. In trismus nascentium (i.e., neonatal tetanus), symptoms usually appear from 4 to 14 days after birth, averaging about 7 days. Based on clinical findings, four different forms of tetanus have been described. It usually occurs through infection of the unhealed umbilical stump, particularly when the stump is cut with a non-sterile instrument. As of 1998, neonatal tetanus was common in many developing countries, and was responsible for about 14% (215,000) of all neonatal deaths. In 2010, the worldwide death toll was approximately 58,000 newborns. As a result of a public health campaign, the death toll from neonatal tetanus was reduced by 90% between 1990 and 2010. By 2013, the disease had been largely eliminated from all but 25 countries. Neonatal tetanus is rare in developed countries. Local tetanus Local tetanus is an uncommon form of the disease, in which people have persistent muscle contractions in the same anatomic area as the injury. The contractions may persist for many weeks before gradually subsiding. Local tetanus is generally milder; only about 1% of cases are fatal, but it may precede the onset of generalized tetanus. and is limited to muscles and nerves in the head. It usually occurs after trauma to the head area, including: skull fracture, laceration, and otitis media, but it has been observed from injuries to other parts of the body. Paralysis of the facial nerve is most frequently implicated, which may cause lockjaw, facial palsy, or ptosis, but other cranial nerves can also be affected. Cephalic tetanus may progress to a more generalized form of the disease. Due to its rarity, clinicians may be unfamiliar with the clinical presentation and may not suspect tetanus as the illness. Treatment can be complicated, as symptoms may be concurrent with the initial injury that caused the infection. Cephalic tetanus is more likely than other forms of tetanus to be fatal, with the progression to generalized tetanus carrying a 15–30% case fatality rate. == Cause ==

s. Pictured is the bacterium alone, with a spore being produced, and the spore alone. Clostridium tetani bacteria cause tetanus. The disease occurs almost exclusively in people who are inadequately immunized. It is more common in hot, damp climates with soil rich in organic matter. Manure-treated soils may contain spores, as they are widely distributed in the intestines and feces of many animals, such as horses, sheep, cattle, dogs, cats, rats, guinea pigs, and chickens. The spores can also be found on skin surfaces and in contaminated heroin. An endospore is a non-metabolizing survival structure that begins to metabolize and cause infection once in an adequate environment. Hence, stepping on a nail (rusty or not) may result in a tetanus infection, as the low-oxygen (anaerobic) environment may exist under the skin, and the puncturing object can deliver endospores to a suitable environment for growth. It is a common misconception that rust itself is the cause; a related misconception is that a puncture from a rust-free nail is not a risk. == Pathophysiology ==

Tetanus neurotoxin (TeNT) binds to the presynaptic membrane of the neuromuscular junction, is internalized, and is transported back through the axon until it reaches the central nervous system. It then leaves the vesicle for the neuron cytosol, where it cleaves vesicle associated membrane protein (VAMP) synaptobrevin, which is necessary for membrane fusion of small synaptic vesicles (SSV's). Tetanus toxin specifically blocks the release of the neurotransmitters GABA and glycine from inhibitory neurons. These neurotransmitters stop overactive motor neurons from firing and also play a role in muscle relaxation after contraction. When inhibitory neurons are unable to release their neurotransmitters, motor neurons fire out of control, and muscles have difficulty relaxing. This causes the muscle spasms and spastic paralysis seen in tetanus infection. The heavy chain has two domains. The N-terminal side of the heavy chain helps with membrane translocation, and the C-terminal side helps the toxin locate the specific receptor site on the correct neuron. The light chain domain cleaves the VAMP protein once it arrives in the inhibitory neuron cytosol. Neurospecific binding The toxin travels from the wound site to the neuromuscular junction through the bloodstream, where it binds to the presynaptic membrane of a motor neuron. The heavy chain C-terminal domain aids in binding to the correct site, recognizing and binding to the correct glycoproteins and glycolipids in the presynaptic membrane. The toxin binds to a site that is taken into the neuron as an endocytic vesicle, which will travel down the axon, past the cell body, and down the dendrites to the dendritic terminal at the spine and central nervous system. Here, it will be released into the synaptic cleft and allowed to bind to the presynaptic membrane of inhibitory neurons in a similar manner to binding to the motor neuron. or that the pore could alter the electrochemical gradient enough, by letting in or out ions, to cause osmotic lysis of the vesicle, spilling the vesicle's contents. Enzymatic target cleavage The light chain of the tetanus toxin is zinc-dependent protease. It shares a common zinc protease motif (His-Glu-Xaa-Xaa-His) that researchers hypothesized was essential for target cleavage until this was more recently confirmed by experiment: when all zinc was removed from the neuron with heavy metal chelators, the toxin was inhibited, only to be reactivated when the zinc was added back in. ==Diagnosis==

There are currently no blood tests for diagnosing tetanus. The diagnosis is based on the presentation of tetanus symptoms. It does not depend upon isolation of the bacterium, which is recovered from the wound in only 30% of cases. C. tetani can be isolated from people without tetanus. Laboratory identification of C. tetani can be demonstrated only by the production of tetanospasmin in mice. The "spatula test" is a clinical test for tetanus that involves touching the posterior pharyngeal wall with a soft-tipped instrument and observing the effect. A positive test result is the involuntary contraction of the jaw (biting down on the "spatula"), and a negative test result would normally be a gag reflex attempting to expel the foreign object. A short report in The American Journal of Tropical Medicine and Hygiene states that, in an affected subject research study, the spatula test had a high specificity (zero false-positive test results) and a high sensitivity (94% of infected people produced a positive test). == Prevention ==

Unlike many infectious diseases, recovery from naturally acquired tetanus does not usually result in immunity. This is due to the extreme potency of tetanospasmin. Tetanospasmin will likely be lethal before it provokes an immune response. Tetanus can be prevented by vaccination with tetanus toxoid. The CDC recommends that adults receive a booster shot every ten years, In children under the age of seven, the tetanus vaccine is often administered as a combined vaccine, DPT/DTaP vaccine, which also includes vaccines against diphtheria and pertussis. For adults and children over seven, the Td vaccine (tetanus and diphtheria) or Tdap (tetanus, diphtheria, and acellular pertussis) is commonly used. Post-exposure prophylaxis Tetanus toxoid can be given in cases of suspected tetanus exposure. In such cases, it can be given with or without tetanus immunoglobulin (also called tetanus antibodies or tetanus antitoxin). The guidelines for such events in the United States for people at least 11 years old (and not pregnant) are as follows: ==Treatment==

Treatment of adult tetanus was covered in a state-of-the-art review in 2025. Mild tetanus Mild cases of tetanus can be treated with: • Tetanus immunoglobulin (TIG), It can be given as intravenous therapy or by intramuscular injection. • Antibiotic therapy to reduce toxin production. Metronidazole intravenous (IV) is a preferred treatment. The antibiotic of choice is metronidazole. It can be given intravenously, by mouth, or by rectum. == Epidemiology ==

In 2013, it caused about 59,000 deaths—down from 356,000 in 1990. In the United States, from 2000 through 2007, an average of 31 cases were reported per year. Nearly all of the cases in the United States occur in unimmunized individuals, or individuals who have allowed their inoculations to lapse. == Other animals ==

Tetanus is found primarily in goats and sheep. The following are clinical symptoms found in affected goats and sheep. Extended head and neck, tail rigors (tail becomes rigid and straight), abnormal gait (walking becomes stiff and abnormal), arched back, stiffness of the jaw muscles, lockjaw, twitching of eyes, drooping eyelids, difficulty swallowing, difficulty or inability to eat and drink, abdominal bloat, spasms (uncontrolled muscular contractions) before death. Death sometimes is due to asphyxiation, secondary to respiratory paralysis. ==History==

Tetanus was well known to ancient civilizations, who recognized the relationship between wounds and fatal muscle spasms. In 1884, Arthur Nicolaier isolated the strychnine-like toxin of tetanus from free-living, anaerobic soil bacteria. The etiology of the disease was further elucidated in 1884 by Antonio Carle and Giorgio Rattone, two pathologists at the University of Turin, who demonstrated, for the first time, the transmissibility of tetanus. They produced tetanus in rabbits by injecting pus from a person with fatal tetanus into their sciatic nerves, and testing their reactions while tetanus was spreading. == Research ==

There is insufficient evidence that tetanus can be treated or prevented by vitamin C. This is at least partially because the historical trials conducted to investigate a possible connection between vitamin C and alleviating tetanus patients were of poor quality. ==See also==