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Bacterial infection characterized by muscle spasms
the disease

Tetanus, also known as lockjaw, is a bacterial infection caused by Clostridium tetani and characterized by muscle spasms. In the most common type, the spasms begin in the jaw, and then progress to the rest of the body. Each spasm usually lasts for a few minutes. Spasms occur frequently for three to four weeks. Other symptoms of tetanus may include fever, sweating, headache, trouble swallowing, high blood pressure, and a fast heart rate. Onset of symptoms is typically 3 to 21 days following infection. Recovery may take months; about 10% of cases prove to be fatal. C. tetani is commonly found in soil, saliva, dust, and manure. The bacteria generally enter through a break in the skin, such as a cut or puncture wound caused by a contaminated object. They produce toxins that interfere with normal muscle contractions. Diagnosis is based on the presenting signs and symptoms. The disease does not spread between people. This is down from 356,000 deaths in 1990. In the US, there are about 30 cases per year, almost all of which were in people who had not been vaccinated. An early description of the disease was made by Hippocrates in the 5th century BC. The cause of the disease was determined in 1884 by Antonio Carle and Giorgio Rattone at the University of Turin, and a vaccine was developed in 1924. 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. However, 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. On the basis of 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 the result of a public health campaign, the death toll from neonatal tetanus was reduced by 90% between 1990 and 2010, and by 2013, the disease had been largely eliminated from all but 25 countries. Neonatal tetanus is rare in developed countries.

Local tetanus is an uncommon form of the disease, in which people have persistent contraction of muscles 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. 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, and that a puncture from a rust free nail is not a risk.

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. Here, it selectively binds to and is transported into inhibitory neurons via endocytosis. 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). The heavy chain has two of the 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.

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 the 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 will be taken into the neuron as an endocytic vesicle that 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 with the presynaptic membrane of inhibitory neurons in a similar manner seen with the 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.

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.

There are currently no blood tests for diagnosing tetanus. The diagnosis is based on the presentation of tetanus symptoms, and does not depend upon isolation of the bacterium, which is recovered from the wound in only 30% of cases, and can be isolated from people without tetanus. Laboratory identification of C. tetani can be demonstrated only by production of tetanospasmin in mice.

Unlike many infectious diseases, recovery from naturally acquired tetanus does not usually result in immunity. This is due to the extreme potency of the tetanospasmin toxin. Tetanospasmin will likely be lethal before it will provoke an immune response. Tetanus can be prevented by vaccination with tetanus toxoid. The CDC recommends that adults receive a booster vaccine 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.

Tetanus toxoid can be given in case of suspected exposure to tetanus. In such cases, it can be given with or without tetanus immunoglobulin (also called tetanus antibodies or tetanus antitoxin
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.

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 of the University of Turin, who demonstrated the transmissibility of tetanus for the first time. 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.

There is insufficient evidence that tetanus can be treated or prevented by vitamin C. This is at least partially due to the fact that the historical trials that were conducted in attempts to look for a possible connection between vitamin C and alleviating tetanus patients were of poor quality.