Tetanus 

(from Ancient Greek: τέτανος tetanos "taut", and τείνειν teinein "to stretch")[1] is a medical

condition characterized by a prolonged contraction of skeletal muscle fibers. The primary
symptoms are caused by tetanospasmin, a neurotoxin produced by the Gram-positive,obligate
anaerobic bacterium Clostridium tetani. Infection generally occurs through wound contamination
and often involves a cut or deep puncture wound. As the infection progresses,
muscle spasms develop in the jaw (thus the name "lockjaw") and elsewhere in the body.
[2]
Infection can be prevented by proper immunization and by post-exposure prophylaxis.[3] Signs
and symptoms

Lock-jaw and risus sardonicusin a patient suffering from tetanus.

An infant suffering from neonatal tetanus.

Tetanus affects skeletal muscle, a type of striated muscle used in voluntary movement. The other type of
striated muscle, cardiac or heart muscle, cannot be tetanized because of its intrinsic electrical properties.
Mortality rates reported vary from 48% to 73%. In recent years, approximately 11% of reported tetanus
cases have been fatal. The highest mortality rates are in unvaccinated people and people over 60 years
of age.[3]

The incubation period of tetanus may be up to several months but is usually about 8 days. [4][5] In general,
the further the injury site is from the central nervous system, the longer the incubation period. The shorter
the incubation period, the more severe the symptoms. [6] In 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.[3]

Generalized tetanus is the most common type of tetanus, representing about 80% of cases. The
generalized form usually presents with a descending pattern. The first sign is trismus, or lockjaw, and the
facial spasms called risus sardonicus, followed by stiffness of the neck, difficulty in swallowing, and
rigidity of pectoral and calf muscles. Other symptoms include elevated temperature, sweating,
elevated blood pressure, and episodic rapid heart rate. Spasms may occur frequently and last for several
minutes with the body shaped into a characteristic form called opisthotonos. Spasms continue for up to 4
weeks, and complete recovery may take months.

Neonatal tetanus is a form of generalized tetanus that occurs in newborns. Infants who have not
acquired passive immunity because the mother has never been immunized are at risk. It usually occurs
through infection of the unhealed umbilical stump, particularly when the stump is cut with a non-sterile
instrument. Neonatal tetanus is common in many developing countries and is responsible for about 14%
(215,000) of all neonatal deaths, but is very rare in developed countries. [7]

Local tetanus is an uncommon form of the disease, in which patients 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.

Cephalic tetanus is a rare form of the disease, occasionally occurring with otitis media (ear infections) in
which C. tetani is present in the flora of the middle ear, or following injuries to the head. There is
involvement of the cranial nerves, especially in the facial area.

[edit]Cause

Tetanus is often associated with rust, especially rusty nails, but this concept is somewhat misleading.
Objects that accumulate rust are often found outdoors, or in places that harbor anaerobic bacteria, but the
rust itself does not cause tetanus nor does it contain more C. tetanibacteria. The rough surface of rusty
metal merely provides a prime habitat for a C.  tetani endospore to reside, and the nail affords a means to
puncture skin and deliver endospore into the wound. An endospore is a non-metabolizing survival
structure that begins to metabolize and cause infection once in an adequate environment.
Because C.  tetani is an anaerobic bacterium, it and its endospores survive well in an environment that
lacks oxygen. Hence, stepping on a nail (rusty or not) may result in a tetanus infection, as the low-oxygen
(anaerobic) environment is provided by the same object which causes a puncture wound, delivering
endospores to a suitable environment for growth.
[edit]Pathophysiology

Facial spasms called Risus Sardonicus-First Symptom of Generalized Tetanus.

Tetanus begins when spores of Clostridium tetani enter damaged tissue. The spores transform into rod-
shaped bacteria and produce the neurotoxin tetanospasmin (also known as tetanus toxin). This toxin is
inactive inside the bacteria, but when the bacteria die, toxin is released and activated by proteases. Active
tetanospasmin is carried by retrograde axonal transport[6][8] to the spinal cord and brain stem where it
binds irreversibly to receptors at these sites.[6] It cleaves membrane proteins involved in neuroexocytosis,
[9]
 which in turn blocks neurotransmission. Ultimately, this produces the symptoms of the disease.
Damaged upper motor neurons can no longer inhibit lower motor neurons (seeRenshaw cells), plus they
cannot control reflex responses to afferent sensory stimuli. [6] Both mechanisms produce the
hallmark muscle rigidity and spasms. Similarly, a lack of neural control of the adrenal glands results in
release of catecholamines, thus producing ahypersympathetic state and widespread autonomic instability.

C. tetani also produces tetanolysin, another toxin whose role in tetanus is unknown.

[edit]Diagnosis

There are currently no blood tests that can be used to diagnose tetanus. The diagnosis is based on the
presentation of tetanus symptoms and does not depend upon isolation of the bacteria, which is recovered
from the wound in only 30% of cases and can be isolated from patients who do not have tetanus.
Laboratory identification of C. tetani can only be demonstrated by production of tetanospasmin in mice. [3]

The "spatula test" is a clinical test for tetanus that involves touching the posterior pharyngeal wall with a
sterile, 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 a patient research study, the spatula test had a high specificity (zero false-
positive test results) and a high sensitivity (94% of infected patients produced a positive test result). [10]

[edit]Prevention

Unlike many infectious diseases, recovery from naturally acquired tetanus does not usually result
in immunity to tetanus. This is due to the extreme potency of the tetanospasmin toxin; even a lethal dose
of tetanospasmin is insufficient to provoke an immune response.

Tetanus can be prevented by vaccination with tetanus toxoid.[11] The CDC recommends that adults

receive a booster vaccine every ten years,[12] and standard care practice in many places is to give the
booster to any patient with a puncture wound who is uncertain of when he or she was last vaccinated, or if
he or she has had fewer than three lifetime doses of the vaccine. The booster may not prevent a
potentially fatal case of tetanus from the current wound, however, as it can take up to two weeks for
tetanus antibodies to form.[13] 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. [11]

[edit]Treatment

The wound must be cleaned. Dead and infected tissue should be removed by surgical debridement.
Administration of the antibiotic metronidazole decreases the number of bacteria but has no effect on the
bacterial toxin. Penicillin was once used to treat tetanus, but is no longer the treatment of choice, owing to
a theoretical risk of increased spasms. However, its use is recommended if metronidazole is not
available. Passive immunization with human anti-tetanospasmin immunoglobulin or tetanus
immunoglobulin is crucial. If specific anti-tetanospasmin immunoglobulin is not available, then normal
human immunoglobulin may be given instead. All tetanus victims should be vaccinated against the
disease or offered a booster shot.

[edit]Mild tetanus
Mild cases of tetanus can be treated with:

 Tetanus immunoglobulin IV or IM,
 metronidazole IV for 10 days,
 Diazepam,
 tetanus vaccination
[edit]Severe tetanus
Severe cases will require admission to intensive care. In addition to the measures listed above for mild
tetanus:

 human tetanus immunoglobulin injected intrathecally (increases clinical improvement from 4% to

35%)
 tracheostomy and mechanical ventilation for 3 to 4 weeks,
 magnesium, as an intravenous (IV) infusion, to prevent muscle spasm,
 diazepam as a continuous IV infusion,
 the autonomic effects of tetanus can be difficult to manage (alternating hyper-
and hypotension, hyperpyrexia/hypothermia) and may require IV labetalol, magnesium, clonidine,
ornifedipine.

Drugs such as diazepam or other muscle relaxants can be given to control the muscle spasms. In
extreme cases it may be necessary to paralyze the patient with curare-like drugs and use a mechanical
ventilator.

In order to survive a tetanus infection, the maintenance of an airway and proper nutrition are required. An
intake of 3500-4000 calories, and at least 150 g of protein per day, is often given in liquid form through a
tube directly into the stomach (Percutaneous endoscopic gastrostomy), or through a drip into a vein (Total
parenteral nutrition). This high-caloric diet maintenance is required because of the increased metabolic
strain brought on by the increased muscle activity. Full recovery takes 4 to 6 weeks because the body
must regenerate destroyed nerveaxon terminals.

[edit]Epidemiology

Tetanus is an international health problem, as C. tetani spores are ubiquitous. The disease occurs almost
exclusively in persons who are unvaccinated or inadequately immunized. [2] Tetanus occurs worldwide but
is more common in hot, damp climates with soil rich in organic matter. This is particularly true
with manure-treated soils, as the spores are widely distributed in the intestines and feces of many non-
human animals such as horses, sheep, cattle, dogs, cats, rats, guinea pigs, and chickens. Spores can be
introduced into the body through puncture wounds. In agricultural areas, a significant number of human
adults may harbor the organism. The spores can also be found on skin surfaces and in
contaminated heroin.[3] Heroin users, particularly those that inject the drug, appear to be at high risk for
tetanus.

Tetanus – particularly the neonatal form – remains a significant public health problem in non-industrialized

countries. The World Health Organization estimates that 59,000 newborns worldwide died in 2008 as a
result of neonatal tetanus.[14] In the United States, 50-100 people become infected with tetanus each year.
[3]
 Nearly all of the cases in the United States occur in unimmunized individuals or individuals who have
allowed their inoculations to lapse.[3]

Tetanus is the only vaccine-preventable disease that is infectious but is not contagious.[3]

[edit]History

Tetanus was well known to ancient people who recognized the relationship between wounds and fatal
muscle spasms.[15] 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, who demonstrated the transmissibility of tetanus for the first time. They
produced tetanus in rabbits by injecting pus from a patient with fatal tetanus into their sciatic nerves. In
1889, C. tetani was isolated from a human victim byKitasato Shibasaburō, who later showed that the
organism could produce disease when injected into animals, and that the toxin could be neutralized by
specific antibodies. In 1897, Edmond Nocard showed that tetanus antitoxin induced passive immunity in
humans, and could be used for prophylaxis and treatment. Tetanus toxoid vaccine was developed by P.
Descombey in 1924, and was widely used to prevent tetanus induced by battle wounds during World War
II.[3]