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Thursday, June 20, 2013


Tetanus 

From Wikipedia, the free encyclopedia

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, rod-shaped, obligate anaerobic bacterium Clostridium tetani.[2] Because of the traditional spasms in the jaw, the disease has been given the generic name of "Lockjaw".

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

Tetanus often begins with mild spasms in the jaw muscles (lockjaw). The spasms can also affect the chest, neck, back, abdominal muscles, and bottom. Back muscle spasms often cause arching, called opisthotonos. Sometimes the spasms affect muscles that help with breathing, which can lead to breathing problems.[3]

Prolonged muscular action causes sudden, powerful, and painful contractions of muscle groups. This is called tetany. These episodes can cause fractures and muscle tears. Other symptoms include drooling, excessive sweating, fever, hand or foot spasms, irritability, swallowing difficulty, uncontrolled urination or defecation.[citation needed]

Mortality rates reported vary from 48% to 73%. In recent years,[when?] approximately 11% of reported tetanus cases have been fatal. The highest mortality rates are in unvaccinated people, people over 60 years of age or newborns.[3]

Mechanism and Action of the Toxin

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.

The tetanus toxin initially binds to peripheral nerve terminals. It is transported within the axon and across synaptic junctions until it reaches the central nervous system. There it becomes rapidly fixed to gangliosides at the presynaptic inhibitory motor nerve endings, and is taken up into the axon by endocytosis. The effect of the toxin is to block the release of inhibitory neurotransmitters (glycine and gamma-amino butyric acid (GABA)) across the synaptic cleft, which is required to check the nervous impulse. If nervous impulses cannot be checked by normal inhibitory mechanisms, the generalized muscular spasms characteristic of tetanus are produced. The toxin appears to act by selective cleavage of a protein component of synaptic vesicles, synaptobrevin II, and this prevents the release of neurotransmitters by the cells.[4]

Incubation period

The incubation period of tetanus may be up to several months but is usually about eight days.[5][6] 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.[7] 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

This 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.[citation needed] Death can occur within four days.

Neonatal tetanus

This 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.[8]

Local tetanus

This 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.[citation needed]

Cephalic tetanus

This is a rare form[9] 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.[citation needed]

Cause

Tetanus is caused by the tetanus bacterium Clostridium tetani.[10] 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 harbour anaerobic bacteria, but the rust itself does not cause tetanus nor does it contain more C. tetani bacteria. The rough surface of rusty metal merely provides a prime habitat for C. tetani endospores to reside in, and the nail affords a means to puncture skin and deliver endospores deep within the body at the site of 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 thrive in environments that lack oxygen. Hence, stepping on a nail (rusty or not) may result in a tetanus infection, as the low-oxygen (anaerobic) environment is caused by the oxidization of the same object that causes a puncture wound, delivering endospores to a suitable environment for growth.[11]

Diagnosis

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 patients without tetanus. Laboratory identification of C. tetani can be demonstrated only 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).[12]

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.[13] The CDC recommends that adults receive a booster vaccine every ten years,[14] 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.[15]

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.[13]

The WHO certifies countries as having eliminated maternal or neonatal tetanus. Certification requires at least two years of rates of less than 1 case per 1000 live borns. In 1998 in Uganda, 3,433 tetanus cases were recorded in new-born babies; of these, 2,403 died. After a major public health effort, Uganda in 2011 was certified as having eliminated tetanus.[16][not in citation given]

Mild tetanus

Mild cases of tetanus can be treated with:[17]


Severe tetanus

Severe cases will require admission to intensive care. In addition to the measures listed above for mild tetanus:[17]


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 (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 nerve axon terminals.

Epidemiology

Tetanus cases reported worldwide (1990-2004). Ranging from strongly prevalent (in dark red) to very few cases (in light yellow) (grey, no data).

Tetanus is an international health problem, as C. tetani spores are ubiquitous. The disease occurs almost exclusively in persons 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.[3]

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 – in particular, 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.[18] In the United States, from 2000 through 2007 an average of 31 cases were reported per 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]

History

Tetanus was well known to ancient people who recognized the relationship between wounds and fatal muscle spasms.[19] 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 patient with fatal tetanus into their sciatic nerves.[3]

In 1891, C. tetani was isolated from a human victim by Kitasato 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]

Notable victims

 

The entire wiki link can be found at:  https://en.wikipedia.org/wiki/Tetanus

 
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