Tetanus pathophysiology: Difference between revisions

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Revision as of 20:25, 22 May 2017

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

The bacteria that causes tetanus, Clostridium tetani is introduced into the human body usually by a wound. The toxins produced by the bacterium, utilize the blood and/or lymphatics to gain access to target tissues. The toxins can act at various places in the central nervous system, including the spinal cord, peripheral motor end plates, and the brain. They can also act on the sympathetic nervous system.

Pathophysiology

Tetanus is caused by an exotoxin from Clostridium tetani that leads to acute, often fatal illness. Generalized, widespread rigidity and skeletal muscle spasms are common presentations of tetanus. The muscle stiffness begins from the jaw (lockjaw) progressing to the neck and then becoming generalized. C. tetani is a terminal spore forming bacteria. The spores is very resistant to extremes of temperature and to the normally used antiseptics. The spores can be found in the soil as well as in the intestines and feces of cattle, dogs, sheep, horses, cats, guinea pigs, rats, and chickens. The soil that has been treated with manure may contain huge amount of spores. Human adults related to agricultural work may also harbor the pathogen.

Pathogenesis

C. tetani gains access to the human body through a wound.
The spores germinate, because of their anaerobic character.
Toxins are produced and spread through the blood and lymphatics.
C. tetani produces two exotoxins
- Tetanolysin, whose function is not well understood and
- Tetanospasmin which is a neurotoxin and is responsible for the clinical symptoms of tetanus. Tetanospasmin among the most potent toxins with respect to weight.
  - The minimum lethal dose for humans, according to an estimate, is around 2.5 nanograms per kg of body weight or 175 nanograms for an individual who weighs 70-kg (154lb).
The release of various neurotransmitters that cause inhibition is altered by the tetanus toxin.
This intern leads to an unopposed contraction of the muscles which manifests as a spasm.
The autonomic nervous system is also targeted leading to a seizure.

Group of Clostridium tetani bacteria, responsible for causing tetanus in humans

References

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 ==Pathophysiology==
-Tetanus is an [[acute]], often [[fatal]], disease caused by an [[exotoxin]] produced by the bacterium Clostridium tetani. It is characterized by generalized [[rigidity]] and convulsive [[spasms]] of [[skeletal muscles]]. The muscle stiffness usually involves the [[jaw]] ([[lockjaw]]) and [[neck]] and then becomes generalized. C. tetani is a slender, [[gram-positive]], [[anaerobic]] rod that may develop a terminal [[spore]], giving it a drumstick appearance. The [[organism]] is sensitive to heat and cannot survive in the presence of [[oxygen]]. The spores, in contrast, are very resistant to heat and the usual [[antiseptics]]. They can survive [[autoclaving]] at 249.8°F (121°C) for 10–15 minutes. The spores are also relatively resistant to [[phenol]] and other [[chemical]] agents. The spores are widely distributed in soil and in the [[intestines]] and [[feces]] of horses, sheep, cattle, dogs, cats, rats, guinea pigs, and chickens. Manure-treated soil may contain large numbers of spores. 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]]. C. tetani produces two exotoxins, [[tetanolysin]] and [[tetanospasmin]]. The function of tetanolysin is not known with certainty. Tetanospasmin is a [[neurotoxin]] and causes the clinical manifestations of tetanus. On the basis of weight, tetanospasmin is one of the most potent toxins known. The estimated minimum human [[lethal dose]] is 2.5 nanograms per kilogram of body weight (a nanogram is one billionth of a gram), or 175 nanograms for a 70-kg (154lb) human.
+Tetanus is caused by an [[exotoxin]] from [[Clostridium tetani]] that leads to [[acute]], often [[fatal]] illness. Generalized, widespread [[rigidity]] and [[skeletal muscle]] [[spasms]] are common presentations of tetanus. The muscle stiffness begins from the [[jaw]] ([[lockjaw]]) progressing to the [[neck]] and then becoming generalized. [[C. tetani]] is a terminal [[spore]] forming bacteria. The spores is very resistant to extremes of temperature and to the normally used [[antiseptics]]. The spores can be found in the soil as well as in the [[intestines]] and [[feces]] of cattle, dogs, sheep, horses, cats,  guinea pigs, rats, and chickens. The soil that has been treated with manure may contain huge amount of spores. Human adults related to agricultural work may also harbor the pathogen.
-{{#widget:SchemaSnippet}}
+===Pathogenesis===
+*C. tetani gains access to the human body through a [[wound]].
+*The spores [[germinate]], because of their [[anaerobic]] character.
+*Toxins are produced and spread through the [[blood]] and [[lymphatics]].
+*C. tetani produces two exotoxins
+**[[Tetanolysin]], whose function is not well understood and
+**[[Tetanospasmin]] which is a [[neurotoxin]] and is responsible for the clinical symptoms of tetanus. Tetanospasmin among the most potent toxins with respect to weight.
+***The minimum [[lethal dose]] for humans, according to an estimate, is around 2.5 nanograms per kg of body weight  or 175 nanograms for an individual who weighs 70-kg (154lb).
+*The release of various [[neurotransmitters]] that cause inhibition is altered by the tetanus toxin.
+*This intern leads to an unopposed contraction of the muscles which manifests as a spasm.
+*The autonomic nervous system is also targeted leading to a seizure.
 [[Image:Clostridium tetani bacteria.jpg|center|thumb|Group of Clostridium tetani bacteria, responsible for causing tetanus in humans]]
-C. tetani usually enters the body through a [[wound]]. In the presence of [[anaerobic]] (low oxygen) conditions, the spores [[germinate]]. Toxins are produced and disseminated via [[blood]] and [[lymphatics]]. [[Toxins]] act at several sites within the [[central nervous system]], including [[peripheral]] motor end plates, [[spinal cord]], and [[brain]], and in the [[sympathetic nervous system]]. The typical clinical manifestations of tetanus are caused when tetanus toxin interferes with release of [[neurotransmitters]], blocking inhibitor impulses. This leads to unopposed muscle contraction and spasm. Seizures may occur, and the autonomic nervous system may also be affected.
 ==References==