Clostridium tetani: Difference between revisions
imported>Sheri Seidenfeld |
imported>Sheri Seidenfeld |
||
| Line 10: | Line 10: | ||
==Pathology== | ==Pathology== | ||
''Clostridium tetani'' spores enter body tissue through wounds, lacerations and burns, settling in dead cells that lack oxygen. Initially unnoticed, the spores are then able to germinate and spread long before diagnosis and pursuit of treatment. All identified strains have been found to produce a common toxin called tetanospasmin. The potent neurotoxin blocks the release of necessary [[neurotransmitter]]s in the central nervous system's transmission of inhibitory nerve impulses. <ref>http://bioweb.uwlax.edu</ref>. It is the inhibitory | ''Clostridium tetani'' spores enter body tissue through wounds, lacerations, and burns, settling in dead cells that lack oxygen. Initially unnoticed, the spores are then able to germinate and spread, long before diagnosis and pursuit of treatment. All identified strains have been found to produce a common toxin called tetanospasmin. The potent neurotoxin blocks the release of necessary [[neurotransmitter]]s in the central nervous system's transmission of inhibitory nerve impulses. <ref>http://bioweb.uwlax.edu</ref>. It is the inhibitory neuron messages that allow the muscles of the body to relax by halting the release of [[acetylcholine]] from exitatory neurons, which stimulate muscle contraction. The resulting effect in humans begins with muscle spasms at the sight of infection. As the infection spreads along neurons of the spinal chord and brain, it could lead to spastic paralysis and may be fatal. The most recognized associated manifistation of the disease is trismus, or lockjaw. The muscles and nerves of the neck and jaw are commonly the first to be affected before spreading to other parts of the body. Death is usually the result of breathing difficulties that arise due to the spasms and lead to respiratory arrest. | ||
Tetanus has been known to take up to 10 years before manifestations | Tetanus has been known to take up to 10 years before manifestations may be observed. Aside from lockjaw, difficulty in swallowing, drooling, and persistent back spasms are among early signs. Later symtoms include perfuse sweating, hyperthermia, cardiac arrythmias and fluctuations in blood pressure. These manifestations indicate the toxic affects of both the somatic and autonomic nervous systems that involve both voluntary and involuntary muscle contractions, respectively. The disease can also be transferred to a fetus by a mother with no immunity through the placenta, where nutrients are absorbed into the blood of the developing baby via the umbilical chord. This is a neonatal infection and the baby is born with the disease <ref>http://student.ccbmd.edu</ref>. | ||
Revision as of 01:35, 19 April 2009
Description and Significance
Clostridium tetani is a rod-shaped, anaerobic, and endospore-forming bacterium that is responsible for the tetanus disease, a condition of the central nervous system affecting an estimated 350,000 people a year worldwide [1]. Single rods have terminal spherical endospores creating a "clubbed appearence" [2]. This bacterium is gram-positive, a characteristic shared by the other related species belonging to the Clostridium genus. The peptoidoglycan structure of the bacteria's cell wall allow it to retain the violet crystals in a gram stain. The resulting appearence under a microscope is often described as resembling a tennis racket or a collection of drumsticks. The organism is an obligate anaerobe found in soil and most often in animal feces.
Genome Structure
Cell Structure and Metabolism
Ecology
Pathology
Clostridium tetani spores enter body tissue through wounds, lacerations, and burns, settling in dead cells that lack oxygen. Initially unnoticed, the spores are then able to germinate and spread, long before diagnosis and pursuit of treatment. All identified strains have been found to produce a common toxin called tetanospasmin. The potent neurotoxin blocks the release of necessary neurotransmitters in the central nervous system's transmission of inhibitory nerve impulses. [3]. It is the inhibitory neuron messages that allow the muscles of the body to relax by halting the release of acetylcholine from exitatory neurons, which stimulate muscle contraction. The resulting effect in humans begins with muscle spasms at the sight of infection. As the infection spreads along neurons of the spinal chord and brain, it could lead to spastic paralysis and may be fatal. The most recognized associated manifistation of the disease is trismus, or lockjaw. The muscles and nerves of the neck and jaw are commonly the first to be affected before spreading to other parts of the body. Death is usually the result of breathing difficulties that arise due to the spasms and lead to respiratory arrest.
Tetanus has been known to take up to 10 years before manifestations may be observed. Aside from lockjaw, difficulty in swallowing, drooling, and persistent back spasms are among early signs. Later symtoms include perfuse sweating, hyperthermia, cardiac arrythmias and fluctuations in blood pressure. These manifestations indicate the toxic affects of both the somatic and autonomic nervous systems that involve both voluntary and involuntary muscle contractions, respectively. The disease can also be transferred to a fetus by a mother with no immunity through the placenta, where nutrients are absorbed into the blood of the developing baby via the umbilical chord. This is a neonatal infection and the baby is born with the disease [4].
The tetanus disease is relatively uncommon in North America and industrialized countries. The condition is more common in underdeveloped countries where immunizations are not widely available and agricultural regions where contact with animal excretion is likely.