Clostridium tetani: Difference between revisions
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=== | === Characteristics === | ||
''Clostridium tetani'' | ''Clostridium tetani'' is a rod-shaped, [[Gram-positive|gram-positive]] bacillus that forms a terminal spore, which is responsible for its drumstick appearance<ref>https://www.cdc.gov/vaccines/pubs/pinkbook/tetanus.html#tetani</ref> . It is the deadliest bacteriological [[Pathogen|pathogen]] after ''[[Clostridium botulinum|Clostridium botulinum]] ''causing [[Tetanus|tetanus]]. The organism is sensitive to changes in heat and cannot survive in the presence of [[Oxygen|oxygen]]. Unlike the organism, the resulting spores are resistant to heat and antiseptics. This spore forming organism is commonly found in the soil or in the [[Gastrointestinal tract|gastrointestinal tract]] of animals, and is obligated to [[Anaerobic|anaerobic]] conditions where it can produce 2 distinctive [[Exotoxins|exotoxins]]<ref>https://www.cdc.gov/vaccines/pubs/pinkbook/tetanus.html#tetani</ref>: | ||
*Tetanolysin | *Tetanolysin | ||
*Tetanospasmin | *Tetanospasmin – is a neurotoxin that affects the [[Nervous system|nervous system]] of victims. | ||
Tetanospasmin is a | Tetanospasmin is a 150 kDa [[Peptide|peptide]] composed of two chains joined by a [[Disulphide bond|disulphide bridge]]; a heavy chain (B) and a light chain (A). The heavy chain is involved in the process of binding to neuronal cells and internalisation, whereas the light chain is a [[Zinc|zinc]] metalloprotease that cleaves the [[Protein|protein]] synaptobrevin, which prevents the release of certain inhibitory [[Neurotransmitters|neurotransmitters]]<ref>https://www.ncbi.nlm.nih.gov/pubmed/7916455</ref>. | ||
=== | === Pathophysiology === | ||
A deep puncture wound infected with | A deep puncture wound infected with ''C. tetani'' will have [[Tetanus|tetanus]] spores that germinate and release tetanospasmin into the bloodstream. Then the [[Toxin|toxin]] enters the [[Motor neuron|motor neurons]] via the terminal buds, travels up the [[Axon|axon]] towards the cell body located in the [[Spinal cord|spinal cord]]. Likewise, inhibitory interneurons are located at the spinal cord, which controls and prevent motor neurons from constantly firing. However, tetanospasmin blocks this mechanism as it gets internalised into these inhibitory interneurons and interferes with the production of inhibitory neurotransmitters [[Glycine|glycine]] and [[GABA|GABA]] by cleaving a vesicle-associated membrane protein (synaptobrevin). Therefore, these [[Motor neuron|motor neurons]] lose their inhibitory control leading to the continual release of [[Acetylcholine|acetylcholine]] neurotransmitters, causing several [[Muscles|muscles]] to simultaneously and constantly contract. This is also known as a state of spastic paralysis<ref>https://www.gtac.edu.au/animation-gallery/clostridium-tetani-and-tetanus/</ref><ref>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3564069/</ref>. | ||
=== | === References === | ||
<references /> | <references /> |
Latest revision as of 13:13, 17 November 2018
Characteristics
Clostridium tetani is a rod-shaped, gram-positive bacillus that forms a terminal spore, which is responsible for its drumstick appearance[1] . It is the deadliest bacteriological pathogen after Clostridium botulinum causing tetanus. The organism is sensitive to changes in heat and cannot survive in the presence of oxygen. Unlike the organism, the resulting spores are resistant to heat and antiseptics. This spore forming organism is commonly found in the soil or in the gastrointestinal tract of animals, and is obligated to anaerobic conditions where it can produce 2 distinctive exotoxins[2]:
- Tetanolysin
- Tetanospasmin – is a neurotoxin that affects the nervous system of victims.
Tetanospasmin is a 150 kDa peptide composed of two chains joined by a disulphide bridge; a heavy chain (B) and a light chain (A). The heavy chain is involved in the process of binding to neuronal cells and internalisation, whereas the light chain is a zinc metalloprotease that cleaves the protein synaptobrevin, which prevents the release of certain inhibitory neurotransmitters[3].
Pathophysiology
A deep puncture wound infected with C. tetani will have tetanus spores that germinate and release tetanospasmin into the bloodstream. Then the toxin enters the motor neurons via the terminal buds, travels up the axon towards the cell body located in the spinal cord. Likewise, inhibitory interneurons are located at the spinal cord, which controls and prevent motor neurons from constantly firing. However, tetanospasmin blocks this mechanism as it gets internalised into these inhibitory interneurons and interferes with the production of inhibitory neurotransmitters glycine and GABA by cleaving a vesicle-associated membrane protein (synaptobrevin). Therefore, these motor neurons lose their inhibitory control leading to the continual release of acetylcholine neurotransmitters, causing several muscles to simultaneously and constantly contract. This is also known as a state of spastic paralysis[4][5].
References
- ↑ https://www.cdc.gov/vaccines/pubs/pinkbook/tetanus.html#tetani
- ↑ https://www.cdc.gov/vaccines/pubs/pinkbook/tetanus.html#tetani
- ↑ https://www.ncbi.nlm.nih.gov/pubmed/7916455
- ↑ https://www.gtac.edu.au/animation-gallery/clostridium-tetani-and-tetanus/
- ↑ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3564069/