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The symptoms of tetanus are due to
Encapsulated Clostridium tetani.
The growth of Clostridium tetani in a wound.
Hemolysins produced by Clostridium tetani.
An exotoxin produced by Clostridium tetani.
All of these.
Hi, Thanks for posting in HCM. Tetanus is an infection characterized by muscle spasms. It is caused by an infection with the bacterium Clostridium tetani. Signs and symptoms of tetanus may appear anytime from a few days to several weeks after tetanus bacteria enter your body through a wound. The average incubation period is seven to eight days. C. tetani is an anaerobic bacterium, it and its endospores thrive in environments that lack oxygen. The symptoms of tetanus is caused due to exotoxin (neurotoxin) produced by the organism. Tetanus toxin initially binds to peripheral nerve terminals and is transported within the axon and across synaptic junctions until it reaches the central nervous system. It becomes rapidly fixed to gangliosides at the presynaptic inhibitory motor nerve endings and block the release of inhibitory neurotransmitters glycine and gamma-aminobutyric acid (GABA) across the synaptic cleft. Due to this, the nervous impulses cannot be checked by normal inhibitory mechanisms which leads to production of generalized muscular spasms characteristic of tetanus. Hope the information provided would be useful. Best wishes.
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Suggest The Cause For Tetanus Infection
Hi, Thanks for posting in HCM. Tetanus is an infection characterized by muscle spasms. It is caused by an infection with the bacterium Clostridium tetani. Signs and symptoms of tetanus may appear anytime from a few days to several weeks after tetanus bacteria enter your body through a wound. The average incubation period is seven to eight days. C. tetani is an anaerobic bacterium, it and its endospores thrive in environments that lack oxygen. The symptoms of tetanus is caused due to exotoxin (neurotoxin) produced by the organism. Tetanus toxin initially binds to peripheral nerve terminals and is transported within the axon and across synaptic junctions until it reaches the central nervous system. It becomes rapidly fixed to gangliosides at the presynaptic inhibitory motor nerve endings and block the release of inhibitory neurotransmitters glycine and gamma-aminobutyric acid (GABA) across the synaptic cleft. Due to this, the nervous impulses cannot be checked by normal inhibitory mechanisms which leads to production of generalized muscular spasms characteristic of tetanus. Hope the information provided would be useful. Best wishes.