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The pathogenesis of tetanus is as follows: Clostridium tetani (C. tetani) spores usually enter the body through a wound or breach in the skin. In the presence of anaerobic conditions, the spores germinate and produce two toxins: oxygen-labile hemolysin also called tetanolysin, and a plasmid-encoded, heat-labile neurotoxin called tetanospasmin. The plasmid carrying the gene for tetanospasmin is non-conjugative. The toxin binds to nerve endings at the site of injury and is transported by retrograde axonal flow to the spinal cord. The toxin then blocks the release of inhibitory neurotransmitters, leading to unopposed muscle contraction.