The pathogenicity of tetanus is primarily associated with a neurotoxin.

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Multiple Choice

The pathogenicity of tetanus is primarily associated with a neurotoxin.

The main idea here is that tetanus disease is driven by a toxin that targets the nervous system. Clostridium tetani produces tetanospasmin, a potent neurotoxin, which is the key factor in the illness. After the wound, the toxin travels into the central nervous system and disrupts inhibitory signaling by cleaving SNARE proteins, which blocks the release of GABA and glycine from inhibitory neurons. With inhibition removed, motor neurons fire too much, leading to the characteristic muscle rigidity and spasms, such as lockjaw and opisthotonos. This toxin-centered mechanism explains why disease severity correlates with toxin activity and why vaccination with tetanus toxoid (which neutralizes toxin) prevents disease. While the bacteria must be present to produce the toxin, the pathogenic effects come from the toxin’s action in the nervous system, not from direct bacterial damage to tissues.

The main idea here is that tetanus disease is driven by a toxin that targets the nervous system. Clostridium tetani produces tetanospasmin, a potent neurotoxin, which is the key factor in the illness. After the wound, the toxin travels into the central nervous system and disrupts inhibitory signaling by cleaving SNARE proteins, which blocks the release of GABA and glycine from inhibitory neurons. With inhibition removed, motor neurons fire too much, leading to the characteristic muscle rigidity and spasms, such as lockjaw and opisthotonos. This toxin-centered mechanism explains why disease severity correlates with toxin activity and why vaccination with tetanus toxoid (which neutralizes toxin) prevents disease. While the bacteria must be present to produce the toxin, the pathogenic effects come from the toxin’s action in the nervous system, not from direct bacterial damage to tissues.

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