How the Toxin Works

Two toxins are released by the bacilli:

Tetanolysin, which causes local tissue damage and may help to optimise conditions for the organism but has no known role in the pathogenesis of the disease.

Tetanospasmin, which is the potent neurotoxin that causes tetanus.

The LD50 of tetanus toxin has been measured to be around 2.5-3ng/kg (albeit in mice), making it the second deadliest toxin known to man after botulinum toxin. [7]

Tetanospasmin enters nerve endings at the neuromuscular junction, by direct infiltration from infected muscle or systemically via vascular and lymphatic routes. Intraneural migration to the neurones of the spinal cord and brainstem follows, where it moves into inhibitory nerve terminals blocking release of neurotransmitters, particularly gamma-aminobutyric acid (GABA) and glycine. [8]

This leads to uncontrolled motor neuron activity, increased muscle tone, and spasms. Spasms may cause dysphagia, respiratory distress, poor suckling in infants, abdominal rigidity, long bone fractures and joint dislocations.

Tetanospasmin also affects neurones of the autonomic nervous system leading to cardiovascular instability.

If the distance from the entry point to the central nervous system is shorter, the onset of symptoms will be quicker, for example in cases with head and neck wounds.

Learning bite

Intra-neural toxin cannot be neutralised and so a patient’s condition may continue to deteriorate after the onset of treatment. Recovery requires new synapse formation which takes 2-4 months.