Kinetics of
the toxin: The toxin is
relatively heat labile being destroyed at 65°C in 5 minutes however, it is
stable in dry state. It is not absorbed
from the gastrointestinal tract and may be inactivated by gastric juice meaning
that there are no receptors for it in the GIT lumen, and the chemical makeup of
the toxin cannot withstand acidic pH. Treatment of this toxin with formaldehyde results in
polymerization of toxin and results into formation of a product (toxoid) which
is non-toxic but antigenic. This is one
basis for prevention of tetanus, where the polymer is formed between
formaldehyde and tetanus toxoid.
Mode of
action of the toxin: The molecular basis for
the action of tetanospasmin is not clearly known. The site of action is the
nerve endings that are high in toxin fixing capacity. The toxin specifically affects the synaptic
junction of nerves by preventing the inhibition or erasing of nerve impulses
once they have crossed the synaptic junctions.
In this case, the nerve continues to send impulses, a condition that
results in spasmodic contraction (tetany) of the involved muscles.
Symptoms of
toxicity by clostridium tetani: Early
symptoms are muscle stiffness with the muscles of the jaw often developing
spasms first. This condition gives the
disease its common name of lockjaw. As
the disease progresses, spasms develop in other muscles. The spasms may be brief but can occur
frequently and cause great pain and exhaustion. Respiratory complications are many and death
rate is high, especially in young children and elderly persons.
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