The toxin acts at the site of interaction of the nerve and the muscle that it stimulates.

This is an area
known as the neuromuscular junction (Xy-Za et al.). In brief, the toxin acts on the human physiology by
amplifying the chemicals signals that are emitted from the nerve to the muscle. This results in the
muscle tightening in a spasm that becomes continuous (Xy-Za et al.) This process needs to be explained
in more detail.

In the first instance the bacteria produce a toxin knows as tetanospasmin. This toxin acts on or binds to
the motor nerves in the human system. It should also be noted that Clostridium tetani is an anaerobic
bacteria and that these bacteria multiply in contaminated wounds. (Xy-Za et al.). The incubation period
of these bacteria varies from three to twenty-one days. This difference is a result of the distance of the
site of the wound or injury through which the bacteria enter, from the central nervous system

(Xy-Za et al.). This is an important aspect of the physiology and process of the disease as, "The shorter
the incubation period, the higher the chance of death" (Xy-Za et al.).

In the presence of anaerobic conditions, the spores therefore germinate. The toxin released includes
both tetanolysin and the Neurotxin tetanospasmin. The latter toxin produced is disseminated through
the bloodstream and lymphatic system. The toxin is "…exclusively taken up by the neuromuscular
junction, where it migrates retrograde transynaptically at the rate 75-250mm/day, a process which takes
3-14 days… (Xy-Za et al.).

The toxin produced by the bacteria also "… enters the axons (filaments that extend from nerve cells),
and travels in the axon until it reaches the body of the motor nerve in the spinal cord or brainstem
"(Tetanus). This is a process known as retrograde intraneuronal transport. The toxin then affects the
space between the nerve cells known as the synapse. The synapse is responsible for the transmission of
signals among the nerve cells. It subsequently impacts the presynaptic nerve terminals and prevents the
release of certain inhibitory neurotransmitters such as glycine and gamma-aminobutyric acid (Tetanus).
This in turn causes the muscle to tightens and lock. This process is explained more fully in the following
quotation:

Its first effect on the motor ganglia of the cord is to render them hypersensitive, so that they are excited
by mild stimuli, which under ordinary conditions would produce no reaction. As the toxin accumulates
the reflex arc is affected, with the result that when a stimulus reaches the ganglia a motor discharge
takes place, which spreads by ascending and descending collaterals to the reflex apparatus of the whole
cord. As the toxin spreads it causes both motor hyper-tonus and hyper-excitability, which accounts for
the tonic contraction and the clonic spasms characteristic of tetanus. (Tetanus: Search Manual of
Surgery)

The Tetanus toxin in essence therefore interferes with the normal inhibitory signals from other nerves,
with an increase in the chemical signal to the motor nerve of the muscle. This subsequently causes the
muscle to tighten into a continuous spasm. Furthermore, "If tetanospasmin reaches the bloodstream or
lymphatic vessels from the wound site, it can be deposited in many different presynaptic terminals
resulting in the same effect on other muscles" (Tetanus). Put more concisely, "General muscle rigidity
arises from uninhibited afferent stimuli entering the central nervous system from the periphery" (Xy-Za
et al.). This disease also results in many complications; among which are… [