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  Oct 17, 2018
Tetanus Pathophysiology
Tetanus Pathophysiology
  Oct 17, 2018

Tetanus is an infectious disease caused by Clostridium tetani bacteria. The active anaerobic bacteria lead to the production of a tetanus toxin, which enters the nervous system via lower motor neurons and travels up to the spinal cord and brain stem.

The presence of the toxin can lead to the initiation of characteristic symptoms of tetanus, such as jaw tightness (lockjaw), dysphagia, opisthotonus and other muscular spasms. This is due to the effect the toxin exhibits on certain parts of the nervous system and neurotransmitters, which interfere with muscular contraction in the body.

Causative Bacteria

The causative bacteria, Clostridium tetani, are widely present in the surrounding environment, particularly in dirt, dust and animal excrement. The spore-producing bacteria can enter the bloodstream via a wound to the skin and germinate in the ideal anaerobic conditions of a deep wound.

The spores then produce two toxins known as tetanolysin and tetanospasmin. Tetanolysin is a hemolysin and does not have any known pathological activity to date. Tetanospasmin, on the other hand, is a potent toxin that enters into the nervous system and has several effects that lead to the symptoms of the disease known as tetanus.

Tetanus is a non-communicable disease and, unlike many other infectious diseases, it is safe to come in close contact with someone that is affected by tetanus. This is because the bacteria need to enter the body via a wound that provides the bacteria with access to the bloodstream. Therefore, only individuals with significant wounds are likely to contract the infection and person-to-person infections are rare.

Tetanus Toxin

It is the tetanus toxin tetanospasmin, which is produced by the causative bacteria in the organism, that is responsible for the symptoms of muscular rigidity and spasms that characterize the disease.

The tetanus toxin enters the nerve terminals through the lower motor neurons, which are usually responsible for activating voluntary muscular movements. It is then transported via the axons to the spinal cord and brainstem.

The toxin then moves throughout the nervous system trans-synaptically into the nerve terminals responsible for the release of inhibitory neurotransmitters. If this vesicular process becomes blocked, the ability to inhibit lower motor neurons is disrupted, which can result in muscle rigidity and spasm.

Tetanus toxin inhibits normal nervous function due to its action as a zinc-dependent metalloproteinase that targets VAMP, a protein that regulates the neurotransmitter release from nerve endings.

The first symptoms to be noted by individuals affected by tetanus are usually localized to the area of the infection and may include flaccid paralysis. This is due to interference at the neuromuscular junction with the release of acetylcholine. From this point, the toxin travels across synapses to inhibitory GABAergic or glycinergic neurons that are responsible for the lower motor neuron activity. The toxin then targets VAMP to inhibit the release of neurotransmitters and affect the function of the motor neurons.