Question

Explain how tetanospasmin functions to cause disease.

Short answer

Tetanospasmin causes tetanus by entering the body through wounds, binding to motor neuron terminals, traveling to the CNS, and inhibiting inhibitory neurotransmitters, resulting in continuous muscle contractions.

Step-by-step solution

Identify the toxin

Tetanospasmin is a toxin produced by the bacterium Clostridium tetani. This bacterium is responsible for the disease tetanus.

Describe the entry into the body

Tetanospasmin enters the body through wounds or cuts that are contaminated with Clostridium tetani spores.

Explain the initial binding

Once inside the body, tetanospasmin binds to motor neuron terminals at the neuromuscular junction.

Describe the transport

After binding, tetanospasmin is internalized and transported retrogradely along the axon to the central nervous system (CNS).

Explain the inhibition mechanism

Within the CNS, tetanospasmin blocks the release of inhibitory neurotransmitters such as glycine and gamma-aminobutyric acid (GABA) by cleaving a protein called synaptobrevin.

Describe the result of inhibition

By inhibiting these neurotransmitters, tetanospasmin causes a failure to regulate motor neuron activity, leading to continuous muscle contractions or spasms.

Summarize the disease symptoms

The continuous muscle activity results in severe muscle stiffness and spasms, which are characteristic symptoms of tetanus.

Key concepts

Clostridium tetani

Clostridium tetani is an anaerobic bacterium, meaning it thrives in low-oxygen environments.
This bacterium produces a potent neurotoxin called tetanospasmin.

Clostridium tetani is typically found in soil, dust, and animal feces, making contamination of wounds possible.
When it enters the body through cuts or puncture wounds, it can lead to tetanus, a serious condition.

The spores of Clostridium tetani are highly resilient and can survive in harsh conditions for extended periods, waiting for an opportunity to infect a host.
Understanding the source and nature of Clostridium tetani helps in effective prevention and treatment.

Neuromuscular Junction

The neuromuscular junction is a critical communication point between nerves and muscles.
When a motor neuron fires, it releases neurotransmitters across this junction, signaling the muscle to contract.

Tetanospasmin, the toxin produced by Clostridium tetani, targets this junction, disrupting normal muscle control.
This especially affects the motor neuron terminals where the toxin binds initially.

The functioning of neuromuscular junctions is essential for voluntary muscle movements.
Any disruption here, like the one caused by tetanospasmin, can lead to severe muscle spasms and rigidity.

Inhibitory Neurotransmitters

Inhibitory neurotransmitters, such as glycine and gamma-aminobutyric acid (GABA), play a key role in controlling muscle activity.
They help relax muscles by inhibiting excessive nerve signals.

Tetanospasmin prevents the release of these neurotransmitters by cleaving synaptobrevin, a necessary protein.
This inhibition leads to the continuous firing of motor neurons.

Without inhibitory neurotransmitters, muscles are unable to relax.
This constant state of contraction causes the painful and severe muscle spasms seen in tetanus.

Tetanus Symptoms

Tetanus is characterized by persistent muscle stiffness and spasms, often starting in the jaw (lockjaw) and progressing to other body parts.

This happens because tetanospasmin stops the muscle relaxation signals in the nervous system.
If left untreated, these spasms can affect breathing, posing a life-threatening condition.

Other symptoms include difficulty swallowing, arching of the back, muscle rigidity, and rapid heart rate.
Tetanus requires prompt medical treatment to prevent severe complications.