tetanus bacteria fester in deep, dark wounds, but how do they travel in neural tissue

Answer 1

Tetanus bacteria, known as Clostridium tetani, do not travel directly in neural tissue. Instead, they produce a potent neurotoxin called tetanospasmin, which is responsible for the clinical symptoms associated with tetanus, such as muscle stiffness and spasms. This toxin travels from the site of infection to the nervous system through different pathways:

1. Retrograde axonal transport: Tetanospasmin can bind to specific receptors on the nerve terminals at the site of infection. After binding, the toxin is taken up by the nerve cell and transported within the nerve axon (long projection of the neuron) towards the central nervous system (CNS). This process is called retrograde axonal transport and occurs in both motor and sensory nerves.

2. Hematogenous spread: Tetanospasmin can also enter the bloodstream, either directly or through the lymphatic system. This allows the toxin to circulate throughout the body and reach tissues with high blood flow, including the nervous system. However, this mode of transport is considered less relevant for the toxin's access to the CNS, as the blood-brain barrier limits the entry of the toxin into the brain.

Once in the CNS, tetanospasmin acts upon inhibitory interneurons, which play a key role in regulating the balance of excitation and inhibition in the nervous system. By blocking the release of inhibitory neurotransmitters, the neurotoxin disrupts this balance, leading to increased excitation and the characteristic muscle stiffness and spasms observed in tetanus.