Let’s learn about tetanus!

A few months ago, I went to visit some college buddies in Washington DC. We hiking around Rock Creek Park, to check out the mysterious Capitol Stones–ruins and rubble from the old dome on the Capitol Building. They were tough to find, but we succeeded!

As we climbed around, we found some stones with nails and rebar protruding. Upon seeing this, I joked, “uh oh, watch out for tetanus!” One of my friends replied, “oh no, there wouldn’t be tetanus there. Tetanus likes to live in wood and in tight crevices, you wouldn’t likely encounter it on exposed metal like this. A nail recently pulled from wood however…”

This. Blew. My mind.

I realized then that I had no knowledge of tetanus, whatsoever, other the excruciating agony that is a booster shot. What is tetanus? Why is it so feared if it’s much harder to come across than we may be inclined to think? Let’s find out!

Tetanus, the condition, is caused by a bacteria Clostridium tetani, a bacillus (rod-shaped) bacteria found in soil, dust and poop. It’s an anaerobic bacteria, which is why you wouldn’t find it in oxygen-exposed surfaces like that rebar in Rock Creek Park. However, it would thrive in a nice, deep puncture wound, like that time when the nail when through Homer Simpson’s foot (“fiddle dee dee, that will require a tetanus shot!”). Deep puncture wounds like that don’t have a lot of air, which encourages C. tetani spores to develop.

If such sporulation should occur, the bacteria develops, invades cells and becomes virulent (uses the cells to reproduce more if itself). The bacteria grow in number, and the chemicals they produce start to affect the organism on a larger scale.

C. tetani produces a neurotoxin called tetanospasmin, which slowly and effectively shuts down nervous system activity. You can, more or less, divide neurons into two classes. There’s excitatory neurons, cells that make all the cells they talk to more likely to also talk. There’s also inhibitory neurons, which make the cells they talk to be quiet. Knowing when talk and when to be quiet is key nervous tsystem function. Diseases like Parkinson’s disease, which can be characterized by an inability to stop tremors in the body, among other awful symptoms, is an example of a system that should be quiet and isn’t.

These classes–excitatory and inhibitory–are defined by the chemicals these neurons produce. Inhibitory neurons produce GABA, which attaches to nearby neurons and encourages silence. Shhhh. Tetanospasmin blocks the production of GABA, specifically in neurons that interface with muscles (the neuromuscular junctioooooon! ::Air horn noises::) The inability to turn off here, means that muscles don’t stop muscling. In other words, spasms. Painful ones.

These muscles promote transport of tetanospasmin to the spinal cord, where it breaks down synaptobrevin, a certain molecule that helps neurons release vesicles (tiny chemical-filled bubbles), effectively stopping communication between neurons. This happens in GABAergic (inhibitory) cells, specifically.

It gets crazier. Tetanus doesn’t just target any muscles, it targets muscles if the neck and jaw. Wassup widdat? Well, it doesn’t. These are the places people experience extreme pain and visible affect, resulting in a focus on the neck and jaw. General tetanus actually produces not only lockjaw ( a spasm of the neck and jaw), but also dysphagia (inability to swallow), opisthotonus (arched neck and back), as well as spasms of the vocal chords, and respiratory and abdominal muscles. Spasms of the respiratory and abdominal muscles can arrest breathing and lead to death by asphyxiation. Yiiiiikes.

Ok so you have tetanus, and you’re feeling… probably extremely awful. What will doctors do? Well, there’s a nonzero chance they’ll give you botulism. Yeah. You read right. Botulism is another bacteria that produces a cocktail of neurotoxins, collectively called botulinum. Botulinum stops neurons from producing acetylcholine, which is predominantly excitatory (making nearby cells talk), but can act as either an excitatory and inhibitory chemical (this is biology, what did you expect, clean delineation?). But wait, doesn’t botulinum sound familiar? Why, yes. Yes it does. You may know botulinum from such things as Botox. Botulinum acts on muscles, causing contraction. When a subclass of botulinum (botulinum A) is applied to muscles just under the skin, it can make the muscles contract, removing appearance of wrinkles for the duration of its presence in the body.

In the case of tetanus, botulinum can be used to counter lockjaw and dysphagia, by being applied to muscles in the area. Like tetanospasmin, botulinum attacks synaptobrevin, preventing vesicle release, but it does it differently, it’s not as good at it, and it affects a certain segment of motor neurons (the neurons that interface muscles via the neuromuscular junction ::more air horn::). So basically, it somehow stops a whole-cell arrest of vesicle release, allowing some GABA to get out and cause the muscles to relax. Aahhh..

If you’re confused, it’s ok. I am, too. The mechinsm isn’t deeply known, and the effect is really counterintuitive. But that’s biology, two spasm-inducing toxins together relax spasms. Go figure!

Well, that’s what tetanus is. Now you and I both know, go forth and nerd out when it’s time to get your booster! And remember when your muscle is aching, that that is a weakened bacteria, and that’s only a ababy spasm, a fraction of the discomfort you’d encounter if you ever contracted tetanus forreal forreal. Be safe!

Primary literature

1. 2. 3.

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