Clostridium tetani (Tetanus)

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Clostridium tetani (Tetanus)



Clostridium tetani (Tetanus)


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USMLE® Step 1 questions

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Clostridium tetani (Tetanus)

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USMLE® Step 1 style questions USMLE

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A 36-year-old woman is brought to the emergency department by a friend for evaluation of muscle pain. The patient is currently undomiciled and has limited access to medical care. A few days ago, the patient developed painful muscle spasms as well as difficulty opening her mouth. Temperature is 37.8 °C (100.0 °F), blood pressure is 127/68 mmHg, and pulse is 100/min. On physical examination, the patient is unable to open her jaw and facial expression appears fixed. There is also backward arching of the neck and head. Multiple deep puncture wounds and superficial lacerations are present on the bilateral feet. Which of the following proteins is targeted by the toxin responsible for this patient’s symptoms?  

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Clostridium tetani p. , 136

exotoxin production p. 130

spore formation p. 129


Clostridium tetani p. , 136

Risus sardonicus

Clostridium tetani p. , 136

Spastic paralysis

Clostridium tetani p. , 136

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Tetanus means “being taut”, which is a good description of the disease caused by bacteria called Clostridium tetani.

Clostridia, as a family, are obligate anaerobes, meaning that oxygen is toxic to them. In nature, they thrive in deep, compact soil, and when they feel the stress of fresh oxygenated air, they often produce spores, which are metabolically inert and extremely resilient to the environment.

Then, when environmental conditions improve, the spores are able to sprout into fully fledged Clostridia.

When doing a Gram stain, Clostridium tetani stains purple, or Gram positive, and it’s a bacillus, meaning that it looks like a big cylinder or rod under the microscope.

Clostridium tetani is notorious for one of its toxins, called tetanospasmin, which can severely disrupt the neuromuscular system of mammals.

Tetanospasmin works by entering special inhibitory neurons called Renshaw cells.

Once they get inside, tetanospasmin cleaves SNARE proteins, which are proteins that pull vesicles that are loaded with neurotransmitters to the neuron membrane.

When the SNARE proteins are cleaved, it prevents the release of inhibitory neurotransmitters, like glycine and GABA.

You can think of SNARE proteins as the rails and the vesicles as trains that are loaded with neurotransmitters.

And tetanospasmin destroys the “rails”, so that the “trains” can’t move.

The role of Renshaw cells and inhibitory neurotransmitters is to fine tune the action of the alpha motor neuron, which is in charge of sending the actual signal for contraction to the muscle.

In tetanus, Renshaw cells fail to work, and the alpha motor neuron keeps firing without any inhibitory control, causing muscle rigidity and spasm.

Spores of Clostridium tetani are most often introduced into the body through penetrating trauma, like a puncture wound. Puncture wounds are usually anaerobic and warm, and are therefore optimal for growth of Clostridium tetani.

And an important point is that the Clostridium spores can get introduced from dirty wounds like a rusty nail, as well as clean wounds like a recently washed kitchen knife.


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