Clostridium tetani (Tetanus)
24,101views

00:00 / 00:00
Assessments
Flashcards
0 / 13 complete
USMLE® Step 1 questions
0 / 2 complete
Flashcards
Clostridium tetani (Tetanus)
0 of 13 complete
Questions
USMLE® Step 1 style questions USMLE
0 of 2 complete
External References
First Aid
2024
2023
2022
2021
Clostridium tetani p. , 136
exotoxin production p. 130
spore formation p. 129
Lockjaw
Clostridium tetani p. , 136
Risus sardonicus
Clostridium tetani p. , 136
Spastic paralysis
Clostridium tetani p. , 136
Transcript
Content Reviewers
Contributors
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.
In fact, any kind of puncture wound or cut brings along a risk of tetanus.
Tetanus usually starts with a delayed onset, about a week to a month after the initial injury.
In the most common form of tetanus, called generalized tetanus, the spasms begin in the face muscles, most notably the lower jaw, and from there the spasms spread throughout the body.
The spasms are sudden, powerful, long lasting and very painful contractions of muscles.
These contractions are so powerful, that they can result in muscle tears or bone fractures.
The classical “tetanic triad” of symptoms involves trismus, or lockjaw, which are mild to severe spasms of the lower jaw, risus sardonicus, or “Sardinian grin”, which is an abnormal looking, sustained grin, caused by facial muscle spasm, and opisthotonos, which is a severe simultaneous spasm of all muscles in the body simultaneously, resulting in a high arched back and patient resting on his heels and the back of his head.
Tetanus only affects skeletal muscle, so smooth muscle and cardiac muscle continue to function normally.
Other symptoms of tetanus involve sympathetic overactivity, which causes drooling, excessive sweating, fever, difficulty swallowing, breathing problems, and irregular urination and defecation.
Rarer forms of the disease include the local tetanus, where the persistent spasm will only be localized around the area of the injury.