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Bacterial structure and functions
Bacillus anthracis (Anthrax)
Bacillus cereus (Food poisoning)
Corynebacterium diphtheriae (Diphtheria)
Clostridium botulinum (Botulism)
Clostridium difficile (Pseudomembranous colitis)
Clostridium tetani (Tetanus)
Streptococcus agalactiae (Group B Strep)
Streptococcus pyogenes (Group A Strep)
Bartonella henselae (Cat-scratch disease and Bacillary angiomatosis)
Legionella pneumophila (Legionnaires disease and Pontiac fever)
Salmonella typhi (typhoid fever)
Yersinia pestis (Plague)
Vibrio cholerae (Cholera)
Bordetella pertussis (Whooping cough)
Francisella tularensis (Tularemia)
Haemophilus ducreyi (Chancroid)
Mycobacterium tuberculosis (Tuberculosis)
Mycobacterium avium complex (NORD)
Gardnerella vaginalis (Bacterial vaginosis)
Coxiella burnetii (Q fever)
Ehrlichia and Anaplasma
Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species
Borrelia burgdorferi (Lyme disease)
Borrelia species (Relapsing fever)
Treponema pallidum (Syphilis)
0 / 13 complete
0 / 2 complete
exotoxin production p. 130
spore formation p. 129
Clostridium tetani p. , 136
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.
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