Clostridium, Actinomyces israelii, Nocardia asteroides, Aeromonas, Plesiomonas Flashcards
Describe the physical structure of Clostridium
G+ Rods, Usually Rounded Ends
Pairs/Short Chains
Sporulatin
Describe the oxygen sensitivity of Clostridium
Anerobic
Clinical presentation of Clostridium botulinum
18-24 hour incubation
Bilateral Cranial Nerve Palsies with Progressive Descending Flaccid Paralysis
How do people die of Clostridium botulinum?
Involvement with heart or diaphragm
Main sources of Clostridium botulinum infection?
Home-Canned Foods, Rarely commercial
Entry Woulds, like needles (botox, black tar heroin)
How does Clostridium botulinum manifest in children?
Rapidly colonizes gut, replaces developing flora
Floppy Baby Syndrome
Caused by spores in honey
Pathogenesis of Clostridium botulinum?
AB neurotoxin
- B binds neuron end plates, A blocks ACh release
No ACh = Flaccid Muscle Paralysis
How does Clostridium botulinum block ACh release?
Cleaving synaptobrevin
How is Clostridium botulinum controlled?
Use Antitoxin from CDC as early as possible
Clinical presentation of Clostridium tetani
Rigid Paralysis
Eventually Death from Inability to Breathe
Epidemiology of Clostridium tetani?
Spores in soil/feces
Introduces by fomites in skin
How do neonates get Clostridium tetani?
Umbilical stump infection
Pathogenesis of Clostridium tetani?
A-B neurotoxin, tetanospasmin
- Absorbed at neuromusc. junction, retrograde transport to motor neuron - Binds irreveribly to and re-uptaken by presynaptic mem. of inhib neurons - Cleaves synaptobrevin, no GABA release
How is Clostridium tetani controlled?
DTaP, Tdap
What can you do for a tetanus patient?
Tetanus Immune Globulin antitoxin avoid stimulation Early tracheostomy to prevent laryngospasm suffication Muscle Relaxants Metronidazole
Describe the presentation of Clostridium perfringens
Infected wound suppurating
Foul Discharge, Tissue Necrosis
Toxemia, Shock Death
Also – can present as food poisoning –> gut necrosis
Epidemiology of Clostridium perfringens
Traumatic Tissue Injury, Esp if anaerobic conditions
Why is Clostridium perfringens typically polymicrobial?
Other infection will produce the anoxic environemnt Clostridium perfringens requires
Pathogenesis of Clostridium perfringens?
Extracellular enzyme secretions destroy tissue, allow invasion
- alpha toxin
- hyaluronidase, collagenase
- beta-toxin
- enterotoxin
Gas from ferm. causes tissue distention, compressed vessels