Flashcards in Clostridium, Actinomyces israelii, Nocardia asteroides, Aeromonas, Plesiomonas Deck (48)
Describe the physical structure of Clostridium
G+ Rods, Usually Rounded Ends
Describe the oxygen sensitivity of Clostridium
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?
- B binds neuron end plates, A blocks ACh release
No ACh = Flaccid Muscle Paralysis
How does Clostridium botulinum block ACh release?
How is Clostridium botulinum controlled?
Use Antitoxin from CDC as early as possible
Clinical presentation of Clostridium tetani
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?
What can you do for a tetanus patient?
Tetanus Immune Globulin antitoxin
Early tracheostomy to prevent laryngospasm suffication
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
Gas from ferm. causes tissue distention, compressed vessels
What does alpha toxin do?
Its a lecithinase (phospholipase)
How is Clostridium perfringens controlled?
Prompt surgical debridement
How is Clostridium perfringens treated?
Metronidazole, Penicillin, and Clindamycin stop growth
Clinical presentation of Clostridium difficile?
Usually following antibiotics
Watery Diarrhea early
Leukocytes penetrate connective tissue of bowel
- Form pseudomembrane
Which anti-biotics are most prone to cause Clostridium difficile development?
Development of Clostridium difficile associated diarrhea requires what two things
1. presence of C diff
2. disruption of native flora
Who gets Clostridium difficile?
People on antibiotics or PPIs
Normal influence of Clostridium difficile on the colon?
Important for T-reg development
Most Clostridium difficile patients are infected where?
A Health Care Setting
Pathogenesis of Clostridium difficile?
Enterotoxin (Toxin A) -- Fluid Acc
Cytotoxin (Toxin B) -- Kills gut epithelial cells