Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/34

Click to flip

34 Cards in this Set

  • Front
  • Back
toxin-mediated disease

invasion and inflammation
2 major mechanisms, how bacteria cause disease
botulism toxin
clostridial toxin, no organisms required in ingestion
Staphylococcus aureus enterotoxin
most common food-borne diarrheal disease in US
Clostridium botulism
toxin preformed in food, ingested
S. aureus enterotoxin
preformed in contaminated food, disease can occur in absence of organism
infant botulism
organisms in honey, toxin formed when in gut, intestinal lumen is anaerobic
vibrio cholerae
intestinal colonization followed by secretion of cholera toxin
Clostridium
obligate anaerobic Gram positive rod, spore-forming, catalase negative, oxidase positive
Clostridium
location of spore in bacterium may aid in species identification
Clostridium botulinum
noninvasive, causing botulism (can be agent of bioterrorism)
Clostridium tetani
generally noninvasive (very limited invasion potential), causative agent of tetanus
Clostridium difficile
noninvasive, secreted toxin causing pseudomembranous enterocolitis (cause of antibiotic-mediated diarrhea)
Clostridium perfringens
very invasive pathogen, gas gangrene
Clostridium septicum
invasive in malignancy
botulism toxin
toxin causes flaccid paralysis

"no fever," "normal mental status"
tetanus toxin
toxin causes tetanus (locked jaw)
exotoxins A and B
toxin causes diarrhea in pseudomembranous colitis due to Clostridium difficile
Alpha toxin
lechithinase which lysed host cell membrane
Alpha toxin
in combination with other degradative enzymes as the cause for "Gas Gangrene" due to Clostridium perfringens
Clostridium botulinum
Gram+ rod with suterminal oval spores (spore location not diagnostic)
Clostridium botulinum
soil organism, spores very resistant to physical and chemical agents
Clostridium botulinum
very heat-labile, cook canned food
Clostridium botulinum
spores found in contaminated food, under anaerobic conditions (canned goods), germinate, grow and produce botulism toxin in 2-3 days

canned veg, smoked fish, preserved fruit
Botulism toxin
extremely potent toxin
heat-labile (inactivated by boiling for 10 min)
not destroyed by stomach acid
7 types (A-G), A,B,E most common
2 subunit toxins (A and B)
Botulism toxin
upon absorption intestine, toxin carried via blood to peripheral nerve synapses, acting as neurotoxin
Botulism toxin
binding of toxin to receptor on nerve synapse, toxin enters cell, blockign release of ACh from cell by interfering with proteolytic processing (toxin is protease) and hence release of ACh
Botulism
incubation period 18-36h

weakness or flaccid paralysis of peripheral nerves including cranial nerves, symmetrical in distribution

no sensory deficit

may affect respiratory muscles

dysphagia, diplopia, dry throat, dilated pupils
Botulism
dysphagia, diplopia, dry throat, dilated pupils
Botulism
usually clinical diagnosis

don't rely on culturing microorganism (preformed toxin is culprit)

toxin in serum, vomitus, feces

bacterial toxin in food with serological tests

electromyography (EMG) - diminished AP of peripheral nerves, suggestive not diagnostic
Botulism
included in differential diagnosis:

myasthenia gravis and Guillain-Barre syndrome (ascending paralysis)
Botulism
therapy:
-removal of toxin from stomach with lavage (if detected early)
-treatment with antitoxin (from horse serum, toxin specific for types A, B, E)
-supportive care, respiratory support
12% fatality rate
Botulism
cook canned food at 100C for 10 min to inactivate toxin
infant botulism
-1-8 months of age
-honey
-bacterial proliferation in gut (immune system immaturity)
-subtle symptoms: constipation, weak head control (flaccid), cranial nerve deficit
-diagnosis by demonstrating toxin and/or organism in stool or organism in food
-treatment used to be supportive due to allergic reaction to old antitoxin, but new human antitoxin Ab against A and B serotypes
wound-associated botulism
spores in soil contaminate wound, germinate and produce toxin

diagnosis by wound culture, demonstration of toxin in serum