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34 Cards in this Set
- Front
- Back
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toxin-mediated disease
invasion and inflammation |
2 major mechanisms, how bacteria cause disease
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botulism toxin
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clostridial toxin, no organisms required in ingestion
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Staphylococcus aureus enterotoxin
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most common food-borne diarrheal disease in US
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Clostridium botulism
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toxin preformed in food, ingested
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S. aureus enterotoxin
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preformed in contaminated food, disease can occur in absence of organism
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infant botulism
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organisms in honey, toxin formed when in gut, intestinal lumen is anaerobic
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vibrio cholerae
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intestinal colonization followed by secretion of cholera toxin
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Clostridium
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obligate anaerobic Gram positive rod, spore-forming, catalase negative, oxidase positive
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Clostridium
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location of spore in bacterium may aid in species identification
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Clostridium botulinum
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noninvasive, causing botulism (can be agent of bioterrorism)
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Clostridium tetani
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generally noninvasive (very limited invasion potential), causative agent of tetanus
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Clostridium difficile
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noninvasive, secreted toxin causing pseudomembranous enterocolitis (cause of antibiotic-mediated diarrhea)
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Clostridium perfringens
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very invasive pathogen, gas gangrene
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Clostridium septicum
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invasive in malignancy
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botulism toxin
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toxin causes flaccid paralysis
"no fever," "normal mental status" |
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tetanus toxin
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toxin causes tetanus (locked jaw)
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exotoxins A and B
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toxin causes diarrhea in pseudomembranous colitis due to Clostridium difficile
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Alpha toxin
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lechithinase which lysed host cell membrane
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Alpha toxin
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in combination with other degradative enzymes as the cause for "Gas Gangrene" due to Clostridium perfringens
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Clostridium botulinum
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Gram+ rod with suterminal oval spores (spore location not diagnostic)
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Clostridium botulinum
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soil organism, spores very resistant to physical and chemical agents
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Clostridium botulinum
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very heat-labile, cook canned food
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Clostridium botulinum
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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 |
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Botulism toxin
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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) |
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Botulism toxin
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upon absorption intestine, toxin carried via blood to peripheral nerve synapses, acting as neurotoxin
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Botulism toxin
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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
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Botulism
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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 |
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Botulism
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dysphagia, diplopia, dry throat, dilated pupils
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Botulism
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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 |
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Botulism
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included in differential diagnosis:
myasthenia gravis and Guillain-Barre syndrome (ascending paralysis) |
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Botulism
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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 |
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Botulism
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cook canned food at 100C for 10 min to inactivate toxin
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infant botulism
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-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 |
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wound-associated botulism
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spores in soil contaminate wound, germinate and produce toxin
diagnosis by wound culture, demonstration of toxin in serum |
