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34 Cards in this Set
- Front
- Back
What do all of these organisms cause? |
Inflammatory diarrhea |
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What do all of these organisms cause? |
Non-inflammatory diarrhea |
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What type of organisms are these? |
Anaerobes |
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What is the definition of acute diarrhea? Chronic diarrhea?
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Acute = 3 or more loose stools per day lasting less than 2 weeks
Chronic = persists for greater than four weeks |
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What is inflammatory diarrhea? What cells will you see in the stool? Is fever common? Is the volume large or small? What part of the GI tract is commonly affected?
Contrast all of this with non-inflammatory diarrhea. |
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How many microbes in the gut?
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Which group is a major contributor to the gut microbiome? Which two types specifically?
Where are these organisms also present? |
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What two enzymes do anaerobes lack (this is why the growth of anaerobes is inhibited by oxygen)? What are these enzymes used to eliminate?
Do anaerobic infections stink? Does lack of a smell rule out anaerobes? |
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Anaerobic flora cause disease (abscesses) when they are introduced into normally _____ sites or when the balance of organisms is upset and pathogenic organisms _____. |
Anaerobic flora cause disease (abscesses) when they are introduced into normally sterile sites or when the balance of organisms is upset and pathogenic organisms overgrow |
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Bacteriodies fragilis:
Gram negative or positive? Predominant organism in what part of the GI tract? Most common cause of what?
What do infections usually arise from? What is an important virulence factor? What plays an important role in abscess formation? |
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What is the organism? |
Bacteriodes fragilis |
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Bacteriodes fragilis:
Clinical findings
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Clinical findings |
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What is the treatment of Bacteroides fragilis? What is it resistant to? |
Treatment: metronidazole, carbapenems, combination beta-lactam/beta-lactamase inhibitors |
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Prevotella melaninogenica:
Gram positive or negative? Where is it commonly found? What type of pathogen? (opportunistic, etc)
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What is the organism? |
Prevotella melaninogenica |
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Clostridium:
Gram stain? What type of rods?
It is the only anaerobic ______ forming bacteria. Resistant to what two things?
What two factors are responsible for pathogenesis?
Where is it found? |
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Describe what you see. What is the organism? |
Large, "boxcar" gram+ bacilli C. perfringens |
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Where is C. perfringens found? What is the clinical syndrome? |
Found in soil and colon Gas gangrene (discussed previously in septic arthritis/myositis lecture) |
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C. perfringens:
Food poisoning: |
Food poisoning |
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Spore found in the soil. Portal of entry is usually a wound site (think nail penetrating foot). Can also be introduced during "skin-popping." What is the bacteria? |
C. tetani |
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How is neonatal tetanus acquired (major problem in developing countries)? |
Organism enters through contaminated umbilicus or circumcision wound |
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What is the pathogenesis of C. tetani? |
Tetanus toxin (tetanospasmin, an AB neurotoxin), enters at neuromuscular junction => transported by motor neurons to ganglia.
Toxin binds irreversibly to ganglioside receptors => blocks release of inhibitory neurotransmitter (glycine and GABA) by cleaving action on membrane proteins (SNARE) involved in exocytosis
Net effect = disinhibition of neurons that modulate excitatory impulses from the motor cortex => increase muscle tone, painful spasms, and widespread autonomic instability. |
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Clinical presentation of Tetanus: |
Clinical presentation |
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Treatment of Tetanus: |
Treatment |
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Different forms of botulism: Type from canned foods (fruits, vegetables, and fish) Type from inhalation or ingestion of spores in carpet or raw honey Type from wounds Type that would be an act of bioterrorism Hospital form
How many cases are reported per year in the US? Most common type?
Why is there a rising incidence in California? |
Cali = black tar heroin users
Babies = raw honey ingestion |
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What is the pathogenies of C. botulinum? |
AB toxins (8 antigenic types and the most potent bacterial toxins) => cleave SNARE proteins and proven the release of acetylcholine => flaccid paralysis |
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Clinical presentation What is this the clinical presentation of? What could have been done to prevent this? |
Classic foodborn botulism
Spores resistant to heat => germinate after cooking and release toxin => subsequent heating will inactivate the toxin! |
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Are antibiotic recommended for infant botulism or for adults with suspected GI botulism? Why? |
No! Lysis of intraluminal C. botulinum => increase amount of toxin available to absorption |
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What is another name for infant botulism? What ages typically?
What are some components of the clinical presentation? |
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How do you treat botulism (think about paralysis of respiratory muscles, anti-toxins depending on ages, and antibiotic therapy for certain types)? How do you PREVENT botulism? |
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What is the organism? |
H. pylori |
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H. pylori: Gram negative or positive, shape? How do they move? Micro___philic.
What is the cytotoxin name? What type of secretion system? What rearranges the cytoskeleton? What enzyme is responsible for damage? |
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What leads to ulcers with H. pylori?
What are some methods of diagnosis? (think instruments, poop, breath, blood)
How do you treat H. pylori? |
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