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34 Cards in this Set
- Front
- Back
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V. cholera bacteriology
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-Gram negative
-Oxidase-positive -Motile -Grown on Thiosulfate CItrate Bile Sucrose (TCBS) agar |
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V. cholera habitat/reservoir
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Salty water
Marine crustaceans |
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V. cholera transmission
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Contaminated food, water
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Virulent V. cholera serogroups
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O1, O139
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V. cholera virulence factors
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Cholera toxin
Toxin concentrated pilus (TCP) |
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V. cholera epidemiology
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-Medium infective dose
-Pandemics common in refugee camps, etc. -Large proportion of the time there aren't sympoms (75%) |
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Cholera symptoms
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-Profuse watery diarrhea
-Vomiting -Leg cramps |
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V. cholera treatment
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Oral rehydration: glucose, NaCl, KCl, NaHCO3
Don't give antibiotics; V. cholera is self-limiting |
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Mechanism of V. cholera pathogenesis
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1. V. cholera in the colon
2. Toxin release 3. A Toxin is endocytoced 4. Toxin + NAD: ribosylation of g-prot--increased AC act. 5. Increased Cl secretion, decreased Na abs 6. Secretory diarrhea |
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Action of cholera toxin
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Crypt cells: increase cAMP increases chlorine secretion
Villus cell: increased cAMP decreases Cl, Na influx |
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Toxin-Co-regulated Pilus (TCP) details
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V. cholera
-Type IV pilus -Essential intestinal colonization factor -On pathogenicity island: from bacteriophage; required for infection. |
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V. cholera life cycle
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In the water: no toxin production
In vivo: ToxR (transcription factor) activates TCP, Toxin production |
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Mechanism of new V. cholera strain toxicity
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O1 was transformed to O139 by horizontal gene transfer --> People can't recognize the antigens any more.
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Prevention of V. cholera
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-Vaccine against the O1 strain
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TCP-ACF horizontal transfer mechanisms
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-The TCP is a receptor for the phage
-On either side of the island there are attachment sites |
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Campylobacter bacteriology
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-Curved gram negative (when young); coccoid after 48 hrs.
-Microaerophilic -Flagellated -Genetic variation |
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Campylobacter genetic variations
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-Variable LOS: missing O antigen
-Variable capsule -Glycosylated flagellin, not recognized by TLR5 |
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Campylobacter reservoir
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-Chicken!
-Water |
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Campylobacter clinical considerations
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-Inflammatory diahhrea
-Diagnosis is made with special agar -Low infectious dose -Only give antibiotics early in the course |
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Campylobacter pathogenesis
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-Flagella required
-Avoidance of lysosomal delivery -CDT Toxin -IL-8 secretion -Avoids innate immune response (antigenic variation, high AT content) |
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Cytolethal distending toxin mechanism
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3 genes:
1. INgestion through clatherin coated pit 2. DNAse activity 3. Cell cycle arrest; cell death |
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Complication of Campylobacter jejuni
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Guillain-Barre syndrome through cross reactivity to the gangliosides
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Diagnosis of Campylobacter jejuni
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-Gram stain stool specimen
-Culture at 42 C -High titer -Hard to culture |
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Salmonella bacteriology
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-Gram negative rods
-Flagellated -Lactose negative -H2S producing -ACID SENSITIVE |
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Diseases caused by Salmonella
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1. Gastroenteritis
2. Focal systemic infections (endocarditis, osteomyelitis) 3. Typhoid fever |
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Salmonella enterica classification
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Typhoid: Systemic, enteric fever
Non-typoid: diarrhea, inflammatory characteristics |
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Salmonella typhi characteristics
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-Not too much diarrhea
-HUMAN SPECIFIC -Very serious systemic infections -Has a Vi capsule |
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Salmonella pathogenesis
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-Infection starts in the small intestine
-Non-typhoid stays, typhoid goes systemic |
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Salmonella virulence factors
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-2 Type III secretion systems
-Virulence regulators -Adherence fimbriae |
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Salmonella secretion system types:
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Type 1: bacterial uptake
Type 2: required for intracellular survival and immune invasion |
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Mechanism of Salmonella activity
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1. Type I secretin system causes entry into cells
2. Type II secretinon system causes inability of lysosomal fusion 3. Multiplication within the vacuoles 4. Once reach critical mass, explode the cell; inflammation 5. Neutrophil recruitment, macrophage activation |
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Who are the most likely people to become carriers of salmonella/typhoid?
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People with gallstones
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Mechanism of Salmonella activity
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1. Type I secretin system causes entry into cells
2. Type II secretinon system causes inability of lysosomal fusion 3. Multiplication within the vacuoles 4. Once reach critical mass, explode the cell; inflammation 5. Neutrophil recruitment, macrophage activation |
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Who are the most likely people to become carriers of salmonella/typhoid?
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People with gallstones
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