Vibrio, Campylobacter, Helicobacter Flashcards
What virulence factors of V. cholerae helps the organism adhere to the intestinal tract and causes the body to dump water into the intestinal lumen, which may lead to dehydration and death?
- Adhesins
- Single polar flagella
- Toxin co-regulated pili (TCP Type IV)
- Hemagglutinin protease
Cholera toxin binds to _____ found on many different cell types.
Ganglioside
How does Cholera toxin cause net excretion of electrolytes then water from cells?
- A1 subunit ADP ribosylates protein Gsa →
- Locks adenylyl cyclase into perpetual on cycle →
- Increase cAMP →
- Net excretion
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T/F Cholera toxin is enoded in V. cholerae’s chromosome
FALSE
Cholera toxin is phage encoded
V. cholerae _____ (a virulence factor) directly correlates with its virulence. Its presence indicates more severe symptoms. What serological group of this factor causes the majority of disease?
- O1 antigen
- Serogroup Inaba (El Tor) causes majority of disease
What is the only non-O1 derivative that does not produce milder illness by V. cholerae?
O139
The serious form of Cholera is acquired by _____
Consumption of contaminated seafood
Patients with cholera produce massive amounts (10-15L) of stool *without fever* that has a characteristic _____ appearance
Rice water stool
T/F V. cholerae invades host cells
FALSE
No invasion → no direct tissue damage → no fever
V. cholerae is sensitive to _____ and _____
- Drying
- Acidic pH
- Pts. with achlorhydria or those taking antacids are more susceptible
When cultured on ____ agar, V. cholerae grows as _____ colonies that ferment _____ and _____
- TCBS agar
- Grows as yellow colonies
- Ferment sucrose and citrate
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Upon gram staining, V. cholerae appear as _____
- Comma shaped gram negative rods
- Look like seagulls in pairs
What is the treatment for Cholera?
- IV fluid/electrolyte replacement
- Tetracycline
- Reduces severity/length
In contrast to V. cholerae, V. parahemolyticus _____ intestinal epithelium with _____
Invades with invasins
In contrast to V. cholerae, the diarrhea caused by V. parahemolyticus is _____
Inflammatory (V. cholerae diarrhea is secretory)
What is the name of the hemolysin produced by V. parahemolyticus?
Kanagawa toxin
V. parahemolyticus is acquired via _____
Consumption of contaminated seafood
In healthy individuals, V. parahemolyticus infection presents as a _____, but immunocompromised patients may develop _____
- Healthy: Self limiting diarrhea
- Immunocompromised: May develop septicemia
How is infection by V. parahemolyticus treated?
- Fluid/electrolyte replacement
- Tetracycline
Infection by V. vulnificus causes a severe _____ and is associated with _____
- Severe cellulitis (“Marsh Death”)
- Assd. w/ raw or undercooked seafood
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What are the four virulence factors of V. vulnificus?
- Acidic capsule - Makes phagocytosis difficult
- Exotoxin
- Proteases - Most serious, causes necrotizing cellulitis
- Siderophores - Hunt for iron, bring it back to organism
What groups are at risk for V. vulnificus infection?
- Older males
- Pts. w/Liver disease or iron storage disease
- Classic exam question: Alcoholic shrimper/fisherman
How is V. vulnificus ID’d clinically?
- Collect blood/wound exudates
- Enrich for growth with alkaline peptone broth
- Culture on TCBS agar
- Green colonies (vs. yellow V. cholerae colonies)
How is V. vulnificus infection treated?
- Tetracyclines
- Fluoroquinolones
- If damage done: Debridement or amputation
What organism is the leading cause of diarrhea in the US and developed world (besided Norovirus)
Campylobacter jejuni
What adhesins are expressed by C. jejuni, allowing it to adhere to intestinal lining?
- CadF
- PEB1
T/F: C. jejuni is a microaerophile that grows at low temps (four degrees Celsius)
TRUE
How is C. jejuni acquired?
- Eating/drinking contaminated foods and beverages
- Unpasteurized milk, undercooked meats
- Fecal-orally from pets
- Dog feces
T/F: Like V. cholerae, C. jejuni does not invade the intestinal epithelium
FALSE
C. jejuni DOES invade and cause damage to the intestinal lining
What three symptoms appear within 2-4 days after acquiring a C. jejuni infection?
- Little/no vomiting
- Intense cramps
- Inflammatory diarrhea
- Lasts 1-2 weeks
T/F C. jejuni infection follows a self-limiting course
TRUE
Antibody to lipooligosaccharide cross-reating with host gangliosides (in myelin) results in the development of _____ 2-3 weeks after infection
Guillain-Barre Syndrome
How is C. jejuni identified clinically?
- Enrich loose stool sample by incubating in cold storage
- Requires microaerophilic environment
- Culture on CAMPY blood agar
- Contains selecting abx
- Oxidase +, Gram -, curved organism
Treatment for C. jejuni infection?
- Erythromycin or Ciprofloxacin
- Reduces severity, does not eliminate symptoms
The virulence factors of H. pylori destroy the protective layer of the stomach leading to _____
Further damage of stomach cells by acid leading to ulcers
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What virulence factor of H. pylori neutralizes stomach acid, providing a protective buffer for the organism?
- Urease
- Converts urea to ammonia
The natural mode of H. pylori transmission is most likely _____
Fecal-oral
What virulence factor of H. pylori induces host cyclooxygenase, triggering apoptosis?
Vacuolating toxin (VacA)
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What is the most characteristic symptoms of H. pylori infection?
Gnawing or burning pain with an empty stomach that is less obvious when full
(Less commonly: Nausea, vomiting, loss of appetite, anemia from blood loss)
What cancers are linked to H. pylori infection?
Adenocarcinoma and MALT B-cell lymphoma
How does H. pylori adhere to the stomach mucosa?
Via pili & glycocalyx
What are the three B’s of H. pylori clinical ID?
- Blood
- Serology for Abs
- Breath
- Measures amount of radioactive CO2
- From urease converting tagged urea to CO2 + NH3
- Measures amount of radioactive CO2
- Biopsy
- Curly rod looking organism
- Urease test positive
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What are the treatment options for H. pylori infection?
- Amoxicillin
- Tetracycline
- Metronidazole
- Bismuth salts
- Proton pump inhibitor