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27 Cards in this Set

  • Front
  • Back
GI host defenses
stomach acid
intestinal motility
resident intestinal flora
innate and adaptive immunity
inflammatory diarrhea
pathogens elicit an immune response
blood and pus in the stool
low volume diarrhea
Bacteria that cause inflammatory diarrhea by INVADING host cells
Salmonella
Shigella
Campylobacter
Bacteria that cause inflammatory diarrhea by colonizing the large intestine and secreting CYTOTOXINS that provoke inflammation
Clostridium difficile
Entero-hemorrhagic E. coli
secretory diarrhea
high volume diarrhea
NO blood nor pus
little cramping, little nausea
Bacteria that cause secretory diarrhea via enterotoxins
Vibrio cholerae
Entero-toxigenic E. coli
Enteroinvasive (enteric) pathogens
Invade host cells
facultative intracellular pathogens
Salmonella enterica
Shigella
Yersinia enterocolitica
Campylobacter jejuni
Listeria monocytogenes
Enter-invasive E. coli
Entertoxigenic (enteric) pathogens
Do NOT invade
Colonize and secrete an enterotoxin
Vibrio cholerae (cholera toxin)
Clostridium difficile (A toxin and B toxin)
ETEC (LT toxin)
Enteropathogenic (enteric) pathogens
Do NOT invade
Bacteria colonize and destroy epithelium
Enteropathogenic E. coli
Enterhemorrhagic E. coli
Helicobacter pylori
diarrhea caused by enteroinvasive pathogens
severe painful cramps
stools contain blood and pus
Zipper mechanism of invading non-phagocytic cells
receptor-mediated endocytosis
Trigger mechanism of invading non-phagocytic cells
Bacteria injects effector proteins into the host cell that induces cytoskeletal rearrangement that lead to the endocytosis of the bacterium
Type 3 secretion system
used by: Salmonella, Shigella, Yersinia, EPEC and EHEC.
Bacteria injectes proteins directly into host cells
Typhoid fever
Salmonella enterica serovar Typhi
Invasive - invades gut epithelial cells and M cells using type 3 secretion system. "Invades" phagocytes (able to survive inside them by preventing phagosome-lysosome fusion)
Can downregulate the expression of MHC II on DCs
Encapsulated - able to evade recognition by immune cells
Disseminates via the RES system to the liver and spleen
Colonizes the biliary duct and is passed in feces (can establish a chronic carrier state)
Treated with long-term antibiotics
2 vaccines available
Non-typhoid Salmonella disease
Zoonotic
Serotypes(vars): Enteritidis, Typhimurium, Cholerasuis
Large infectious dose (100,000,000)
Symptoms: intestinal inflammation, cramping, diarrhea, fever
Septicemia is rare (does not disseminate)
Invades M cells
Highly resistant to killing by macrophages - prevents phagosome-lysosome fusion
No capsule
Shigellosis
(Shigella sonnei, flexneri and dysenteriae)
Bacilliary dysentery
Low infectious dose (10)
fecal-oral transmission
incubation period: 1-7 days
Shigella invades M cells and spreads to neighboring cells using actin-based motility
Symptoms range from mild to dysentery (abd pain, cramping, fever, water, bloody, low volume stools with pus, nausea and vomiting
Rare - HUS (hemolytic uremic syndrome)
Treat with rehydration and antibiotics
Secretes Shiga toxin - inhibits host cell protein synthesis
Campylobacter jejuni
gram-negative, curved rod, microaerophlic, motile, selective growth on charcoal
Most common bacterial cause of diarrhea in the US
Low infectious dose (500)
Symptoms: inflammatory diarrhea (sometime bloody), with cramps and fever
Lasts ~1 weeks
Secretes a genotoxin - a cytolethal distending toxin that arrests the host cell cycle and causes cell death
Listeria monocytogenes
gram-postive bacillus
host range: humans, mammals, birds, fish, crustaceans
Uses actin-based motility to spread from cell to cell.
Grows well at 4 degrees Celsius (fridge temp)
Associated with soft cheeses and processed meats
Symptoms: fever, myalgia, vomiting (diarrhea not common)
Pregnant women, fetuses and neonates: Pregnant women experiences mild flu-like symptoms. Can experience miscarriage, stillbirth and pre-term labor
Symptoms in neonates are similar to GBS: meningiits and encephalitis
Vibrio cholerae
gram-negative, comma shaped rod
polar flagellum that gives it darting mobility
found in aquatic environments
high infectious dose (100,000,000)
Low infectious does when in the hyperinfectious state (when the bacteria exit the infected person they are "primed" to infect
incubation period: 1-3 days
"rice water stool" - 10-15L/day
hypovolemia, hypokalemia
secretes cholera toxin
Cholera toxin
Secreted by Vibrio cholerae
A-B toxin
B subunits binds to GM1 ganglioside and leads to endocytosis of the toxin
A subunit is activated inside the cell - cleaved into A1 and A2. A1 locks adenylate cyclase in the active stage - increasing intracellular cAMP. Increase cAMP increases ion secretion into the lumen. Water follows, causing diarrhea
Clostridium difficile
gram-positive rod; obligate anaerobe
SPORES
asymptomatically colonizes a small proportion of people
can lead to pseudomembranous colitis and toxic megacolon
Toxins A and B disrupt host cell actin which rounds out the cell, killing them. Infected cells secrete loads of cytokines and chemokine that recruit neutrophils. This increases the permeability of the colonic epithelium (diarrhea)
Enterotoxigenic E. coli
difficult to distiguish from cholera (rice water stool)
lacks darting motility, however
ST and/or LT toxins - LT is identical to the cholera toxin
Helicobacter pylori
Flagellar motility is essential for colonization of the stomach - pushes its way through the mucus barrier
Produces urease that converts urea to NH3 and CO2, raising the pH
Increased pH allows bacteria to replicate
Produce mucinases that break down the mucus barrier - stomach acid and contents (like pepsin) damage exposed epithelial cells and induce inflammation
Treat with PPIs, antibiotics adn bismuth subsalicylate
Diarrheagenic E. coli
Gram-negative rod
ferments lactose
Critical virulence factors are encodes on plasmids, lysogenic phage and/or pathogenicity islands
EIEC
Resembles Shigellosis (dysentery), but does NOT produce a toxin
invades colonic cells and causes inflammatory diarrhea
fecal oral transmission
EPEC
"traveler's diarrhea"
Attaching and effacing lesions that damage the intestinal epithelium (pedestals)
Uses Type 3 secretion system
EHEC
Highly virulent
Reservoir: GI tract
Symptoms - hemorrhagic colits with bloody diarrhea
ex strain, O157:H7
Produces shiga or shiga-like toxin
Uses Type 3 secretion system