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28 Cards in this Set

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Diarrheagenic types of E. Coli
-Enterotoxigenic (ETEC)
-Enteropathogenic (EPEC)
-Enterohemorrhagic (EHEC) and other toxin producign (STEC)
-Enteroaggretagtive
Extraintestinal types of E. Coli
-Uropathogenic (UPEC)
-Neonatal meningitis (MAEC)
ETEC plasmid virulence factors
-Colonozation factor antigens
-Heat-labile enterotoxin
-Heat stable enterotoxin
Mechanism of heat labile enterotoxin entry
1. Heat labile toxin binds to cell wall via the B subunit
2. A subunit enters intot he cell
3. A subunits ADP ribosylates adenylate cyclase
4. Cell is unable to take in sodium; constituitively secreted Cl
5. Water flows out of cell; diarrhea
Structure of heat stable exotoxin
Small peptide; very similar to gyanalyn

Many conserved cystine residues within; gives stability in heat
Mechanism of heat stable toxin virulence
1. Heat stable toxin binds to cell wall via the B subunit
2. A subunit enters intot the cell
3. A subunits ADP ribosylates GUANYLATE (G-C bonds are more STABLE than A-T bonds) cyclase
4. increased levels of cGMP
5. Inhibition of Na absorption, increase of Cl secretion
6. Water efflux into lumen
Do ETEC cause damage to the cells?
No! They only cause an efflux of water. Think through the mechanisms...
Colonization factor antigens mechanism
Mediate attachment ot the intesitinal epithelium
EPEC (enteropathogenic E. Coli) pathogenesis
-Localized adherence: plasmid encoded pilus
-Attaching and effacing: Type III secretion system on pathogenicity island
EPEC LEE
-Pathogenicity island
-Required for virulence
-Type III secretion
-Intimin/Tir Adhesin/receptor pair (makes receptor and its ligand)
-Derived from flagella
EPEC: LEE mechianims of pathogenicitiy
1. BFP contributes to the initial adherence
2. Host cytoskeleton rearranges
3. Tir protein is inserted into the membrane
4. Intimin binds to the Tir protein
5. Injection of contents into cytosol
EHEC Epidemiology
Reservoir: cattle

Ways we get it: Contaminated food, water, petting zoos, person to person (low innoculating dose)

Low infectious dose
EHEC culture details
Lactose fermenting
Sorbitol nonfermenting
EHEC mechanisms of pathology
Chromosomal LEE
Phage Shiga-like toxin
Plasmid hemolysin
Chromosomal LEE mechanism of pathology
-On a pathogenicity island
-Type III secretion system
-Intiin/Tir Adhesin/receptor pair
Phage Shiga-like toxin mechanism of pathology
-EHEC
-Cleavage of an adenosin in the 23S rRNA - stops protein synthesis
-Causes cell death; damaged epi; hemorrhage
-Cause enough for pathogenic traits
Plasmid hemolysin mechanism of pathology
Causes lysis of RBCs
EAEC pathogenesis
-Aggregative adherence mediated by plasmid encoded fimbriae
-Damage to intestinal cells
-Toxins: Pet (protease), EAST (enteroaggregated stable toxin)
EAEC mechanism of pathology
-Fimbriae mediate attachment to epithelium
-Flagellin trigers an inflammatory response via TLR5
-Biofilm formation
Enteroinvasive E. Coli mechanism of pathology
1. Endocytosis of the cells
2. Actin rocket propels the cell into the adjacent cell

Encoded by a pathogenicity island; Type III secretion
Shigella distinguishing characteristics
-Gram - bacillus
-Non-lactose fermenter
-Non-motile
-Invades colonic epithelium
-Causes dysentery
Species of Shigella
-S. sonnei (US)
-S. flexneri (most common worldwide)
-S. dysenteriae (MOST SEVERE!!!)
-S. boydiii (least common)

HUMANS ARE ONLY RESERVOIR
Does Shigella need a high or low dose to cause infection?
Low
When do Shigella infectons usually occur
July-December
What cells do Shigella enter into the epithelium through?
M cells
Mechanism of Shigella pathogenesis
1. Shigella enters M cells
2. Crossing over to the basolateral side of the cell
3. Infection of the macrophage; cause it to die; cytokine release (IL-1,8,18)-->PMNs
4. Reentry into Epithelium
5. Go laterally through epi. via actin polymerization
Shigella type III secretion system effectors
Encoded by mxi-spa genes

Secreted effectors:
-IpaC (activates Cdc42, Rac)
-Vir A (tubulin)
-IpaA (vinculin)
-IpgD (seals vesicles)
Symptoms secondary to a S. dysenteriae infection
-Severe colitis
-Neurologic complications
-Hemolytic Uremic Syndrome