L47

Question 1

E.Coli:
GN or GP
Shape
Air status
Grow on MacConkey agar?
Ferment lactose?
Where part of normal flora
Motile?

Answer 1

GN rod - typical of GI flora
Facultative anaerobe 
YES grows on MacConkey
YES ferments lactose
Motile w/ flagella

Question 2

What the 2 characteristics that E.Coli are serotyped on?

Answer 2

O antigen = repeating polysaccharides @ end of LPS

H antigen = flagellar antigen (highly variable)

Question 3

What is the serotype of the most common pathogenic strain of E.Coli?

Answer 3

O157:H7

Question 4

How can E.coli both be normal GI flora AND cause so many diseases?

Answer 4

Virulence factors on:
Plasmids
Bacteriophages
PIs

Question 5

What is ETEC? What are the clinical features/picture?

Answer 5

ETEC = entero-toxigenic E.Coli
WATERY diarrhea (short)
*Developing countries - children + travelers

Question 6

How is ETEC transmitted?

Answer 6

Fecal-oral

Need high inoculum for disease

Question 7

What are the virulence factors for ETEC?

Answer 7

Plasmid w/:
1. Colonization factor = pili for GI adhesion, unique to each strain!!
2. Heat labile enterotoxin (aka destroyed by heat)
3. Heat stable enterotoxin
Aka secreting enterotoxin at pretty much any temp

Question 8

How do you gain immunity against ETEC?

Answer 8

Immunity vs pili (colonization factor)

But b/c this variability changes with each stain, immunity is UNLIKELY

Question 9

Explain how heat-labile enterotoxin works.

Answer 9

B subunit uptake into GI cells
Retrograde transport to golgi
A subunit is ejected and moves to the BL surface of the cell
A ADP ribosylates Gs –> activates adenylate cyclase
Increased cAMP production
Turn on PKA –> open CFTR = open Cl- channel
Na blocked + Cl moving from cells into lumen = NaCl in lumen
H2O follows
WATERY diarrhea

Question 10

Explain the heat-stable enterotoxin mechanism.

Answer 10

Elevated cGMP (this is the difference!!)
Same down stream effects

Question 11

Treat ETEC (traveler’s diarrhea).

Answer 11

Oral rehydration
Antimicrobial to shorten duration only:
- Fluoro +/- antimotility agent
- Non-absorbable rifaximin

Question 12

What is EPEC? What are the clinical symptoms/picture?

Answer 12

EPEC - entero-pathogeneic E.Coli
Watery diarrhea + vomiting!! 
(Problematic for oral rehydration)
Infants - only - @ developing countries
Can be DEADLY!

Question 13

How is EPEC transmitted?

Answer 13

Person-person

Question 14

What is EPEC’s disease mechanism/virulence factors?

Answer 14

Both REQUIRED for VIRULENCE
Adherence - pili,
- On plasmid
- Bacteria aggregate in microcolonies
T3SS - modifies cytoskeleton for attachment
- On PI
- Intimin (bacterial ligand)/tir (host receptor)

Question 15

What is tir?

Answer 15

Translocated intimin receptor
In the host (target) cell
Binds intimin –> actin polyermization
Net = pedestal for bacterial attachment to gut (vs normal pili)

Question 16

How do you treat/prevent EPEC?

Answer 16

Prevent: babies drink breast milk!
Treat: oral/IV rehydration

Question 17

What is EHEC? What is the reservoir? Transmission?

Answer 17

Entero-hemorrhagic E.Coli
Reservoir = cattle (petting zoos)
Transmitted:
- Contaminated beef, spinach, water 
- Unpasteurized juice
- Person-person (low inoculum)

Question 18

Which toxin does EHEC secrete? How did it get this virulence factor?

Answer 18

Shiga toxin
From bacteriophages
B + A subunits
Retrograde transport to ER
Depurinates 28S ribosome subunit 
X protein synthesis 
Cell DIES --> initiates CLOTTING

Question 19

What triggers EHEC shiga toxin production?

Answer 19

Body’s SOS signals
- Antibiotics
- Oxidative stress
Otherwise laying latent in lysogenic phase of bacteriophage
- SOS turns on late genes –> into lytic
TAKE HOME = antibiotics may be associated with higher complication rates

Question 20

How did EHEC evolve?

Answer 20

EPEC + bacteriophage w/ Shiga toxin = EHEC

Question 21

What is EHEC’s other main virulence factor?

Answer 21

Attaching & effacing

Question 22

Describe the clinical progression/presentation of EHEC.

Answer 22

Cramps/pain
Watery –> bloody diarrhea
Progression = HUS

Question 23

What is HUS?

Answer 23

Hemolytic uremic syndrome
Clots in capillaries (thrombocytopenia) + hemolysis as RBCs lysed
Increased risk w/ ANTIBIOTICS
Brought on by EHEC - could cause permanent kidney damage

Question 24

How do you diagnose EHEC?

Answer 24

1. MacConkey agar
   - Non-O125H7 stains = most = ferment sorbitol
2. ELISA for Shiga toxin
   NEED BOTH

Question 25

What is EAEC? Describe the clinical symptoms/presentation.

Answer 25

Entero-aggregative E.Coli
Kids w/ growth retardation
Traveler’s diarrhea
HIV patients

Question 26

What are the virulence factors for EAEC?

Answer 26

Adhesion = fimbrae (plasmid)
Damages intestinal cells
Toxins:
- Pet
- EAST

Question 27

What are the pathogenic mechanisms by which E.Coli can cause neonatal meningitis?

Answer 27

K1 capsule
Fimbriae
Invasiveness - crosses BBB

Question 28

Klebsiella encapsulated?

Answer 28

YES & mucoid

Question 29

Infections caused by Klebsiella

Answer 29

UTI
Severe pneumonia
Nosocomial infections

Question 30

Which drugs is Klebsiella resistant to?

Answer 30

ALWAYS resistant to penicillins

Question 31

Enterobacter and serratia encapsulated?

Answer 31

YES & mucoid

Question 32

What infections do enterobacter and serratia cause?

Answer 32

NOSOCOMIAL infections

Question 33

What drug is easily induced to be resistant in enterobacter and serratia?

Answer 33

Cephalosporins - don’t use them!! Even if report says susceptible

Question 34

What are 4 virulence factors of proteus?

Answer 34

1. Urease + (makes urine alkaline)
2. Swarming motility
3. Fimbriae
4. Hemolysin

Question 35

Which drugs are proteus resistant to?

Answer 35

Tigecycline & polymixin

Question 36

How do you treat P.mirabilis?

Answer 36

Same way you'd treat E.Coli
Ampicillin
TMPX-SMX
Cephalo
Fluoro

Question 37

How do you treat P.vulgaris?

Answer 37

More likely to be resistant, so…
3rd gen cephalo
Fluoro