Gram Negative Rods Flashcards

1
Q

Biochemical and growth properties of Pseudomonas aeruginosa

A

Opportunistic aerobe, makes pigments in humans and agar (green), oxidase positive

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2
Q

What types of diseases does Pseudomonas aeruginosa cause?

A

Opportunistic infection and nosocomial (hospital acquired infections)

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3
Q

What is Pseudomonas relationship to cystic fibrosis and burns?

A

CF: Cl- transporter (CTFR) pumps little Cl- = thick mucous due to no water released to thin it out

Burns: can get deeper into body bc no barrier (sepsis)

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4
Q

What are the 3 major bacterial structures used for attachment/colonization in Pseudo?

A
  1. Type 4 Pili: adhesions that attach to surface sialic acid
  2. Flagella: adhesions that attach to surface mucins
  3. Alginate Slime: thick polysacc that surrounds mucin (binds mucins to host lung cells)
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5
Q

What does Type IV pili do in Pseudo?

A

Helps with movement (pili shrinks and grows), proteases degrade fibronectin (exposes sugars for pili)

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6
Q

What are the host targets of the bacterial structures used for attachment in Pseudo?

A
  1. Type 4 Pili: surface sialic acid
  2. Flagella: surface mucins
  3. Alginate Slime: mucins on host lung cells
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7
Q

How does Pseudo obtain iron, phosphate, and other nutrients?

A

Iron: Siderophores that scavenge Fe to bacteria (pyochelin and pyoverdin)
Phosphate: Phospolipases that destroys phospo bilayer that releases phosphate
Other: Lemolysins that destroy tissues = releases lots of nutrients

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8
Q

What is the function of elastase, phospholipase, and exotoxin A in Pseudo?

A

Elastase: secreted and destroys ECM (collagen, elastin, fibronectin)
Phospholipase: destroy eukaryotic cells (blood cells)
ExoA: MOST TOXIC stops translation and cell dies

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9
Q

What do ExoS, T, U, and Y proteins do and how do they get into the cell in Pseudo?

A

Toxins in Type 3 secretions systems that injects directly into target cell (not exposed to immune invasion)

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10
Q

What is the role of inflammation in the damage of Pseudo?

A

Endotoxin can cause Lipid A to activate TNFa = hypertension, shock, death

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11
Q

How do the bacteria evade host attack in Pseudo?

A
  1. Production of biofilm
  2. Elastase destroying antibodies
  3. Exoenzymes alter cytoskeleton structure
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12
Q

How is Pseudo diagnosed?

A

Grow on blood agar OR EMB (look for florescence)

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13
Q

How is Pseudo treated?

A

Multiple antibiotics bc resistant and avoids easily

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14
Q

How is Pseudo prevented?

A

Common in hospitals so clean throughly
- Clean contacts, wounds, jacuzzi, etc

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15
Q

What is the role of Type III secretion in the pathogenesis of Pseudo?

A

Helps avoid immune response (phagocytosis and endocytosis) bc injected directly into target cell

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16
Q

Biochemical and growth properties of Helicobacter pylori

A

Spiral rod, fastidious, and causes ulcers

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17
Q

What types of diseases does H. pylori cause?

A

ulcers, gastritis, different forms of stomach cancer (only bacteria found to cause stomach cancer)

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18
Q

How prevalent is H. pylori in the population and how is it thought to be transmitted?

A

1/3 of world infected (higher in elderly/developing countries) - clinical is 10-15%
Transmission thought to be person to person or fecal-oral (not sure)

19
Q

How does H. pylori survive the pH of the stomach?

A

Produces urease that turns urea into ammonia (ammonia inc pH to more basic)

20
Q

How does H. pylori attach to the mucus above the epithelium?

A

Via a membrane-bound form of urease (replicates well and can survive for a long time)

21
Q

Why does H. pylori move through the stomach mucus and how does it do so (how does it know where to go)?

A

Why: Certain genes only turned on when bound to cell (moves with flagella like corkscrews)

How: Follows concentration gradient of urea and mucins

22
Q

How does H. pylori attach to the stomach cells directly?

A

BabA , HopZ, Alp proteins that target sugars on cell surface = triggers binding in both cells

23
Q

What is a Type IV secretion system and what is it used for?

A

Type 4 secretion system is used to inject other virulence factors (CagA and VacA)

24
Q

What is the role of cagA and vacA in H. pylori?

A

CagA: disrupts cell junctions, turns on cell signaling that alters cell division, cell death

VacA: induces vacuolation and increased membrane permeability that leads to cell death and release of nutrients (more holes in them that kills cells)

25
How does the host cells respond to CagA and VacA in H. pylori?
Damage and inflammation, neutrophils do more damage than good
26
How are the host cells damaged in H. pylori? (apical vs basal)
Apical: exposed tissue damages by toxic acid Basal: inflammatory mediators
27
How does prolonged bacterial growth and inflammation lead to stomach cancer with H. pylori?
mutated cells don't die, rapid cell division
28
How is H. pylori diagnosed?
ELISA, PCR, biopsy
29
How is H. pylori prevented?
Not completely understood yet but don't damage epithelium (smoking)
30
How is H. pylori treated?
H2 blocker (reduces stomach acid) Bacteria elimination needs 2 antibiotics
31
Why is Vibrio cholera resistance to base important?
Able to grow in harsh environments
32
What disease does V. cholera cause?
Severley watery diarrhea, can lose a lot of fluid very fast
33
How come people can be infected multiple times with V. cholera (e.g. do not gain protective immunity)?
Mutates quickly and multiple new strains
34
How is V. cholera transmitted?
Ingestion of contaminated food/water
35
Why does V. cholera have to have a high infectious dose?
No actual protection from immune system other than safety in numbers
36
How does V. cholera get through intestinal mucus?
Flagella and protease that break down mucous with water
37
How does V. cholera attach to cells (and how does that relate to toxin production)?
Uses a toxin-coregulated pilus to adhere, forms micro colonies on surface
38
How invasive is V. cholera?
Does NOT invade epithelium, multiplies without killing host cells
39
Mechanism by which CT binds to cells in V. cholera
Cholera toxin binds to GM1 ganglioside in epithelial cells
40
How does V. cholera turn on cAMP production?
Overactivated G protein continually activates cAMP = high levels
41
How does V. cholera open the CFTR channel (how does that lead to water loss)?
high cAMP levels = CFTR protein stays open and chlorine continuously leaves the cell Chlorine leaving cell also causes water to leave = WATER LOSS
42
How is V. cholera diagnosed?
Cholera-specific dipstick (like pregnancy test)
43
How is V. cholera treated?
Rehydration (water or IV), NO antibiotics bc toxin is doing the damage
44
How is V. cholera prevented?
Vaccine not that effective, avoid contaminated food/water