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Micro Patho > Gram Negative Rods > Flashcards

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
Q

How does the host cells respond to CagA and VacA in H. pylori?

A

Damage and inflammation, neutrophils do more damage than good

26
Q

How are the host cells damaged in H. pylori? (apical vs basal)

A

Apical: exposed tissue damages by toxic acid

Basal: inflammatory mediators

27
Q

How does prolonged bacterial growth and inflammation lead to stomach cancer with H. pylori?

A

mutated cells don’t die, rapid cell division

28
Q

How is H. pylori diagnosed?

A

ELISA, PCR, biopsy

29
Q

How is H. pylori prevented?

A

Not completely understood yet but don’t damage epithelium (smoking)

30
Q

How is H. pylori treated?

A

H2 blocker (reduces stomach acid)

Bacteria elimination needs 2 antibiotics

31
Q

Why is Vibrio cholera resistance to base important?

A

Able to grow in harsh environments

32
Q

What disease does V. cholera cause?

A

Severley watery diarrhea, can lose a lot of fluid very fast

33
Q

How come people can be infected multiple times with V. cholera (e.g. do not gain protective immunity)?

A

Mutates quickly and multiple new strains

34
Q

How is V. cholera transmitted?

A

Ingestion of contaminated food/water

35
Q

Why does V. cholera have to have a high infectious dose?

A

No actual protection from immune system other than safety in numbers

36
Q

How does V. cholera get through intestinal mucus?

A

Flagella and protease that break down mucous with water

37
Q

How does V. cholera attach to cells (and how does that relate to toxin production)?

A

Uses a toxin-coregulated pilus to adhere, forms micro colonies on surface

38
Q

How invasive is V. cholera?

A

Does NOT invade epithelium, multiplies without killing host cells

39
Q

Mechanism by which CT binds to cells in V. cholera

A

Cholera toxin binds to GM1 ganglioside in epithelial cells

40
Q

How does V. cholera turn on cAMP production?

A

Overactivated G protein continually activates cAMP = high levels

41
Q

How does V. cholera open the CFTR channel (how does that lead to water loss)?

A

high cAMP levels = CFTR protein stays open and chlorine continuously leaves the cell

Chlorine leaving cell also causes water to leave = WATER LOSS

42
Q

How is V. cholera diagnosed?

A

Cholera-specific dipstick (like pregnancy test)

43
Q

How is V. cholera treated?

A

Rehydration (water or IV), NO antibiotics bc toxin is doing the damage

44
Q

How is V. cholera prevented?

A

Vaccine not that effective, avoid contaminated food/water

Micro Patho (2 decks)

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