Gm- Opportunists Flashcards

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1
Q

List 7 commonly isolated Gram negative bacteria that often grow as opportunists in debilitated
patients.

A
Escherichia coli
Pseudomonas aeruginosa
Klebsiella pneumoniae
Enterobacter cloacae
Serratia marcesens
Proteus vulgaris & Proteus mirabilis
Acinetobacter baumanii
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2
Q

Explain how specific known properties of each organism can contribute to its ability to cause infections.

A

Antibiotic resistance

Biofilms

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3
Q

List three diagnostic critera for diagnosis of Gram negative opportunists.

A

Diagnostics:

  • –Colony morphology
  • –Selective medium
  • –Biochemical tests
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4
Q

Explain how infections by Gram negative opportunists are prevented and the role of antibiotics in controlling infections.

A

Treatments: Abx used dependent on infecting microbe and site of infection

Prevention: many things in combination need to be used to prevent infections

  • –Control underlying compromising factors
  • –Reduce catheter usage, increase hygiene
  • –Decontamination of medical equipment
  • –Cleaning of hospital spaces
  • –Handwashing and glove use!
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5
Q

List three things that can increase risk of infection by opportunistic pathogens

A
  1. Decreased/altered immune function: chronic disease, chemo/immunosuppressive therapies, antibiotics
  2. Alterations in innate protective mechanisms
  3. Breach of physical barriers: surgery, indwelling catheters
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6
Q

What are opportunistic pathogens? What bacteria typically cause them?

A

Pathogens that can only cause disease in compromised people

Typically caused by Gm- bacteria

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7
Q

What are some sources of opportunistic pathogens?

A

Everywhere! Water, soil, vegetables, us

HOSPITALS!

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8
Q

What general virulence factors are associated with opportunistic infections? (4)

A

LPS -> systemic response if in bloodstream
Adhesins: cell-surface structures that mediate colonization
Nutrient acquisition factors
Toxins

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9
Q

What can contribute to pneumonia from opportunistic pathogens? (5)

A
Lung/heart disease, cancer
Surgery
Lying on back for a long time
Mechanical ventilation
Sedation
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10
Q

What are nosocomial infections? How can they be prevented?

A

Infections acquired in hospitals

Handwashing!

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11
Q

Name two important opportunistic pathogens with high INNATE resistance to antibiotics. Why are they so resistant?

A

Pseudomonas aeruginosa
Acinetobacter baumanii

Resistant because they grow in soil and have to compete with Abx producers in soil

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12
Q

What are biofilms? Why are they important? Where do they form?

A

Single or mixed species films of bacteria on a surface that increase their resistance to Abx

Form on catheters, sutures, chronic wounds, lung infections, endocarditis, UTIs
–65% of nosocomial infections are biofilm-related

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13
Q

How are biofilms formed?

A

Organic layer on catheter -> surface-associated cells -> ECM -> induction of biofilm Abx resistance genes

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14
Q

What is quorum sensing? What does it have to do with virulence factors?

A

A way for bacteria to talk to one another using chemicals that will indicate that they are surrounded by a certain number of organisms of the same type

Bacteria generally only induce virulence factors when they are at high density

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15
Q

What are three infections that can be caused by commensal E. coli?

A

UTIs
Bacteremia
Meningitis

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16
Q

Uropathogenic E. coli: epidemiology, including number of serotypes

A

Cause most UTIs
-Catheters important source of infection
-Women more susceptible than men
Only a few serogroups cause infection

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17
Q

Uropathogenic E. coli: how does infection occur?

A

Invasion and spread of bacteria into UT
Uses adhesins to aid in colonization and ascension of urethra
—Different strains = diffferent types = different colonizable locations
Form biofilms -> persistent infections

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18
Q

Uropathogenic E. coli: what are clinical symptoms? How many bacteria must be present to have a diagnosable infection?

A

Need 10^5 bacteria/ml in urine

Cystitis (inflammation of bladder)

  • -Dysuria (burning during urination)
  • -Frequent/urgent urination

Acute pyelonephritis (kidney infection)

  • -Flank pain and tenderness
  • -Fever
  • -Dysuria (burning during urination)
  • -Frequent/urgent urination
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19
Q

Uropathogenic E. coli: how is it treated?

A

Acute and self-limiting
Treat pyelonephritis with Abx

Commonly reoccur: human behavioral, biofilm formation

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20
Q

Uropathogenic E. coli: what is the P-pili? What does it bind to?

A

Binds to glycolipids found on human P blood group (Gal-Gal moiety)

  • -Common in PYELONEPHRITIS
  • -Different individuals have different P blood groups -> different susceptibility to P-pili/E. coli UTIs
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21
Q

Uropathogenic E. coli: what are type I pili?

A

Mannose-binding pili - allow them to bind mannose on host uroepithelial cells
–Common in CYSTITIS

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22
Q

E. coli bacteremia: epidemiology, pathogenesis

A

Leading cause of nosocomial bacteremia

–Commonly invades through IV catheters or UTIs with obstructed urine flow

23
Q

E. coli bacteremia: how does it resist serum?

A

Produces K1 capsule: polysialic acid capsule (same as N. meningitidis)
–Sialic acid is on host glycoproteins/lipids, so no effective immune response

24
Q

E. coli bacteremia: what is its most dangerous virulence factor?

A

LPS! Life-threatening

25
Q

E. coli meningitis: what is it? What virulence factors are important for it? Briefly describe its pathogenesis.

A

Causes meningitis in neonates
Main virulence factor = K1 polysialic acid capsule (escapes phagocytosis)
–Siderophores very important
Proliferates in CSF -> inflammation, tissue damage

26
Q

Pseudomonas aeruginosa: what range of infections can it cause?

A

Infections of burns, eyes, wounds, catheters, implants
Pneumonia, especially ventilator-associated
Bacteremia in immunocompromised patients

27
Q

Pseudomonas aeruginosa: role in cystic fibrosis

A

Forms biofilms -> recalcitrance and resistance
Infects more than 80% of CF patients
Die in mid-30s due to inflammation/infection
Cannot be cleared

28
Q

Pseudomonas aeruginosa: how does it evolve in chronic infections (CF)? (may not be important)

A

Produces alginate slime that may block phagocytosis (very mucousy)

29
Q

Pseudomonas aeruginosa: virulence factors (5)

A

LPS
Extracellular elastases (proteases) and phospholipases
T3SS exotoxins:
–ExoA. Inhibits protein synthesis.
–ExoS and ExoT. Exoenzymes that modify host cell regulatory proteins
–ExoU. Phospholipase activity within host cell
Pyocyanin

30
Q

Pseudomonas aeruginosa: why does it produce a green color?

A

Blue-green pigment = toxin called pyocyanin

–Affects host cell function, generates ROS

31
Q

Klebsiella pneumoniae: clinical syndromes

A
Pneumonia when other conditions are present
--Associated with alcoholism
--Red currant jelly sputum
UT, wound infections
Diarrhea by enterotoxigenic strains
Bacteriemia and meningitis
32
Q

Klebsiella pneumoniae: virulence factors

A

CAPSULE:

  • -Reduced phagocytosis and complement susceptibility
  • -Produces mucoid phenotype
33
Q

Enterobacter cloacae: epidemiology

A

Hospital-associated!

  • –Associated with burns, wounds, respiratory/UT/catheter associated infections
  • –Forms biofilms

Virulence factors unknown

34
Q

Serratia marcesens: epidemiology, virulence factors

A
Very common enterobacteriaciae
---Produces a red color when grown (pink color on showers, water bottles!) - likes water
Most common in respiratory/UT infections
---Can colonize joints, most tissues
Generally seen secondary to immune problems, instrumentation, Abx use
Virulence factors:
---MS-fimbrae
---Proteases
---Siderophores
---Swarming motility (see Proteus)
35
Q

Proteus vulgaris & mirabilis: clinical syndromes, virulence determinants (2)

A

Commonly causes UTIs
Virulence determinants:
–Flagella (swarm motility- make a surfactant, then swim through it)
–Urease production: can contribute to stone formation due to urine pH change

36
Q

Acinetobacter baumanii: characteristics, epidemiology

A
Similar to P. aeruginosa (non-fermenter)
---Oxidase negative
---Short rod
---Increasingly multi-drug resistant
Causes nosocomial infections, especially with indwelling devices
37
Q

UPEC: virulence factors (5)

A
Pili
LPS
Capsule
Motility
Exotoxins (including hemolysin)
38
Q

Classify P. aeruginosa’s oxygen usage.

A

Obligate aerobe (cannot ferment sugars)

39
Q

Acinetobactor baumanii: virulence factors (4)

A

Capsular polysaccharides
Adhesins
Proteolytic/lipolytic enzymes
LPS

40
Q

E. coli: energy metabolism

A

Facultative anaerobe

41
Q

E. coli: lactose fermenting?

A

Positive

42
Q

K. pneumonia: energy metabolism

A

Facultative anaerobe

43
Q

K. pneumonia: lactose fermenting?

A

Positive

44
Q

S. marcescens: energy metabolism

A

Facultative anaerobe

45
Q

S. marcescens: lactose fermenting?

A

Negative

46
Q

E. cloacae: energy metabolism

A

Facultative anaerobe

47
Q

E. cloacae: lactose fermenting?

A

Positive

48
Q

P. mirabilis: energy metabolism

A

Facultative anaerobe

49
Q

P. mirabilis: lactose fermenting?

A

Negative

50
Q

A. baumanii: energy metabolism

A

Non-fermenter

51
Q

A. baumanii: lactose fermenting?

A

Negative

52
Q

P. aeruginosa: energy metabolism

A

Obligate aerobe

53
Q

P. aeruginosa: lactose fermenting?

A

Negative

54
Q

What is CRE?

A

Carbapenem-resistant enterobacteriaceae