Pseudomonas and ICU GRNs Flashcards

1
Q

What drugs can treat pseudomonas infections ?

A

1) Piperacillin + Tazobactam
2) 3rd Generation Cephalosporins: ceftriaxone, ceftazidime
3) 4th generation Cephalosporins: cefepime
4) Ciprofloxacin
5) Aminoglycosides: gentimycin, amikacin (used in combination, nephrotoxinc)
6) polymyxins (used with gentimycin, highly nephrotoxic)
7) aztreonam – but usually a bad choice; only if pen allergic

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2
Q

What are the common Manifestations of Pseudomonas?

A
  • Pneumonia - HCAP, VAP, CAP
  • Bacteremia, which can lead to endocarditis
  • Ecthyma Grangrenosum (but not specific)
  • Skin and soft tissue infections (burn patients)
  • Wound infections
  • Hot tub folliculitis
  • Otits Externa (Swimmer’s ear; specific)

Rare: Osteomyelitis, UTI, eye infections

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3
Q

Microbiology/Biochemistry of Pseudomonas

A
  • Gram Negative Rod
  • Aerobic
  • Non lactose Fermenting
  • Oxidase Positive
  • Grape like odor
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4
Q

Describe the microbiology and biochemistry of Pseudomonas?

A
○ Aerobic
		○ Gram Negative Rod 
		○ Non-lactose fermenting
		○ Glucose fermenting
		○ Oxidase Positive
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5
Q

Epiemiology of Pseudomonas:

  • where is it found
  • who is at risk?
  • where can it colonize ?
A

○ Ubiquitous in the environment
○ Throughout hospital environment
§ fluids (dialysis, ophthalmic, rinses, water taps)
§ equipment (whirlpools, respiratory, endoscopes, humidifiers, catheters)
- Airway is colonized by pseudomonas

Risk:
Disrupted physical barriers
Immune deficiencies
Chronic Lung disease (CF)

can colonize respiratory tract

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6
Q

Pathogenesis of Pseudomonas:

  • Describe virulence factors
  • How does it form biofilms
  • what toxins does it secrete?
A
Virulence: 
	 Adherence: pili, flagella 
	LPS - endotoxin -- biggest inducer of cytokine storm -- sepsis 
	Polysaccharide capsule, slime 
		○ 

Biofilm formation: Type IV pili; deposit glycopeptide

Exotoxin A - ADP Ribosylating EF2 (similar to diphtheria toxin)

Type II Secretions (Exoenzymes – ExoS)

Degredative Enzymes:
PLC, Elastase, Cytotoxin, Proteases

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7
Q

What are the clinical Manifestations of Psuedomonas?

A
  • PNA: (HCAP, VAP, CAP) – primarily nosocomial, possibly from hospital equipment
    worse with aspiration
  • Bacteremia – which may lead to endocarditis
  • Echthyma gangrenosum
  • § Pseudomonas Skin and Soft tissue infections (burn patients, hot tub folliculitis, wound infections)

Otitis Externa

Osteomyelitis, Cath-UTIs, Eye infections

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8
Q

Describe the biochemistry of Acinetobacter baumanii

A
- 		○ Gram Negative Coccobacillus 
		○ Non motile 
		○ Aerobic 
		○ Non-lactose fermenter 
		○ Glucose fermenter 
		○ Oxidase Negative (unlike pseudomonas)
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9
Q

Epidemiology of Acinetobacter:

  • where does it colonize?
  • risks for infection?
A
  • Colonizes the skin, respirtaory and GI tracts
  • Nosocomial pathogen of the ICU
  • Opportunistic

-

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10
Q

Pathogenesis of Acinetobacter

A
  • Survives for longer periods in dry conditions

- Polysaccharide capsule

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11
Q

Clinical Presentations of Acinetobacter

A

ICU patients

	○ VAP 
	○ CAUTI  -- cathater associated blood stream infection 
	○ CLABSI -- Central line associated blood stream infection 
	○ Wound infections 
	○ Sacral decubitous ulcers
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12
Q

Treatment for Acinetobacter

A

• Treatment of Acinetobacter — often use combination therapy

	○ 3rd and 4th generation cephalosporins 
	○ Carbapenems 
	○ Beta Lactams w/ beta lactamase inhibitor 
		§ Ampicillin/sulbactam 
		§ Sulbactam has activity by itself 
	○ Fluoroquonones 
	○ Aminoglycosides 
	○ Polymyxins -- high toxicity 
	○ Tigecyclin -- gets into bone and abscesses well, but leaves the blood stream too quickly for bacteremia
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13
Q

name two other GN Rods of the ICU

what is the go to treatment

A

Stenotrophomonas maltophila
• Often colonizes respiratory tract (CF, Vents, etc)
Treated with TMP/SMX

  • Burkholderia cepacia
    • seen mostly in CF
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