describe the shape, location, mobility, and need or O2 of Pseudomonas aeruginosa.
- G- bacilli (rods)
- ubiquitous (found everywhere): soil & water
- motile: one/several polar flagella, polar pili (twitching)
- aerobic (this species): some strains anaerobically grow with nitrate
what do the pseudomonas aeruginosa colonies produce?
- water soluble pigments that function as antibacterials
- pyocyanin (blue-green)
- pyoverdin (green)
- fluorescein (yellow fluorescence)
- fruity or grape like odor to colonies (or near wounds)
pseudomonas aeruginosa grows rapidly and is very robust… does it have nutritional requirements?
- minimal nutritional requirement
- do not ferment (oxidize sugars): indophenol oxidase (like Neisseria sp.)
- need only acetate and ammonia as carbon and nitrogen sources (most organic compounds can provide this including petroleum and toxic wastes
- can survive in hand creams, soaps, and dilute antiseptics
name the persistence virulence factors of pseudomonas.
- mucoid polysaccharide capsule (alginate) shields from immune system
- siderophores
- elastase
- exotoxin A
- phopholipase C
name the dissemination virulence factors of pseudomonas.
- toxin A
- collagenase
- elastase
- exoenzymes
- flagella
- heat stable hemolysin
- tissue damage by proteases and toxins
which 3 of the dissemination factors are considered spreading factors?
- collagenase
- elastase
- exoenzymes
which 2 virulence factors are nutritional aids? describe them
- siderophores (iron binding compounds): complete with transferrin for iron, iron limitation causes increase production of elastase and exotoxin A
* damages tissue/creates conditions that make iron more accessible - phospholipase C: hydrolyzes phospholipids (lecithin) in the eukaryotic membrane, releasing usable phosphate
where and how do we encounter pseudomonas?
- where = soil and water
- how:
- adheres to vegetables and plant matter
- in water taps, drains, wet surfaces: otis externa (swimmer’s ear)
- hot tubs! (folliculitis, dermatitis): hot tub rash
pseudomonas is an OPPORTUNISTIC pathogen… how does it enter into a host cell?
- local or systemic breach of immune system
- immunocompromised patients
- *org does not adhere well to healthy epithelium:
- can enter thru abrasions, cuts, etc.
- usually they don’t get far unless in large #s
**after entry of pseudomonas the ability of it to spread and multiply depends on what two things?
- avoiding phagocytosis
2. successful adherence to a surface
**adherence of pseudomonas to epithelia is mediated by what 2 things?
- flagella
- pili
* interactions with glycolipid (cleaves sialic acid to create asialo GM1; receptor for Type 4 pili) on host cells and toll like receptors (TLR5)
what kind of phenotype is the pseudomonas polysaccharide capsule (alginate)?
mucoid phenotype
what components of the pseudomonas polysaccharide capsule (alginate) helps with its spread and multiplication?
- major adhesin and component of biofilm in cystic fibrosis patients
- production is highly regulated
what are the two key factors in pseudomonas spread and multiplication?
- polysaccharide capsule (alginate)
2. numerous cytolytic exotoxins
how do pseudomonas spp cause damage?
- LPS
- exotoxins (cause local inflammation)
- multifunctional enzymes (proteases)
- type III secretion system
how does LPS cause damage?
- adhesin
- lipid A = endotoxin; which interacts with host TLR4 to initiate inflammatory response
* fever, hypotension, G- sepsis
* less inflamm than e. coli or s. typhimurium - core oligosaccharide interacts with CFTR (an ATP-binding cassette transporter; cystic fibrosis transmembrane conductance regulator)
* bacterial internalization, initiation of immune resistance - Long O-antigen side chains
* responsible for resistance to human serum, antibiotics, detergents
how do endotoxins cause damage?
- they cause local inflammation
- some kill host tissue (exotoxin A): ADP-ribosylation of EF-2 (similar to diptheria toxin)
- all are tightly regulated
how do multifunctional enzymes (proteases) cause damage?
- elastase:
- cleaves elastin & colllagen: direct tissue damage
- cleaves proteinase inhibitors
- cleaves immune system components: complements Ig’s
- LasA:
- serine protease that works with elastase to degrade elastin
how does the type III secretion system cause damage?
- delivers virulence factors directly into host cells
- transfer from bacterial cytosol to host cytoplams
- similar to flagella
- targets specific proteins on host cells
- induced by host cell contact or low calcium levels
-secretion effectors include ExoS, ExoT, ExoU, and ExoY which are transcriptionally controlled by ExsA
what type of epithelium does P. aeruginosa adhere to best?
- does not adhere well to normal intact epithelium
- piliated strains adhere better than non-pilated strains
why do cystic fibrosis respiratory cells bind more P. aeruginosa than those of normal cells?
- cystic fibrosis transmembrane conductance regulator (CFTR)
- dysfunctional in CF patients:
- loss of Cl- transport
- hereditary
- can be rescued with normal copy of gene
what can CFTR cause?
-decreased sialylation of surface glycolipids: p. aeruginosa binds to these asialo-glycolipids
what happens to mucous production in cystic fibrosis and p. aeruginosa?
- thick mucous produced which impairs mucociliary system
- dehydration of respiratory secretions
how is p. aeruginosa shielded from the immune system?
- mucoid exopolysaccharide (alginate) shields organism from immune system
- however these alginate strains produce less protease and toxins
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G- pathogens of mucosal surfaces pt.155
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G-pathogens of mucosal surfaces pt.269
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Neisseria (G-)33
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Haemophilus (G-)10
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Pseudomonas (G-)31
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Listeria monocytogenes (G+)9
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Small G- Pathogens (chlamydiae, rickettsiae, ehrlichia)72
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Clostridia (G+)66
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Virus Classification, Structure & Replication84
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Neurological Viruses38
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Retroviruses, AIDS, & Tumor Viruses52
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