LECTURE - Pseudomonas aeruginosa & non-fermenters Flashcards
non-fermenter
uses glucose, or other sugar, oxidatively, if it uses sugar as an energy source at all
- all gram neg rods
- O/F test
What is a “non-fermenter”?
collection of gram neg bacilli that, in contrast to Enterobacteriaceae:
- do not ferment sugars
- oxidase positive typically
- found in many environments (ubiquitous) but are rarely normal flora in humans
- cause opportunistic, hospital-acquired (nosocomial infections)
- antibiotic resistant
most common patient isolates if non-fermenters (3)
- P.aeruginosa
- Acinetobacter spp. (esp. multidrug resistant A. baumanii = emerging problem)
- Stenotrophomonas maltophila
Characteristics of P. aeruginosa
- can grow with most simple carbon and nitrogen sources
- found in soil, plants, water, ubiquitous!
- motile by a polar flagellum
- oxidase pos
- produces dyes: pyoverdin and pyocyanin
- biofilmformation
cystic fibrosis
- Caucasian newborns
- autosomal recessive
- defective cystic fibrosis transmembrane conductance regulator (CFTR)
- ATP- and cAMP-dependent Cl- conductance channel
- thick mucus, impairs mucociliary clearance, lungs and gut
- chronic colonization (takes advantage) = P. aeruginosa, S. aureus, Burkholderia cepacia
- colonization by early adolescence
- chronic carrier state
- Antibiotics do not clear infection
- extensive lung damage
seven key virulence factors of Pseudomonas
- pyocyanin
- adhesins (type IV pili)
- type III secretion and associated effector proteins
- exotoxin A
- quorum sensing and biofilms
- alginate
- multidrug efflux
alginate
- produced by mucoid strains
phenotype of CF isolates (as if the mucus from defective CFTR wasn’t enough) - complex regulation
- polymer of mannuronic and guluronic acids
- part of biofilm matrix
T or F. P. aeruginosa has a small genome
F! it’s pretty large = lot of possibilities!
- two-component regulatory system proteins
pyocyanin
- “blue pus”
- secondary metabolite
- non-essential (not every strain produces it)
- regulated by quorum sensing
- causes cellular damage in vitro
type IV pili
- adhesin
- twitching motility
- binds to asialo-Gm1 with help of neuramindase
- cell adherence
- natural transformation (pick up DNA)
- site for bacteriophage infection
- DNA binding
non-pilus adhesins of P. aeruginosa
- flagellum binds to mucin
- Pseudomonas LPS two types:
> A band, a rhamnose homopolymer
> B band, 2-6 sugar repeat units of O antigen, that confers serum resistance and serotype specificity
> outer core binds to CFTR, which triggers innate immune response; CF = this trigger is compromised
non-pilus adhesins of P. aeruginosa
- flagellum binds to mucin
- Pseudomonas LPS two types:
> A band, a rhamnose homopolymer
> B band, 2-6 sugar repeat units of O antigen, that confers serum resistance and serotype specificity
> outer core binds to CFTR, which triggers innate immune response; CF = this trigger is compromised
T3SS can be functionally divided into five components
- needle complex
- translocation apparatus
- regulatory proteins
- effector proteins
- chaperones
** work together to inject effector proteins into host cells in a highly regulated manner **
secreted effector enzymes of T3SS 94)
- ExoS: impairs phagocytic killing by PMNs
- ExoT: similar to Exo S but inhibits macrophages
- ExoU: toxic to macrophages, but not PMNs; aids in dissemination
- ExoY: adenylate cyclase (converts cellular ATP to cAMP)
ExoA (exotoxin A)
- NOT a T3SS effector; secreted independently
same as diphtheria toxin… - ADP-ribosylates elongation factor 2
- induced by low iron conditions
BUT different - amino acid sequence
- receptor on host cells (300 kDa glycoprotein)
- most clinical isolates produce ExoA
- mutants are less virulent in animal models
- contributes to tissue destruction, inflammation, and inhibition of phagocytosis by PMNs