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94 Cards in this Set

  • Front
  • Back
How many Pseudomonas species are there?
~140 (know by rRNA studies)
General characteristics of Pseudomonads?
Rod shaped
Polar flagellum
Gamma proteobacteria
Very diverse genus
Metabolic capabilities
Mostly aerobic (some facultative anaerobes)
Diverse ecological niches
Imp role in nature's C and N cycle
What is a characteristic feature of Pseud.?
fluorescent siderophore production
Pigment production
What kind of pathogen is Pseud?
What does P. fluorescens do?
Plant growht properties
Plant pathogen control (biocontrol)
What does P. putida do?
Degradation of polycyclic hydrocarbon (bioremediation)
What does P. syringae do?
Plant pathogen (tomatoes, tobacco)
Ice-nucleation properties cause frost damage
What does P. stutzeri do?
Degradation of aromatic compunds, carbon tetrachloride (a CFC), crude oil and other hydrocarbons, biocides, metal cycling
P. aeruginosa general characteristics:
Tests it's positive for?
Pigment production?
Motile (polar flagellum)
Ubiquitous in soil and water
NON-spore forming
Tests: Oxidase +, Beta hemolytic
Grows on laboratory medium and blood agar
Blue (pyocyanin), Yellow (pyoverdin), Brown (pyomelanin)
Where can P. aeruginosa colonize?
Different ecological habitats
Can contaminate water sources, medical equpment (can cause disease)
What O2 env't does it like?
facultative anaerobe
(NO3 is terminal acceptor)
What kind of metabolism does P. aeruginosa have?
highly diverse
Minimal nutritional requirements
Growth on many dicerse organic cmpds
Optimal growth of P. aeruginosa?
37 degrees
but can grow btw 15-42 degrees
=>Versatile physiology
Tolerance to env't stimuli?
V/ tolerant to env't and physiological stresses
ex: osmolar, pH, metals, weak antiseptics, starvation
Colony morphology?
Depends where its being isolated from
Distinctive phenotypic variants
(mucoidy w/ alginate over production, small colony variants, pigment overproduction/loss, autolysis)
What kind of a pathogen is P. aeruginosa?
Who does P. aeruginosa cause disease in?
Compromised hosts
->immuno-suppression, compromised mucosal barrier, damaged tissues
Nearly alll tissues and organs can be affected
4th most common nosocomial (hospital acq'd infection) pathogen (10%)
What kind of infection can P. aeruginosa cause?
Example of acute infections caused by P. aeruginosa?
Nosocomial pneumonia
Corneal infection
Bacteremia and sepsis
Example of subacute infections by P. aeruginosa?
Soft tissue, skin infection
Bone and joint infection
Examples of P. aeruginosa chronic infections?
Chronic airway infection (CF)
Otitis media
What are virulence factors important for?
Pathogenesis of acute and subacute infections
What are virulence factors involved in?
Tissue colonization
Cell/tissue damage
Invasion and dissemination
Activation of local and systemic inflammatory responses
What defines the type of virulence factors ass't with the bacteria?
Host model systems
-Plant model
What kind of virulence factors are there?
Type III secretion systems and effector ptns
Flagellum, Type IV pili, non-pilus adhesins
Pyocyanin, siderophores, rhamnolipids, HCN
Protease, elastase, lipase, phospholipase
Whats the first step require for cells associate virulence factors?
Adherence to epithelial cellls
How does P. aeruginosa's virulence factors bind epithelial cells?
Usually mediated by Type IV pili
-distal end contcts various surfaecs in a non-specific way (inert surfaces) or receptor specific way (galactose or mannose binding ptns to glycosphingolipids) on mammalian host cell surfaces
How does P. aeruginosa draw itself cloer to the host after it attaches?
Retracts pilus
Mediates twitching (surface) motility
What part of P. aeruginosa can bind mucin in host?
Flagellar cap ptn ( P. aeruginosa has a single polar flagellum)
Describe LPS (cell ass't virulence factor)
Embedded in OM
LPS can be a ligand to bind CFTR and enter epithelial cells
This response might be protective (engulf and destroy)or pathogenic depending on cell type
Does the O-ag of LPS cause a protective response in the host?
Probably not, even though it is highly immunogenic
What does the Lipid A region of LPS do?
Induces prod'n of inflammatory cytokines
-> mainly through CD14 and TLR4 mechanisms
What happens if too much TNF-alpha and IL-1 is released?
Septic shock
What can secreted extracellular virulence factors do?
Cause tissue damage
What are examples of secreted extracellular virulence factors of P. aeruginosa?
Alkaline protease
Protease V
Exotoxin A
Elastases LasA and LasB
Phospholiase C
Lipase LipA and LipC
What do Alkaline protease and protease IV do?
Degrade complement components and cytokines
Hydrolyzes fibrin and fibrinogen
What does Exotoxin A do?
Enter euk cells by receptor mediated endocytosis
Catalyzes ADP-ribosylation and inactivation of EF-2
.: inhibits ptn biosynthesis and causes cell death
-Causes local tissue damage, bacterial invasion, can impair host defenses
What do Elastases Las A and Las B do?
Destroy elastin (imp in lung tissue and bld vessels), fibrin and collagen, human surfactant, IgG/IgA
What does phospholipase C do?
Cleaves phospholipids
Induces release of inflammatory cytokine
Vascular permeability and tissue damage
What do lipases LipA and LipC do?
Degrade phospholipid (imp in lung surfactant)
Induce inflammatory cytokines
(lipases are highly immunogenic)
Describe how the Type III secretion system and its effector ptns work.
Exoptns secreted through T3SS
->require close contact with target cells to be toxic
-T3SS injects its effector ptns directly into the target cells
What type of infections is T3SS responsible for?
ACUTE infections
-> Kills host quickly
->invasive infections more than subacute or chronic infections
What are the 4 exoenz/toxins belonging to T3SS?
Exoenz S
Exoenz T
Exotoxin U
Exotoxin Y
What do exoenzymes S/T do?
ADP-ribosyltransferase that disrupts actin filaments, intracellular GTP-binding ptns
May impair wound healing and tissue repair
Induce inflammation
What does exotoxin U do?
Highly cytotoxic to mammalian cells
Likely due to phospholipase activity that destroys eukaryotic cell mbs
What does exotoxin Y do?
When do T3SS cause chronic infections?
When the T3SS is mutated
Why does the bacteria have such a wide range of tools of infection at its disposal?
Doesn't always want to kill the host (i.e. in mutant T3SS)
Extracellular virulence factors
Rhamnose-containing glycolipids biosurfactant with detergent like properties
Can dissolve lung surfactant
May be important in biofilm formation
Cytotoxic to PMNs
Extracellular virulence factors
Redox active phenazine pigment that generates ROS
->Causes oxidative stress to host cells
-> Can induce inflammatory response and apoptosis of neutrophils
Extracellular virulence factors
HCN (hydrogen cyanide)
Cytochrome oxidase inhibitor
Causes arrest of mitochondrial respiration
Causes death of C.elegans
Unclear role in human infection
Extracellular virulence factors
Siderophores: Pyoverdin and pyochelin
Iron scavengers
Compete with transferrin for iron
Iron metabolism regulates expression of other virulence factors, bacterial growth and motility
Extracellular virulence factors
Exoplosaccharide and alginate
Important in biofilm formation
What is quorum sensing/
Mode of bacterial communication
Where was quorum sensing first seen?
in V. fischeri (symbiont)
->at high cell density, bacterial cells re luminesent through expression of lux genes
How is QS (quorum sensing) mediated in P. aeruginosa and most other G- bact?
Acyl-HSL (homoserine lactone) molecules
-> Auto inducers
How are acyl-HSL produced?
LuxI-like ptn
When bound to their cognate transcription activator LuxR-like ptn, LuxR activates the transcription of many target genes
Describe QS.
Low density: don't turn on genes
When reaches quorum (critical mass), turns on genes
Cell has synthetases that are LuxI-like ptns
->synthesizes signals that diffuse out into the env't
-After reaching a certain density, bind to LuxR-like receptors
->Induce T on target genes
(after reach a critical density, turn on genes)
What are the 2 acyl-HSL signals in P. aeruginosa?
3-oxo-C12-HSL (LasI-LasR system)
C4-HSL (RhII-RhIR ststem)
(there's also a third non-acyl-HSL system that has the PQS signal: pseudomonas quinolone signal)
What does the QS result in
Coordinated expression of virulence genes (among others) at high cell density that is growth phase dependent
How many genes in Psuedomonas aeruginosa are regulated by QS?
~350 (6%)
This includes virulence factors genes (encoding elastase, rhamnolipids, pyocyanin......)
What does the massive attack model explain?
As single cells (low density), bacteria can't cause disease
However, expression of their virulence factors can alert the host defense/immune system
.: virulence factors are only induced when bacteria has reached a critical density
(As cell density increases, target gene expression inc as well)
In best interest of bacteria to lay low and replicate, without alerting host
->Turn on virulence factors all at once when reach a critical mass so that you can have a longer effect
Why can QS modulate the inflammatory response?
Subvert host responses and cause persistent infection
(ex: 3-oxo-C12-HSL can inhibit IL-12 prod'n from T cells and modulate away from a Th1 response. It cam also inhibit TNF-a (monocytes) and NF-kB signalling)
BUT, 3-oxo-C12-HSL can also induce inflammation by inducing IL-8 in airway epithelial cells
What is another role of QS?
Biofilm formation (critical to persistent chronic infections, particularly in CF patients)
What is cystic fibrosis(CF)?
Autosomal recessive disease
Caused by mutation in CFTR gene (encodes a transmb chloride channel)
Most common Caucasian genetic disease (1/3000 ppl)
How is CF related to P. aeruginosa?
Most CF patients are chronically infected with
->modeldisease for chronic P. aeruginosa infections
What do CFTR mutations cause?
Abnormal NaCl transport across the epithelium
What is the most common mutation in CFTR?
dF508 mutation
->Causes abnormal trafficking of the CFTR ptn
(ptn is there, but doesn't reach the surface, because it is targeted and destroyed)
What do mutations in CFTR end up causing (due to abnormal NaCl transport)?
Thick and dehydrated mucus in airways, GI tract and other exocrine organs
->affects multiple organs, but nowadays, the main cause of disease and death is lung disease
When are ppl with CF infected with P. aeruginosa?
At an early age
They become chronically infected with P. aeruginosa eventually
This chronic infection causes destruction of the lungs and can cause death
What is the difference btw an intermittent P. aeruginosa infection and chronic infection?
- Low bacterial burden
- Normal Lung fct
- Bacterial phenotype similar to environmental strains
- Can be cleared by early aggressive antibiotic treatment
-up to 10^10 bacteri/mL,
-DECREASED lung fct,
-bacteria have adapted to the CF lung env't
-Cannot be eradicated by antibiotic treatment
What's the main difference between a chronic and intermittent P. aeruginosa infection?
In chronic infection, can't be treated
Bacteria never completely go away, even if given antibiotics
Need to cstly take antibiotics
What is a key reason for bacterial persistence in CF patients?
-Clusters of bacteria embedded in a matrix
Why are biofilms so important in bacterial persistance?
Form of bacterial resistance to antibiotics and host defenses
Where does P. aeruginosa form biofilms in CF patients?
In the sputum of their airways
What is a biofilm?
Structure communities of bacterial cvells growing to high densities, encased in an extracellular matric
Where do biofilms attach?
Attach to a surface
They are ubiquitous in the natural env't
What does the biofilm extracellular matrix consist of?
Secreted polysacs, ptns, DNA, bacterial and host cellular debris
What kind of diseases are caused by biofilm infections?
Corneal infections
Peridontal disease
Sinusitis and otitis media
Endobronchial infections in patients with CF
Prosthetic device and catheter-ass't infections
Why are chronic and subacute infections difficult to treat?
Long, aggressive antibiotic treatment
Need to remove the infected tissue and/or foreign body
May be impossible to eradicate (ex: chronic airway infection in CF patients)
--> Seen with a wide range of bacteria: staph, strep, E. coli, NTHi
How do biofilms form?
Individual cells attach to the surface and remain immobile
Bacteria divide to form aggregates, secrete polysac and form an extracellular matrix
Aggregates grow and mature: change cellular metabolism and gene expression, cell-to-cell communication (QS), sub-specialization of the bacterial population, disintegratioin and release of cells
(get a heterogenous population of genes, since dif genes are expressed in a biofilm than under other circumstances)
What does biofilm growth require (based on in-vitro studies)?
Type IV pilus for surface attachment and motility
Exopolysac production, including alginate
What are the benefits of a biofilm for the bacteria?
At high cell density, cell-to-cell communication allow bacteria to regulate genes differently than at low density (virulence and toxins)
Cell physiology and metabolism change and allow the bacteria to withstand more stresses
Bacterial population differentiates phenotypically and genetically into specialized sub-population
What is the difference btw acute and chronic infections?
Acute: Invade ad disseminate, but are more susceptible to host defense and antibiotics
Chronic: Localized and persits, but are more resistant to host defenses (won't cuase septicemia)
How are biofilms less invasive than plaktonic bacteria?
Biofilms: bacteria are encased in tenacious matrix
-> may limit spread of bacteria
-> encased bacteria may provoke less inflammation
Invasion and motility genes are turned off in biofilms
(Damper acute virulence, create niche to replicate in)
What happens once bacteria form a biofilm?
Bacteria are protected from the host's immune response
->Greater resistance to oxidants (such as NO and peroxidase) and AMPs
-> More difficult to phagocytose, do not activate PMNs as much as planktonic bacteria
-> PMNs can be immobilized by the biofilm matrix and host cells have difficulty penetrating its structure
-> Ab can be trapped in the biofilm matrix and fail to mediate opsonic killing
Can Ab kill biofilm bacteria?
Even at very large Ab doses, can't kill them off completely
(A significant fraction of biofilm bacteria are not killed by antibiotics)
->This is because bact in a biofilm are heterogenous, .: some cells different from others
How are biofilms physiologically heterogeneous?
Biofilm growth produces gradients in nutrients, oxygen and metabolic waste
What is ana important bacterial nutrient?
Important to biofilm formation at several stages for dev'p
-> Bacteria are starving for iron within biofilms
Do biofilms produce genetic variants?
Describe the genetic variants in biofilm growth.
CF patients are often infected with multiple genetic variants (morphotypes)
In-vitro biofilm growth also generates genetic varients at a high frequency
Increased genetic diversity due to oxidative stress, endogenous to biofilm growth generating DNA breaks
What is the benefit of this diversity?
Confers strength to bacterial populations and contribute to persistence
-> Diverse populations have a greater chance of survival than homogenous populations
->Will have some resistant strains
P. aeruginosa is an opportunistic pathogen
Highly versatile
Multiple virulence factors important in the pathogenesis of acute and subacute infections
Complex regulation of virulence factors through a QS system and integration of multiple regulators
CF chronic airway disease presents an important and unique paradigm of chronic infection
Biofilm growth presents a different paradigm of infection pathogenesis and is o chronic infections
P. aeruginosa: pathogenic?
Not meant to be a pathogen, but they are when they come into contact with humnand
Probably behaves differently in nature