Flashcards in Virulence factors Deck (48):
component G- bacterial cell wall
released when bacterial cell die
LPS (or LOS)
Portion of LPS.
highly conserved endotoxin forming outer leaflet of outer membrane.
if cell can't make lipid A, can't survive
antigenic portion of LPS. Non-toxic.
adhesion to host lectins
G- immune response
Lysis of G- bacteria --> LPS --> Lipid A binds to CD14 and TLR4 on macrophage --> cytokines (IL-1, IL-6, IL-8, TNFalpha, PAF)
G+ immune response
Lysis of G+ bacteria --> Peptidoglycan fragments & Lipotechoic acid --> binds to TLR2 and TLR6 on macrophage --> activates transcription --> cytokines (IL-1, IL-6, IL-8, TNFalpha, PAF)
free of LPS endotoxin (lipid A)
How do you vizualize a bacterial capsule?
What is the Quellung reaction?
antibodies bind to the bacterial capsule
The antibody rxn allows these species to be seen under microscope.
If reaction is positive, the capsule becomes opaque and appears to enlarge.
Streptococcus pneumoniae, Klebsiella pneumoniae, Neisseria meningitidis, Haemophilus influenzae, Escherichia coli, and Salmonella.
how do capsules block phagocyte receptor binding? (3 ways)
1)negative charge (acidic) capsules repel phagocyte
2) cover components of baterial cell surface recognizable to phagocyte receptor
3) reduce complement activity --> sialic acid
what is sialic acid?
component of some bacterial capsules. It binds factor H & chews up complement so complement can't destroy bacteria.
It is NOT antigenic
protein secreted by bacterial cell --> disease symptoms
binds MHCII & TCR w/o antigen present (non-specific T cell activation). It is a type of exotoxin.
What are three examples of superantigen exotoxins?
1) staphylococcal enterotoxins
2) TSS toxin
3) streptococcal pyrogenic toxins
what is quorum sensing?
in biofilms, bacteria secrete "autoinducer" which activates transcriptional regulators when reaches sufficient concentration.
ex: G- bacteria grow together.
@low density --> QS can't bind
@high --> QS signal-receptor complex forms
staph aureus's exotoxin virulence factor?
pore-forming toxin. Alpha-toxin inserts into membrane, oligomerizes and forms pores which leads to cell lysis
What bacteria and exotoxin lead to gas gangrene?
alpha toxin = PLC enzyme
it degrades cell membrane which leads to lysis of cell. This leads to decrease in muscle blood flow which leads to occlusive plugs and results in low oxygen environment which is favorable for bacteria.
B binds cell membrane, A breaks off and inactivates (ADP-ribosylates) elF2 which is necessary for protein synthesis inside of cells.
What bacterium has same MOA as diptheria exotoxin?
Vibrio cholerae toxin
toxin permanently activates Gs which INCREASES cAMP --> CFTR channel continually activated --> Diarrhea
type of intracellular exotoxin
encoded in pathogenicity islands
injected into host cell by type III "Injectisome"
"floppy baby", flaccid paralysis
what medium do Neisseria meningitides grow?
Chocolate agar or thayer martin
what is the main virulence factor for neisseria meningitides & Pathogenesis?
Invasion and growth in blood stream via capsule --> LOS released while organism is intact --> Lipid A released which blebs --> inflammatory response --> increases permeability of capillaries --> shock & DIC
which serogroups on capsule in neisseria meningitidis most commonly cause serious disease?
B, C, Y (causes most), W-135, A
what are the clinical features of meningitis?
-common in college aged students
- neck stiffness, rash
- fever, nausea, vomiting, myalgia
- petechial rash!
What color does Pseudomonas aeruginosa stain?
blue-green pigment with fruity odor (pus can be colored and useful for diagnosis)
what is the main virulence factor of pseudomonas aeruginosa and what is the pathogenesis?
ADP ribosylates elF2 on diphthamide residue
A functions same as diptheria
B has different specificity
what are the cytolysins of P. aeruginosa?
1) Phospholipase C
What type III exotoxins exist with P. aeruginosa?
1) ExoS (alters cell shape and prevents DNA synthesis) & ExoT (inhibits phagocytosis)
2)ExoU- Phospholipase that causes cell necrosis and is associated with more virulent, fulminant disease
what are exoenzymes and what bacteria are they important for?
"spreading factors" responsible for signficant tissue damage and faciliate spread through tissue by degrading immune components and reducing effeective response
ex: elastases-- lung damage)
CFTR mutation exacerbated by which bacteria?
chronically infects by age 20. causes chronic inflammation and bouts of pneumonia. Causes most inflammation and is major cause of morbidity and mortality
pathogenesis in CF lung (P. aeruginosa)
forms biofilm with other species and this leads to persistent infection, chronic inflammation and impedes gas change.
exacerbation with fever and increases sputum production
eventually lungs fail
polysaccharide virulence factor associated with p. aeruginosa.
it is a component of mature biofilm that initially isolates from CF infections that are non-mucoid. It switches to mucoidy. It is linked to severe disease
what exopolysaccaride virulence factors are associated with P. aeruginosa?
Pel and Psl polysaccharides
regulated by quorum sensing
what reservoir does staph aureus colonize?
hand hygene is shown to cut down infection rates in hospitals of what bacteria?
which types of capsule are linked to severe illness in S. Aureus?
5 and 8
Protein A is major virulence factor for what bacteria and how does it work?
Binds Fc portion of IgGs. Prevents complement from binding same region, prevents phagocytosis
which cytolysins are important virulence factors for staph aureus?
alpha-toxin = forms pore in membrane, targets PMNs in infection
beta-toxin = sphingomyelinase
gamma-toxin = Planton-Valentine Leukocidin (PVL), pore forming that is carried most often by strains causing community-causing infection and more severe symptoms (takes out WBCs)
Staphyloccal food poisoning is caused by what?
ingestion of preformed staph enterotoxins (SEA, SEB, SEC)
Toxic Shock syndrome is caused by what? and is associated with which bacteria?
hyperabsorbant tampon use
S. aureus already present in vagina.
bacteria induced to produce: TSST-1!!! = pyrogenic exotoxin C, enterotoxin F
bacteria not found in bloodstrea-- toxin migrates through mucosa
colonization of infection somewher ein body (i.e. nose-- usually deep tissue, bacteremia)
half of cases due ot strains producing TSST-1 and other half produce SEB/SEC
Staph. Scalded skin syndrome
most seen in infants
EXFOLIANTS produced by colonizing and infecting bacteria.
Bind GM4 ganglioside and degrade desmosomes (top layer of skin separates)
localized form of scalded skin syndrome. Toxin (exfoliantins) limited to site of production by anti-exfoliatin Abs, bacteria present in blisters can be cultured. Vs. Generalized form where you cannot culture causative agent.
What is Listeria's virulence factor? and what is its mechanism of action?
Listeriolysin O, a phospholipase, punches hole in phagosome allows pathogen to escape from phagolysosome.