virulence factors Flashcards
elastin, collagen, fibronectin binding proteins; clumping factor
MSCRAMMs (S. aureus)
cleaves fibrin to fibrinogen to evade phagocytic cells
coagulase (S. aureus)
binds heavy chain Fc region of natibody (in reverse) to block opsonization
protein A (S. aureus)
multi-subunit pore forming cytotoxin
alpha toxin (S. aureus)
damages membrane in leukocytes, erythrocytes, fibroblasts; responsible for B hemolysis on BAP
beta toxin (S. aureus)
multi-subunit pore forming cytotoxin that effcets leukocytes
leukocidin (S. aureus)
quorum snesing sytem that determines what genes will be expressed based on cell density
AGR system (S. aureus)
loosens junctions of stratum granulosum resulting in sloughing off of top layer of dead keratinocytes (stratum corneum)
exfoliative toxin (S. aureus)
lancefield group A antigen
group specific carbohydrate (S. pyogenes)
allow attachment to host tissues
fimbriae (S. pyogenes)
binds fibronectin allowing for adherence to respiratory cells
F protein (S. pyogenes)
contributes to adhesion by binding fibronogem, inhibits C3b binding which inhibits complement binding, opsonization
M protein (S. pyogenes)
allows to be recognized as “self”
hyaluronic acid capsule (S. pyogenes)
protease that deactivates C5a so that it cannot attract phagocytic cells
C5a peptidase (ScpA) (S. pyogenes)
oxygen-stable, non-immunogenic, cytotoxin that disruots membranes of leukocytes, erythrocytes, platelets
Streptolysin S (S. pyogenes)
oxygen-labile, immunogenic pore forming cytotoxin, monomers bind cholesterol
Streptolysin O (S. pyogenes)
(S. pyogenes) act as superantigens (not all strains)
streptococcal pyrogenic exotoxins (SpeA-D) (S. pyogenes)
facilitate breakup of blood clots to allow for spread
Streptokinases (S. pyogenes)
(S. pyogenes) breakdown DNA to reduce viscosity of pus to allow for spread
Streptodornases (S. pyogenes)
(S. pyogenes) cleave hyaluronic acid in host connective tissue to facilitate spread
Hyaluronidase (S. pyogenes)
(S. pyogenes) break down cellular NAD+ which can lead to death via depletion or inhibition of immune system
NADase (S. pyogenes)
(S. pneumoniae) binds platelet active factor (PAF) receptors found on surfcae of endothelial cells, leukocytes, platelets, epithelial cells to allow bacteria to be transcytosed (apical to basolateral side for release)
phosphorylcholine (S. pyogenes)
(S. pneumoniae) host traps IgA in mucous and protease cleaves antibody to allow escape from mucous = capsule disruption, freeing phosphorylcholine to bind PAF receptors
IgA protease (S. pyogenes)
(S. pneumoniae) pore forming cytotoxin, binds host cell cholesterol and kills ciliated epithelial cells
pneumolysin (PLY) (S. pyogenes)
(S. pneumoniae) release cell wall techoic acids, phosphorylcholine in techoic acid allows for binding of PAF receptor, bound techoic acid is recognized by C3b to activate alternative complement pathway, increased inflammatory response and lysis results in tissue destruction
autolysins (S. pyogenes)
glycocalyx, made up of poly D glutamic acid; non-toxic on its own but necessary for organism to be pathogenic; prevents opsonization, complement activation
capsule (B. anthracis)
binds to receptors, cell surface furin cleaves into two subunits (83 > 63, 20); 63 multimerizes and interacts with EF or LF, once endocytosed low pH in endosome causes conformation change to allow pore formation, delivey of LF, EF to cytoplasm
protective antigen (PA) (B. anthracis)
Ca2+, calmodulin dependent AC, rapid efflux of fluid by increasing cAMP
edema factor (EF) (B. anthracis)
Zn2+ dependent metalloprotease, snips of n terminase of MAPK kinase - only affects macrophages, intereferes w/ cell signaling pathways, leads to apoptosis
lethal factor (LF) (B. anthracis)
protein products of 26 genes required for intracellular growth
Dot/ICM Type IV secretion system (L. pneumophila)
secreted through DOT/ICM system, not all required
Effector proteins (L. pneumophila)
interactions with each other and host Met trigger cell signaling events that promote cytoskeletal rearrangements, uptake
Internalins, E-cadherins (L. monocytogenes)
binds cholersterol and multimerizes in membrane to form pore and lyse phagosome
listeriolysin O (L. monocytogenes)
anchors on pole of cell to acitvte Arp2/3 comlex to induce formation of filaments that push listeria from infected to uninfected cell
ActA/F-actin (L. monocytogenes)
(M. tuberculosis) type of secretion system
Type VII
suppresses T-cell activation, interferon induced expression of macrophage activation
lipoarabinomannan (M. tuberculosis)
link mycolic acid to cell wall, potent antigens
Fbp A, B, C (M. tuberculosis)
binds host cell heparin-binding epidermal growth factor, A subunit binds EF-2 altering it so it cannot interact with ribosome, inhibiting translation
diptheria toxin (C. diphtheriae)
A subunti ADP-ribosylates alpha subnits of G proteins which inhibits recruitment of immune cells
pertussis toxin (B. pertussis)
inhibits antigen presentation, proinflammatory cytokine release, complement mediated phagocytosis, immune cell recruitment by increasing cAMP levels
AC toxin (B. pertussis)
facilitates attachment to ciliated epithelial cells
filamentous hemagglutinin (B. pertussis)
inhibits cilia movement at low concentrations and kills ciliated epithelial cells at higher concentrations; sloughed dead cells contribute to thickening of mucous/ spread of bacteria
tracheal cytotoxin (B. pertussis)
pilus that binds glycoprotein receptor on surface
colonizing factor adhesin (CFA) (ETEC)
heat labile, AB enterotoxin that upregulates AC = cAMP up, H2O, Na2+, Cl- out of cell which results in electrolyte imbalance and watery diarrhea
LT-1 (ETEC)
heat stable enterotoxin, upregulates GC = CGMP up, H2O, Na2+, Cl- out of cell which results in electrolyte imbalance and watery diarrhea
ST-a (ETEC)
allows for aggregation of organisms to avoid phagocytosis
bundle forming pilus (BFP) (EPEC)
inserts into cell membrane and binds bacterial protein intimin to induce pedestal formation which results in effacement of microvilli
Tir (EPEC, EHEC)
disrupts tight junctions between cells leading to fluid loss, induces cell apoptosis
EspF (EPEC, EHEC)
inhibits protein translations resulting in lysis of renal endothelial cells, RBCs, can lead to platelet activation, formation of blood clots, renal failure
Shiga toxin (EHEC, S. dysentariae)
sequester iron
siderophores (UPEC)
bind uroplakin receptor on superficial bladder cells to initiate cytoskeletal rearrangement, invasion of superficial bladder cells, activation of immune celsl
FimH (UPEC)
(UPEC) resist phagocytosis and complement protein
capsule (K antigen) (UPEC)
alpha, beta hemolysins
exotoxins (UPEC)
chromosomal encoded pore-forming cytotoxin (only in certain strains)
ShET-1 (Shigella spp.)
virulence plasmid encoded AB toxin - cAMP up, Cl-, Na2+, H2O out = electrolyte imbalance = watery diarhhea
ShET-2 (Shigella spp.)
form pores in phagosome membrane to allow escape
IpaB/C (Shigella spp.)
localizes to one pole to promote formation of filaments that propel bacteria through cell
IcsA (Shigella spp.)
depolymerize microtubules in host cell
VirA (Shigella spp.)
zinc endopeptidase that inhibits interaction of SNARE with vesicles containing excitatory neurotransmitter acetylcholine to prevent fusion with membrane
botulinum toxin (C. botulinum)
zinc endopeptidase that inhibits interaction of SNARE with vesicles containing inhibitory neurotransmitter gamma-aminobutyric acid to prevent fusion with membrane
tetanus toxin (tetanospasmin) (C. tetani)
glycotransferases that inactivate Rac, Rho, Cdc42 to depolymerize actin cytoskeleton, disrupt tight junctions, induce apoptosis
Tcd A/B (C. difficle)
pathogenicity island required for intracellular multiplication in nonphagocytic intestinal epithelial cells
SP-1 (S. enterica ssp. enterica)
pathogencity island required for formation of replicative vacuole
SP-2 (S. enterica ssp. enterica)
phospholipase C, interacts with C-terminus of phosphatidylcholine, triggers conformational change that brings down N-term to cleave phsophatidylcholine, results in membrane damage leading to cell lysis
alpha toxin (C. perfringens)
sequester iron from host binding proteins
Tbp A, B, Fbp A (N. gonorrheae, N. meningitis)
blebs of this act as decoys for immune system
lipooligosaccharide (N. gonorrheae, N. meningitis)
allow nutrient and waste exchange, act as adhesins, interfere with phagolysosome fusion, inhibit complement mediated killing
PorA/B (N. gonorrheae, N. meningitis)
bind factor H to inhbit complement activation
factor H binding protein (fHbp) (N. gonorrheae, N. meningitis)
allow for movement by twitching motility
pili (N. gonorrheae, N. meningitis)
trancytose organism from apical to basolateral side to allow for extracellular multiplication
Opa (N. gonorrheae, N. meningitis)
promotes survival on mucosal surface
IgA protease (N. meningitidis)
fibronectin may be a receptor for attachment to host cells, complex with host antibodies resulting in destructive immune response in which fibronectin is recognized as foreign
virulence of T. pallidum
contain RNA genome
matrix proteins (influenza, measles)
coat RNA segments
nucleocapsid proteins (NP) (infleunza)
facilitates release during budding
neuramidnidase (NA) (influenza)
binds viral receptor (sialic acid) on host cell
hemagglutinin (influenza)
nucleocapsid, inteacts with M protein
N protein (measles)
prevents N from binding cellular RNA, tether viral polymerase to viral RNA-N complexes
D protein (measles)
suppress host innate immune response by interefering w/ IFN signaling proteins
V, C proteins (measles)
facilitates membrane fusion
F protein (measles)
attachment of virions to host cell
hemagglutinin (measles)
RNA-dependent RNA polymerase, caps and polyadenylates mRNAs for translation
L protein (measles)
inhibits MAPK kinase signaling cascade
Yop J/P (Y. pestis)
inhibits cytoskeletal rearrangement
Yop H (Y. pestis)
adhesin, allows binding to collagen, fibronectin, mucous, inhbits complement binding
YadA (Y. pestis)
antiphagocytic
proteinaceous capsule (F1, LcrV) (Y. pestis)