Download Most important VF Table for Board Review

Most Important Virulence Factor for Board Review
Below are listed some diseases that are associated with specific virulence factors that can often
be found in case scenario questions. Please fill out the specific virulence factor next to the
disease. In addition, case scenarios often focus on the mechanism of action of the virulence
factor. If you have trouble finding these (after trying of course), feel free to ask me.
Disease
Acute glomerulonephritis
Virulence Factor
(previously thought to be
Streptococcal M-protein,
may be what they are
looking for on the
boards)
Anthrax (Bacillus anthracis)
Anthrax toxin 2A + B
Mechanism of Action
A streptococcal neuraminidase
may alter host immunoglobulin G
(IgG). IgG combines with host
antibodies. IgG/anti-IgG immune
complexes are formed and then
collect in the glomeruli. In
addition, elevations of antibody
titers to other antigens, such as
antistreptolysin O or
antihyaluronidase, DNAase-B, and
streptokinase, provide evidence of
a recent streptococcal infection.
(http://emedicine.medscape.com/article/239278-overview#a0104)
Protective antigen B
Edema factor A
Lethal factor B
Bacillus cereus food poisoning
Botulism
Cereulide
Enterotoxin
Botulinum toxin AB
(Neurotoxin)
Cholera (Vibrio cholera)
Cholera toxin AB5
Diphtheria
Diphtheria toxin AB
Escherichia coli meningitis
Capsular antigen K1
Escherichia coli UTI (UPEC)
P fimbriae
(pyelonephritisassociated pili)
Receptor-binding domain
Required for other toxins
Adenylate cyclase
Edema
Protease
Pulmonary edema
 vomiting
 Diarrhea
Inhibits synaptic vesicle
fusion in the plasma
membrane at the
neuromuscular junction,
flaccid paralysis
Hormone-independent
activation of adenyl
cyclase
Diarrhea
ADP ribosylates
Elongation Factor-2
Kills cells
Neonates lack IgM and
the K1 antigen resembles
cerebral glycopeptides
Binds to D-galactose-Dgalactose moieties to colonize
urothelial cells.
UPEC also produces alpha and
beta hemolysins that lyse cells in
the urinary tract
Gas gangrene (Clostridia spp.)
α-toxin
β-toxin
Enterotoxin
Gonorrhea
Gram-negative septic shock
Endotoxin =
Lipopolysaccharide
(LPS)
Hemolytic uremic syndrome
Cytotoxin
Kidney stones
Urease
Klebsiella pneumoniae pneumonia
K antigen (capsular
polysaccharide)
Listeriosis
LPS
Listeriolysin
Meningococcal meningitis
Endotoxin
Meningococcal septic shock
Pneumococcal pneumonia/meningitis
(Streptococcus pneumoniae)
Endotoxin
Peptic ulcers
cagA gene
Pneumolysin
Phospholipase C
(Lecithinase)
Necrosis in gas gangrene,
cytolytic, lethal
Necrotic enteritis
(unknown mech)
Cytotoxin, damages
membranes
Food poisoning, diarrhea
Antigenic variation
Also inhibits the alternative
complement pathway
LPS is a component of the
gram negative cell walls.
Lipid A is most antigentic
property of LPS.
Stimulates cytokines.
Like Shiga toxin,
Inactivates 60S ribosomes
Kills cells
Hemorrhagic diarrhea
Proteus mirabilis
Stones also provide
seeding for further
infections
K antigen protects against
complement activation.
Like Streptolysin O
(cytolysin, pore forming
toxin)
Membrane damage, allows
release of ingested bacteria
from endosomes into
cytoplasm
However, Capsule aids in
reaching the CSF
LPS from gram neg
Cytolysin, pore forming
toxin
Similar to streptolysin O
Helicobacter pylori
(pathogenicity island)
vacA (Vacuolating
cytotoxin A)
Pseudomembranous colitis
(Clostridium difficile)
Pseudomonal pneumonia
Pseudomonal wound infection
Pseudomonas aeruginosa
cagA = codes a complex type IV
secretion system
vacA = a protease
Other factors include: oxidase,
catalase, urease, flagellum, LPS
etc…
Toxin A
Glucosylation of small
GTP-binding proteins
Fluid secretion, mucosal
damage
Toxin B
Glucosylation of small
GTP-binding proteins (in
conjugation with toxinA)
Cytotoxin,
mucosal
damage
See pseudomonas aeruginosa
Exotoxin A
Type III cytotoxins
Like diphtheria toxin (ADP
ribosylates EF-2)
Kills cells
Inhibit actin cytoskeletons
(modulate host cell
physiology)
Rheumatic fever
M-protein
Highly antigenic, antibodies to Mprotein can cross-react with myosin
in cardiac muscle cells (molecular
mimicry)
Scalded skin syndrome
(Staphylococcus aureus)
Shigellosis
Exfoliating toxin
Protease
Sloughing of skin
Inactivates 60S ribosomes
Kills cells
Staphylococcal food poisoning
Enterotoxin
Heat-stable, resistant to digestive
proteases
Intoxication locally irritates the intestine
and may stimulate the vagus nerve
Strep throat (Streptococcus pyogenes)
Streptolysin O
Scarlet fever (Streptococcus
pyogenes)
Erthrogenic toxin
(SpeA)
Tetanus
Tetanus toxin AB
(neurotoxin)
Toxic shock syndrome
Toxic shock syndrome
toxin
Cytolysin
Pore-forming toxin
Mediated through IL-1
Fever, neutropenia, rash of
scarlet fever
Inhibits synaptic vesicle
fusion in the plasma
membrane nerve terminals
at inhibitor synapses,
spastic paralysis
Activates host antibody
and cytokine synthesis by
an antigen-independent
mech
Superantigen
Shiga toxin
Traveler’s diarrhea
LT - Enterotoxin
ST - Enterotoxin
Tuberculosis
Mycolic acid wall
Fever, headache, arthralgia,
neutropenia, rash
Similar to cholera toxin
(Hormone-independent
activation of adenyl
cyclase)
Causes accumulation of
cGMP in cells and -> in
loss of fluids and
electrolytes into intestinal
lumen
PREVENTS KILLING
FROM MACROPHAGES
Unclear VFs
Isotuberculosinol
Prevents fusion of the
phagosome with the
lysosome
Also prevent acidification
of phagosome
INDUCTION OF
GRANULOMAS
Whooping
cough
(Bordetella Adenylate cyclase
Adenylate cyclase, pore
pertussis)
formation in membranes
Inhibits and kills while
cells
Pertussis toxin AB5
ADP ribosylation of G
protein
Many hormonal effects
Tracheal cytotoxin
Peptidoglycan fragment
that kills cilia bearing cells
(unknown)
Legionella pneumonphila
Cytotoxin
Lyses cells (unknown
mech)
Type
IV
secreted Interfere with Rab protein
proteins
function.
Inhibit endosome
maturation