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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