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Virulence factors
Toxins, adhesins
| Term | Definition |
|---|---|
| Protein A | Staph aureus -> binds IgG Fc -> prevent opsonisation/phagocytosis |
| IgA protease | Staph pneumoniae, Hemophilus influenzae type b, Neisseria -> cleave IgA in mucus membranes -> allow bacterial adhesion/colonisation of mucus membranes |
| M protein | Group A Strep -> sequence homology w/ human tropo/myosin (molecular mimicry) -> prevent phagocytosis |
| Diphtheria toxin secretion? | Corynebacterium diphtheriae -> DTX gene carried on corynephage integrated in bacterial chr -> Fe binding to DTX receptor represses expression -> Fe sequestered by lactoferrin -> DTX secretion |
| Diphtheria toxin mechanism? | B component binds to HB-EGF -> toxin endocytosed -> nicked by host furin protease -> endosomic acidification -> AB translocation -> disulfide bond reduced in cytosol -> A subunit ADP ribosylates EF-2 -> blocks host cell protein synthesis |
| Exotoxin A | Pseudomonas aeruginosa -> ADP ribosylation of EF2 -> block host cell protein synthesis |
| Shiga toxin | Shigella -> removes adenine from human 60S ribosome 28S rRNA -> block host cell protein synthesis |
| ETEC heat labile toxin | E. coli -> overactivates AC -> increase cAMP -> increase Cl- secretion in gut -> H2O efflux |
| ETEC heat stable toxin | E. coli -> overactivates GC -> increase cGMP -> activate PKG II -> Cl- efflux -> H2O follows |
| Anthrax toxin | Bacillus anthracis -> protective Ag (mediates toxin cell entry), lethal factor (tissue necrosis), oedema factor (CaM-dependent adenylyl cyclase -> elevates cAMP -> PKA -> open Cl- channels -> H2O efflux) |
| Cholera toxin | Vibrio cholerae -> hyperactivates G-alpha s -> adenylyl cyclase overactive -> high cAMP -> PKA -> opens Cl- channels -> H2O efflux |
| Pertussis toxin | Bordetella pertussis -> inactivates G-alpha i -> adenyly cyclase uninhibited -> high cAMP -> PKA -> opens Cl- channels -> H2O efflux |
| Tetanus toxin | Clostridium tetani -> cleaves synaptobrevin at CNS neurons -> inhibit inhibitory GABA release from spinal cord Renshaw cells-> spastic paralysis |
| Botulinum toxin | Clostridium botulinum -> cleaves synaptobrevin at PNS neurons -> inhibit excitatory ACh release from NMJ -> flaccid paralysis |
| Alpha toxin | Clostridium perfringens -> lecithinase phospholipase -> degrades tissue/cell membranes, Staph aureus -> lyse cell membranes -> cell death |
| Streptolysin O | Strep pyogenes -> degrades cell membrane -> lyse RBCs -> beta hemolysis |
| Superantigen | Staph aureus -> binds APC MHC II to TCR outside of Ag binding site -> inappropriate T cell activation -> cytokine storm |
| Erythrogenic exotoxin A | Strep pyogenes -> binds APC MHC to TCR outside of Ag binding site -> inappropriate T cell activation -> cytokine storm |
| Endotoxin release? | Lipid A component of LPS -> infected cell lysis/cell membrane blebs detach from living cells |
| Endotoxin mechanism? | LPS recognised by TLR4 -> macrophage activation -> IL-6/TNF-alpha/NO, complement activation -> C3a (histamine)/C5a (neutrophil chemotaxis), tissue factor activation -> DIC |
| Pneumolysin | Strep pneumoniae -> pore-forming toxin in cell surface membrane -> disrupt ion gradients |
| DNase | Strep pyogenes, Campylobacter jejuni, Salmonella typhi -> trigger G2/M cell cycle arrest -> enlarged/distended cells -> apoptosis |
| Bacillus anthracis capsule | Poly D-Glu capsule -> weakly immunogenic -> -ve charge disguises vegetative bacterium from host immune system |
| Toxin A/B | Clostridium difficile -> glycosylate intracellular small GTPases -> subvert actin cytoskeleton, disrupt tight junctions -> leaky epithelium |
| Internalins | Listeria monocytogenes -> zipper protein -> bacterial internalins mimic eukarytic fibronectin ligand -> bind to host cellular integrins -> receptor-mediated endocytosis |
| Listeriolysin O/phospholipase | Listeria monocytogenes -> pore-forming toxin -> degrade single membrane entry vacuole |
| 2nd phospholipase | Listeria monocytogenes -> pore-forming toxin -> sequestered in double-membrane vacuole -> lysis -> released into 2nd cell |
| Pilus protein | Neisseria, EHEC -> adheres bacteria to cell surface, sex pilus forms for conjugation |
| What is the clinical use for Haemophilus influenzae capsule? | Type B polysaccharide added w/ tetanus toxoid -> subunit vaccine for meningitis (2-18 months) |
| Cytolysin | Bordetella pertussis -> disrupt cell membranes |
| Bacterial proteins | Legionella pneumophilla -> modify host phagosome -> block lysosomal/vacuole fusion, prevents oxidative burst, stimulates cytokine release |
| Mucoid capsule | Pseudomonas aeruginosa -> alginate polysaccharide -> biofilm formation |
| Pyoverdin | Pseudomonas aeruginosa -> green fluorescent siderophore -> sequester iron into aqueuous solution -> increase iron bioavailability for bacteria |
| Pyocyanin | Pseudomonas aeruginosa -> blue protein -> oxidises/reduces molecules -> ROS generation -> kills competing microbes/mammalian lung cells during CF |
| Tripartite efflux pumps | Pseudomonas aeruginosa -> eject Abx via unique TolC exit duct spanning periplasm/outer membrane |
| Vi capsule | Salmonella typhi -> inhibit phagocytosis, inhibit C3b opsonin binding |
| SipA/C | Salmonella typhi -> binds actin -> directly forces cellular entry via distal ileum/proximal colon epithelial cell apical surface |
| SPI-2 genes | Salmonella typhi -> effectors inhibiting phagolysosome maturation, effectors conferring resistance to defensins/oxidative burst (pumps, superoxide dismutase, catalase) |
| Typhoid toxin | Salmonella typhi -> cytolethal-distending toxins -> DNase -> trigger G2/M cell cycle arrest -> enlarged/distended cells -> apoptosis |
| p30 | Salmonella typhi -> p30 on typhoid toxin -> potent CD4+ T helper cell epitope -> enhance CD8+ CTL response -> increase inflammatory damage |
| What is the clinical use for Salmonella typhi capsule? | Vi capsular polysaccharide -> IM vaccine for Salmonella |
| Fimbriae pilli | UPEC (P pilli) -> cystitis, pyelonephritis -> allows UTI spread up ureters, prevent bacterial removal during micturition |
| K capsule | E. coli -> pneumonia, neonatal meningitis |
| Tir | EHEC -> bacterial injectosomes inject Tir into host cell -> present on host CSM -> bacterial intimin binds Tir -> subverts host cell signal transduction -> Tir phosphorylated -> protein recruitment -> actin polymerisation -> pedestal formation |
| Cholera toxin secretion? | CTX gene on bacteriophage integrated into bacterial chr -> binds to GM1 ganglioside in gut lumen brush border |
| Urease | Helicobacter pylori -> produce ammonia -> creates alkaline environment in acidic gastric mucosa -> lower mucus viscosity -> easier flagella mvmt around epithelium |
| Flagella | Campylobacter jejuni (polarised), vibrio cholerae (single), helicobacter pylori (several) |
| VacA | Helicobacter pylori -> pore-forming cytotoxin -> hexameric -> inserts into host cell membrane anion-selective channels -> endocytosed -> disturb late endosome balance -> H2O influx -> swelling endosome -> vacuole formation (replicative niche) |
| Tarp | Chlamydia trachomatis -> translocated actin recruiting phosphoprotein -> rearrangement of host actin cytoskeleton via injectosome |
Created by:
vykleung
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