Micro Summary: Virulence Factors Flashcards
Bacteriodes: Bacilus, Prevotella, Porphoryngeus
LPS, capsule, enterotoxin
Histotoxic Clostridia: C. perfringens, C. septicum
Exotoxins, α toxin
C. tetani
Tetanus toxin
C. botulism
Exotoxin (neurotoxin), Botulinum toxin (type A most serious, persists the longest in the neuron), Spores: heat-resistant (toxin is heat-sensitive)
C. difficile
Toxins A & B: enterotoxins, render intestinal epithelial cells nonfunctional & leaky, chemoattractants for neutrophils, provoke inflammation, Binary toxin: causes cytoskeletal effects
Campylobacter jejuni
Adhesions, LPS
Haemophilus influenzae
Capsules, Hib, LOS, IgA, obtain iron from transferrin
Mycoplasma pneumoniae
Adhesins, CARDS toxin, peroxides, inflammation
Escherichia coli
(1) Fimbrial & afimbrial adhesins: All produce a common (type 1) pili that attach to mannose receptors, Pathogenic E. coli have a unique pili (CFA for ETEC) to bind unoccupied receptors; (2) Iron acquisition: Produce siderophores w/ high affinity for iron; (3) Toxins: Endotoxin (LPS): outer membrane, Hemolysin: pyelonephritis, Heat-stable enterotoxin: increases cGMP, Heat-labile enterotoxin: increases cAMP, Shiga toxin: inactivates ribosomes
Salmonella
LPS: inflammation, Type III secretion system & effectors: Inv/Spa (entry) & Spi/Ssa (survival in macrophages), Pho/PhoQ: controls gene expression, PagC & outer membrane proteins: resist antimicrobial peptides, Adhesins, Typhoid toxin: damages hot DNA, Vi antigen: capsular polysaccharide, Flagella
Shigella
LPS, Ipa proteins, Mxi-Spa TTSS needle, IcsA, IcsB, Shiga toxin
Yersinia pestis
LPS, TTSS, plasminogen activator
Rickettsia rickettsii
Direct actin reorganization (filopodia enhances spread), Phospholipases, proteases, and membrane peroxidation result in host cell damage, Energy parasites
Borrelia burgdorferi
Osps (surface lipoproteins, differentially expressed, important for attachment/adhesins)
Bacillus anthracis
Capsule, Exotoxins (Edema toxin, Lethal toxin)
Francisella tularensis
Capsule, FPI
Helicobacter pylori
Urease & flagella (for higher pH), VacA, cag pathogenicity island (type IV secretion system & CagA), LPD, & inflammation/urease
Staphylococcus aureus
Multiple adhesion molecules, exotoxins, cell wall components (LTA, peptidoglycan), exotoxins (hemolysins, enterotoxins, exfoliative epidemolytic scalded skin syndromes, toxic shock syndrome toxin), protein A, polysaccharide capsule, peptidoglycan, LTA, resistance molecules
Acinetobacter baumanii
Endotoxin
Neisseria meningitidis
*Capsule, outer membrane proteins, pili, LOS, IgA-protease, complement-binding proteins
Neisseria gonorrhoeae
Pili, Opa proteins, LOS
Streptococcus pyogenes
M protein, LTA, cell wall components: hyaluronic acid (disguise molecular mimicry), C5a peptidases (complement), exotoxins: hemolysisn, streptokinase steptodornase, hyaluronidase, erythrogenic toxin
Streptococcus pneumoniae
Adherence: neuraminidase, Immune evasion: IgA protease, Inflammation: LTA, Immune evasion: capsule, Defense damage: pneumolysin
Listeria monocytogenes
phagosome, a toxin (listeriolysin O; gene: hlyA) which breaks open the phagosome and allows the bacterium to enter the cytoplasm, an actin tail by actA which propels the microbe around the cell, and sometimes into a neighboring cell, allowing cell to cell spread without leaving the cell (eliminates exposure to antibodies)
Legionella pneumophila
Intracellular, (1) replication phase (abundant nutrients) & (2) transmission (limiting nutrients), Inhibition of phago-lysosome fusion by remodeling phagosome to look like the RER by recruiting host secretory vesicles from the ER, Type IV secretion system may allow rapid secretion of effector molecules to modulate phagosome and prevent fusion with lysosomes
Pseudomonas aeruginosa
exotoxin A: necrosis, endotoxin: shock, pili: adhesion, enzymes (proteases, elastase): tissue damage, leucocidin: inhibits/kills WBCs, phospholipase C: hemolysin, affects WBCs, capsule (slime layer/biofilms): antiphagocytic, contributes to cystic fibrosis, inferferes w/ antibiotic actio+K32n
Mycobacterium tuberculosis
mycolic acids, lipids, liparabinomannan (~LPS), cytolysin, adhesin/invasin genes, secretion systems (ESX loci), allow survival & replication of M. tuberculosis within macrophages using complement receptor
Mycobacterium leprae
lipid-rich outer “capsule” contains phenolic glycolipid 1 (PGL-1), acid fast, slow-growing, resides within macrophages & Schwann cells (tropism for peripheral nerves)
Corynebacterium diphtheria
Adhesins, diphtheria toxin: responsible for the disease, inhibits hot cell protein synthesis by ADP-ribosylating elongation factor 2
Vibrio cholera
Cholera toxin: causes increased cAMP levels in intestines –> fluid & electrolyte loss, Zonula occludens toxin (affects tight junctions) & accessory enterotoxin (forms ion channels),Toxin-coregulated pilus, biofilm production, other adhesins, & other colonization factors
Bordetella pertussis
adhesins: fliamentous hemagglutinin, pertussin toxin, pili, pertussis toxin: A-B exotoxin, increases cAMP, adenylate cyclase: increases cAMP, tracheal cytotoxin derived from peptidoglycan: kills ciliated cells, heat-labile toxin: local damage
Poliovirus
CNS spread, unenveloped for GI acid, 2A protein (inhibits protein translation), 2BC/3A protein (inhibits vesicle transport), 3C protease (inhibits transcription)
HBV
4 genes (surface, core, pol, X), chronic infection, HBsAG immune decoy
HCV
High mutation rate of viral RNA polymerase, protease
HSV
envelope: acquired from host, tegument: surrounds capsid, capsid: icosahedral, DNA genome: linear dsDNA, Viral DNA synthesis: maintain nucleotide pools in quiescent cells (thymidine kinase & ribonucleotide reductase), Control host cell function: shut-off protein synthesis and block apoptosis (UL41 & g34.5),Control host cell function: toxicity/apoptosis (ICP0), Immune regulation: block complement, antibody and Ag recognition (gE/gI, gC, & ICP47)
HPV
Enter and remain in latency in keratinocytes, Inactivation of E1 or E2 genes –> integration into host DNA –> up-regulation of E6 &E7 oncogenes –> transformation
Norovirus
Capsid
Rotavirus
Nonstructural protein (NSP4): enterotoxin
Adenovirus
Early genes hijack normal growth resources for viral replication, Immune evasion by blocking cell signaling (E3), Cell destruction (cytopathic effect) releases new virions
Hantavirus
Envelope glycoproteins
Rabies
Neuronal tropism, targets ACh receptor
EBV
Infects B cells or nasopharyngeal cells by CD-21(-like), receptor, Latency & immortalized human B cells
Influenza
Hemagglutinin (HA) protein: binds carbohydrates, causes fusion for entry into cell, releases viral RNA inside cell, Neurominidase: releases new viral particles to infect new cells, prevents viral aggregation
