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Lecture 6
Fichas del conjunto (38)
- 1Pili of Gram+ Bacteria- mostly found in oral colonizers and Corynebacterium spp.
- important for biofilm formation and in pathogenic strains (adhesion and invasion) - 2Formation of Gram+ Pili- pilin subunits covalently attached to each other and to the peptidoglycan later
- done by Sortases
- @ first pili are bound to the membrane, active site cleaved, sorted, anchored to the cell wall, repeated - 3Non-Fimbrial Adhesins of Gram+ Bacteria + Example- hair like protrusions that resemble pili but are not
- many bind to ECM and connective tissue
E.g. Streptococcus pyogenes
-> pilus like structures made of M protein
-> fibronectin-binding protein to avoid complement and phagocytosis - 4Afimbrial Adhesins- cell surface proteins used for adherence but do not assemble themselves into pilus like structures
- like glue patches on microbes
- tighter binding than pili
- allow for attachment and invasion
- less known - 5What is meant by "attachment triggers downstream events?"- no matter how a pathogen attaches to a host cell, it generally produces a signal transduction event
- 6Downstream event in... - Host - BacteriaH: triger endocytosis of bacteria, can alter gene expression
B: activate virulence genes once in contact with target cell - 7Evading the immune system. In order to maintain a persistent infection and be successful, bacteria must...be able to combat immune defenses of the host
innate: complement, phagocytosis
adaptive: antibodies, CTLs - 8Capsules- loose, unstructures network of polymers that covers the surface of bacterium
- 9Capsules help avoid complement by...preventing alternative activation by inhibiting formation of the C3 convertase by binding factor H rather than factor B which deactivates C3b that might bind with them
- 10Complement: Alternative Activation1. C3 binds to surface of bacterium
2. Spontaneously forms C3a and C3b
3. Factor B combines with C3b forming C3 convertase
4. More C3a and C3b are produced - 11Capsules can prevent what two things and how?1. opsonization by binding to factor H, stealing the hosts protection system
2. MAC from forming holes in the membrane, preventing direct lysis - 12Capsule Caveat- not 100% effective at stopping complement
- capsules can still be targets for antibodies - 13"Host Mimicry"-> make yourself look like the host by making capsules out of sialic or hyaluronic acid
-> modify LPS O-Ag to look like host Ags - 14Sialic Acid vs. Hyaluronic AcidS: found in relatively high amount sin all animal tissue, on surface
H: Glycosaminoglycan + NAG, "goo" molecule that binds well to water - 15Modifying LPS O-Ag to look like host antigensO-Ag = immunogenic
-> C3b target
-> MAC formation
-> Ab binding
--> attach sialic acid, carbs like the hosts to it - 16By attaching common chemical groups found in host cells to outer surface structures...they can avoid detection by complement, phagocytes, and antibodies
- 17H. pylori + Modifying LPS O-AgGastric epithelial cells produce Ags, the Lewis Ags X,Y on H. pylori look VERY similar
--> can be protection for H. pylori, and extra destructive to us - 18How altering LPS can prevent MAC from forming- change lenth of LPS, creating a longer distance for the MAC to travel, preventing the MAC from forming near the outer membrane
- become serum resistant, becoming immune to complement - 19Biowarfare- secrete enzymes that destroy complement proteins
-> C5a for instance by some Gram+
- produce toxins
-> kill, inactivate, immobilize, reduce strength of immune cells
-> prevent cytokine signaling - 20Why become intracellular?- pathogens that live inside the host cell are not directly exposed to the immune system
- 21Intracellular pathogens produce ______ that are what? + ExamplesInvasins: surface proteins that provoke phagocytic ingestion of the bacterium by host cells
Examples: Y. pseudotuberculosis - M cells
L. monocytogenes - uses internalins to target E-cadherin receptors - 22Surviving Phagocytosis - Prevent Phagolysosomal Fusion- creates a breeding compartment
-> examples: legionella, salmonella, mycobacterium = all remodel phagosome to +/- proteins that prevent normal acidification
L - removes proteins
S - makes own vesicle out of hosts' actin
M - lives in macrophages - 23Surviving Phagocytosis - Survive the Phagolysosomal Compartment- Change structure of your cell membrane (LPS, capsule)
- avoid defensins, resist low pH, proteases, lysozyme - 24Surviving Phagocytosis - Resist RORs and NO- ROR = primary way the oxidative burst kills bacteria
- produce enzymes that neutralize oxygen radicals
Catalase: hydrogen peroxide -> oxygen, water
Superoxide dismutase: reactive O2 spp. to water and oxygen - 25S. enterical Typhimurium produces _____ superoxide dismutases4
- 26NO exists in many cells. _______ uses normal respiratory coumpound _______ to detoxify itE. coli
- flavohemoglobin aka nitric oxide dioxygenase - 27Surviving Phagocytosis - Escape the Phagosome- produce toxins that disrupt, degrade, or make holes in host membrane
E.g. Listeria monocytogenes - 28Listeria monocytogenes & escaping the phagosome- produces a pore forming hemolysin called Listeriolysin (LLO)
- similar to other Gram+ cholesterol-binding cytotoxins
- active only in low pH (5.5) of phagolysosome
- Cloning LLO into non-path strain of B. subtilis made it able to escape and grow in macrophages - 29BEING INTRACELLULAR Cell-to-Cell Spread- many pathogens can direct endocytosis and can manipulate the actin cytoskeleton once inside
- use actin-based motility
-> push themselves around the cell and into neighboring cells - 303 spp. that use Cell-to-Cell SpreadListeria monocytogenes
Shigella flexneri
Ricketsia ricketsii - 31Listeria monocytogenes as model for intracellular immune evasion- enters cell via invasins called internalins (InIA/B)
- uses toxins to escape phagosome to replicate (LLO, PIcA)
- uses ActA to polymerize acting and proper itself into neighboring cels
- uses toxins to escape new "pushed in" vesicle (LLO, PIcB)
- repeat - 32BEING INTRACELLULAR Avoiding the Ab Response- intracellular
- Ag/Phase variation
- Host mimicry
- bind and create layer of host proteins on surface
-> S. pyogenes bind to fibrinogen, use Ab against host - 33BEING INTRACELLULAR Stealing Host Abs/Proteins- S. pyogenes: protein G
- S. aureus: protein A
-> bind Fc region of Abs creating coating of Abs facing outward - 34Dissemination - Tissue Penetration1. Breakdown pus
2. Secrete meat tenderizers
3. Secrete blood thinners - 35Breakdown pus- thick substance, tends to breakdown bacteria
-> secrete DNAses to thin it - 36Secrete meat tenderizers- collegenases, elastases, hyaluronidases, other proteases
-> break down connective tissue and ECM protein - 37Secrete blood thinners- streptokinase degrades fibrin
-> escape from blood clots - 38The Opportunists = the "real" hitchhikers- some have few to no VFs, some have many
- mostly harmless, rely on defective host to be pathogenic
B. fragilis: capsule activates immune response
Staph epi: adhesins stick better to plastic than other cells
- commonly antibiotic resistant
- host generally immunocompromised
- infectiosn difficult to treat
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- College Pathogenic Microbiology Fichas sobre Lecture 6, creado por Bella Paniagua el 27/10/2015.
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- Bella Paniagua
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