Lecture2 Flashcards
How do bacteria avoid host defense?
Hide within the host cells
Spread intracellularlly
Avoid phagocytes, complement & antibodies
How do bacteria replicate intracellularly and spread from cell to cell?
Enter cell—> break out of vacuole—> replicate in the cytosol —> assemble host actin & use the energy to move & encounter new cells —-> engulf new vacuole
What are key molecules/ proteins for intracellular replication of bacterium?
InIA and InIB—> internalins
LLO—-> listeriolysin (pore forming)
PlcA and PlcB—> phospholipases
ActA—> actin assembly inducing protein
How are microbes cleared by phagocytes?
Chemotaxis —> recognition and attachment on microbe via opsonins (C3b) OR antibodies that tag the bacteria
Phagocytes engulfs the microbe
Phagosome- lysosome fusion—-> destruction of the microbe
Lastly, exocytosis
How do microbes prevent encounter + uptake with phagocytes via protease and pore forming toxins?
Protease—- destroys chemoattractant like C5a
-destroy antibodies
Lysis of phagocytes
How do microbes avoid destruction by phagocytes via escaping from phagosome & preventing phagosome-lysosome fusion OR avoid recognition & uptake?
Phagosome: produce toxins that forms pores in the membrane
Phagosome-lysosome: produce proteins that block the fusion or interfere with signaling
Uptake: capsule, Fc receptor, M protein
How do microbes avoid recognition & uptake by phagocytes?
Mimic host molecules—> they cover theirselves with molecules similar to those found on host cells, so they wont bind because the microbes appear to be self
How do bacteria produce Fc receptors to avoid uptake, what is changed?
Examples?
Usually: Fab region of antibody binds to bacterium
Bacteria with Fc receptor: Fc receptor on bacterium, so binds the Fc region of the antibody—> not recognized
S. Aureus + Strep Pyogenesis
Where are toxins, where do they act and what kinds of exposure?
Surface localized + secreted to the extracellular environment
—act locally or systematically
-exposure:
-bacterial colonization followed by toxin
-ingestion of pre-formed toxin (rapid food poisionig)
What are the components of AB toxins and what are their functions?
What are their receptors?
Examples?
B binds the toxin to cells before entry
A has enzymatic activity damaging to cells or tissues
Receptors: glycoproteins OR glycoproteins
Ex: tetanus toxin, diphtheria toxin, cholera toxin
What are membrane damaging toxins?
What are their functions two types?
Pore forming: insert into membrane and make holes, disrupting & lysine the cell
Phospholipases: enzyme that cleave phospholipid—-> damaging the membrane
What do super antigens bind to?
What happens after binding?
What can their binding lead to?
Bind MHC 2 + TCR—> non specifically
T cell interprets the super antigen binding as an antigen, so it’s produces a cytokines from Th—> which is very inflammatory
Fever,rash, shock, death
S. aureus causes toxic shock syndrome toxin (TSST)
What are hydrolysis enzymes?
Example?
Proteases, collagenases, lipases that break down connective tissues & other tissues like muscle
—-> necrotizing fasciitis
What is E. Coli and what is the difference between the pathogenic strains of it?
Member of normal intestinal micro biota
Have different adhesion, invasiveness & toxins
What are the layers of the skin & what is the skin function?
Epidermis (skin)—> dermis (ski)—> hyperdermis
Has glands and hair—> restricts hair loss, reg body temp & sense environment
What are part of the skin microbiota & what are their features?
How do they inhibit growth of others?
Bacteria + fungi, adapted to dry, acidic, salty, cool habitat
Use sweat + sebum as nutrients
—degradation of products can inhbit growth of other microbes
C. Acnes is a member of the skin microbiota, what type of microbe is it, how does it grow, how does acne happen?
Aerotolerant
—uses sebum as nutrients in sebaceous glands (lipases)—>
increased sebum increases bacterium growth—> inflammation—> pimple ( pus with neutrophils,bacteria, debris)
S. Aureus is part of the skin,
what kind of bacterium is it,
where does it survive,
where it is usually found
and what can it cause?
Gram positive
In Salty conditions
Usually in the nose
Boils
Food poisioning
Pneumonia
Wound + blood infections
Skin is a good barrier, but what allows pathogens to enter?
What is the leading bacteria for wound infection ?
Cuts, wounds, bug bites, burn
S. Aureus
Why is S aureus able to produce food poisoning?
Has toxins that mediate its virulence
It is resistant to heat
What are cell surface features + secreted proteins of S. Aureus ?
Capsule prevents phagocytosis
-Fc receptor protein A binds Fc portion of antibodies
Coagulase that binds fibrinogen
Protease + hylureonidase—> degrade tissue
What are the toxins produced by S aureus ?
What are the resistant to?
Pore forming toxins—->Leukocidin kills leukocytes
Super antigens—> toxin shock, food poisoning
Protease (exfoliatin)—> cleaves proteins that connects cells layers, so cause separations of the skin
—> SSS in infants
90 percent penicillin resistant, all resistant to methicillin
What type of bacteria is S. Pyogenes and what can it cause?
Gram positive chain forming
Superficial skin infection (impetigo)
Strep throat
Rheumatic fever
What are parts of S pyogenes cell wall that contribute to its pathogenicity?
Capsule—- has hyaluronic acid that mimic host molecule
Fc receptor (protein G)—-> bins Fc portion of antibodies
Antiphagocytic protein (M protein) —> prevents opsonization by C3b
