Micro Lec 2

Front 1

What influences the type of host defense encountered by bacteria?

Back 1

Site of infection AND lifestyle of pathogen (where the bacteria lives)

Front 2

What is the difference between septicemia and bacteremia?

Back 2

septicemia has a host response while bacteremia does not

Front 3

What is the hallmark of bacterial infection and if none is present then we lean toward a viral infection?

Back 3

Inflammation

Front 4

How does bacterial invasion promote inflammatory response?

Back 4

TLRs on epithelial cells (induction of proinflammatory cytokines); Complement (alternative pathway C5a produced); Anti-microbial peptides released from epithelial cells; Resident phagocytes ingest bacteria and secrete cytokines

Front 5

What three cytokines play the biggest role in inflammation?

Back 5

TNFa, IL-6 and IL-1

Front 6

Which WBC will be increased during a bacterial infection?

Back 6

Neutrophils (band form)

Front 7

What are the classic manifestations of inflammation?

Back 7

swelling, erythema, heat, pain, loss of function

Front 8

What kind of exudate is seen with infections of pyogenic bacteria (staphylococci, streptococci, Neisseria)?

Back 8

Purelent exudate (neutrophils, dead cells etc…)

Front 9

What MUST happen for neutrophils to be able to uptake bacteria?

Back 9

opsonization (alternative or classical pathway)

Front 10

What is the primary complement factor that plays a major role in opsonization of bacteria?

Back 10

C3b

Front 11

Which bacteria is generation of C3b by the alternative and classical pathways CRITICAL for clearing?

Back 11

Gram Positive (helps with gram-negative)

Front 12

How are C3b bound microbes recognized by phagocytes?

Back 12

Via Complement Receptor (CR1)

Front 13

This external structure produced by some bacteria (streptococcus pneumonia, klebsiella pneumonia) inhibits deposition of C3b?

Back 13

Capsule

Front 14

What do encapsulated bacteria more often cause?

Back 14

meningitis, pneumonia, system infections (dissemination through blood and lymph)

Front 15

What do M protein, Porin protein, fHBP, OspE protein, and PspC protein all have in common?

Back 15

All allow bacteria to evade complement mediated opsonization

Front 16

How does factor H binding protein allow bacteria to escape opsonization?

Back 16

Factor H binding protein allow Factor H to bind and inactivate C3b

Front 17

How do bacteria evade oxygen-dependent defenses of phagocytes?

Back 17

Enzymes (directly detoxify like catalase, peroxidase, superoxide dismutase; Repair enzymes); Location in anaerobic areas of the body

Front 18

Why are diabetics more prone to infection?

Back 18

Poor circulation deprives phagocytes the ability to perform oxygen-dependent destruction of bacteria (NADPH-oxidase_

Front 19

What are some oxygen-independent defenses of phagocytes?

Back 19

lysozyme M, lactoferrin (iron sequestering), serine proteases, antimicrobial peptides (defensins, cathelicidin, hepcidin)

Front 20

What are some ways that bacteria evade oxygen-independent defenses?

Back 20

Capsules, LPS, active efflux pumps

Front 21

What are neutrophil extracellular traps (NETs)?

Back 21

produced from neutrophil death (release of granules, toxic oxygen species, DNA and histones

Front 22

What are some mechanisms used by bacteria to evade NETs?

Back 22

detoxifying enzymes, surface charges, DNAses (emphasis teacher)

Front 23

T/F uptake of microbes via Fc receptor cannot be blocked by capsules?

Back 23

TRUE; (classical pathway eventually overcomes the encapsulated bacteria)

Front 24

What complement components are required for complement-mediated bacterial lysis of bacteria?

Back 24

C5-C9 (MAC)

Front 25

The membrane attack complex is critical for which type of bacteria (gram negative or gram positive)?

Back 25

Gram Negative (outer membrane allows MAC formation)

Front 26

T/F membrane attack complex is not effective for Gram Positive bacteria?

Back 26

TRUE;

Front 27

What are some methods that bacteria use to evade complement-mediated bacteriolysis (MAC)?

Back 27

Capsule/LPS (only if target antigen is different than capsule or LPS); molecular mimicry, antigenic variation, C4BP surface molecules

Front 28

These are some surface molecules that can bind C4b-binding protein to downregulate the classical pathway?

Back 28

Porins, M proteins, Filamentous Hemeagglutin (FHA)

Front 29

This molecule is a cofactor for Factor-I mediated inactivation of C4b to C4d, effectively inhibiting the classical pathway?

Back 29

C4BP

Front 30

Gram-negative bacteria are killed by (opsonophagocytosis, bacteriolysis, Both)?

Back 30

BOTH

Front 31

What are some ways that the host response to bacterial surface components is harmful?

Back 31

Cross reaction (rheumatic fever); Immune complex (arthritis/rickettsia); Chronic Inflammation (helicobacter pylori)

Front 32

Exposure to this causes gram-negative shock?

Back 32

endotoxin/LPS

Front 33

Which part of LPS is biologically active and induces gram-negative toxic shock (O-antigen, Core, Lipid A, ALL)?

Back 33

Lipid A

Front 34

Briefly explain the process of Gram-Negative Sepsis>Toxic Shock?

Back 34

LPS binds to TLR4 and CD14 on macrophage> systemic release of TNFa> vascular permeability increases in all tissues> systemic edema > decreased volume, hypoproteneimia, neutropenia followed by neutrophilia > collapse of vessels (due to decreased volume) > widespread clotting (DIC) > multiple organ failure and death

Front 35

What is the difference between continous and intermittent septicemia?

Back 35

Continuous = Intravascular, Intermittent = Distal site, Blood cultures are generally positve in continuous septicemia

Front 36

How does systemic exposure to endotoxin occur?

Back 36

Deep-seeded gram negative infection (kidney, heart, lung); Bloodstream pathogen (Nesseira meningitidis); Nosocomial (hospital-aquired) exposure

Front 37

T/F endotoxin cannot be inactivate dby autocleaving?

Back 37

TRUE;

Front 38

T/F only gram-negative bacteria are capable of producing septic shock?

Back 38

False; Gram positive also due to host response to G+ wall component (peptidoglycan or techioic acid)

Front 39

What are the clinical signs of gram negative sepsis?

Back 39

fever, shills, hypotension, mental confusion