Microbiology Lectures 21-23

Front 1

Humoral branch of adaptive immunity

lecture 21

Back 1

involves antibodies (made by B cells)

attacks extracellular pathogens

Front 2

Cell-cell mediated branch

Back 2

involves T cells

attacks intracellular pathogens

Front 3

Class I MHC

Back 3

all nucleated cells'

present peptides that originate in cytoplasm from intracellular pathogens

e.g. CD8 and cytotoxic T cells

Front 4

Class II MHC

Back 4

Professional antigen-presenting cells only

present peptides from extracellular paths taken up by phagocytosis (e.g. CD4 and helper t cells)

Front 5

Helper T cells

Back 5

make cytokines, activate B cells, macrophages, or other T cells

Front 6

Cytotoxic T cells

what they do and two things they use

Back 6

kill cells expressing foreign antigen using:

1, granzymes and 2. perforins

Front 7

perforins

Back 7

form pores, involved in cytotoxic t cells

Front 8

granzymes

Back 8

induce apoptosis

Front 9

Cluster of Differentiation (CD) molecules

Back 9

membrane proteins that function as coreceptors on immune cells

can help determine a cell's identity

e.g. helper t cell: CD4

cytotoxic t cell: CD8

Front 10

T-cell receptors (TCR's)

Back 10

recognize a peptide and an MHC containing said peptide NEED BOTH!

bind the peptide

are expressed from gene segments rearranged in the thymus

Front 11

MHC (major histocompatibility complex)

Back 11

a collection of genes encoding cell surface molecules for self/nonself recognition

Front 12

what is human version of MHC?

Back 12

human leukocyte antigen (HLA) complex. get 1 from each parent.

Closer 2 people are related, more similar HLA

important for organ/tissue donation

Front 13

pathogen

Back 13

organism that produces disease

Front 14

opportunistic pathogen

Back 14

infects host with weakened immune system

Front 15

carrier

Back 15

infected individual, potential source of infection (no observable symptoms)

Front 16

zoonoses

Back 16

disease transmitted to humans from animals

Front 17

vectors

Back 17

organisms that transmit disease to humans e.g. mosquitos, fleas, ticks

Front 18

pathogenicity

Back 18

ability to produce disease

Front 19

virulence

Back 19

degree of pathogenicity

Front 20

latency

Back 20

pathogen stops reproducing. Dormant, CAN become active again

Front 21

pathogenicity islands

Back 21

large groups of genes which encode virulence determinants. Present in virulent, absent in non-virulent strains.

DNA based composition differs for rest of genome, often flanked by phage or plasmid genes

Front 22

how is virulence measured?

Back 22

Infections dose 50 (ID50): # of paths required to cause clinical disease in 50% of inoculated hosts

Lethal dose 50 (LD50): # of paths required to KILL 50% of inoculated hosts

Front 23

viral attachment example

watched in lecture and biochem lecture

Back 23

capsid and viral spike proteins mediate viral atta.

e.g.

GP120 of HIV binds CD4 and CCR5

and Hemagglutinin of influenza binds sialic acid

Front 24

through what bodily systems can viruses be spread?

Back 24

blood, neural, and lymphatic

Front 25

tropism

Back 25

cell tissue, organ specificity

determine by host cell receptors

Front 26

how do viruses evade adaptive immune response?

Back 26

block antigen processing, MHC export

evade antibody (Antigenic variation)

e.g. aa changes in virion spikes, common of RNA viruses

Front 27

how do viruses evade innate immune response?

Back 27

block, breakdown complement,block interferon production

Front 28

mechanism of bacterial pathogenicity

(4 steps)

Back 28

1. attachment

2. invasion and spread

3. colonization

4. evade innate and adaptive IRs

Front 29

#1 bacterial attachment

Back 29

pili

capsules: Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitidis

certain strains of P. aeruginosa make capsules, called mucoid strains. Is an opportunistic path in burn/cystic fibrosis patients

Front 30

#2 invasion and spread

Back 30

Active penetration of host mucous membranes or epithelium

Passive penetration also possible: wounds/bites

once below mucous membrane, can spread to deeper tissue or even blood **bacteremia

Front 31

Bacterial virulence factors (6 of them)

Back 31

coagulase

streptokinase

IgA protease

hemolysins

siderophores

Dnase

Front 32

coagulase

Back 32

clots fibrinogen in plasma, clot protects pathogen

Front 33

streptokinase

Back 33

activates plasmin, digests fibrin clots- pathogen moves from clotted areas

Front 34

IgA protease

Back 34

destroy antibody

Front 35

hemolysins

Back 35

digest RBCs, release iron

Front 36

siderophores

Back 36

released, bind iron

Front 37

DNase

Back 37

lowers viscosity of secretions, spread nutrition

Front 38

3 ways for bacterial pathogens to evade innate immune responses

Back 38

1. capsules-block opsonization, membrane attach complex

2. proteases- degrade C3b (opsonin) or C5a (chemoattractant)

3. type III systems- inject proteins into macrophages & other cells & block TLR signaling and NFkB

Front 39

3 ways for bacterial pathogens to evade ADAPTIVE immune responses

Back 39

capsules

IgA proteases

Antigenic variation: ∆ cell surface outer membrane or pilli proteins

Front 40

what are NETs?

lecture 22

Back 40

Neutraphil extracellular traps

DNA & antimicrobial proteins/enzymes

Front 41

4 examples of bacterial intracellular paths

Back 41

1. Mycobacterium tuberculosis

2. Legionella

3. Chlamydia

4. Listeria monocytogenes

Front 42

Listeria monocytogenes

Back 42

Gram +, food borne path

psychrophile, so bad cause fridge doesn't slow growth or kill

can cross placenta

Front 43

what bacteria use the virulence factor biofilm?

Back 43

Streptococcus pneumoniae: Otitis Media

Pseudomonas in cystic fibrosis lung

Staphylococcus & Enterococcus on heart valves -endocarditis

Front 44

toxins

Back 44

substances that damage the host

exotoxins (unstable, neutralized by antibodies) and endotoxins

Front 45

4 types of exotoxins

Back 45

1. membrane disrupting

2. superantigens

3. AB

4. specific host site

Front 46

membrane-disrupting exotoxins

Back 46

pore forming exotoxins e.g. Leukocidins and Hemolysins

Front 47

superantigens (exotoxins)

Back 47

cause T cells to overexpress, release cytokines

(connects MHC II w/antigen to T cell receptor)

failure of multiple host organs

TSS caused by Staphylococcus aureus

Front 48

AB exotoxins

Back 48

2 subunits

A: toxic effect

B: binds target cell receptor

many are ADP ribosyltransferases which remove ADP ribose group from NAD& attach it to host cell protein making it fxn abnormally or inactivate

Front 49

diptheria toxin

Back 49

Corynebacterium diptheriae

Binds growth factor receptor.

enters by endocytosis

ADP ribosyltransferase attaches ADP ribose from NAD onto Elongation factor 2 (EF2)

Front 50

specific host site exotoxins

Back 50

many AB toxins are also host site specific

Front 51

Vibrio cholerae

Back 51

ENTEROtoxin

ADP ribosylates a host G protein that controls cAMP levels and keeps protein on.

increase of cAMP means loss of control of ion flow- massive H20 loss

Front 52

Clostridium botulinum

Back 52

NEUROtoxin

blocks Ach release at neuromuscular joints

flaccid paralysis

Front 53

sepsis

Back 53

systemic response to microbial infection, elevated temp, heart & respiratory rate, leukocyte count

Front 54

shock

Back 54

sepsis with hypotension (low bp)

Front 55

bacteremia

sepsicemia

Back 55

viable bacteria in blood

disease associated with pathogens or toxins in blood

Front 56

Type III secretion systems

Back 56

'hand to hand combat'

Gram - paths of plants and humans

the bad bois all use em

Front 57

features of type III

Back 57

1. injectisome has hollow basal body

proteins from bacteria inject into host

Injector proteins inject effectors (e.g. yops, sops, and bops

their genes are found on pathogenicity island

Front 58

Targets for typeIII effectors

Back 58

1. host cell cytoskeleton (actin)

promotes invasion, blocks phagocytosis

2. Host cell signaling (NFkB)

blocks cytokine production, induces apoptosis

Front 59

enteropathogenic E. coli (EPEC)

Back 59

TIIISS

major cause of infantile diarrhea

Binds host cell using bundle-forming pill, the delivers effectors via injectisome

MOA includes TIR

Front 60

Translocated Intimin Receptor (TIR)

Back 60

presented on host cell surface, binds bacterial intimin

Front 61

autoclave stats

Back 61

15 lbs/square inch, 121 C 15 min

Front 62

pasteurization

Back 62

63C for 30 min, rapid cool

72C for 15 sec, rapid cool

Doesn't sterilize, kills most pathogens

e.g. Listeria, Salmonella, Campylobacter

Front 63

Paul ehrlich

Back 63

selective toxicity

Front 64

Alexander Flemming

Back 64

accidentally redsicovered penicillin

Front 65

florey, chain, and heatley

Back 65

purified and injected penicillin into mice which survived

Front 66

selman Waksman

Back 66

cultured 10,000+ strains of soil bacteria and identified streptomycin

Front 67

targets of antimicrobial agents

Back 67

1. cell wall

2. plasma membrane

3. metabolic enzymes

4. Nucleic acid synthesis

5. protein synthesis

Front 68

penicillins

MOA, structural features, spec

Back 68

cell wall inhibitors.

mostly narrow spec G+ and cidal

structural features:

B lactam ring and R group (stability and spectrum)

MOA: inhibit bacterial Penicillin binding proteins (PBPs) used for transpeptidation

Front 69

ampicillin

Back 69

broad spec G + and G -

Front 70

where do penicillinases attack and inactivate the drug?

Back 70

draw plz

B lactam ring bond

Front 71

penicillin and cephalosporins end result for bacteria?

Back 71

stop cell wall synthesis creating osmotic lysis!

Front 72

vancomycin MOA

Back 72

binds terminal D-alanine on NAM, also blocking transpeptidation

Front 73

where in the cell are Nag and NAM made?

Back 73

cytoplasm, carrier moves them across membrane to become part of cell wall

Front 74

Bacitracin MOA

Back 74

blocks carrier of NAG & NAM across membrane

* topically applied e.g. neosporin

Front 75

plasma membrane inhibitors

3 types

Back 75

1. polymyxins

2. Miconazole

3. Nystalin

Front 76

Polymixins MOA, spec

Back 76

cidal, narrow spec mostly G-

bind LPS, disrupt outer/plasma membrane

e.g. colistin

Front 77

Miconazole, MOA, conditions treated

Back 77

blocks sterol synthesis

treats athletes foot/candida yeast infections

Front 78

Nystalin MOA, condition

Back 78

binds sterols

candida yeast infections

Front 79

4 types of protein synthesis inhibitors

Back 79

1. AMinoglucosides

2. Tetracyclines

3. Macrolides

4. Chloramphenicol

Front 80

aminoglycosides MOA, 2 examples of drugs

Back 80

cidal

bind 30s, cause misreading of mRNA codons

e.g. streptomycin, kanamycin

Front 81

tetracycline MOA

Back 81

static

also bind 30s, block tRNA + aa binding to A site

Front 82

macrolides MOA

Back 82

static

Bind 23s rRNA of 50s, block peptide bond formation

Front 83

chloramphenicol MOA

Back 83

same MOA as macrolides

toxic, only used in life-threatening situations