Pod: Bacterial Pathogenesis

Front 1

What are the three organism/host relationships?

Back 1

1. commensalism
2. mutualism
3. paratisism

Front 2

What's the relationship between pathogenicity and virulence?

Back 2

Virulence is a quantitative measure of pathogenicity.

Front 3

Virelence factors are not always expressed. What mechanism does bacteria use to regulate virulence expression?

Back 3

Quorum sensing.

Front 4

The following virulence factors are under quorum sensing regulation:
A. Exoprotease/exotoxin
B. Siderophores
C. Biofilms
D. All the above

Back 4

D

Front 5

The concentration of what molecules bacteria quorum sensing is based on?

Back 5

autoinducers

Front 6

What are the five general steps in the establishment of a bacterial infection?

Back 6

1. Entry and attachment
2. multiplication
3. local/general spread
4. evasion of host defense
5. exit from body

Front 7

Group A streptococcus (strep throat) attach to respiratory epithelium through what molecules on the bacterial cell wall?

Back 7

LPA
M protein - antiphagocytic
F-protein
finronectin

Front 8

Group A streptococcus (strep throat) is cleared by which immune response?

Back 8

Antibodies opsinize and induce phagocytosis.

Front 9

Give one example of bacteria that enter human body via the following pathway:
1. ingestion
2. inhalation
3. trauma
4. needlestick
5. arthropod bite
6. sexual transmission

Back 9

1. E.Coli
2. TB
3. Staphycoccus aureus
4. syphilis
5. lyme disease
6. gonorhea

Front 10

What molecules on human cell do the following bacterial adhesins stick onto:
1. fimbriae
2. M protein
3. intimin protein

Back 10

1. lectin
2. CD46
3. cytoskeleton (internalization)

Front 11

What method does some bacteria lacking adhesins use to attach to host cells?

Back 11

Secret its own receptor which is internalized and expressed by the host cell.

Front 12

Why cranberry juice is good at treating E coli infection?

Back 12

Contain lectin used by E coli to adhere to uroepithelium.

Front 13

What type of epithelium does Chlamydia trachomatis bind to?

Back 13

nonciliated columnar, cuboidal, or transitional: genital, ocular.

Also bind to macrophage.

Front 14

What are the two purposes of biofilm production from bacteria?

Back 14

1. adhesion to other cell surface.
2. provide resistance to antibiotics (phagocytic cells, immune cells)

Front 15

Which bacteria tend to flourish in cyctic fibrosis patients?

Back 15

psudomonas aeruginosa

Front 16

Why are psudomonas aeruginosas resistant to antibiotics?

Back 16

Production of biofilm triggered by low levels of peroxide from PMNs in the lung.

Front 17

Which human cells do salmonallas bind to?

Back 17

M cells.

Front 18

Which molecule is responsible for uptake of salmonella into M cells?

Back 18

invasin

Front 19

Where are the genes of p-fimbriae, hemolysin in uropathogenic E. Coli located on the chromosome?

Back 19

Pathogenicity island (by transposition or site-specific recombination).

Front 20

Sites of bacteria exit.

Back 20

1. respiratory tract
2. GI tract
3. urogenital tract
4. skin (shedding)
5. blood
6. mother to fetus

Front 21

What is the essential nutrient for bacterial multiplication?

Back 21

iron

Front 22

Virulence factors that obtain iron for bacteria:
1. siderophores
2. receptors for transferrin
3. hemolysins
4. all the above

Back 22

4.
siderophores: iron chelators
receptor for tranferrin: remove iron at cell surface
hemolysin: release iron from cell.

Front 23

Endotoxin trigger which type of immune response:
A. innate
B. adaptive

Back 23

innate.
Endotoxins are signals to host that there is infection.

Front 24

Give an example of toxin that is a strucural component of bacteria.

Back 24

LPS(lipid A)

Front 25

Give an example of bacterial toxin that is an excreted enzymatic protein.

Back 25

1. tetnus
2. diptheria

Front 26

How does macrophages and dendritic cells sense the presence of invading bacteria?

Back 26

1. Toll-like receptors (TLR)
2. CD14
3. nucleotide-binding pliogomerization domain (NOD) protein

Front 27

Describe how GN endotoxin LPS released from bacterial lyse induce inflammation.

Back 27

1. LPS bind to LPS binding protein
2. complex bind to CD14 on macrophage
3. complex passed ontp TLR4
4. transcription of cytokines: TNF-α, IL1, IL6, IL12.

Front 28

(T/F): High levels of endotoxin could result in sepsis and multisystem organ failure.

Back 28

T.

Front 29

How many exotoxin types are there?

Back 29

Four.
1. superantigen: bind but not translocate
2. destroy host membrane
3. intracellular toxin A-B: bind and translocate
4. use type III,IV secretion system of bacterial cell

Front 30

T/F: Diptheria toxin and S. pyrogenes exotoxin genes are carried on lysogenic phages.

Back 30

T.

Front 31

T/F: E.Coli and tetnus toxin genes are carried in plasmids.

Back 31

T.

Front 32

What mechanism do bacteria use to trigger expression of exotoxin genes?

Back 32

quorum sensing

Front 33

Examples of exotoxin enzymatic molecular mechanism of action

Back 33

1. adenylate cyclase toxins
2. ADP-rybosylating toxin
3. deamidating toxins
4. glusylating toxin
5. metalloprotease toxin
6. RNA glycosidase toxin

Front 34

Why does superantigen cause massive immune response (massive cytokine release by CD4 cells)?

Back 34

No need for processed antigen.

Front 35

IL-2 triggers release of what cytokines?

Back 35

TNF-α, IL-1, chemokines

Front 36

Other than endotoxin, which exotoxin can also cause sepsis?

Back 36

superantigens.

Front 37

Superantigen toxins are from GP or GN organisms?

Back 37

GP

Front 38

Give 2 examples of GP bacteria that release superantigen toxin.

Back 38

1. Staphylococcus aureus
2. Streptococcus pyrogenes

Front 39

What symptom is associated with staphylococcus aureus?

Back 39

diarrhea
toxic shock

Front 40

What symptom is associated with streptoococcus pyrogene?

Back 40

scarlet fever
necrotizing fascitis
toxic shock

Front 41

Pore-forming toxins and phoapholipases are what type of exotoxin?

Back 41

Type II: membrane disrupting

Front 42

An example of bacteria that uses phospholipase (lecithinase) to disrupt host membranes:

Back 42

Clostridium perfringens α toxin: lyse erythrocytes, platlets, leukocytes, endothelial cells.

Front 43

What exotoxin cause massive hemolysis, tissue destruction, hepatic toxicity, and myocardial infarction?

Back 43

Clostridium perfringens α toxin

Front 44

Two bacteria that uses intracelluar toxins A-B:

Back 44

Cholera
Diptheria

Front 45

What are A and B stand for in intracelluar toxins A-B?

Back 45

A: active portion
B: binding portion

Front 46

T/F: Diptheria(Corynebacterium diptheriae) colonization in the pharnx need lysogenic phage.

Back 46

T.
Gene incorporated as prophage onto bacterial chromosome during lysogenic conversion.

Front 47

Which portion of intracelluar toxins A-B contain translocation region?

Back 47

B(binding portion)

Front 48

A portion of intracelluar toxins A-B bind to what molecule of susceptible cells?

Back 48

HB-EGF (heparin-binding epidermal growth factor.

Front 49

How does portion A of intracelluar toxins A-B of diptheria kill the host cell?

Back 49

ADP-ribosylates EF-2->protein synthesis stopped

Front 50

How might the toxin-mediated effects of diptheria toxin best be prevented in humans?

Back 50

1. give anti-toxin.
2. prevent toxin binding with HB-EGF on human cell (heart, nerve).
3. cure the bacteria by target the bacteriophage.

Front 51

Where does the vaccine designed for diptheria bind: binding portion or active portion of the toxin?

Back 51

binding portion. Vaccine no longer contain active enzymatic function.

Front 52

What is the formalin-inactivated toxin in the diptheria vaccine called?

Back 52

toxoid

Front 53

What is toxoid?

Back 53

toxoid is a bacterial toxin Bacterial toxin whose toxicity has been weakened or suppressed either by chemical (formalin) or heat treatment.

Front 54

Exotoxin produced by Pseudomonas aeruginosa has the same mechanism of action as extotoxin of diptheria. Why is Pseudomonas aeruginosa less virulent?

Back 54

Difference lies in receptors and their cellular distribution.

Front 55

List some examples of type IV exotoxin which is secreted directly into cells by gram negative bacteria.

Back 55

1. Apoptotic toxins
2. protein kinases and phosphorylases

Front 56

What is "by-stander" damage to host cells?

Back 56

Damage due to the presence of inflammatory cells at site of reation:
1. enzymatic: byproductes of neutrophils, macrophages, complement reactions
2. replacement of normal tissue with inflammatory response tissue: granulomas

Front 57

What are some examples of damage due to cross reactive antibodies?

Back 57

1. Rhumatic fever (s. pyogene): damage to heart
2. mycoplasma pneumoniae: damage joint, CNS, Blood antigens
3. Guillian_Barre syndrome(campylobacter jejuni): damage to gangliosides

Front 58

What are the 8 ways extracellular pathogens avoid phagocytosis?

Back 58

1. capsules
2. antigenic masking
3. antogenic shift/variation
4. production of IgA protease
5. serum resistence
6. destroy phagocytes
7. inhibit phagocytosis/chemotaxis
8. hide in normal cells

Front 59

How do our body clear intracellular pathogens that dwell in phagocytic cells?

Back 59

Th1 response

Front 60

How does capsula bacteria avoid activation of alternative complement system?

Back 60

shedding the capsule to mask the deposited C3

Front 61

How does human body clear capsular bacteria?

Back 61

Produce antibody to opsonize or activate complement

Front 62

3 examples of capsular bacteria:

Back 62

1. Neisseria meningitis
2. Streptocossus pneumoniae, agalactiae
3. Haemophilus influenzae

Front 63

Why do people develop spleenomegaly with hyper IgM syndrome?

Back 63

Spleen works extra hard to take out encapsulated bacteria since antibody is not sufficient to clear the infection.

Front 64

How does bacteria mimic host cell?

Back 64

Coat themself with host antigens.

Front 65

What molecule does Staphylococcus aureus use to mask themself from antibodies?

Back 65

Protein A: binds to Fc region of IgG so that phagocytes can no longer bind to Fc of IgG.

Front 66

What is serum resistence referring to as a immune avoidance mechanism?

Back 66

resistance to lytic effect of complement.

Front 67

What molecule on GN bacilli that activates the complement system?

Back 67

LPS

Front 68

What methods do bacteria use to become resistant to lytic effect of complement system?

Back 68

1. failure to bind and activate complement
2. shedding of surface molecule that activate complement
3. interrupt complement cascade before formation of membrane attack complex.

Front 69

How does M protein prevent the activation of complement system?

Back 69

Bind to factor H which destabilized C3b.

Front 70

What two immune-avoidance mechanisms does staphylococcus aureus use?

Back 70

1. protein A mask IgG from binding to phagocytic cells.
2. produce proteolytic enzymes that destroy phagocytes: leukocidin

Front 71

How do bacteria inhibit chemotaxis?

Back 71

1. procude catalase that reduce the effect of neutrophils's oxidative burst
2. form abcesses, granulomas

Front 72

How does intracellular bacteria survive inside phagocytes?

Back 72

1. revent fusion of endosome wuth lysozome
2. resistance to lysosomal enzymes
3. escape lysosome and replication in cytosol