Host Microbe Interactions Flashcards

1
Q

What are the 3 ways that normal microbiota contribute to the first line of defense?

A
  1. colonization resistance (occupying surfaces/receptor)
  2. producing inhibitors (bacteriocins and acids)
  3. competitive exclusion (competing for nutrients)
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2
Q

What are the 4 conditions under which a commensal microbe can become and opportunist pathogen?

A
  1. immune competency compromised or deficient
  2. Presence of the microbe in unaccustomed sites
  3. Following broad spectrum antibiotic therapy
  4. After medical device or implants put in that allows for biofilm formation
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3
Q

(briefly) what are the 6 strategies employed by pathogens in avoiding host immune system

A
  1. Protective structural components and products
  2. Mimicry of host antigens
  3. Antigenic variation
  4. Suppression of host responses
  5. Survival in macrophages
  6. Growth in areas isolated from immune responses
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4
Q

What are the 2 kinds of structural components/products that pathogens can make?

A
  1. anti-phagocytic (capsules)

2. Degradative (IgA proteases)

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5
Q

What are 8 diseases caused by S. pyogenes (group A strep)

A
  1. Pharyngitis (strep throat)
  2. Scarlet fever
  3. Impetigo
  4. Erysipelas
  5. Sepsis
  6. Toxic shock like syndrome
  7. Necrotizing fasciitis
  8. Post streptococcal disease (rheumatic fever and glomerulonephritis)
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6
Q

What’s one example of a secreted virulence factor of S. pyogenes?

A

DNases

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7
Q

What are the 3 systems (briefly) that are involved in virulence factor control?

A
  1. Mga
  2. CovRS
  3. Catabolite control protein A (CcpA)
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8
Q

How does the CcpA system work? (under glucose limiting/not limiting conditions)

A
  1. Under glucose-limiting conditions, HPr is not phosphorylated and the CcpA-HPr-P complex is not formed.
    - Genes that are normally repressed by the CcpA-HPr-P complex are now able to be transcribed.
  2. Under conditions where glucose is present the CcpA-HPr-P complex binds to cre (catabolite response element) sites in the promoter regions or within target genes to repress gene expression.
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9
Q

Whats the morphology of salmonella enterica?

A

gram neagtive motile rods

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10
Q

What is the main reservoir of Salmonella?

A

poultry products

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11
Q

What 2 diseases does Salmonela enterica cause?

A

typhoid fever and salmonellosis

** acute diarrhea

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12
Q

Where does S. enterica invade the body from

A

the GI tract

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13
Q

How does Salmonela enterica survive the acidic pH of the stomach ?

A

through an acid tolerance response

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14
Q

How does Salmonela enterica colonize the distal ileum?

A

either by invasion of epithelial cells or uptake by M cells

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15
Q

What happens to Salmonela enterica once it is engulfed by macrophages? what system is used?

A

it can survive within them

done through the PhoPQ and PmrAB 2 component regulatory systems

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16
Q

Where are the genes for the type III secretion system used by Salmonela enterica encoded?

A

Salmonella pathogenicity island 1 (SPI-1)

17
Q

How do effector proteins enter into host cells?

A

Injected via the needle complex

18
Q

What is an example of an effector Salmonella protein and what does it do?

A

SopE: alter host cell cytoskeletal structure (e.g. actin rearrangement) resulting in engulfment of the bacteria

19
Q

What activates PhoQ?

A

acidic pH and cationic antimicrobial peptides

20
Q

What does activated PhoQ do?

A

phoshphorylates PhoP (RR)

21
Q

what does PhoP-P do? what is the result?

A

Phosphorylated PhoP binds to DNA to control expression of phoP-activated and phoP-repressed genes leading to resistance to cationic antimicrobial peptides

22
Q

What other virulence trait does the PhoPQ system control?

A

LPS modification

- masking negative charge to evade cationic microbial peptides

23
Q

What does Mga do?

A

gene expression of M protein, C5a peptidase, and Immunoglobulin-binding proteins (and others)

24
Q

What does the CovRS system do?

A

Negatively regulates capsule synthesis, cysteine protease SpeB, streptokinase, streptolysin S, and DNase production