3.8 Flashcards

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1
Q

skipped

The Parasite’s Way of Life - Chapter 8 (6)

A
  1. Surface colonization
  2. Finding a nutritionally compatible niche
  3. Surviving host defenses
  4. Intracellular life
  5. Subverting host immune responses
  6. Transmission to a new host
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2
Q
  1. Surface colonization (3)
A
Preference of bacteria for particular locations in body
bacteria vary in specificity
tissue tropism
Adhesins on bacterium
Receptors on host cell
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3
Q

bacterial proteins on the tips of fimbriae and/or

pili often interact with

A

glycolipids and/or

glycoproteins of host epithelial cells

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4
Q
  1. intimins (bacterial
    proteins at the the cell
    surface) interact with
A

their
own translocated intimin
receptor (TIR)

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5
Q

Surface colonization (continued)
Examples:
gram-positive bacteria (e.g. Staphylococcus aureus)
often bind host — (epithelial cells), which binds to

A

fibronectin

integrins

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6
Q

fibronectin binding proteins =

A

subclass of a large
family of bacterial adhesins referred to as Microbial
Surface Components Recognizing Adhesive Matrix
Molecules or MSCRAMMS

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7
Q

Other MSCRAMM targets:

A

fibrinogen and collagen

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8
Q

many individuals in poor health are —deficient

A

fibronectin

  • balance shifts in favors of gram negatives
    e. g. greater incidence of pneumonias caused by gramnegative bacteria
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9
Q
  1. Surface colonization (continued)
    Examples:
    gram-positive bacteria
    serine rich repeat proteins (SRRPs) (= bacterial adhesins)
    contain a domain of hundreds of alternating serine residues
    Extend a unique non-repeat (NR) domain that mediates adhesion
    NR domain binds
A

sialic acid moieties, keratin, and other NR domains

of a similar SRRP

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10
Q

sialic acid binding adhesins =

A

serine rich repeat proteins (SRRPs)

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11
Q

Finding a nutritionally compatible niche (2)

A

Intermittent availability of food for some bacteria
e.g. intestinal bacteria
Adaptation to particular location

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12
Q

Surviving host defenses

A

Defending against complement

masking and inhibition

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13
Q

Defending against complement

masking and inhibition: Activation of complement Figure 6-1 (3)

A

C3a is an anaphylatoxin
(inducer of acute inflammation)

C3b is an opsonin and part of
C3 convertase (alt. pathway)
and C5 convertase

C5a is a chemotactic protein
for neutrophils and an
anaphylatoxin

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14
Q
Microbial mechanisms to defend
against complement (4)
A

long chain smooth LPS limits access of MAC to the organisms surface
polysaccharide capsule masks surface compenents that can activate complement via the alternative pathway
addition of sialic acid to lipooligosaccaride inhibits complement fixation
c3b peptidase cleaves the component into inactive fragments

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15
Q
  1. Surviving host defenses

Subverting phagocytosis

A

inhibiting phagocyte recruitment and function
C5a peptidase production (see figure)
Increasing cAMP to inhibitory levels

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16
Q

killing phagocytes:

A

leukocidins

17
Q

escaping ingestion:

A

protein A (Staphylococci and Streptococci)
expressed on bacterial cell surface
binds Fc portion of IgG (wrong end)
these bound antibodies cannot act as opsonins

18
Q

surviving inside phagocytes (4)

A
inhibit lysosomal fusion with
phagosome
escape into the cytoplasm
(form pores in phagosome)
resist lysosomal enzymes
inhibit phagocyte’s oxidative
pathway (respiratory burst)
19
Q

Penetration of nonphagocytic host cells:

A

Some bacteria enter host cells by stimulating host cell membrane protrusion

20
Q

internalins

A

(bacterial
proteins at the the cell
surface) interact with
host E-cadherin

21
Q

invasins

A

(bacterial
proteins at the the cell
surface) interact with
host integrins

22
Q

. Transmission to other cells (2)

A

tissue damage

cell-to-cell transmission

23
Q

Subverting immune responses (4)

A

immunosuppression
superantigens (diverting lymphocyte function)
changing antigenic coats
proteolysis of antibodies

24
Q

Transmission to a new host

A

judgment of transmission as passive or active can be arbitrary
consider effects on host