Pathogenesis Flashcards

1
Q

innate immunity is ____ and ____

A

quick and nonspecific

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2
Q

Innate immunity is ____ and ____

A

quick and nonspecific

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3
Q

Innate immune cells are…

A

phagocytes (neutrophils and macrophages)

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4
Q

Adaptive immune cells are…

A

T and B cells

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5
Q

Adaptive immunity is ____ and ____

A

slow and specific

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6
Q

Which cells make antibodies?

A

B cells

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7
Q

What is a pathogenicity island?

A

a section of bacterial chromosome that differs from the surrounding “ocean” of DNA sequences as a result of horizontal genetic exchange

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8
Q

Type 3 bacterial secretion system = ?

A

a virulence factor! can inject into host cells

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9
Q

How can one pathogen cause different diseases?

A

All pathogens have a core genome in common within their species, but the addition of variable elements (like phage DNA or plasmids) can introduce new virulence factors and accessory machinery

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10
Q

Role of pili in adherence?

A

different pili have different subunits (tip of tail) that bind to different receptors

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11
Q

What is facultative adherence?

A

some pathogens can have both extracellular and intracellular means of adherence/invasion depending on conditions/host

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12
Q

Advantages of intracellular lifestyle?

A

protection from extracellular immune response, protection from abx, “trojan horse” transportation, get host nutrients from cytoplasm

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13
Q

Disadvantages of intracellular lifestyle?

A

exposed to intracellular defenses, spatial limits on growth, limited to one host/harder to transmit to new host, inflammatory damage when host cell is damaged

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14
Q

How do enveloped viruses attach to host cell receptors?

A

via envelope glycoproteins

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15
Q

Do nonenveloped viruses have glycoproteins?

A

No!

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16
Q

HA on flu virus binds ___ on respiratory epithelial cells

A

sialic acid

17
Q

GP120 (glycoprotein) on HIV binds ___ on host immune cells

A

CD4

18
Q

How do nonenveloped viruses attach to host cell receptors?

A

via capsid components, i.e. spike structures

19
Q

How do spikes on nonenveloped viruses confer diversity?

A

Difference in spikes –> different serotypes that bind to different receptors and determines what tissue infected

20
Q

What is the purpose of antigenic variation?

A

swap out surface antigens periodically to evade host immune responses launched against them by the host

21
Q

Antigenic variation vs serotypes

A

AV: short time scale, rapid evolution within life of a single organism or population
S: much longer time scale!

22
Q

How can some capsules evade the human immune system?

A

By being too similar to human polysaccharide antigens for immune system to distinguish between self and pathogen

23
Q

What are the functions of the A and B subunits of exotoxin?

A
A = enzymatic activity
B = binding
24
Q

Difference between alpha, beta, and gamma hemolysis?

A
alpha = partial hemolysis
beta = complete hemolysis
gamma = no hemolysis
25
Q

An example of a pore-forming exotoxin is ?

A

hemolysin

26
Q

Exotoxin vs endotoxin - secreted from cell?

A

Exo: yes, actively from viable microbes
Endo: no, part of bacterial architecture

27
Q

Exotoxin vs endotoxin - chemical makeup?

A

Exo: polypeptide
Endo: lipopolysaccharide

28
Q

Exotoxin vs endotoxin - relative toxicity?

A

Exo: very toxic
Endo: variable toxicity

29
Q

Exotoxin vs endotoxin - relative antigenicity?

A

Exo: very antigenic (triggers immune response easily)
Endo: poorly antigenic

30
Q

What is meant by an “exfoliative toxin?”

A

Literally skin peels, i.e. scalded skin syndrome

31
Q

5 main ways pathogens can avoid clearance by immune system:

A
  1. protective polysaccharide coat
  2. attaching to host cells/tissues
  3. invading host cells
  4. latency
  5. changing antigenic characteristics
32
Q

Main role of pili?

A

adherence

33
Q

Main role of capsule?

A

anti-phagocytosis mechanism

34
Q

Main role of toxins?

A

inflict cell and tissue damage