Microbiology Flashcards

1
Q

Peptidoglycan cell wall

A

+ thick

- thin

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2
Q

Teichoic acid

A

+ present

- absent

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3
Q

Periplasmic space

A

+ absent

- present

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4
Q

Outer membrane

A

+ absent

- present

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5
Q

LPS

A

+ absent

- present

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6
Q

Porin

A

+ absent

- present

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7
Q

Why is gram - bacterial infection harder to treat?

A

Bc gram - bacteria have outer membrane

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8
Q

What is color of gram - bacteria when stained?

A

Pink

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9
Q

What is color of gram + bacteria when stained?

Hint: thick cell wall

A

Violet-blue

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10
Q

Characteristics of atypical bacteria

A
  1. Lack cell wall e.g., mycoplasma

2. Composition of cell wall is atypical

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11
Q

Acid-fast staining stains A acid on cell wall of mycobacterium tuberculosis. The resulting color is B.

A

A: mycolic
B: yellowish-red

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12
Q

Mycolic acid makes mycobacterium tuberculosis A & B resistant.

A

A: chemical
B: aridity

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13
Q

Why is mycoplasma resistant to B-lactam?

A

Bc it has no cell wall & B-lactam kills bacteria by inhibiting synthesis of cell wall

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14
Q

E.g. of B-lactam

A

Penicillin

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15
Q

Pathogenicity

A

Ability - organism - cause disease

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16
Q

What make an organism pathogenic/have pathogenicity?

A
  1. Transmissibility: ability - transfer - host to host
  2. Infectivity: ability - breach - defense
  3. Invasiveness: spread - diff parts of body
  4. Virulence: capacity - cause disease (quantitative measure of pathogenicity)
17
Q

How can pathogen invade/spread to diff parts of body?

A
  1. Direct extension: adjacent wound/infection
  2. Lymph
  3. Blood
  4. Nerves
18
Q

As LD & ID50 increase, virulence ___.

A

decreases

19
Q

Bacterial pili & fimbriae

A

Adherence

20
Q

Bacterial capsule

A

Anti-phagocytic allowing survival in host cell

21
Q

Endospores are only formed by gram ___ bacteria but not all gram ___ bacteria can form endospores.

A

+

22
Q

Clinical effects of LPS are (systemic/local)?

A

systemic

23
Q

Effects of endotoxin/LPS

A
  1. Activates macrophages via CD14/TLR4 –> TNF-a, IL-1, IL-6 & NO released
  2. Alternatively activates complement system –> histamine released & neutrophil recruited
  3. Activation of coagulation cascade –> disseminated intravascular coagulation (DIC)

Overall: hypotension, fever, septic shock, edema & DIC

24
Q

Clinical effects of exotoxin are ___ for each toxin.

Give an e.g..

A

specific

E.g., botulinum exotoxin causes muscle paralysis

25
Q

List 6 differences between endotoxin/LPS & exotoxin

A
  1. LPS: lipopolysaccharide; exotoxin: protein
  2. LPS: heat-stable; exotoxin: heat-labile (protein denatures at 60 ‘C)
  3. LPS: component of outer membrane; exotoxin: synthesized in cytoplasm & secreted
  4. LPS: gram - bac; exotoxin: gram + bac
  5. LPS not as toxic as exotoxin
  6. LPS: can’t; exotoxin: can be used as toxoid vaccine bc protein
26
Q

List 6 differences between endotoxin/LPS & exotoxin

A
  1. LPS: lipopolysaccharide; exotoxin: protein
  2. LPS: heat-stable; exotoxin: heat-labile (protein denatures at 60 ‘C)
  3. LPS: component of outer membrane; exotoxin: synthesized in cytoplasm & secreted
  4. LPS: gram - bac; exotoxin: gram + bac
  5. LPS not as immunogenic & toxic as exotoxin
  6. LPS: can’t; exotoxin: can form toxoid which can be modified into toxoid vaccine bc protein
27
Q

Components of exotoxin

A

A: A for active
B: B for binding

28
Q

Immunogenic component of LPS

A

O antigen

29
Q

Toxic component of LPS

A

Lipid A

30
Q

Modes of transmission

A
  1. Zoonoses (animals)
  2. Vector transmission (arthropods like mosquitoes)
  3. Aerosol (respiratory tract diseases like diphtheria, Legionnaire’s disease & TB)
  4. Indirect (food, water & surgical instruments)
  5. Direct (sex & transplacental)
31
Q

Incubation period

A

Time between encounter w/ pathogen & onset of symptoms

32
Q

Subclinical infection

A

No symptoms

33
Q

Carrier state

A

During incubation period or subclinical infection where pathogen is latent/dormant in both states