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USMLE > Microbiology - general and antibiotics > Flashcards

Microbiology - general and antibiotics Flashcards

1
Q

Gram + cell membrane component

A

Lipoteichoic acid

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2
Q

2 unique features of Gram - bac cell wall

A
  1. Periplasm

2. Outer membrane

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3
Q

3 components of outer cell membrane of Gram - bacteria

A

Polysaccharide
Lipid A
O antigen

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4
Q

2 components of peptidoglycan sheets of bacterial cell wall

Which one connects peptides?

A

NAG

NAM (connects peptides)

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5
Q

Make up of capsule

Which bacteria is the exception?

A

Polysaccharide

Exception - Bacillus anthracis - poly D glutamate peptide capsule (major virulence factor)

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6
Q

3 conjugated vaccines with capsule polysaccharide

A

Strep pneumonia
H influenzae b
N meningitidis

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7
Q

Bacteria using glycocalyx

A

Staph epidermidis - forms biofilm

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8
Q

2 key bacteria using pili/fimbria

A 
E. Coil
Neisseria gonorrhoea (antigenic variation —> risk subsequent infection
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9
Q

3 components of bacteria spores

A

Keratin-like outer coating
Dipicolinic acid
Peptidoglycan cortex/core wall

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10
Q

2 main spore-forming groups of bacteria

A

Bacillus

Clostridium

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11
Q

Name the microbes that poorly Gram stain.

A 
‘These Little Microbes May Unfortunately Lack Real Colour But Are Everywhere’
Treponema (too thin to visualise)
Leptospirosis (too thin to visualise)
Mycobacterium (high lipid content)
Mycoplasma (lack cell wall)
Ureaplasma (lack cell wall)
Legionella (primarily intracellular)
Rickettsia (primarily intracellular)
Chlamydia (primarily intracellular; lacks muramic acid)
Bartonella (primarily intracellular)
Anaplasma (primarily intracellular)
Ehrlichia (primarily intracellular)
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12
Q

Giemsa staining microbes (4)

A 
‘Ricky got Chlamydia as he tried to Please the Bored Geisha’
Rickettsia
Chlamydia
Plasmodium
Borrelia
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13
Q

Staining for Cryptococcus (2)

A

India ink

Mucicarmine (stains capsule red)

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14
Q

Chocolate agar

A

H influenzae

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15
Q

Thayer Martin agar

A

Neisseria gonorrhoea

Neisseria meningitidis

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16
Q

Bordet Gengou agar

A

Bordatella pertussis

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17
Q

Tellurite agar

A

C diphtheria

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18
Q

Loffler medium

A

C diphtheria

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19
Q

Lowenstein Jensen agar

A

M TB

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20
Q

Eaton agar

A

Mycoplasma

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21
Q

MacConkey agar

A

Lactose-fermenting enteric

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22
Q

Eosin-methylene blue (EMB) agar

A

E. Coil

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23
Q

Charcoal yeast extract agar buffered with cysteine and iron

A

Legionella

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24
Q

Sabouraud agar

A

Fungi

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25
Q

Silver stain (3)

A

PCP (fungi)
Legionella
H pylori

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26
Q

Most cocci are Gram +

Name 2 cocci that are Gram -

A

Neisseria meningitidis/gonorrhoea

Moraxella

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27
Q

Most rods are Gram -ve

Name the G+ rods (4)

A

Corynebacterium
Clostridium
Listeria
Bacillus

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28
Q

Branching/filamentous

A

Nocardia

Actinomyces

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29
Q

Sorbitol culture

A

Used to detect E.coli 0157 (colourless colonies instead of pink)

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30
Q

Facultative aerobes (3)

A

Staph
Strep
Enteric gram -

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31
Q

Obligate aerobes (3)

A

Pseudomonas
M TB
Nocardia

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32
Q

Key obligate intracellular organisms (2)

A

Rickettsia

Chlamydia

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33
Q

Facultative intracellular (8)

A 
‘Some Nasty Bugs May Live FacultativeLY’
Salmonella
Neisseria
Brucella
Mycobacterium
Listeria
Francisella
Legionella
Yersinia
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34
Q

Urease +ve organisms

A 
‘Pee CHUNKSS’
Proteus
Cryptococcus
H pylori
Ureaplasma
Nocardia
Klebsiella
S epidermidis
S saprophyticus

Predisposes to struvite stones

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35
Q

Catalase +ve organisms

A

‘Cats Need PLACESS to Belch their Hairballs’

E.g.s
Nocardia
Pseudomonas
Listeria
Aspergillus
Candida
E. coli
Staph
Serratia
B cepacia 
H pylori
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36
Q

Name 3 key virulence factors.

A

Protein A
IgA protease
M protein

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37
Q

MOA protein A virulence factor.

Which bacteria?

A

Binds FC portion of IgG —> prevents opsonisation and phagocytosis
Staph aureus

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38
Q

MOA IgA protease.

Which bacteria?

A

Cleaves IgA —> adhere and colonise mucous membranes

SHiN bacteria

  • S pneumonia
  • H influenzae type b
  • Neisseria
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39
Q

MOA M protein virulence factor

Expressed by which bacteria?

A

Helps prevent phagocytosis (binds factor H, break down of C3 convertase)
Gp A Strep

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40
Q

MOA diphtheria toxin

A

ADP ribosylation of EF-2 —> prevents protein synthesis

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41
Q

MOA exotoxin A of Pseudomonas

A

ADP ribosylation of EF-2 —> prevents protein synthesis

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42
Q

MOA Shiga toxin

A

Inactivated 60S ribosome by removing adenine residue from rRNA

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43
Q

MOA EHEC toxin

A

Inactivated 60S ribosome by removing adenine residue from rRNA

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44
Q

What causes the HUS with enterohaemorrhagic E. coli?

A

Shiga-like toxin enhances cytokines release.

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45
Q

MOA ETEC heat labile toxin

A

Overactivation adenyulate cyclise —> increases cAMP —> increased chloride secretion into gut

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46
Q

MOA EHEC heat stable toxin

A

Overactivates cGMP —> increased cGMP —> reduced resorption of NaCl and water in gut

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47
Q

MOA oedema toxin of Bacillus anthracis

A

Mimics adenylate cyclase —> increased cAMP

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48
Q

MOA Vibrio cholera’s toxin

A

Activates Gs —> increased cAMP —> increased chloride secretion into gut

Voluminous ‘rice water’ diarrhoea

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49
Q

MOA Pertussis toxin

A

Disables Gi —> increased cAMP —> impaired phagocytosis

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50
Q

MOA tetanospasmin

A

Cleaves SNARE (soluble NSF attachment protein receptor; required for neurotransmitter release via vesicular fusion) —> prevent release of inhibitory GABA and glycine from Renshaw cells —> spastic paralysis

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51
Q

MOA Boutlinum toxin

A

Cleaves SNARE (soluble NSF attachment protein receptor; required for neurotransmitter release via vesicular fusion) —> prevents release stimulators (ACh) signals at NMJ —> flaccid paralysis

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52
Q

MOA of alpha toxin (Clostridium perfringens)

A

Phospholipase (lecithinase) —> degrades tissue and cell membranes

Myonecrosis and double zone haemolysis on blood agar

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53
Q

MOA Strep pyogenes Streptolysin O

A

Degradation cell membrane

RBC lysis, contribute to beta haemolysis

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54
Q

MOA TSST-1 of Staph aureus and erythrogenic exotoxin A of Strep pyogenes

A

Cross-links beta region TCR to MHCII outside of antigen binding site —> overwhelming release IL-1, IL-2, IFN-gamma, TNF-alpha

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55
Q

3 main effects LPS of outer membrane of Gram -

A
  1. Macrophage activation (TLR4/CD14)
  2. Complement activation
  3. Tissue factor activation
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56
Q

Bacterial transformation

A

Uptake of DNA from surrounding environment

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57
Q

What prevents bacterial transformation?

A

Add deoxyribonuclease (degrades naked DNA)

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58
Q

Bacteria using bacterial transformation (3)

A

‘SHiN’

S pneumonia
H influenza type b
Neisseria

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59
Q

Bacterial conjugation

A

DNA t/f of plasmids via sex pili

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60
Q

High frequency strains in bacterial conjugation

A

Allow gene mapping

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61
Q

Bacterial transduction

A

Transfer of DNA via bacteriophage

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62
Q

What are the two types of bacterial transduction?

A
  1. Generalised (lytic phage)
    - virus infects bacteria and multiplies randomly picking up host DNA —> transfer to another bacteria
  2. Specialised (lysogenic phage)
    - virus DNA inserts into host DNA, some host DNA then excised with phage DNA
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63
Q

Name the bacteria whose toxins are formed from lysogenic phages.

A

‘ABCDS’

Group A erythrogenic toxin
Botulinum toxin
Cholera toxin
Diphtheria toxin
Shiga toxin
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64
Q

What is the term given to phages only replicating in the lytic cycle?

A

Virulent

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65
Q

What is the term given to phages replicating in both the lytic and lysogenic forms?

A

Temperate

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66
Q

Bacterial transposition

Give an example.

A

Transposons excised and re-integrated in new locations
Mechanism of abx resistance

E.g. Tal456 with vanA gene from VRE —> Staph aureus

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67
Q

What do penicillin binding proteins do?

A

Cross link alanine residues in bacterial cell wall

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68
Q

MOA penicillins

A

Mimic alanine residues (D-ala-D-ala) —> breakdown >creation of cell wall —> autolysis —> cell death

Therefore bacteriocidal

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69
Q

Name 2 natural penicillins

A

Penicillin G

Penicillin VK

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70
Q

Which drug increases the concentration of pen G/VK when co-administered?

A

Probenecid (usually used in gout)

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71
Q

Name 3 mechanisms by which bacteria develop resistance to penicillins.

A
  1. Modify PBPs e.g. Strep pneumonia
  2. Reduced bacterial cell penetration (G- outer cell membrane has poor penetration; reduced porins)
  3. Beta lactamase enzymes
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72
Q

Which bacteria produce beta-lactamase enzymes? (2)

A
  1. Gram negative (present in periplasm)

2. Staph aureus (no periplasm therefore secretes)

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73
Q

Name 3 inhibitors of beta lactamase.

A
  1. Clavaulanic acid
  2. Sulbactam
  3. Tazobactam
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74
Q

How many hours after administration of penicillin does the Jarisch-Herxheimer reaction occur?

A

2 hours

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75
Q

Name examples for each hypersensitivity reaction in penicillin.
(Similar for cephalosporins)

A

Type 1 - acute (IgE) anaphylaxis
Type 2 - haemolysis (IgG)
Type 3 - serum sickness (IgG)
Type 4 - skin reaction, interstitial nephritis

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76
Q

What type of T cell mediates the SJS and TEN reactions that you see with penicillin use?

A

CD8

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77
Q

With which abx can you see SJS/TEN?

A

Aminopenicillins
TMP-SMX
Cephalosporins

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78
Q

Name 3 anti-staph penicillins. Why are they anti-staph?

A

Oxacillin
Naficillin
Dicloxacillin

Side chain protects from Staph penicillinase.

79
Q

Name 3 uses of anti-staph penicillins.

A

Community-acquired cellulitis
Impetigo
Staph endocarditis (once sensitivities confirmed)

80
Q

Name 2 aminopenicillins

A

Amoxicillin (po)

Ampicillin (iv - poor bioavailability)

81
Q

MOA resistance to penicillin G & V

A

Beta lactamase cleaves beta lactam ring

82
Q

Name the 8 bacteria where aminopenicillins are used.

A

‘HHELPSS kill Enterococci’

H influenzae (G-)
H pylori (G-)
E coli (G-)
Listeria monocytogenes (G+)
Proteus mirabilis (G-)
Salmonella (G-)
Shigella (G-)
Enterococci (G+)
83
Q

Mechanism of resistance to aminopenicillins.

A

Penicillinase (type of beta lactamase) - cleaves beta lactam ring

84
Q

Why is MRSA resistant to penicillinase-resistant penicillins (anti-staph penicillins)?

A

Altered PBP target site

85
Q

Name 2 antipseudomonal penicillins.

A

Piperacillin

Ticarcillin

86
Q

MOA of antipseudomonal penicillins (ticarcillin, pipercillin).

A

Increase porin channel penetration

87
Q

Which 3 abx groups are ESBL resistant to?

A

Penicillins
Cephalosporins
Aztreonam

88
Q

In which type of bacteria do you find ESBL?

89
Q

MOA of cephalosporins

A

Beta lactam drugs that inhibit cell wall synthesis (less susceptible to penicillinases)

90
Q

Cephalosporins - bacteriostatic or bactericidal?

A

Bactericidal

91
Q

Which organisms are not covered by 1-4th generation cephalosporins?

A

‘LAME’

Listeria
Atypicals (Chlamydia, Mycoplasma)
MRSA
Enterococci

92
Q

Name the 2 1st generation cephalosporins

A

Cefazolin

Cephalexin

93
Q

Name the 4 2nd generation cephalosporins

A

Cefaclor
Cefoxitin
Cefuroxime
Cefotetan

94
Q

Name the 8 bacteria in which 2nd generation cephalosporins are effective

A

‘HENS PEcK’

Gram + cocci
H influenzae
Enterobacter aerogenes
Neisseria spp.
Serratia marcesens
Proteus mirabilis
E coli 
Klebsiella
95
Q

Name the 4 organisms which can be treated with 1st generation cephalosporins

A

‘PEcK’

Gram +
Proteus mirabilis
E coli
Klebsiella

96
Q

Which cephalosporin might you use prophylactically prior to surgery to prevent S aureus wound infections?

A

Cefazolin (1st generation)

97
Q

Name 4 3rd generation cephalosporins

A

Ceftriaxone
Cefotaxime
Cefpodoxime
Ceftazidime

98
Q

Name 3 conditions in which you would use ceftriaxone

A

Meningitis
Gonorrhoea
Disseminated Lyme disease

99
Q

When might you use ceftazidime

A

Pseudomonas

100
Q

Name a 4th generation cephalosporin

101
Q

Coverage of cefepime

A

Gram - with increased activity against Pseudomonas and G+

102
Q

List the following according to beta lactamase sensitivity from most sensitive to most resistant

1-4th generation cephalosporins
Carbapenems
Aztreonam
Penicillins

A
  1. Penicillins (anti-staph penicillins resistant to staph penicillinases)
  2. 1st gen ceph
  3. 2nd gen ceph
  4. 3rd gen ceph
  5. 4th gen ceph
  6. Aztreonam
  7. Carbapenems
103
Q

Name a 5th generation cephalosporin

A

Ceftaroline

104
Q

Which two microbes is ceftaroline (5th gen cephalosporin) particularly effective against?

105
Q

Name 5 adverse reactions seen with cephalosporins and their mechanisms

A

HS reactions
Vitamin K deficiency - reduced K2 (reduced GI bacteria)
Hypoprothrombinaemia - NMTT side chains inhibit epoxide reductase; mainly seen in malnourished patients
Nephrotoxicity with aminoglycosides
Disulfiram reaction - inhibits acetaldehyde dehydrogenase

106
Q

What are the 3 mechanisms of resistance to cephalosporins?

A
  1. Modified PBPs
  2. Altered cell permeability
  3. Inactivation by cephalosporinases (type of beta lactamase)
107
Q

What is the name of the drug co-administered with impenem and what is its purpose?

A

Cilastatin - reduce inactivation of drug in renal tubules

108
Q

What is the MOA of cilastatin?

A

Inhibits dehydropeptidase I

109
Q

Where do carbapenems act?

A

Bacterial cell wall - affect peptidoglycan cross-linking

110
Q

Name a monobactam and state its MOA

A

Aztreonam - affects peptidoglycan cross-linking

111
Q

Name the 3 main SEs of carbapenems

A

Rash
GI distress
Neurotoxicity (seizures)

112
Q

What is the mechanism of neurotoxicity of carbapenems?

A

Inhibit GABA

113
Q

When are you more likely to get the neurotoxicity effects of carbapenems? (2)

A

High doses

Renal failure

114
Q

What is the MOA of aztreonam?

A

Binds PBP 3 (found in G-)

115
Q

Is there any cross reactivity of aztreonam with penicillin allergies?

116
Q

Which type of bacteria is aztreonam effective against?

117
Q

What is the MOA of sulphonamides?

A

Inhibit dihydropterate synthase

118
Q

3 mechanisms of resistance to sulphonamides

A

Increased PABA synthesis
Reduced uptake
Altered dihydropterate synthase

119
Q

What is the MOA of trimethoprim and pyrimethamine?

A

Inhibition of DHF reductase

120
Q

What is the main toxic effect of TMP/pyrimethamine and how can this be prevented?

A

BM suppression; leucovorin (avoids need of DHF reductase to convert to THF)

121
Q

Name the main SEs of sulphonamides and their mechanisms where applicable. (6)

A

Hypersensitivity - due to NH2 group at N4 and N ring at N1
SJS/TEN
Photosensitivity - drug interaction with UV light
Haemolysis in G6PD deficiency
Kernicterus - displaces other albumin bound substances; increased unconjugated bilirubin
Raised INR if taking warfarin - displaces other albumin bound substances

122
Q

What is the MOA of dapsone?

A

Inhibition of DHF reductase

123
Q

Is dapsone bactericidal or bacteriostatic?

A

Bacteriostatic

124
Q

Name 2 uses of dapsone

A
  1. Leprosy

2. PCP prophylaxis

125
Q

Name 2 adverse effects of dapsone

A

Haemolysis if G6PD deficient

Methaemoglobinaemia

126
Q

MOA of sulfonamide abx

A

Mimic PABA —> competitive inhibition of dihydropterate synthase (PABA —> dihydropteric acid)

127
Q

Mechanisms of resistance to sulfonamides (3)

A
  1. Increased PABA production
  2. Altered dihydropterate synthase
  3. Reduced uptake
128
Q

Which microbes does TMP-SMX not cover?

A

PsA
B fragilis
Most anaerobes

129
Q

What are the main problems with the use of TMP-SMX in pregnancy? (2)

A

Sulfonamides —> kernicterus

TMP —> NTDs

130
Q

Name the 3 stages of protein synthesis that protein inhibitors affect and name the abx acting in each one.

A
  1. Initiation - aminoglycosides, linezolid
  2. Add tRNA - tetracyclines
  3. Add peptides - chloramphenicol, macro lives, clindamycin
131
Q

MOA of aminoglycosides

A

Block initiation by binding 30S subunit of ribosomes

132
Q

Are aminoglycosides effective against anaerobes?

A

No - require transport into cells

133
Q

Are aminoglycosides effective against intracellular bacteria?

134
Q

Mechanisms of resistance to aminoglycosides (2)

A

Phosphorylation aminoglycoside kinases

Adenylation/acetylation of transferases

135
Q

Main SEs with aminoglycosides (3)

A

Ototoxicity
Nephrotoxicity
Neuromuscular blockade (blocks ACh release at NMJ) - mainly occurs with pre-existing neuromuscular disease/high levels

136
Q

MOA macrolides

A

Blocks tRNA translocation (from A site, where peptide bond catalysed to P site) by binding to P site of 50S subunit

137
Q

Cover of macrolides

A

G+ cocci
Some G-
Intracellular pathogens - Chlamydia (obligate), Legionella (facultative)

138
Q

Why is erythromycin used in gastroparesis?

A

Binds to motilin rec in GIT —> smooth muscle contraction

139
Q

Mechanism of resistance of macrolides

A

Alter 23S rRNA (component of 50S) by methylation

140
Q

3 main SEs of macrolides

A 
Increased motility
Increased QT (blocks K+, especially erythromycin)
Cholestatic hepatitis
141
Q

Why do macrolides —> raised theophylline/warfarin levels?

A

P450 inhibitor

142
Q

MOA tetracyclines

A

Binds 30S ribosome —> prevent attachment tRNA

143
Q

Are tetracyclines transported into the cell?

144
Q

What type of drugs impair the absorption of tetracyclines?

A

Minerals and antacids (Ca, Mg, Fe, dairy) - chelate drug

145
Q

Mechanisms of developing resistance to tetracyclines (1)

A

Reduced influx/increased efflux from cells via plasmid-encoded transport pumps

146
Q

Main SEs tetracyclines (4)

A

GI
Photosensitivity
Teeth discolouration (in under 8 year olds)
Inhibit bone growth in children

Chelates calcium

147
Q

MOA chloramphenicol

A

Inhibition peptidyl transferase

148
Q

Main SEs of chloramphenicol (3)

A

Anaemia (BM suppression)
Aplastic anaemia (irreversible and often fatal)
Grey baby syndrome (babies lack UDP glucoryltransferase that is required for excretion) - grey skin, hypotension, fatal

149
Q

MOA clindamycin

A

Similar MOA to macrolides - bind to 23S rRNA of 50S ribosomes —> prevent translocation

150
Q

Mechanism resistance to macrolides

A

Methylation of 23S rRNA binding site

151
Q

Why use metronidazole over clindamycin for ‘below the diaphragm’?

A

B fragilis - high resistance

152
Q

Main SE of clindamycin

A

Diarrhoea (C. Difficile, abx-associated)

153
Q

MOA linezolid

A

Binds to 50S ribosome, blocking initiation

154
Q

Main use of linezolid

155
Q

MOA streptogramins

A

Act at 50S ribosome

156
Q

Uses of streptogramins (quinipristin, dalfopristin)

157
Q

Aminoglycosides - bactericidal/bacteriostatic?

A

Bacteriocidal

158
Q

Macrolides - bactericidal/bacteriostatic?

A

Bacteriostatic

159
Q

Tetracyclines - bactericidal/bacteriostatic?

A

Bacteriostatic

160
Q

Chloramphenicol - bactericidal/bacteriostatic?

A

Bacteriostatic

161
Q

Clindamycin - bactericidal/bacteriostatic?

A

Bacteriostatic

162
Q

Linezolid - bactericidal/bacteriostatic?

A

Bacteriostatic (mostly)

163
Q

MOA quinolones

A

Inhibit DNA synthesis - DNA grasses, topoisomerase IV

164
Q

Quinolones - bactericidal/bacteriostatic?

A

Bactericidal

165
Q

Mechanism of resistance to quinolones (3)

A

Altered DNA gyrase and topoisomerase IV
Altered cell permeability
Efflux of drug

166
Q

3 main uses of quinolones (3)

A

UTI
Pneumonia
Abdo infection (enteric G-)

167
Q

Order of PsA cover for cipro, levo and moxi

A

Cipro>levo>moxi

168
Q

Levofloxacin use

A

Strep pneumonia
MSSA

Therefore use in pneumonia

169
Q

MOA vancomycin

A

Inhibits peptidoglycan (cell wall) formation by binding D-ala-D-ala peptides and preventing cross-linking (vs beta lactams, which inhibit transpeptidases)

170
Q

Mechanism of resistance to vanc

A

Terminal acid change

E.g. D-ala-D-ala —> D-ala-D-lactate in VRSA

171
Q

Cover of vancomycin

A

G+ (too large to enter cell)

172
Q

2 main uses of vanc

A

MRSA

C diff

173
Q

3 main SEs of vanc

A

Nephrotoxicity
Ototoxicity
Red man syndrome

174
Q

What is red man syndrome?

A

Seen with vanc infusion (if given too fast)
Histamine release from mast cells
Prevent with slow infusion
NOT a hypersensitivity reaction

175
Q

MOA metronidazole

A

Reduced form = activated —> free radicals —> interact with DNA —> DNA breakage/destabilisation —> cell death

176
Q

Main SEs metronidazole (3)

A

Metallic taste
Non-specific GI/neuro (e.g. neuropathy)
Disulfiram-like reaction ?MOA

177
Q

Nitrofurantoin - bactericidal/bacteriostatic?

A

Bactericidal

178
Q

In which condition might nitrofurantoin cause haemolysis?

A

G6PD deficiency

179
Q

4 bacteria resistant to cephalosporins and reason for resistance

A

Resistant PBP

  • Listeria
  • MRSA
  • Enterococci

No cell wall
- atypicals e.g. Mycoplasma, Chlamydia

180
Q

Name 10 granulomatous infections.

A

Mycobacterium - TB and leprosy
Fungal pneumonias - Histo, Blasto, Coccidio
Zoonotic - Bartonella, Brucella
Listeria in infants (granulomatosis infantiseptica)
Shistosomiasis
Syphilis

181
Q

3 infections causing a rash involving palms and soles

A
  1. Secondary syphilis
  2. Rocky Mountain Spotted Fever (Rickettsia)
  3. Coxsackie
182
Q

All DNA viral genomes are double-stranded except for?

A

Parvovirus

183
Q

All DNA viral genomes are linear except for? (3)

A

‘PPH’
Papilloma
Polyoma
Hepadnavirus

184
Q

Name the 4 groups of naked DNA viruses.

A

Parvo
Adeno
Papilloma
Polyoma

185
Q

Name the 3 groups of enveloped DNA viruses.

A

Hepadna
Herpes
Pox

186
Q

DNA viruses - icosahedral or helical? Which virus is the exception?

A

Icosahedral

Pox virus does not have icosahedral capsid

187
Q

Where do DNA viruses replicate? Which virus is the exception?

A

Nucleus

Pox virus - replicates in cytoplasm

188
Q

All RNA viruses are single stranded except for _____?

A

Reovirus (dsRNA)

189
Q

All RNA viruses are linear except for? (3)

A

‘BAD’
Bunyavirus
Arenavirus
Delta virus

190
Q

All RNA viruses replicate in the cytoplasm except for? (2)

A

Influenza

Reovirus

191
Q

Name the 4 viruses that have segmented genomes.

A 
‘BOAR’
Bunyavirus
Orthomyxovirus
Arenavirus
Reovirus
192
Q

Name the 4 + sense naked viruses.

A 
CHRP
Calci
Hepe
Reo
Picorna
193
Q

Name the 4 +ve sense enveloped viruses.

A 
CFTR
Corona
Flavi
Retro
Toga
194
Q

Name the 5 -ve sense enveloped virus families.

A 
BROAD FP
Bunya
Rhabdo
Orthomyxo
Arena
Delta
Filo
Paramyxo

USMLE (3 decks)

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