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Micro Midterm Flashcards

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1
Q

What color are gram positive bacteria on a typical gram stain? What about gram negative?

A

Gram positive: blueish or purple; gram negative: pink

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2
Q

Are these bacteria gram positive or gram negative?

A

Gram positive, note the purple color. This is bacillus.

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3
Q

What shape are cocci bacteria?

A

Typically spherical, in clusters, pairs, or chains

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4
Q

Can all bacteria be visualized with the gram stain?

A

No, some need other stains e.g. spirochetes

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5
Q

Do bacteria have organelles?

A

No, they are prokaryotes

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6
Q

What is the outermost coat of the gram-negative cell wall?

A

A phospholipid membrane (there are two of them, one for the cell well and one that functions as the plasma membrane)

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7
Q

What is the cell wall of gram-positive bacteria made of?

A

Peptidoglycan: peptide cross links between polysaccharide chains

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8
Q

Are lipopolysaccharides characteristic of gram positive or gram negative bacteria?

A

Gram negative, as they integrate into the outer phospholipid membrane

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9
Q

Does Staphylococcus epidermidis normally cause disease on the skin?

A

No, it is benign. Staph aureus is the more virulent strain that can cause acne and other skin infections.

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10
Q

Is the peptidoglycan layer of the cell wall thicker in gram positive or gram negative bacteria?

A

Gram positive bacteria have thicker peptidoglycan

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11
Q

Bacteria can be colonize or can cause disease. The ability to cause disease is determined by

– […] factors

– Host factors

– Environmental factors

A

Bacteria can be colonize or can cause disease. The ability to cause disease is determined by

– Virulence (bacterial) factors

– Host factors

– Environmental factors

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12
Q

Bacteria can be colonize or can cause disease. The ability to cause disease is determined by

– Virulence (bacterial) factors

– […] factors

– Environmental factors

A

Bacteria can be colonize or can cause disease. The ability to cause disease is determined by

– Virulence (bacterial) factors

– Host factors

– Environmental factors

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13
Q

Bacteria can be colonize or can cause disease. The ability to cause disease is determined by

– Virulence (bacterial) factors

– Host factors

– […] factors

A

Bacteria can be colonize or can cause disease. The ability to cause disease is determined by

– Virulence (bacterial) factors

– Host factors

– Environmental factors

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14
Q

Besides direct damage caused by the organism, what can infectious disease symptoms manifest via?

A

The immune response mounted by the host

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15
Q

What is hemolysis as it relates to bacteria?

A

The pattern that the colonies form on a blood agar plate, related to their ability to break down blood cells

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16
Q

Is this α or β hemolysis?

A

β: halo like growth around streaks

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17
Q

What kind of typing is this? Which side is positive?

A

Lancefield typing; left is positive

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18
Q

What are non-suppurative complications?

A

When the host response causes the clinical manifestations of the disease

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19
Q

What bacterium causes pharyngitis, cellulitis, impetigo, and necrotizing fasciitis?

A

Streptococcus pyogenes

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20
Q

Is Streptococcus pyogenes α or β hemolytic?

A

β hemolytic

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21
Q

What clinical manifestation is this? What bacterium is immediately suspect?

A

Pharyngitis; Streptococcus pyogenes

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22
Q

What clinical manifestation is this? What bacterium is suspected?

A

Erypsipelas; Streptococcus pyogenes

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23
Q

What skin condition is this? What bacterium is immediately suspect?

A

Impetigo; Streptococcus pyogenes

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24
Q

What does it mean to talk about suppurative complications of an infection?

A

Clinical manifestations directly caused by the organism itself; e.g., pharyngitis or a rash

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25
Q

Are acute rheumatic fever, glomerulonephritis, scarlet fever, and toxic shock suppurative or non-suppurative complications?

A

Non-suppurative

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26
Q

What does the word “suppurative” derive from (e.g. what does suppuration refer to?)

A

Pus formation

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27
Q

Is acute rheumatic fever more rare or less rare over the age of 30 than below?

A

It is very rare over 30

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28
Q

Does acute rheumatic fever associate with a preceding S. pyogenes throat infection, or a skin infection, or both?

A

Only throat infections

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29
Q

When a bacteria is said to belong to Group A, B, etc. what grouping system is being referenced?

A

The Lancefield grouping system

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30
Q

What is the Lancefield grouping system based on? Does it apply to α hemolytic or β hemolytic bacteria?

A

The carbohydrate composition of bacterial antigens in their cell walls; Lancefield only worked on β hemolytic bacteria

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31
Q

Clinical manifestations of acute rheumatic fever include:

  • […]
  • Carditis (heart failure, new murmur,

pericarditis)

  • Sydenham’s chorea
  • Erythema marginatum
A

Clinical manifestations of acute rheumatic fever include:

  • Painful, migratory arthritis
  • Carditis (heart failure, new murmur,

pericarditis)

  • Sydenham’s chorea
  • Erythema marginatum
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32
Q

Clinical manifestations of acute rheumatic fever include:

  • Painful, migratory arthritis
  • […] (heart failure, new murmur,

pericarditis)

  • Sydenham’s chorea
  • Erythema marginatum
A

Clinical manifestations of acute rheumatic fever include:

  • Painful, migratory arthritis
  • Carditis (heart failure, new murmur,

pericarditis)

  • Sydenham’s chorea
  • Erythema marginatum
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33
Q

Clinical manifestations of acute rheumatic fever include:

  • Painful, migratory arthritis
  • Carditis (heart failure, new murmur,

pericarditis)

  • Sydenham’s […]
  • Erythema marginatum
A

Clinical manifestations of acute rheumatic fever include:

  • Painful, migratory arthritis
  • Carditis (heart failure, new murmur,

pericarditis)

  • Sydenham’s chorea
  • Erythema marginatum
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34
Q

Clinical manifestations of acute rheumatic fever include:

  • Painful, migratory arthritis
  • Carditis (heart failure, new murmur,

pericarditis)

  • Sydenham’s chorea
  • […] marginatum
A

Clinical manifestations of acute rheumatic fever include:

  • Painful, migratory arthritis
  • Carditis (heart failure, new murmur,

pericarditis)

  • Sydenham’s chorea
  • Erythema marginatum
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35
Q

What is the pathogenesis of post-streptococcal glomerulonephritis?

A

Antibodies, complement components react with streptococcal antigens to form immune complexes which deposit in the renal glomerulus

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36
Q

Does post-streptococcal glomerulonephritis most often affect children or adults?

A

Children

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37
Q

What are these clinical manifestations characteristic of? Hint: this patient had a known exposure to Streptococcus pyogenes.

A

Scarlet fever

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38
Q

What toxins cause streptococcal toxic shock syndrome?

A

Pyrogenic exotoxins (SPEA, SPEB, SPEC)

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39
Q

If a patient is in shock and undergoing multi-organ system failure following a streptococcal infection, what syndrome may be occurring?

A

Streptococcal toxic shock syndrome

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40
Q

What do the exotoxins involved in streptococcal toxic shock bind to? What does this cause the release of?

A

T lymphocytes and class II MHC complexes of antigen-presenting cells; leads to massive cytokine release

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41
Q

Is Streptococcus agalactiae in group A or B? Is it α hemolytic or β hemolytic?

A

Group B; β hemolytic

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42
Q

What bacterium is highly associated with neonatal sepsis and maternal sepsis, as well as soft-tissue infection in diabetics?

A

Streptococcus agalactiae

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43
Q

Are enterococcal species more resistant or less resistant to cephalosporins and β-lactam based drugs?

A

More resistant

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44
Q

Enterococcus can cause:

  • […]
  • Biliary tract infection
  • Peritonitis
  • Bacterial endocarditis
  • Nosocomial superinfection: particularly bacteremia
A

Enterococcus can cause:

  • Urinary tract infection
  • Biliary tract infection
  • Peritonitis
  • Bacterial endocarditis
  • Nosocomial superinfection: particularly bacteremia
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45
Q

Enterococcus can cause:

  • Urinary tract infection
  • Biliary tract infection
  • Peritonitis
  • Bacterial […]
  • Nosocomial superinfection: particularly bacteremia
A

Enterococcus can cause:

  • Urinary tract infection
  • Biliary tract infection
  • Peritonitis
  • Bacterial endocarditis
  • Nosocomial superinfection: particularly bacteremia
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46
Q

Enterococcus can cause:

  • Urinary tract infection
  • Biliary tract infection
  • Peritonitis
  • Bacterial endocarditis
  • Nosocomial superinfection: particularly […]
A

Enterococcus can cause:

  • Urinary tract infection
  • Biliary tract infection
  • Peritonitis
  • Bacterial endocarditis
  • Nosocomial superinfection: particularly bacteremia
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47
Q

Are strep viridans species α hemolytic or β hemolytic? How are they distinguished from pneumococci?

A

α hemolytic; distinguished from pneumococci with the optochin test, which strep viridans are not sensitive to

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48
Q

What is the major agent causing bacterial endocarditis?

A

Streptococci, in particular strep viridans

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49
Q

Can Staphylococcus aureus cause bacterial endocarditis?

A

Yes

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50
Q

Are streptococcal strains gram positive or negative?

A

Gram positive

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51
Q

S. mutans and S. sanguis are both streptococcal bacteremia that comprise what group?

A

Strep viridans, or α hemolytic streptococci

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52
Q

How many kinds of hemolysis are there for a bacterial culture on blood agar? What are they?

A

Three: α, β, γ

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53
Q

Is Streptococcus pyogenes sensitive to bacitracin? Does an antibody to M protein enhance immune response?

A

Yes, it is sensitive to bacitracin; yes, antibody to M protein is protective

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54
Q

What are three pyogenic consequences of streptococcus pyogenes infection?

A

Pharyngitis, cellulitis, impetigo

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55
Q

What does “pyogenic” mean?

A

Causes creation of pus

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56
Q

What genus do E. faecalis and E. faecium belong to?

A

Enterococcus

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57
Q

How are enterococci divided by Lancefield grouping?

A

They are divided into group D and non-group D

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58
Q

What streptococcal bacteria normally colonize the oropharynx?

A

Strep viridans

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59
Q

What bacterium most typically causes dental caries (cavities)?

A

S. mutans

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60
Q

What is the hardest genus of streptococcus to kill with antibiotics?

A

Enterococcus

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61
Q

What is a mnemonic for three common causes of S. pyogenes based on “PH”?

A

PHaryngitis to rheum PHever and glomerulonePHritis

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62
Q

What is a mnemonic for rheumatic fever symptoms?

A

JONES:

  • Joints
  • Heart (is round like an O)
  • Nodules
  • Erythema marginatum (pink rings on the trunk)
  • Syndenham’s Chorea (abnormal involuntary movement disorder)
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63
Q

Is Staphylococcus aureus gram positive or negative? Does it form chains or clusters?

A

Positive; clusters

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64
Q

Is S. aureus coagulase positive or negative?

A

Positive

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65
Q

What bacteria are these?

A

Staphylococcus aureus; clusters + gram positive

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66
Q

Virulence factors for S. aureus include […], surface factors, and secreted proteins.

A

Virulence factors for S. aureus include biofilm, surface factors, and secreted proteins.

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67
Q

Virulence factors for S. aureus include biofilm, […], and secreted proteins.

A

Virulence factors for S. aureus include biofilm, surface factors, and secreted proteins.

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68
Q

Virulence factors for S. aureus include biofilm, surface factors, and […] proteins.

A

Virulence factors for S. aureus include biofilm, surface factors, and secreted proteins.

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69
Q

What protein in S. aureus correlates with virulence and binds to the Fc terminal of IgG inhibiting complement fixation? What else does this inhibit?

A

Protein A; phagocytosis

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70
Q

S. aureus can surround their cell walls with a […] capsule, which inhibits opsonization.

A

S. aureus can surround their cell walls with a polysaccharide capsule, which inhibits opsonization.

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71
Q

S. aureus can surround their cell walls with a polysaccharide capsule, which inhibits […].

A

S. aureus can surround their cell walls with a polysaccharide capsule, which inhibits opsonization.

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72
Q

What part of S. aureus is protein A integrated into?

A

The cell wall

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73
Q

Are coagulase positive staphylococci more or less virulent than coagulase-negative ones?

A

More virulent

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74
Q

Do staphylocci infections typically produce pus?

A

Yes

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75
Q

What is the primary host immune response to staphylococcus infection?

A

Primarily mechanical and in the epidermis, but opsonization and neutrophil phagocytosis are also significant

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76
Q

Can S. aureus cause skin and soft tissue infections? What about endocarditis? Septic arthritis?

A

Yes to all

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77
Q

What toxin does S. aureus produce that causes toxic shock syndrome?

A

TSST1

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78
Q

What bacteria produces an abscess like this?

A

S. aureus

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79
Q

Can impetigo be caused by S. aureus?

A

Yes

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80
Q

What color is the crust around impetigo lesions?

A

Golden

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81
Q

What is skin infection is this picture characteristic of?

A

Cellulitis, probably by S. aureus

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82
Q

What is this infection called? Is this the same as a stye? What bacterium is it associated with?

A

Chalazion; it is different from a stye (it is a cyst blocking a tarsal gland, not a sebaceous gland); S. aureus

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83
Q

What are these?

A

Microemboli associated with endocarditis

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84
Q

What are serious neurologic targets of metastatic infection caused by S. aureus?

A

Brain abscesses or spinal epidural abscess

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85
Q

Can S. aureus cause knee arthritis?

A

Yes, it can infect it causing septic arthritis

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86
Q

What does “nosocomial” mean?

A

Hospital-acquired (usually referring to an infection)

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87
Q

What does MRSA stand for? What infection source is it associated with?

A

Methicillin-resistant Staphylococcus aureus; nosocomial infections

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88
Q

What bacteria commonly causes acute food poisoning? How long does this illness last?

A

Staphylococcus aureus; 24 hours

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89
Q

How long is an S. aureus bacteremia usually treated? What is the reasoning behind this?

A

4 weeks; undertreating a bacteremia can lead to the development of a resistant strain

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90
Q

How do you treat MRSA?

A

Synthetic cell-wall active penicillins: Oxacillin, nafcillin, cefazonin; or vancomycin

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91
Q

Does vancomycin work on gram positive or gram negative bacteria?

A

Gram positive

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92
Q

Is S. epidermidis coagulase positive or negative?

A

Negative

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93
Q

Does S. epidermidis typically cause any disease while inhabiting the skin?

A

No, but it is important in association with medical devices

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94
Q

What is the thick, multilayered slime created by *S. epidermidis *that covers catheters during invasion and protects it from antibiotics called?

A

Biofilm

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95
Q

What bacterium is associated with infections from intravascular devices?

A

S. epidermidis

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96
Q

What location of infection is S. saprophyticus commonly associated with?

A

Urinary tract infection

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97
Q

*S. saprophyticus *most likely has unique surface proteins that permit it to bind to which receptors in the genitourinary tract?

A

Mucosal receptors

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98
Q

What drug is this?

A

Vancomycin

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99
Q

Wha tis the mechanism of Vancomycin?

A

It inhibits bacterial cell wall synthesis by binding firmly to D-ala-D-ala of the peptidoglycan, preventing elongation and cross-linking

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100
Q

What are two mechanisms of resistance to vancomycin?

A
  • Altered peptidoglycan binding site: D-ala-D-ala to D-ala-D-lactate
  • Thickened cell wall
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101
Q

Is vancomycin active against gram-positive or gram-negative bacteria or both?

A

Gram-positive

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102
Q

What is the drug of choice for treating MRSA and penicillin-resistant pneumococcus?

A

Vancomycin

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103
Q

What are two major toxic side effects of vancomycin?

A

Nephrotoxicity and hypersensitivity (red man syndrome or anaphylaxis)

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104
Q

Why is vancomycin given slowly?

A

To avoid histamine reactions resulting from rapid infusion, such as red man syndrome

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105
Q

Why might a pretreatment of antihistamine be used before a rapid infusion of vancomycin?

A

To avoid anaphylaxis or red man syndrome

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106
Q

Is vancomycin bactericidal or bacteriostatic?

A

Slowly bactericidal, mostly bacteriostatic

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107
Q

What drug is this?

A

Daptomycin

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108
Q

Does daptomycin act against gram-positive or gram-negative bacteria?

A

Gram-positive

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109
Q

What is the mechanism of daptomycin?

A

It binds the cytoplasmic membrane and causes rapid depolarization

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110
Q

Is daptomycin bactericidal or bacteriostatic?

A

Rapidly bactericidal

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111
Q

Does daptomycin have gram-negative activity?

A

No

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112
Q

What ion does daptomycin use to bind to the cytoplasmic membrane?

A

Ca++

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113
Q

If an enterococcus is vancomycin resistant, what cyclic lipopeptide antibacterial can be used?

A

Daptomycin

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114
Q

What is the interaction between daptomycin and pulmonary surfactant? Can daptomycin be used to treat pneumonias?

A

Pulmonary surfactant breaks it down; no

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115
Q

Does daptomycin have adverse musculoskelatal effects?

A

Yes, including myalgias, weakness, rhabdomyolysis, and cramps

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116
Q

What serum levels can be measured to monitor musculoskeletal adverse effects of daptomycin?

A

Creatinine phosphokinase

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117
Q

What is a protein synthesis inhibitor in gram-positive cocci that acts on…

  • Initiation?
  • Elongation?
  • Transpeptidation?
A
  • Initiation: linezolid
  • Elongation: doxycycline
  • Transpeptidation: clindamycin
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118
Q

Are protein synthesis inhibitors for gram positive cocci bactericidal or bacteriostatic?

A

Bacteriostatic

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119
Q

What drug family do doxycycline, minocycline, and demeclocycline belong to? What is their mechanism?

A

Tetracycline; inhibitor against protein elongation

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120
Q

What dietary substance should not by consumed with doxycycline?

A

Dairy, because it forms nonabsorbable chelates with Ca++

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121
Q

Doxycycline binds to which tissues undergoing calcification?

A

Teeth and bones

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122
Q

Is doxycycline excreted in the urine? Metabolized in the liver?

A

Yes to both

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123
Q

What effect on teeth can occur with doxycycline?

A

Discoloration of teeth or stunting of growth

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124
Q

Does clindamycin affect enterococcal bacteria?

A

No

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125
Q

Does clindamycin affect aerobic or anaerobic bacteria?

A

Anaerobic

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126
Q

Can clindamycin treat an infection in the CNS?

A

No, it does not reach therapeutic levels in CSF

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127
Q

The disc on the left is erythromycin, and the one on the left is clindamycin. What is significant about the flattened part of the area of impeded growth facing the erythromycin disc? Is this bacteria resistant to clindamycin?

A

This indicates that erythromycin is activating genes that provide resistance to clindamycin; therefore, this bacteria is inducibly clindamycin resistant.

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128
Q

What are two side effects of clindamycin?

A

Rash and clostridium difficile colitis

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129
Q

What is the bioavailability of oral linezolid?

A

100%

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130
Q

What is the mechanism of linezolid?

A

Inhibits protein synthesis initiation in gram positive bacteria

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131
Q

What are three main safety concerns with linezolid?

A

Thrombocytopenia/neutropenia, metabolic acidosis, serotonin syndrome

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132
Q

What side effect of linezolid is characterized by mental status changes, fever, hypertension, tachycardia, hyperreflexia, myoclonus, and tremor?

A

Serotonin syndrome

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133
Q

Is hyperthermia a more severe toxicity finding than altered mental status?

A

Yes

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134
Q

What is the mechanism of trimethoprim-sulfamethoxazole?

A

It is a folic acid antagonist

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135
Q

How do humans acquire folic acid? How do bacteria acquire folate?

A

Humans ingest it; bacteria synthesize it

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136
Q

What synthesis process requires folate-derived cofactors in bacteria?

A

Synthesis of DNA and RNA

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137
Q

Are folic acid antagonists bacteriostatic or bactericidal?

A

Bacteriostatic

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138
Q

What is the drug of choice for treatment of Pneumocystis jirovecii and Nocardia?

A

TMP-SMX, a combo of sulfamethoxazole and trimethoprim

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139
Q

Can TMP-SMX reach the CSF?

A

Yes

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140
Q

Side effects of TMP-SMX include: […], rashes, hemolytic anemia, and kernicterus (a bilirubin-induced brain dysfunction)

A

Side effects of TMP-SMX include: hypersensitivity, rashes, hemolytic anemia, and kernicterus (a bilirubin-induced brain dysfunction)

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141
Q

Side effects of TMP-SMX include: hypersensitivity, […], hemolytic anemia, and kernicterus (a bilirubin-induced brain dysfunction)

A

Side effects of TMP-SMX include: hypersensitivity, rashes, hemolytic anemia, and kernicterus (a bilirubin-induced brain dysfunction)

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142
Q

Side effects of TMP-SMX include: hypersensitivity, rashes, hemolytic […], and kernicterus (a bilirubin-induced brain dysfunction)

A

Side effects of TMP-SMX include: hypersensitivity, rashes, hemolytic anemia, and kernicterus (a bilirubin-induced brain dysfunction)

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143
Q

Side effects of TMP-SMX include: hypersensitivity, rashes, hemolytic anemia, and […] (a bilirubin-induced brain dysfunction)

A

Side effects of TMP-SMX include: hypersensitivity, rashes, hemolytic anemia, and kernicterus (a bilirubin-induced brain dysfunction)

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144
Q

What bacterium causes this skin infection?

A

Staphylococcus aureus

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145
Q

What genus of bacterium causes this infection?

A

Staphylococcus species

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146
Q

What six antibacterials can be used to treat MRSA?

A

Vancomycin, daptomycin, clindamycin, doxycycline, linezolid, TMP-SMX

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147
Q

What is the common mechanism for penicillin, cephalosporin, carbapenems, and monobactam?

A

They are inhibitors of peptidoglycan crosslinking

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148
Q

Which side is gram +, and which is gram -?

A

Left is gram + (thick peptidoglycan); right is gram - (two cell membranes)

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149
Q

What drugs are these?

A

Top: penicillin; bottom: cephalosporin. Notice the CH3R1 group and six-membered ring on cephalosporin, distinguishing it from other β-lactams. Penicillin has a five-membered ring with a dimethyl group.

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150
Q

What drug derived from mold acts on this crosslinking process in peptidoglycan? What enzyme is being inhibited?

A

Penicillin; a transpeptidase

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151
Q

What is the most common method of resistance to penicillin?

A

Beta-lactamase, a gene that breaks penicillin down

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152
Q

Where does beta-lactamase cleave penicillin?

A

The beta-lactam four atom ring

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153
Q

Can plasmids contain multiple resistance factors?

A

Yes

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154
Q

What channels do β-lactams use to enter the peptidoglycan layer of gram negative bacteria?

A

Porin channels

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155
Q

What is the mechanism of vancomycin and bacitracin?

A

Both inhibit peptidoglycan synthesis

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156
Q

Do vancomycin and bacitracin inhibit peptidoglycan crosslinking?

A

No, they inhibit polymerization of the peptide to the polysaccharide chain

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157
Q

Are gram negative and gram positive bacteria equally susceptible to vancomycin treatment? Why or why not?

A

Gram negative are intrinsically resistant; vancomycin cannot cross the outer membrane

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158
Q

What do enterococci synthesize instead of the terminal D-ala-D-ala on peptidoglycan to prevent vancomycin from binding?

A

D-ala-D-lactic acid

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159
Q

What is another name for transpeptidases in bacteria named after the drug that affects them?

A

Penicillin-binding proteins

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160
Q

What class of drugs does erythromycin belong to? What is their mechanism? How is resistance generated?

A

Macrolides; they inhibit protein synthesis by acting on the bacterial ribosome; the 50S subunit is modified so the drug cannot bind

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161
Q

How can resistance to tetracyclins be generated by bacteria?

A

They actively transport it out of the cell

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162
Q

What is the mechanism of metronidazole?

A

It enters bacteria and is metabolized by bacterial enzymes that allow it to cause DNA damage

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163
Q

What are two antibiotics that are DNA-dependent RNA polymerase inhibitors?

A

Rifampicin and actinomycin D (the latter is only a laboratory reagent)

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164
Q

Why do folic acid antimetabolites like sulfonamides and trimethoprim have antibacterial activity?

A

Bacteria need to metabolize folic acid to synthesize nucleotides (humans can acquire them from the diet)

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165
Q

How might resistance to trimethoprim develop, unrelated to modifications in the target enzyme itself?

A

Overproduction of the target enzyme can prevent the inhibitor from sufficiently affecting folic acid metabolism

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166
Q

What kind of antibiotic-antibiotic interaction is this? (The y-axis is log bacterial cell count)

A

Indifference

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167
Q

What kind of antibiotic-antibiotic interaction is this?

A

Antagonism

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168
Q

What is the best possible antibiotic-antibiotic interaction?

A

Synergy

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169
Q

Can aminoglycosides still kill bacteria without protein synthesis?

A

No

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170
Q

What antibiotic (whose mechanism is still unclear) is used against TB?

A

Isoniazid

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171
Q

Is the number of antibiotics discovered per year increasing or decreasing?

A

Decreasing

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172
Q

Why is it less profitable to build a new antibiotic than, for instance, a new anti-cholesterol drug?

A

Antibiotics are usually not taken chronically and so patients and hospitals will almost always spend less on them than other drugs

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173
Q

What experiment did Avery et al. perform in 1944 to show that bacterial virulence is a genetic property?

A

Virulent bacteria could be non-encapsulated and mixed with encapsulated non-virulent bacteria which would then be able to infect and kill mice

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174
Q

Are bacteria typically haploid or diploid?

A

Haploid

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175
Q

How do bacteria normally exchange genetic material with other cells, conferring antimicrobial resistance?

A

Plasmids

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176
Q

What is the spontaneous frequency of a mutation that knocks out or knocks in an operon in bacteria, per replication?

A

10-6

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177
Q

What are three methods of genetic exchange used by bacteria?

A

Transformation, conjugation, and transduction

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178
Q

Could mutations alone explain the rapidity at which bacteria acquire resistance to drugs?

A

No, the exchange of genetic material is also significant

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179
Q

Can all bacteria use transformation to take up DNA from the environment?

A

No

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180
Q

How is bacterial conjugation different from transformation?

A

During conjugation, an extension of the membrane from one bacterium to another (a pillus) whereby the cytoplasms of the two cells can mix allows genetic material to move from one cell to the other. Transformation involves uptake of extracellular DNA.

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181
Q

As double-stranded DNA enters the bacterium during transformation, what happens to it?

A

One strand of it is degraded, and then it forms a triple-strand with genomic DNA

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182
Q

During conjugation of two bacteria, are the cell walls of each organism interrupted?

A

Yes

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183
Q

What process is being observed here via EM? What is the significance of one cell looking “hairy” while the other is not?

A

Conjugation of bacteria; the hairy cell is the F+ cell and the other is the F- cell

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184
Q

Can plasmids be exchanged during conjugation?

A

Yes, along with chromosomes

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185
Q

What structures allow transduction to occur between bacteria?

A

Bacteriophages

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186
Q

What are these? What genetic exchange process for bacteria do they facilitate?

A

Bacteriophages; transduction

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187
Q

When bacteriophages add DNA to a bacterium, is it necessarily killed?

A

No, it is only killed in the lytic cycle, not the lysogenic cycle

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188
Q

What are phages capable of only the lytic cycle called?

A

Virulent

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189
Q

Can all phage species undergo the lytic cycle? What happens to the bacterium in this cycle?

A

Yes; it is killed

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190
Q

If bacteriophages create and replicate their own DNA during the lytic cycle, how could it be used to transfer host genetic material to another bacterium (transduction)?

A

Host genetic material (e.g. part of a chromosome) could be packaged by accident into a phage created within a bacterium, which goes on to inject it into another cell

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191
Q

What genetic studies can be facilitated by measures of cotransduction?

A

Linkage, or an estimate of how far apart two bacterial genes are to each other on a chromosome

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192
Q

What are DNA sequences that can jump from one position to another called?

A

Transposons

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193
Q

How long are insertion sequences (IS elements), a type of transposon? What is encoded by them?

A

1-3kb; a transposase protein that facilitates the transposition action, along with regulatory proteins

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194
Q

What sort of DNA element is this?

A

A transposon, specifically an insertion sequence (note IS elements)

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195
Q

What are DNA elements that encode a site-specific recombinase along with its recognition region called? What public health issue are they relevant for?

A

Integrons; multiple antibiotic resistance

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196
Q

What can destroy DNA that enters a bacterium?

A

Nucleases, or it can be inherently unstable and self-destruct

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197
Q

What type of recombination does RecA facilitate?

A

Homologous recombination

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198
Q

What is the most frequent cause of genetic variation in bacteria? How frequently does it occur per generation?

A

Homologous recombination, with a frequency of 10-1 to 10-2 per generation

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199
Q

Is plasmid transfer in bacteria more frequent per generation than transposition?

A

Generally more frequent

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200
Q

What was the first bacterial genome sequenced?

A

Haemophilus influenzae in 2003

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201
Q

Are aminoglycosides, fluoroquinolones and lipopeptides like daptomycin time-dependent or concentration-dependent?

A

Concentration-dependent

202
Q

For concentration-dependent drugs, is a large bolus administered, or frequent smaller doses?

A

A large bolus

203
Q

What is the minimum inhibitory concentration of an antibiotic/bacteria combination?

A

The lowest concentration that will inhibit the visible growth of bacteria in vitro

204
Q

Can broth microdilution measure minimum inhibitory concentration (MIC)?

A

Yes

205
Q

What method is microdilution (to measure minimum inhibitory concentration) based on?

A

Broth macrodilution

206
Q

Is the epsilometer more or less accurate than broth macrodilution at measuring minimum inhibitory concentration (MIC)?

A

Less

207
Q

Does Kirby Bauer disc diffusion produce the minimum inhibitory concentration of a drug-bacteria combination?

A

No

208
Q

Is the zone size measured by Kirby Bauer proportional to bacterial resistance or susceptibility?

A

Proportional to susceptibility

209
Q

Can an antibiotic be bactericidal against some organisms and bacteriostatic against others?

A

Yes, e.g., vancomycin

210
Q

Would a person already severely ill from bacterial infection preferably receive a bactericidal or bacteriostatic agent?

A

Bactericidal

211
Q

What is the identifying prefix for cephalosporin antibiotics?

A

Cef- or Ceph-

212
Q

What are the four families of β-lactam antibiotics?

A

Penicillins, cephalosporins, carbapenems, and monobactams

213
Q

What is the unifying suffix for penicillin-class β-lactam antibiotics?

A

NAME?

214
Q

Name the two rings in this generalized antibiotic structure. What family does this structure describe?

A

Top, thiazolidine ring; bottom, β-lactam ring; penicillins (identified by the thiazolidine ring)

215
Q

Where is penicillin-binding protein located within a bacterium?

A

The cell membrane (the inner one, for gram-negative bacteria)

216
Q

Do natural penicillins have activity against streptococci? What about staphylococci?

A

Yes against streptococci; usually not against staphylococci

217
Q

Are there synthetic penicillins that act against staphylococci?

A

Yes

218
Q

What penicillin is very completely absorbed after oral administration?

A

Amoxicillin

219
Q

Which penicillin is not cleared renally?

A

Nafcillin

220
Q

What diagnoses are penicillin still used for today?

A

Group A and Group B Strep, caused by *S. pyogenes *and S. agalactiae, respectively, and syphilis, caused by Treponema pallidum

221
Q

What is the oral formulation of pencillin called? What is the IV forumation called?

A

Penicillin V - oral; penicillin G - intravenous

222
Q

What bacteria causing skin infections is mostly resistant to penicillin because of the production of β-lactamases?

A

Staphylococcus aureus

223
Q

Can anti-staphylococcal penicillins be cleaved by β-lactamases (penicillinases)?

A

Usually, no.

224
Q

What are three anti-staphylococcal penicillins? What is the route of administration?

A

NOD: Nafcillin, oxacillin, dicloxacillin; oral

225
Q

Is methicillin still used clinically?

A

Usually no, because of nephrotoxicity

226
Q

What common infection are NOD (Nafcillin, oxacillin, dicloxacillin) used to treat?

A

Skin or bloodstream infections with Staphylococcus aureus

227
Q

What is another name for extended-spectrum penicillins?

A

Amino-penicillins

228
Q

What are two extended-spectrum penicillins taken orally?

A

Ampicillin and amoxicillin

229
Q

Do ampicillin and amoxicillin have gram-negative activity?

A

Yes, although Klebsiella is resistant

230
Q

What penicillins have good activity against enterococci?

A

Amino-penicillins like ampicillin and amoxicillin

231
Q

What is the drug of choice for listeria monocytogenes?

A

Amino-penicillins: ampicillin, amoxicillin

232
Q

What should this 12 year old patient be tested for? What is the treatment for the common infection that results in this appearance of the tonsils?

A

Strep type A (S. pyogenes); it can be treated with penicillin or amoxicillin

233
Q

Why is Mycoplasma resistant to penicillins?

A

It has no cell wall

234
Q

What two penicillin resistance strategies can a gram-negative bacteria develop that a gram-positive bacteria cannot?

A

Change in the outer membrane porins, or an efflux pump in the outer membrane

235
Q

What mutation commonly causes the resistance to penicillins seen in MRSA?

A

An alteration to penicillin-binding protein (transpeptidases) that decreases affinity for β-lactams

236
Q

What drug is this? What bond would be broken by a β-lactamase?

A

Ampicillin; this bond would be broken:

237
Q

What is the point of a β-lactamase inhibitor?

A

It inhibits the β-lactamases that break down β-lactam antibiotics, so the β-lactam can inhibit transpeptidases

238
Q

What class of drugs do clavulanic acid, sulbactam, and tazobactam belong to?

A

β-lactamase inhibitors

239
Q

What three drugs can be combined with penicillins to increase gram-negative activity by inhibiting β-lactamases?

A

Clavulanic acid, sulbactam, and tazobactam

240
Q

What does the sulbactam in an ampicillin-sulbactam combination do?

A

It inhibits β-lactamases that would break down the ampicillin

241
Q

What does the clavulanic acid in the amoxicillin-clavulanic acid combination formulation do?

A

It is a β-lactamase inhibitor that inhibits breakdown of the amoxicillin

242
Q

What are two common adverse reactions to penicillin that present as skin symptoms?

A

Hypersensitivity and rash

243
Q

Can penicillins cause anaphylaxis?

A

Yes

244
Q

What is this patient experiencing after administration of penicillin?

A

Angioedema, an adverse reaction do to hypersensitivity of the immune system

245
Q

Are rash and hypersensitivity reactions to penicillin common? What other drug allergies can be suspected after such a reaction?

A

Yes; increased chance of reactivity to other β-lactams (cephalosporins, carbapenems) excepting monobactams

246
Q

Almost 100% of patients with what viral infection develop a maculopapular rash to amoxicillin?

A

EBV-associated mononucleosis

247
Q

What kidney-related adverse reaction can occur with penicillins? What antibiotic is no longer used because of this risk?

A

Nephritis (acute kidney injury); methicillin

248
Q

What kind of colitis can result from penicillin administration?

A

Clostridium difficile colitis

249
Q

What type of antibiotic is this? What are its identifying features?

A

Cephalosporin; β-lactam 4-membered ring in center, and 6-membered dihydrothiazine ring to the right

250
Q

How many generations of cephalosporins have been made? What increases over the generations?

A

5; gram-negative activity

251
Q

Can cephalosporins cross the blood-brain barrier?

A

Yes, after the 3rd and 4th generation

252
Q

Do cephalosporins treat Enterococcus or Listeria?

A

No

253
Q

Can cephalosporins treat MRSA?

A

Only the “5th” generation, ceftaroline

254
Q

What is the 1st generation cephalosporin? What is its oral formulation called?

A

Cefazolin; cephelexin is the oral formula

255
Q

Can cefazolin be used against group A and group B strep, and S. viridans?

A

Yes

256
Q

Are cephalosporins affected by β-lactamases?

A

No, they are not β-lactam drugs

257
Q

Is cefazolin more active against gram-positive or gram-negative bacteria?

A

Gram-positive

258
Q

Can cefazolin be used for UTIs and skin infections?

A

Yes

259
Q

Do cephalosporins have similar adverse reactions as penicillin?

A

Yes

260
Q

What is the cross-reactivity of cephalosporins with people that have penicillin allergies? Should they be used in a patient that has had hives in reaction to penicillin?

A

About 1-10%; no

261
Q

What does this patient have on his arm, given the following culture?

A

Staphylococcus aureus

262
Q

If a patient who has a history of IV drug abuse has high fevers and a methicillin susceptible S. aureus infection, what are some reasonable treatments?

A

Anti-staphylococcal penicillins: Nafcillin

Cephalosporins: Cefazolin

These will kill methicillin-susceptible S. aureus, and both drugs are unaffected by penicillase (most S. aureus harbors penicillase)

263
Q

Besides age and allergies, what else should be evaluated before prescribing β-lactam or cephalosporin antibiotics?

A

Kidney function

264
Q

If a skin infection has gram positive cocci that are identified as β hemolytic, what bacterium related to the one causing strep throat should be suspected?

A

S. pyogenes

265
Q

What are examples of non-suppurative consequences of a S. pyogenes infection?

A

Scarlet fever, acute rheumatic fever, glomerulonephritis

266
Q

Are penicillins bacteriostatic or bactericidal?

A

Bactericidal

267
Q

What potential problem when treating abscesses with oral antibiotics, assuming the right one was prescribed at the right dosage and the organism is susceptible?

A

Distribution of the drug into the abscess, since the neutrophils surrounding the abscess can block access of the antibiotic to the area with the most bacteria

268
Q

When the serum C3 complement level is measured as low, what does this indicate?

A

It has been consumed (broken down to C3b and C3a), so the immune system was exposed to an antigen that activated the complement pathway (alternatively: there is a C3 deficiency, but this is rare)

269
Q

Acute rheumatic fever is most often associated with streptococcal strains rich in what protein?

A

Protein M

270
Q

Are streptococcal strains rich in M protein more or less virulent? Why?

A

They are relatively resistant to phagocytosis and multiply quickly in tissues

271
Q

What exotoxin is secreted by extra-virulent S. pyogenes that causes necrotizing fasciitis? What life-threatening syndrome can this exotoxin cause?

A

Superantigen, which hyperactivates T cells; it can cause toxic shock syndrome

272
Q

What is the course of treatment for necrotizing fasciitis?

A

Aggressive surgical debridement, and secondarily, IV antibiotics

273
Q

Which researcher on tuberculosis developed postulates that led to a new understanding of infectious disease and a Nobel?

A

Robert Koch

274
Q

What is the property of tuberculosis bacteria’s cell wall that makes it resistant to disinfectants and traditional stains?

A

It is lipid rich

275
Q

What is the major component of mycobacterium’s cell wall?

A

Mycolic acid

276
Q

Why do mycobacteria clump together?

A

Hydrophobicity of the cell wall

277
Q

Are mycobacteria motile? Are they spore-forming?

A

No to both

278
Q

What is the gram staining of mycobacteria?

A

Gram null to weakly gram positive

279
Q

What kind of staining, also called Ziehl-Neelsen or Kinyoun, reveals mycobacteria?

A

Acid fast staining

280
Q

Of the four Runyon classes of mycobacteria, which grows fastest?

A

Runyon class IV

281
Q

Is mycobacterium tuberculosis in a Runyon class? If so, which one?

A

No, it is not in a class.

282
Q

Do mycobacteria encourage or discourage phagocytosis by immune cells? What happens to a phagosome containing a mycobacteria?

A

Phagosome formation is encouraged; phagosome maturation is blocked, so the bacterium can survive

283
Q

What fusion event is inhibited after phagocytosis of mycobacteria to allow them to survive?

A

Phagosome-lysosome fusion is inhibited

284
Q

What immune proteins that normally surround intruders to aid in their destruction are rendered ineffective by mycobacterium?

A

Antibody and complement proteins

285
Q

Is the incidence of TB in the United States among native-born persons still declining?

A

Yes

286
Q

Approximately what fraction of the world’s population carries mycobacterium tuberculosis?

A

One third

287
Q

The spread of what disease in the 1980’s led to an uptick in tuberculosis infection?

A

HIV/AIDS

288
Q

What can a tuberculosis patient do to expose other people to the bacterium, besides blood-to-blood contact? Can TB bacilli remain infectious in the air?

A

Coughing, sneezing, speaking, or singing; yes, it can remain suspended in the air for several hours

289
Q

During the primary infection process for mycobacterium tuberculosis, is there a host immune response?

A

No, the bacteria replicate freely in alveolar macrophages

290
Q

What channels does the tuberculosis bacterium use to spread after infection of the alveoli?

A

Lymphatics and bloodstream

291
Q

What immune response (humoral or cell-mediated) contains the primary infection by TB? What histological immune structures form in the lungs during the killing of the bacilli?

A

Cell-mediated immune response; granulomas

292
Q

What is this histological feature, characteristic of TB infection?

A

A granuloma

293
Q

Within caseating centers of granulomas, does TB replicate faster or slower? Why?

A

Slower; because of the lower pH and the anoxic environment.

294
Q

In 90% of patients, what is the endpoint of primary tuberculosis? Is it symptomatic?

A

Latent tuberculosis; usually it is not

295
Q

Is latent tuberculosis contagious?

A

No

296
Q

What is the common test for latent TB infection? What is a requirement for this test, without which it will return a false negative?

A

PPD (the tuberculin skin test); you need a functional immune system

297
Q

How long does it take for delayed hypersensitivity reactions to tuberculins to be detectable by a PPD after the initial infection? How long are the tuberculins implanted in the skin before reading?

A

6-8 weeks; 48-72 hours

298
Q

What is a more sensitive assay for past exposure to tuberculosis bacterium? How does it work?

A

Interferon γ release assay; it is an ELISA test that detects release of interferon γ from sensitized patients after incubation with two peptides from TB

299
Q

What is the standard approach to latent tuberculosis?

A

Chest x-ray, sputum analysis, and Isoniazid for 9 months

300
Q

What are the common presenting symptoms of active tuberculosis?

A

Cough, hemoptysis (bloody cough), night sweats, anorexia, weight loss

301
Q

Can tuberculosis infect tissues besides the longs?

A

Yes, including the bones, lymph nodes, brain, GI tract…

302
Q

This sample is from a TB patient. What has occurred that is characteristic of its pathology?

A

Caseating necrosis

303
Q

What staining is used here to visualize bacteria? Which bacterium is this characteristic of?

A

Acid fast staining; mycobacterium, particularly tuberculosis

304
Q

What is common in HIV patients with tuberculosis infections?

A

It spreads to other tissues quickly, e.g., the fingers

305
Q

What is visible on a CT scan of the lungs of most tuberculosis patients?

A

Nodules (they can be bilateral or unilateral and in any lobe, as the following CT shows)

306
Q

What is the mnemonic for the 4-drug regimen to treat active tuberculosis?

A

RIPE:

  • Rifampin
  • Isoniazid
  • Pyrazinamide
  • Ethambutol
307
Q

Which part of the bacterium does isoniazid act upon?

A

The cell wall

308
Q

What dietary warning is given to people on prolonged isoniazid for tuberculosis infection?

A

Do not consume alcohol

309
Q

What is the mechanism of Rifampin? Is it bactericidal or bacteriostatic?

A

It inhibits DNA-dependent RNA polymerase in mycobacteria; bactericidal

310
Q

What is the primary adverse effect of Rifampin? Why?

A

Hepatotoxicity; it induces hepatic cytochrome p450 enzymes

311
Q

What is the primary adverse affect of isoniazid, requiring a dietary warning?

A

Hepatotoxicity

312
Q

Production of what component of mycobacterium is inhibited by isoniazid? Is it bacteriostatic or bactericidal?

A

Mycolic acid synthesis, the main component of the cell wall; bactericidal

313
Q

Is pyrazinamide bacteriostatic or bactericidal? What globally common infection is it used to treat?

A

Bacteriostatic; tuberculosis

314
Q

What does ethambutol inhibit that makes it a good treatment for tuberculosis? Is it bacteriostatic or bacteriocidal?

A

Cell wall polysaccharide synthesis

315
Q

What is the primary adverse effect of ethambutol?

A

Optic neuritis

316
Q

Are certain strains of TB resistant to isoniazid and/or rifampin?

A

Yes

317
Q

What can be used to supplement treatment for MDR or XDR tuberculosis?

A

Other antibacterials: streptomycin, linezolid, fluoroquinolones, kanamycin, …

318
Q

Why are multiple antibiotics administered concurrently to eradicate a TB infection in a patient?

A

To prevent development of a resistant strain

319
Q

What is the most significant gram-negative microbe in the GI tract?

A

E. coli

320
Q

Can E. coli cause neonatal sepsis or meningitis?

A

Yes

321
Q

What bacterium is this?

A

E. coli, identified by gram negative rods and fermentation of lactose on MacConkey agar

322
Q

There are 3 important surface antigens on E coli. How are they named?

A

O, H, and K

323
Q

In the strain serotype E. coli O157:H7, what is the meaning of the second part of this name?

A

It refers to surface antigens O and H

324
Q

When a patient complains of dysuria and changes in frequency of urination, a UTI is suspected. What is significant about a co-presentation with flank pain and cost-vertebral angle tenderness?

A

An upper UTI may be suspected as opposed to a lower UTI. This might include e.g. pyelonephritis

325
Q

What is the most common cause of UTIs?

A

E. coli

326
Q

What does dysuria mean?

A

Painful urination

327
Q

Which pili on E. coli allows certain strains to adhere to the urinary epithelium?

A

P-pili

328
Q

What is the typical IV therapy for pyelonephritis?

A

Fluroquinolones (e.g. Ciprofloxacin) or ceftriaxone

329
Q

What is the typical course of treatment for a lower UTI?

A

Fluoroquinolones, ceftriaxone, or trimethoprim-sulfamethoxazole

330
Q

What is the typical cause of “traveler’s diarrhea”?

A

E. coli, caused by a lack of immunity to bacteria in the local water

331
Q

ETEC, EPEC, EIEC, EHEC, STEC, and EAEC are all strains of…

A

Diarrhea-causing E. coli

332
Q

In enterotoxigenic E. coli, is the mucosa of the GI tract disrupted?

A

No

333
Q

What long structures surround E coli, mediating its attachment to various surfaces?

A

Pili

334
Q

Which pili mediates adhesion of ETEC to the GI tract?

A

CF pili

335
Q

What other microbial toxin is the Heat Labile Toxin of ETEC similar to?

A

Cholera toxin

336
Q

What enzyme is stimulated by Heat Labile Toxin and what doe sthis cause? What organism secretes this toxin?

A

Adenylate cyclase, causing export of Na+, K+, and water into the GI lumen (diarrhea); enterotoxigenic E. coli (ETEC)

337
Q

What enzyme is stimulated by Heat Stable Toxin, released by enterotoxigenic E. coli?

A

Guanylate cyclase

338
Q

Enterotoxigenic E. coli secretes two toxins abbreviated LT and ST. What are their full names?

A

Heat labile toxin and heat stable toxin

339
Q

What does the stimulation of guanylate cyclase by heat stable toxin cause? What organism secretes it as an exotoxin?

A

Secretion of Cl-, HCO3- and water; ETEC (enterotoxigenic E. coli)

340
Q

What organism causes hemolytic-uremic syndrome (HUS)?

A

Enterohemorrhagic E. coli

341
Q

What has happened to these RBCs? What strain of E. coli can do this?

A

Fragmentation (happens in small blood vessels); Enterohemorrhagic E. coli

342
Q

How is enterohemorrhagic E. coli acquired?

A

Consumption of raw beef, food contaminated by animal feces, or animal contact

343
Q

What is the hallmark symptom of enterohemorrhagic E. coli infection?

A

Bloody diarrhea

344
Q

What are two common abbreviations for the organism that causes hemolytic uremic syndrome?

A

EHEC or STEC, both referring to enterohemorrhagic E. coli

345
Q

What toxin is produced by EHEC that triggers hemolytic uremic syndrome?

A

Shigatoxin

346
Q

What is the best way to test for EHEC infection?

A

Test for Shiga toxin in the stool

347
Q

Can sorbital agar reliably identify EHEC?

A

It can only identify the O157:H7 strain—it will not identify other strains of EHEC

348
Q

Where are the typical genomic locations for virulent factors of E. coli strains, like exotoxins?

A

Phages, plasmids, or pathogenicity islands

349
Q

What does enteroinvasive E. coli cause (EIEC)?

A

Dysentery

350
Q

When E. coli is suspected for a case of dysentery, what can be used on the stool to diagnose it?

A

A stool smear to reveal WBCs

351
Q

Is there disruption of the mucosa in EIEC?

A

Yes, bacteria invade the enterocytes (enteroinvasion)

352
Q

What do enteroaggregative E. coli form on the wall of the GI epithelium?

A

A biofilm, inhibiting proper absorption across the intestinal membrane

353
Q

Why is bacterial neonatal sepsis and meningitis treated with ampicillin in addition to cefotaxime?

A

Cefotaxime is for E. coli, but the ampicillin is intended to kill listeria, another top bacterial etiology for these symptoms

354
Q

What is notable about the strains of E. coli that cause nosocomial infections?

A

They are typically resistant to many antibiotics

355
Q

What bacterium is seen here, in this sampling of CSF from a patient with altered mental status?

A

Gram negative; probabably meningococcus

356
Q

Is meningitis more common in children or adults?

A

Children under 2 years of age

357
Q

Removal of what organ can cause in increase in risk for meningitis?

A

Spleen

358
Q

How is neisseria meningitidis transmitted?

A

Respiratory droplets, which is why it is more likely to cause epidemics in overcrowded conditions

359
Q

What is “meningococcus” an abbreviation for?

A

Neisseria meningitidis

360
Q

What does N. meningitidis secrete to allow survival in the respiratory tract?

A

IgA protease

361
Q

What is the function of the pili on N. meningitidis in the respiratory tract, besides conjugation?

A

Attachment to the respiratory epithelium

362
Q

What is the capsule of N. meningitidis made of?

A

Polysaccharides

363
Q

What form of endotoxin is secreted by N. meningitidis that can cause sepsis?

A

Lipooligosaccharide

364
Q

What is the defining feature of the rashes caused by meningococcemia?

A

They are all non-blanching

365
Q

Which serogroup of N. meningitidis has no vaccine? Why not?

A

Serogroup B, because it has a polysaccharide capsule similar to human sialic acid

366
Q

Is LOS different from LPS? If so, how?

A

Yes; they are a subtype of LPS present in bacteria that colonize mucosal surfaces not bathed in bile, such as N. meningitidis

367
Q

What is the difference with the conjugate vaccine for meningitis as opposed to the polysaccharide vaccine?

A

The conjugate vaccine has proteins, which are more immunogenic

368
Q

Does N. meningitidis produce β-lactamases?

A

No

369
Q

What can be used to treat N. meningitidis?

A

Penicillin works, but ceftriaxone is more common

370
Q

Empiric treatment of bacterial meningitis in adults when nothing is seen on gram stain consists of what drugs?

A

Ceftriaxone (against meningococcus, Haemophilus and pneumococcus), vancomycin (against β-lactam pneumocci), and sometimes ampicillin (against Listeria monocytogenes)

371
Q

Is Listeria gram positive or negative? What is its shape?

A

Gram positive; rod (bacillus)

372
Q

What is the motility style of Listeria?

A

Tumbling, end over end

373
Q

Which age groups does Listeria affect? What other population is particularly at risk?

A

Infants and the elderly (bimodal); the immunocomprised, such as pregnant women

374
Q

Is ceftriaxone used to treat L. monocytogenes?

A

No, ampicillin is more reliable

375
Q

What can be used to prevent spread of meningitis to those in close contact?

A

Chemoprophylaxis

376
Q

What is a nickname for N. gonorrhoeae?

A

Gonococcus

377
Q

What is the difference in the capsule between N. meningitidis and N. gonorrhoeae?

A

N. gonorrhoeae does not have a true polysaccharide capsule

378
Q

What is the energy source for N. gonorrhoeae in culture? Is this different from N. meningitidis?

A

Glucose only; yes, N. meningitidis can also use maltose

379
Q

What part of N. gonorrhoeae makes development of a vaccine difficult?

A

Antigenic variability of the pili

380
Q

Is the age distribution of N. gonorrhoeae infections modal or bimodal?

A

Modal, with the highest range around 15-25 years of age

381
Q

What inflammatory disease can be caused by chronic N. gonorrhoeae infection?

A

Pelvic inflammatory disease

382
Q

Which diagnostic tool is used most often in clinical practice for gonococci?

A

DNA amplification probes

383
Q

What is the mainstay of therapy for N. gonorrhoeae? Do they have β-lactamase? What co-infection is assumed?

A

Cephalosporins, e.g., ceftriaxone; yes; Chlamydia

384
Q

When a patient presents with respiratory symptoms, and a cultured bacterium grows on chocolate agar and with VX factor, what organism is suspected?

A

Haemophilus influenzae

385
Q

What is this feature seen on a blood agar plate? What organism is it significant for?

A

Satellite colonies; Haemophilus influenzae

386
Q

Is the present vaccine for Haemophilus influenzae a polysaccharide vaccine or a conjugate vaccine?

A

Conjugate

387
Q

Does the Haemophilus genus cause any STDs?

A

Yes, chancroid, by Haemophilus ducreyii. It is characterized by painful fluid-filled lesions on the genitals

388
Q

What can Moraxella catarrhalis cause? Is it gram negative, or gram positive? Is it anaerobic or aerobic?

A

Otitis, sinusitis, and pneumonia (particularly with underlying emphysema); gram positive; aerobic

389
Q

What is the gram negative coccobacillus that causes whooping cough?

A

Bordetella pertussis

390
Q

Which vaccine was built to eliminate Bordetella pertussis?

A

DPT: diphtheria, pertussis, tetanus

391
Q

Are incidents of pertussis on the rise or declining since the introduction of the DPT vaccine?

A

They are still rising

392
Q

What capsulated bacterium produces a purpuric, petechial rash?

A

N. meningitidis

393
Q

How many capsule serogroups of N. meningitidis are there? Does the vaccine cover all of them?

A

13; no, the vaccine covers 4 of the most common

394
Q

What is the vaccine protecting against Haemophilus influenzae called?

A

HiB vaccine

395
Q

Are N. gonorrhoeae susceptible to quinolones?

A

No, resistance has developed

396
Q

What is used to combat B. pertussis in severe cases of whooping cough?

A

Azithromycin

397
Q

What type of organisms is the spleen an important defense organ for?

A

Encapsulated organisms, e.g. N. meningitidis and Listeria

398
Q

Can fats and sugars within the outer membrane of a gram negative bacterium trigger a fatal response?

A

Yes, because of inflammation

399
Q

What is notable about this CT that is suggestive of S. pneumoniae?

A

The infection is well contained to one lobe

400
Q

What bacterium is this?

A

Strep pneumoniae: a gram-positive, encapsulated diplococci, note the thick cell wall.

401
Q

What is the hemolysis pattern of S. pneumoniae? Is it optochin sensitive or resistant? Does it have a Lancefield antigen?

A

α hemolysis; optochin sensitive; no Lancefield antigen

402
Q

How is S. pneumoniae transmitted? What is colonized transiently that leads to no symptoms in most adults? Is smoking a risk factor?

A

Through droplets; the nasopharynx; Yes

403
Q

What is the distribution of ages for S. pneumoniae infection? What other significant risk factor must be considered, which e.g. asplenia could contribute to?

A

Very young and very old; immunosuppression

404
Q

Besides age, immunosuppression, and smoking, what are two other risk factors for S. pneumoniae infection?

A

CSF leaks and cochlear implants

405
Q

How many serotypes of S. pneumoniae exist?

A

Over 90

406
Q

Did a vaccine for pneumococcus exist in 1998?

A

No

407
Q

What is serotyping of S. pneumoniae based on? Are antibodies against these molecules protective?

A

The capsular polysaccharide; Yes

408
Q

Do symptoms of S. pneumoniae present acutely or chronically compared to a TB patient?

A

Acutely

409
Q

What are nuchal rigidity, Kernig and Brudzinsky signs all indicative of?

A

Meningitis

410
Q

What infection with a high mortality can cause fever, photophobia, headache, and altered mental status?

A

Meningitis

411
Q

What physical exam procedure is this? What does it test for?

A

Kernig sign; meningitis

412
Q

What physical exam technique is this? What is it testing for?

A

Brudzinski sign; meningitis

413
Q

What is this a picture of? What condition is present?

A

The eardrum; otitis media. The following is a normal eardrum:

414
Q

Can S. pneumonia cause bacteremia, sinusitis, and peritonitis?

A

Yes

415
Q

What type of antibody can prevent adherence of S. pneumoniae, preventing infection?

A

Secretory IgA (sIgA)

416
Q

What is the main virulence factor of S. pneumoniae?

A

The capsule

417
Q

What is binding of the pneumococcus to an epithelial cell mediated by?

A

Adhesins

418
Q

What can pneumococci secrete to defeat secreted IgA and adhere to epithelial cells anyway?

A

IgA protease

419
Q

Which pathway for complement activation is inhibited by the capsule of S. pneumoniae?

A

The alternate pathway

420
Q

What bacterium contains pneumolysin? Where is it stored in the bacterium? What is its function?

A

S. pneumonia; in the cytoplasm; it lyses phagocytic cells

421
Q

Which system unrelated to the capsular specific antibodies is critical for clearing S. pneumoniae from the bloodstream?

A

The lymphoreticular system of the spleen

422
Q

Why is the spleen more important for clearing capsulated organisms?

A

Phagocytosis by neutrophils is less efficient, so filtration in the spleen is a more significant way for these organisms to be cleared

423
Q

What class of drugs is used to treat S. pneumoniae? How does resistance usually present?

A

β-lactams; resistance is usually from altered penicillin binding proteins

424
Q

Do clavulinic acid or sulbactam help β-lactam treatment of S. pneumoniae that are becoming β-lactam resistant? Why or why not?

A

No; they are β-lactamase inhibitors, but this is not the typical way that resistance develops in S. pneumoniae

425
Q

Can you overcome the weak binding of β-lactams to PBP’s in somewhat resistant S. pneumoniae by increasing the dose?

A

Sometimes, yes

426
Q

Which β-lactams are most often used against S. pneumoniae?

A

Amoxicillin, ampicillin, cefotaxime and ceftriaxone

427
Q

Why is ceftriaxone particularly effective against S. pneumoniae, particularly with regard to preventing serious complications?

A

It can get into the CSF, and does well against the three most common causes of bacterial meningitis

428
Q

What cause of meningitis is not covered by cephalosporins?

A

Listeria monocytogenes

429
Q

Can ceftriaxone be administered orally? Can vancomycin be administered orally?

A

No to both

430
Q

How is ceftriaxone excreted?

A

Biliary ducts

431
Q

How is cefotaxime excreted? Does it have a shorter or longer half-life than ceftriaxone?

A

Kidneys; shorter half-life (8h) compared to ceftriaxone (12-24h)

432
Q

What do fluoroquinolones inhibit causing bacterial death? Which fluoroquinolone cannot be used against respiratory infections?

A

Bacterial topoisomerase and DNA gyrase, thereby inhibiting DNA synthesis; Ciprofloxacin has no activity against gram positive organisms and thus is not indicated for respiratory infections (where S. pneumoniae is suspect)

433
Q

What athletic activity is dangerous during administration of fluoroquinolones?

A

Weight lifting and running, because of the adverse effect of tendonitis and/or tendon rupture

434
Q

If S. pneumoniae is resistant to β-lactams, what antibiotic can be used? Is it active against gram negatives, gram positives, or both?

A

Vancomycin

435
Q

What is the empiric treatment for bacterial meningitis?

A

Vancomycin and ceftriaxone, which both reach the CSF and in conjunction combat β-lactam sensitive and resistant gram positive and gram negative bacteria

436
Q

What oral treatment is given for pneumococcal pneumonia?

A

Amoxicillin and/or azithromycin, and levofloxacin

437
Q

If an IV drug user comes in and reports symptoms indicating bacterial pneumonia, what else must be suspected?

A

Immunodeficiency, e.g. AIDS

438
Q

What would otitis media or sinusitis with a suspected bacterial cause be treated with?

A

Amoxicillin (oral)

439
Q

Why isn’t the pneumovax vaccine immunogenic in children under 2? What vaccine is given to them instead, and why does that one work better?

A

It is a purified capsular polysaccharide antigen, which children of this age will not recognize as foreign (it is a T-cell independent antigen); the PCV-13 (Prevnar-13) vaccine has the polysaccharide conjugated to a diphtheria toxoid (T-cell dependent antigen), which the immune system will recognize as foreign at this age

440
Q

After recommendation of the PCV7 vaccine in 2000, did rates of S. pneumoniae decrease in children, or across all age groups? What is this phenomenon called?

A

All age groups; herd immunity

441
Q

What are environmental sources of pseudomonadaceae?

A

Soil, water, plant material, and environmental surfaces

442
Q

What is this bacterium, which grows aerobically in immunocompromised hosts, particularly within burn injuries?

A

Pseudomonadaceae (gram negative bacilli)

443
Q

Does P. aeruginosa ferment lactose?

A

No (right), which is different from E. coli (left)

444
Q

Does Pseudomonas produce oxidase?

A

Yes

445
Q

Is this a positive or negative oxidase test?

A

Positive

446
Q

What is this morphology on agar to the right called?

A

Mucoid: it indicates formation of a biofilm

447
Q

What features of P. aeruginosa are shown here?

A

Unipolar flagellum and adherence mediating pili

448
Q

What can render a host particularly susceptible to Pseudomonas infections?

A

Neutropenia (e.g. by chemotherapy), severe burns, diabetes/foot ulcers, cystic fibrosis

449
Q

What kind of Pseudomonas infection is most likely to manifest in a neutropenic patient?

A

Bacteremia or sepsis

450
Q

What risk factors for P. aeruginosa infection associate a respiratory infection?

A

Cystic fibrosis or mechanical ventilation

451
Q

What organism is associated with “hot tub folliculitis”?

A

P. aeruginosa

452
Q

What condition caused by P. aeruginosa is seen here?

A

Ecthyma gangrenosum, a result of bacteremia

453
Q

What are these two manifestations of P. aeruginosa, from left to right?

A

Hot tub folliculitis and infected pressure sore

454
Q

What manifestation of P. aeruginosa is this?

A

Otitis externa

455
Q

What injurious infection of P. aeruginosa can be seen here, which follows trauma to the eye, including that caused by contact lenses?

A

Corneal ulcers or endophthalmitis

456
Q

What is the clinical (not genetic) marker of cystic fibrosis, which relates especially to P. aeruginosa?

A

They present with chronic lung infections and inflammation

457
Q

With chronic infection by P. aeruginosa in cystic fibrosis patients, what are the two typical infections that precede it? Does the mucoid P. aeruginosa precede the non-mucoid, in the sequence of infections or the other way around?

A

S. aureus and H. influenzae; non-mucoid is typically first

458
Q

Are cephalosporins useful against Pseudomonas aeruginosa? What about carbapenems? Monobactams? Fluoroquinolones?

A

Yes to all, with various resistance factors seen in the wild

459
Q

What two organisms (excepting P. aeruginosa) are linked to catheter-associated bacteremia and ventilator-associated pneumonia?

A

Burkholderia cepacia and Stenotrophomonas maltophilia

460
Q

What classes of bacteria are aminoglycosides useful for treatment? Are they usually used as primary or secondary therapy?

A

Gram negative, aerobic bacteria, e.g. P. aeruginosa; usually secondary to another antibiotics

461
Q

What is the basic structure of an aminoglycoside?

A

Amino sugar linked to a central hexose

462
Q

What are the host cell entry, CSF, and tissue penetration characteristics of aminoglycosides? Why is this?

A

All are poor; they are polycationic and highly polar

463
Q

What is the mechanism of action of aminoglycosides?

A

Interference with bacterial protein synthesis (initiation, see the A pathway here)

464
Q

What is the most common mechanism of resistance to aminoglycosides?

A

Drug modification (acetylation or adenylation of parts of the drug by the bacterium)

465
Q

What kind of antibiotic is kanamycin? Is it currently administered?

A

Aminoglycoside; no longer used

466
Q

What is a common topical aminoglycoside?

A

Neomycin

467
Q

What class of drugs are streptomycin, gentamicin, tobramycin, and amikacin?

A

Aminoglycosides

468
Q

What are four aminoglycosides that can be administered intramuscularly? Are oral forms available?

A

Streptomycin, gentamicin, tobramycin, and amikacin; no

469
Q

What are the main adverse toxicities of aminoglycosides?

A

Nephrotoxicity and ototoxicity, along with neuromuscular blockade

470
Q

Important agents of nosocomial infection include:

– […] (e.g., RSV, Parainfluenza, Influenza, Adenovirus)

– Methicillin-resistant Staphylococcus aureus

– Vancomycin-resistant Enterococcus faecium

– Multiresistant Gram-negative bacilli

– Clostridium difficile

A

Important agents of nosocomial infection include:

– Respiratory Viruses (e.g., RSV, Parainfluenza, Influenza, Adenovirus)

– Methicillin-resistant Staphylococcus aureus

– Vancomycin-resistant Enterococcus faecium

– Multiresistant Gram-negative bacilli

– Clostridium difficile

471
Q

Important agents of nosocomial infection include:

– Respiratory Viruses (e.g., RSV, Parainfluenza, Influenza, Adenovirus)

– […]-resistant Staphylococcus aureus

– Vancomycin-resistant Enterococcus faecium

– Multiresistant Gram-negative bacilli

– Clostridium difficile

A

Important agents of nosocomial infection include:

– Respiratory Viruses (e.g., RSV, Parainfluenza, Influenza, Adenovirus)

– Methicillin-resistant Staphylococcus aureus

– Vancomycin-resistant Enterococcus faecium

– Multiresistant Gram-negative bacilli

– Clostridium difficile

472
Q

Important agents of nosocomial infection include:

– Respiratory Viruses (e.g., RSV, Parainfluenza, Influenza, Adenovirus)

– Methicillin-resistant Staphylococcus aureus

– […]-resistant Enterococcus faecium

– Multiresistant Gram-negative bacilli

– Clostridium difficile

A

Important agents of nosocomial infection include:

– Respiratory Viruses (e.g., RSV, Parainfluenza, Influenza, Adenovirus)

– Methicillin-resistant Staphylococcus aureus

– Vancomycin-resistant Enterococcus faecium

– Multiresistant Gram-negative bacilli

– Clostridium difficile

473
Q

Important agents of nosocomial infection include:

– Respiratory Viruses (e.g., RSV, Parainfluenza, Influenza, Adenovirus)

– Methicillin-resistant Staphylococcus aureus

– Vancomycin-resistant Enterococcus faecium

– […] bacilli

– Clostridium difficile

A

Important agents of nosocomial infection include:

– Respiratory Viruses (e.g., RSV, Parainfluenza, Influenza, Adenovirus)

– Methicillin-resistant Staphylococcus aureus

– Vancomycin-resistant Enterococcus faecium

– Multiresistant Gram-negative bacilli

– Clostridium difficile

474
Q

Important agents of nosocomial infection include:

– Respiratory Viruses (e.g., RSV, Parainfluenza, Influenza, Adenovirus)

– Methicillin-resistant Staphylococcus aureus

– Vancomycin-resistant Enterococcus faecium

– Multiresistant Gram-negative bacilli

– […] difficile

A

Important agents of nosocomial infection include:

– Respiratory Viruses (e.g., RSV, Parainfluenza, Influenza, Adenovirus)

– Methicillin-resistant Staphylococcus aureus

– Vancomycin-resistant Enterococcus faecium

– Multiresistant Gram-negative bacilli

– Clostridium difficile

475
Q

What two major classes of gram-negative bacilli are associated with nosocomial infections?

A

Enterobacteriaceae and Pseudomonodaceae

476
Q

What units are most at risk for nosocomial infections?

A

Burn units, NICU, MICU/SICU, and oncology

477
Q

What is the mean attributable cost to the hospital of a nosocomial bloodstream infection?

A

$36k

478
Q

What standard precaution must be taken by all hospital workers with all patients to prevent nosocomial infections?

A

Hand hygiene

479
Q

How long should we wash our hands with soap and water or Purell to prevent nosocomial infections?

A

>15 seconds

480
Q

What is the usual suspect for “typical” pneumonia?

A

Streptococcus pneumoniae

481
Q

Is there a productive cough and copious sputum with typical or atypical pneumonia?

A

Typical pneumonia

482
Q

What extrapulmonary symptoms typically manifest in atypical pneumonia? Do most patients seek medical care?

A

Muscle aches and headache, low fever; most do not

483
Q

Is an elevated WBC more indicative or typical or atypical pneumonia?

A

Typical

484
Q

What are the three major suspect bacteria for atypical pneumonia?

A

Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Legionella

485
Q

What bacterium causing atypical pneumonia is seen in this EM?

A

Mycoplasma pneumoniae

486
Q

What is the incubation period of M. pneumoniae?

A

2-3 weeks

487
Q

How is M. pneumoniae transmitted? Can it spread between people across a room?

A

Respiratory droplet; no, it requires close contact

488
Q

What structural feature makes M. pneumoniae an unusual bacterium?

A

It lacks a cell wall

489
Q

What is the shape of M. pneumoniae? Is it visible on a gram stain?

A

Short and rod-shaped; invisible on gram stain

490
Q

Is M. pneumoniae easy to grow quickly in culture?

A

No, it has a long doubling time (6h)

491
Q

Why was M. pneumoniae initially assumed to be a virus, in 1918?

A

It could pass through filters that only viruses could pass through

492
Q

What is the age distribution of typical M. pneumoniae infections?

A

Unimodal, around adolescents and young adults

493
Q

Do most patients survive M. pneumoniae infection without treatment?

A

Yes

494
Q

Does M. pneumoniae grow inside or outside of cells?

A

Inside of them

495
Q

What blood cell abnormality is a risk factor for Mycoplasma pneumoniae?

A

Sickle cell

496
Q

Why does sickle cell predispose patients to M. pneumoniae?

A

Cold-agglutinins produced by polyclonal T cells and B cells during the immune response to M. pneumoniae bind to the I antigen on the RBC surface area, which is smaller for patients with sickle cell

497
Q

What skin manifestation is associated with M. pneumoniae?

A

Erythema multiforme

498
Q

Can M. pneumoniae cause meningitis?

A

Yes

499
Q

Where in the respiratory tract does M. pneumoniae infection start?

A

Usually in the upper part, but it can spread anywhere within the tract

500
Q

Is a cold-agglutinin test useful in diagnosing M. pneumoniae?

A

No, it is not sensitive or specific enough

Microbiology (4 decks)

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