Micro of Strep - Cross Flashcards

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1
Q

Generalized morphology of streptococci?

A

spherical gram (+) cocci in pairs or chains; catalase(-), varying hemolysis

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2
Q

Group A strep also known as?

A

Strep Pyogenes

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3
Q

Group B strep also known as?

A

Strep agalactiae

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4
Q

3 bugs in Group D strep?

A

Enterococcus faecalis, Enterococcus faecium, and Strep bovis (gallolyticus)

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5
Q

Diagnosis of GAS?

A

Do a rapid swab and a culture at time of presentation

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6
Q

Diseases that GAS most commonly causes?

A

Pharyngitis (most common cause), cellulitis/impetigo, necrotizing fasciitis, TSS, scarlet fever, rheumatic fever, glomerulonephritis

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7
Q

GAS virulence factors (there are 9)

A

1) Hyaluronidase 2) Streptokinase 3) DNase 4) C5a peptidase 5) Streptococcal chemokine protease 6) Steptolysin O 7) Strepolsyin S 8) Protein M 9) Polysaccharide capsule

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8
Q

Action of Hyaluronidase

A

Degrades hyaluronic acid in the subQ tissue; known as spreading factor, facilitates cellulitis/skin infection

GAS pyogenes

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9
Q

Action of Streptokinase

A

Plasminogen–>Plasmin; role in infection unclear

GAS pyogenes

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10
Q

Action of DNase

A

Degrades DNA exudate to prevent bacteria from being trapped in neutrophil extracellular traps (NETs)

GAS pyogenes

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11
Q

Action of C5a peptidase

A

Cleaves C5a; significantly impedes influx of neutrophils early in infection

GAS pyogenes

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12
Q

Action of Streptococcal chemokine protease

A

Prevents migration of neutrophils to infection site by degrading IL-8

GAS pyogenes

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13
Q

Action of Streptolysin O

A

cytotoxic, protects GAS from phagocytic killing

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14
Q

Strepolysin O hemolysis characteristics (on agar)

A

Oxygen labile, beta hemolysis only when UNDER the surface of blood agar

GAS pyogenes

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15
Q

Streptolysin S hemolysis characteristics (on agar)

A

Oxygen stable, beta hemolysis ON THE SURFACE of blood agar

GAS pyogens

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16
Q

2 distinguishing physical exam findings/symptomology of GAS phraygnitis

A

Tender, enlarged cervical lymph nodes and ABSENCE of uri symptoms (cough, rhinorrhea)

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17
Q

Specificity/Sensitivity of GAS rapid screen?

A

High specificity, low sensitivity (false negatives common)

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18
Q

Typical course of GAS pharyngitis abx?

A

10 days, patient must finish the abx

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19
Q

Why do you treat GAS pharygnitis? Most cases are self limiting

A

To prevent complications; Rheumatic fever, otitis media, mastoiditis, meningitis, retropharyngeal abscess

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20
Q

What type of GAS illness does rheumatic fever follow?

A

Only follows a pharyngitis

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21
Q

How does mastoiditis normally occur?

A

Due to an untreated otitis media and subsequent local spread

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22
Q

What is erysipelas?

A

A rapidly spreading, erythematous cutaneous swelling on the face. Sometimes in a butterfly distribution

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23
Q

Contrast necrotizing fasciits vs. cellulitis?

A

The necrotizing fasciitis won’t look that bad on physical exam; cellulits looks erythematous, swollen, etc.

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24
Q

Physical exam finding on necrotizing fasciitis (this is on the test)?

A

PAIN OUT OF PROPORTION TO EXAM

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25
Q

Difference in diagnosis of toxic shock with S. aureus vs. GAS?

A

S. aureus doesn’t require isolation of bactria; for GAS, you must isolate bacteria from a normally sterile site (blood, CSF, etc)

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26
Q

Treatment for necrotizing fasciits?

A

Surgical debridement (emergency)

27
Q

What strains of GAS are more associated with necrotizing fasciits?

A

Protein M types 1 and 3

28
Q

Immune response at site of necrotizing fasciitis?

A

Paucity of neutrophils due to GAS degradation of IL-8

29
Q

Symptoms of advanced necrotizing fasciitis infection?

A

Fever, tachycardia, systemic toxicty

30
Q

What does crepitus indicate?

A

There is a necrotizing fasciits; anaerobes are producing CO2 in the subQ

31
Q

What toxin causes scarlet fever?

A

Erythrogenic toxin (superantigen)

32
Q

What GAS toxin causes TSS?

A

Pyrogenic exotoxin A

33
Q

What GAS toxin causes necrotizing fasciits (most commonly)?

A

Exotoxin B

34
Q

Who does scarlet fever affect?

A

Children

35
Q

Clinical findings with scarlet fever?

A

Skin feels like “sand paper” (small papules rough to the touch), rash desquamates, STRAWBERRY TONGUE, normally occurs in association with pharyngitis

36
Q

Post-strep glomerulonephritis commonly occurs after which type of infection?

A

Skin infetion, not pharyngitis

37
Q

Does early treatment of inection prevent PSGN?

A

It is unclear

38
Q

Do most cases of PSGN come to clinical attention?

A

No, most are self limiting and relatively asymptomatic

39
Q

Physical exam/clinical findings with PSGN

A

HTN, facial edema, LE edema, dakr urine

40
Q

Onset of rheumatic fever?

A

Normally 2 weeks post untreated GAS pharyngitis

41
Q

Mechanism/Pathophysiology of acute rheumatic fever?

A

Molecular mimicry, antibodies cross react with host antigens

42
Q

JONES criteria for acute rheumatic fever diagnosis?

A

J- Joints, polyarthitis

O-Cariditis (O looks ike a heart)

N- Nodules (subQ)

E- Erythema Nodosum (pink rash on the trunk)

S- Sydenham chorea (abrupt involuntary movement)

43
Q

What lab finding aids in the diagnosis of rheumatic fever?

A

ASO titer; correlates to recent GAS infection

44
Q

Strep agalactiae (GBS) morphology

A

Narrow zone of beta hemolysis; lacks hydolysis on bile esculin agar; hydrolyzes hippurate; bacitracin RESISTANT; CAMP test (+)

45
Q

Bacitracin test. What are you distinguishing between?

A

GAS (sensitive) and GBS (resistant)

46
Q

Where is GBS normally found?

A

Genital tract of some women, also the colon

47
Q

How are neonates infected with GBS?

A

Acquired in utero or directly when passing through the vagina

48
Q

What diseases do GBS cause in neonates?

A

Meningitis, sepsis, and PNA

49
Q

Prevention of GBS infection in neonates

A

Screen women at 35-37 weeks gestation; Penicillin G/Ampicillin at time of delivery for those positive

50
Q

Charactersitic appearance of GDS (enterococcus) on bile-esculin agar?

A

Hyrdolyzes esculin producing black pigment

51
Q

Growth in hypertonic saline is characteristic of enterococcus or strep bovis?

A

Enterococcus

S. bovis will not grow in hypertonic saline.

  • both will lyse bile
52
Q

What infections do enterococcus faecalis/faecium commonly cause?

A

Hospital-acquired UTIs (extremely common), blood stream infections (line-related), endocarditis, and intra-abdominal infection

53
Q

Patient has a Strep bovis/gallolyticus infection. What do you do next?

A

Screen them for Colon cancer; extremely high association

54
Q

Growth of streptococcus bovis/gallolyticus in hypertoni saline?

A

Will NOT grow

55
Q

Most common cause of ACUTE bacterial endocarditis?

A

Staph aureus

56
Q

Virdans group strep morphology

A

Alpha hemolytic; resistant to lysis by bile; optochin RESISTANT

57
Q

Where do you normally find virdans group strep?

A

Normal flora of the mouth and colon

58
Q

What does streptococcus mutans (Virdans group) commonly cause?

A

Dental caries and subacute bacterial endocarditis after oral surgery

59
Q

Optochin test. What are you distinguishing between?

A

Strep pneumo (SENSITIVE) and Virdans group (RESISTANT)

60
Q

Most common cause of SUBACUTE bacterial endocarditis?

A

Virdans group strep

61
Q

Are abscesses normally monomicrobial or polymicrobial?

A

Polymicrobial

62
Q

Brain abscess from oral source. Which 2 bacteria?

A

Virdans group or peptostreptococcus

63
Q

Describe Janeway lesions

A

Microabscesses caused by septic emboli (seen in endocarditis); NOT PAINFUL

64
Q

Describe Osler Nodes

A

Immune complex deposition on the fingers and toes; PAINFUL