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Flashcards in Micro of Strep - Cross Deck (64):
1

Generalized morphology of streptococci?

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

2

Group A strep also known as?

Strep Pyogenes

3

Group B strep also known as?

Strep agalactiae

4

3 bugs in Group D strep?

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

5

Diagnosis of GAS?

Do a rapid swab and a culture at time of presentation

6

Diseases that GAS most commonly causes?

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

7

GAS virulence factors (there are 9)

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

8

Action of Hyaluronidase

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

GAS pyogenes

9

Action of Streptokinase

Plasminogen-->Plasmin; role in infection unclear

GAS pyogenes 

10

Action of DNase

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

GAS pyogenes 

11

Action of C5a peptidase

Cleaves C5a; significantly impedes influx of neutrophils early in infection

GAS pyogenes 

12

Action of Streptococcal chemokine protease

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

GAS pyogenes 

13

Action of Streptolysin O

cytotoxic, protects GAS from phagocytic killing

14

Strepolysin O hemolysis characteristics (on agar)

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

GAS pyogenes 

15

Streptolysin S hemolysis characteristics (on agar)

Oxygen stable, beta hemolysis ON THE SURFACE of blood agar

GAS pyogens 

16

2 distinguishing physical exam findings/symptomology of GAS phraygnitis

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

17

Specificity/Sensitivity of GAS rapid screen?

High specificity, low sensitivity (false negatives common)

18

Typical course of GAS pharyngitis abx?

10 days, patient must finish the abx

19

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

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

20

What type of GAS illness does rheumatic fever follow?

Only follows a pharyngitis

21

How does mastoiditis normally occur?

Due to an untreated otitis media and subsequent local spread

22

What is erysipelas?

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

A image thumb
23

Contrast necrotizing fasciits vs. cellulitis?

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

24

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

PAIN OUT OF PROPORTION TO EXAM

25

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

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

26

Treatment for necrotizing fasciits?

Surgical debridement (emergency) 

27

What strains of GAS are more associated with necrotizing fasciits?

Protein M types 1 and 3

28

Immune response at site of necrotizing fasciitis?

Paucity of neutrophils due to GAS degradation of IL-8

29

Symptoms of advanced necrotizing fasciitis infection?

Fever, tachycardia, systemic toxicty 

30

What does crepitus indicate?

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

31

What toxin causes scarlet fever?

Erythrogenic toxin (superantigen)

32

What GAS toxin causes TSS?

Pyrogenic exotoxin A

33

What GAS toxin causes necrotizing fasciits (most commonly)?

Exotoxin B

34

Who does scarlet fever affect?

Children

35

Clinical findings with scarlet fever?

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

36

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

Skin infetion, not pharyngitis 

37

Does early treatment of inection prevent PSGN?

It is unclear 

38

Do most cases of PSGN come to clinical attention?

No, most are self limiting and relatively asymptomatic

39

Physical exam/clinical findings with PSGN

HTN, facial edema, LE edema, dakr urine 

40

Onset of rheumatic fever?

Normally 2 weeks post untreated GAS pharyngitis 

41

Mechanism/Pathophysiology of acute rheumatic fever?

Molecular mimicry, antibodies cross react with host antigens 

42

JONES criteria for acute rheumatic fever diagnosis?

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

What lab finding aids in the diagnosis of rheumatic fever?

ASO titer; correlates to recent GAS infection

44

Strep agalactiae (GBS) morphology

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

45

Bacitracin test. What are you distinguishing between?

GAS (sensitive) and GBS (resistant)

46

Where is GBS normally found?

Genital tract of some women, also the colon

47

How are neonates infected with GBS?

Acquired in utero or directly when passing through the vagina 

48

What diseases do GBS cause in neonates?

Meningitis, sepsis, and PNA

49

Prevention of GBS infection in neonates

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

50

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

Hyrdolyzes esculin producing black pigment

51

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

Enterococcus

S. bovis will not grow in hypertonic saline. 

- both will lyse bile

52

What infections do enterococcus faecalis/faecium commonly cause?

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

53

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

Screen them for Colon cancer; extremely high association 

54

Growth of streptococcus bovis/gallolyticus in hypertoni saline?

Will NOT grow

55

Most common cause of ACUTE bacterial endocarditis?

Staph aureus

56

Virdans group strep morphology

Alpha hemolytic; resistant to lysis by bile; optochin RESISTANT 

57

Where do you normally find virdans group strep?

Normal flora of the mouth and colon

58

What does streptococcus mutans (Virdans group) commonly cause?

Dental caries and subacute bacterial endocarditis after oral surgery

59

Optochin test. What are you distinguishing between?

Strep pneumo (SENSITIVE) and Virdans group (RESISTANT)

60

Most common cause of SUBACUTE bacterial endocarditis?

Virdans group strep 

61

Are abscesses normally monomicrobial or polymicrobial?

Polymicrobial

62

Brain abscess from oral source. Which 2 bacteria?

Virdans group or peptostreptococcus 

63

Describe Janeway lesions

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

64

Describe Osler Nodes

Immune complex deposition on the fingers and toes; PAINFUL