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Cardio > Strep Micro Lecture 2 > Flashcards

Strep Micro Lecture 2 Flashcards

1
Q

The three strep that are most important human pathogens are:

A

Streptococcus pyogenes (group A strep)
S. agalactiae (group B strep)
S. pneumoniae

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2
Q

Strep grows in what conformation?

A

chains

if very short = diplococci

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3
Q

What types of strep are alpha hemolytic?

A

S. pneumococci

viridans strep such as S. mitis, S. mutans

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4
Q

What types of strep are beta hemolytic?

A

S. pyogenes

S. agalactiae

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5
Q

What types of strep are gamma hemolytic?

A

S. salivarius

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6
Q

What are the growth requirements for strep?

A

Facultative anerobes (can make ATP by aerobic respiration when oxygen is present, but can switch to fermentation if oxygen is not present)

Fastidious (need amino acids, vitamins, etc.)

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7
Q

S. pyogenes is group ____ strep and ____-hemolytic

A

A

beta

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8
Q

S. agalactiae is group ____ strep and ____-hemolytic

A

B

beta

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9
Q

What isn’t typable by the Lancefield system?

A

S. pneumoniae (pneumococcus)

viridans strep (S. mutans, S. sanguis, S. mitis, S. salivarius, etc.)

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10
Q

Strep are catalase (+/-) and oxidase (+/-)

What is the significance?

A
  • and -
    staph are catalase +
    neisseria are oxidase +
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11
Q

Viridans and enterococci are ___-hemolytic

A

alpha

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12
Q

What are some pretty freaking serious Group A Streptococcal Diseases?

A

toxic shock

necrotizing fasciitis

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13
Q

What causes rheumatic heart disease?

A

pharyngitis from S. pyogenes

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14
Q

What causes acute glomerulonephritis?

A

S. pyogenes (often) following skin infection

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15
Q

What are SLO and SLS?

A

potent virulence factors

SLS is oxygen stable; responsible for hemolysis surrounding colonies on the surface of blood agar plate

SLO is oxygen sensitive; responsible for the clearings below the surface of the agar

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16
Q

What is hyaluronic acid capsule?

A

group A strep virulence factor which prevents phagocytosis

Structurally similar to human hyaluronic acid, thus there are no antibodies produced against it

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17
Q

What is M protein?

A

group A strep virulence factor which is:

  1. a major antiphagocytic factor in most strains; binds fibrinogen and other host proteins that mask the bacteria from the immune system
  2. an adhesin
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18
Q

What is lipoteichoic acid?

A

group A strep virulence factor which is thought to be an adhesin

aids in group A strep binding to mucosal surfaces in the host, but it is also a PAMP (activates innate immune system)

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19
Q

What is the difference between the N and C terminus in protein M?

A

C-terminal half is conserved

N-terminus varies under immune pressure, forms the basis for serotyping

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20
Q

What are the strep superantigens?

A

Streptococcal pyrogenic exotoxin A
Streptococcal pyrogenic exotoxin B
(there are others)

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21
Q

How does pharyngitis spread?

A

droplets, especially in a crowd (asymptomatic carriage rates are 15-30%)

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22
Q

Should you treat strep pharyngitis?

A

it’s self-limiting, but you should treat with penicillin to decrease the risk of developing ARF

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23
Q

Acute rheumatic fever follows:

A

strep pharyngeal infections, not skin infections

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24
Q

How does M protein relate to recurrence of strep pharyngitis?

A

When pharyngitis occurs again, it will be from a different M type strain of S. pyogenes

The patient has antibodes against the previous strand’s M (which bind to the amino terminus of the M protein)

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25
Q

Why is endometritis, or puerperal fever, uncommon now?

A

we wash our hands…

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26
Q

Who common becomes infected with group A strep impetigo?

A

kids, especially after insect bites (kids have strep on their fingers, then scratch the bites)

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27
Q

What is a pyoderma?

A

an infection of the skin that produces pus

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28
Q

How does group A strep impetigo present?

A

weeping vesicles with honey-colored crusts

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29
Q

What is ecthyma?

A

a form of impetigo that has invaded more deeply, forming round lesions with pus and ulceration in the center

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30
Q

What is erysipelas? What does it look like?

A

form of strep cellulitis that involved both the dermis and epidermis

“fiery red” erythema and edema with rapidly advancing, well-demarcated edges

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31
Q

What are the symptoms of erysipelas? (4)

A

rapid-onset of cheek redness
pain
fever
lymphadenopathy

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32
Q

Erysipelas normally affects:

A

kids and elderly

33
Q

How are staph and strep cellulitis different?

A

staph: usually associated with localized infection (folliculitis, foreign body, etc)
strep: spreads more rapidly and usually has fever and lymphangitis

34
Q

What are the symptoms of strep cellulitis?

A

localized pain
erythema
swelling
heat

35
Q

Why would a strep cellulitis have a negative blood culture?

A

a small number of bacteria secreting toxins can cause this

36
Q

What is necrotizing fasciitis? How serious is it?

A

deep tissue infection that spreads along the fascial planes

can be life threatening–40-70% mortality

37
Q

What causes strep toxic shock and necrotizing fasciitis, and how does it progress from there?

A 
innocuous infection (bruise,  skin trauma)
Necrosis then progresses quickly (~1 inch per hour)
38
Q

What symptoms is very indicative of strep toxic shock and necrotizing fasciitis?

A

extreme pain out of proportion to the appearance of the lesion
(crescendo pain: rapid ramping up of the degree of pain)

39
Q

What are the early and later signs of strep toxic shock and necrotizing fasciitis?

A

early:
flu-like symptoms
brawny edema
extreme pain out of proportion to lesion

later:
spreading erythema
eccymosis (hematoma) with vesicles enlarging to purple bullae

40
Q

What is the proper treatment for strep toxic shock and necrotizing fasciitis?

A

Debridement

Aggressive use of broad spectrum abx immediately–penicillin and clindamycin if S. pyogenes is detected

Massive amounts of IV fluids may be needed

Monitor CO closely

41
Q

What causes the shock related to strep TSS and necrotizing fasciitis?

A
  1. streptococcal pyrogenic exotoxins

2. peptidoglycan fragments, lipoteichoic acid, etc

42
Q

Why is clinda very useful in strep TSS?

A

protein synthesis inhibitor – does not break down cell walls.

Therefore: less peptidoglycan, LTA and other cell wall substances released (innate immune system is not activated so broadly)

43
Q

What is usually different about the appearance of strep TSS versus staph TSS?

A

Streptococcal toxic shock causes a widespread rash that blanches when pressure is applied

44
Q

How do you confirm a diagnosis of strep TSS?

A
  1. Isolate GAS from a clinically significant specimen in a hypotensive pt (SBP <90)
  2. Two/more of the following:
    - -renal impairment
    • -coagulopathy
    • -liver dysfunction
    • -acute respiratory distress syndrome
    • -generalized eryth macular rash
      • -soft-tissue necrosis (NF, myositis or gangrene)
45
Q

What is a fulminant infection?

A

one occurring suddenly and quickly, and one that is intense and severe to the point of lethality

46
Q

What are the non-suppurative sequelae of S. pyogenes?

A

ARF and AGN

47
Q

Usually develops in young children after pharyngitis:

A

ARF

48
Q

What are the major manifestations listed in the guidelines for diagnosis of ARF (Jones Criteria)?

A

*Carditis
*Polyarthritis
Chorea
Erythema marginatum
Subcutaneous nodules (uncommon)

49
Q

What are the minor manifestations listed in the guidelines for diagnosis of ARF (Jones Criteria)?

A 
Arthralgia
		Fever
		elevated ESR
		elevated CRP
		Prolonged PR interval
50
Q

Non-suppurative sequelae of S. pyogenes are most frequent in:

A

children 5-15

51
Q

Usually develops after throat or skin infection:

A

acute glomerulonephritis

52
Q

What titer is high in non-suppurative sequelae of S. pyogenes?

A

anti-SLO

53
Q

What are the major clinical findings listed in the guidelines for diagnosis of AGN?

A

Edema
Hypertension
Malaise, headache
Back pain

54
Q

What are the major lab findings listed in the guidelines for diagnosis of AGN?

A 
Ig 
complement C3 
strep antigens
Hematuria (rust-colored urine)
Proteinuria
55
Q

How are kidneys affected by AGN?

A

Increased glomerular intracapillary cellularity

Almost all glomeruli involved, some tubules

56
Q

Treatment of AGN:

A 
Benzathine penicillin (slow-release)
**no treatment alters long-term prognosis, treat to manage acute kidney problems
57
Q

Treatment of most S. pyogenes infections:

A

penicillin

For patients with allergies: clindamycin, azithromycin

58
Q

Treatment of serious/invasive S. pyogenes infections:

A

Initiate broad spectrum abx if Group A strep is identified: high levels of penicillin and clindamycin (which is more effective in deep infections)

Surgical debridement required

IVIG (may protect against superantigens)

SUpportive therapy (fluids to treat hypotension, dialysis for renal failure, etc)

59
Q

What does GBS cause (but this is declining)?

A

septicemia and meningitis in neonates and infants <3mo

pregnancy-related morbidity

60
Q

GBS are resistant to:

A

Bacitracin

61
Q

What is CAMP factor?

A

GBS factor which synergizes with S. aureus hemolysin to cause increased lysis of red cells

62
Q

What substance is hydrolyzed by GBS (thus a useful test)?

A

Bile esculin

63
Q

What is an example of a GBS?

A

S. agalactiae

64
Q

5 VFs in GBS?

A
  1. Capsule (serves as an antiphagocytic factor and reduces adhesion); *major
  2. Adhesins:
    a-protein
    fibrinogen-binding proteins (FbsA, FbsB)
  3. Surface beta-protein (binds factor H and downregulated complement deposition)
  4. beta-hemolysin (damage cells if bacteria evade phagocytosis)
  5. peptidoglycan and lipotechoic acid (stimulate cytokine secretion)
65
Q

What does neonatal GBS cause? Who is infected?

A

Septicemia, respiratory distress, meningitis

7 days or younger (often pre-term) whose mothers had intraamniotic infection

66
Q

What does early GBS cause? Who is infected?

A

Bacteremia
Meningitis
Permanent neurologic sequelae

2wks to 2mos, 50% pre-term

67
Q

What has reduced incident of GBS in neonates and infants?

A
  1. Prenatal screening (35-37 weeks)

2. intrapartum IV penicillin to infected mothers and mothers with risk factors

68
Q

Viridans Streptococci are ___-hemolytic and are commonly found in:

A

alpha

plaque biofilm on teeth (normal oral flora)

69
Q

Viridans Streptococci are distinguished from enterococci by:

A

inability to grow in 6.5% NaCl

70
Q

Viridans Streptococci are distinguished from pneumococci by:

A

resistance to optochin (ethylhydrocupreine)

71
Q

Viridans Streptococci contribute to what conditions?

A

caries, periodontal disease and endocarditis (if you have damaged heart valves)

72
Q

Why do patients with damaged heart valves require prophylactic antibiotics before dental procedures?

A
  1. Transient bacteremia occurs after dental procedures (S. sanguis and other viridans strep)
  2. Damage of heart valves leads to exposure of fibronectin and deposition of fibrin and platelets
  3. Viridans strep have adhesins for fibronectin, fibrin and other host proteins that accumulate on injured valves.
  4. Once they adhere, form biofilms (vegetations)
73
Q

_____ shows reaction for Lancefield antigens, but _____ do not.

A

Enterococcus

Viridans

74
Q

What do enterococcus cause?

A

nosocomial infections, many of which are vanc-resistant

75
Q

Why are enterococcus infections problematic after a course of antibiotics?

A

killing competing organisms with antibiotics leads to overgrowth

Once they increase in number, they can gain access to lymphatics or blood

76
Q

Why are enterococci a big problem, in terms of drug resistance?

A

extremely proficient at taking up DNA (plasmids, transposons) and passing it along to other species

77
Q

When is intrapartum prophylactic penicillin not necessary?

A

planned c-section in absence of membrane rupture or negative GBS screen

78
Q

When is intrapartum prophylactic penicillin necessary?

A

Unknown GBS with:
Intrapartum temp >100.4
Amniotic membrane rupture >18h
Delivery at <37 weeks

Previous infant with GBS

Current GBS bacteremia

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