Streptococci Flashcards

1
Q

How to diff staph and strep

A

Staph is cat +

Strep is cat -

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2
Q

What enhances strep growth?

A

Blood or serum enhances growth

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3
Q

Which strep are a-hemo and which are B-hemo?

A

a-hemo:

  1. S. pneumoniae
  2. S. veridans

B-hemo:

  1. S. pyogenes (GAS)
  2. S. agalactiae (GBS)
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4
Q

Both S. pneumoniae +

S. veridans are a-hemolytic bacteria, how do you diff them?

A
  1. S. pneumoniae
    - optochin sensitive
  2. S. veridans
    - optochin resistant
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5
Q

Hemolysis type of E. faecalis

- where are they found

A

None

-found in intestinal tract of man and animals

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6
Q

Major virulence of S. pyogenes

A

M protein

  • Phagocytes do no ingest and kill strains w/ M protein
  • Primarily at N terminus
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7
Q

How do we kill M protein?

A

Antibody against Mprotein allows killing

  • Ab protection is serotype specific
  • 80 diff M protein serotypes =(
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8
Q

Streptolysin O

A

oxygen labile hemolysin (hemolytic)

Binds to RBC membranes –> polymerize into polymer –> inserts into pore –> cell lysis –> release lysosomal enzymes

Cardiotoxic in animals

Antistreptolysin I (ASO) antibody increases after infxn –> implies greater risk for ARF (not APSGN).

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9
Q

Spreading factors of GAS

A
  1. Streptokinase
  2. Hyaluronidase
  3. DNAse
  4. Proteinase
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10
Q

Streptolysin S of GAS are virulent how?

A

Hemolytic

Cytotoxic

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11
Q

Pyrogenic exotoxins A, B, C of GAS are virulent how?

A

Fever
Rash
Shock

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12
Q

Streptokinase of GAS are virulent how?

A

Activates plasminogen –> plasmin

Plasmin lyses thrombin + fibrin clots

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13
Q

Hyaluronidase of GAS are virulent how?

A

dissolves ground substance of connective tissue

–> facilitate spread through tissue planes

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14
Q

DNAase of GAS are virulent how?

A

Dissolves DNA

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15
Q

Proteinase of GAS are virulent how?

A

proteolytic destruction

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16
Q

Well demarcated deep erythema is due to what?

A

GAS probably

17
Q

GAS infxns manifest as what?

A

Pus forming infxns
- pneumonia, osteomyelitis, cellulitis

Acute rheumatic fever

Post strep glomerulonephritis

18
Q

Acute rheumatic fever (ARF)

A

Nonsuppurative complication of S. pyogenes

Inflammation of heart valve, skin, joints, CNS

Models like AUTOIMMUNE disease (Type II)
- S. pyogenes is not recovered from site of inflammation

19
Q

PSGN

A

Nonsuppurative complication of S. pyogenes

Onset 2-4 weeks after infxn/inflammation of kidney (glomeruloneph)

Models like IMMUNE COMPLEX disease (type III)
- S. pyogenes is not recovered from site of inflammation

20
Q

Prevention by therapy of acute infection can prevent which, ARF or PSGN?

A

ARF

Cant really prevent PSGN with preventive therapy

21
Q

Which is genetic, ARF or PSGN? What seasons?

A

ARF is familial- winter/spring

PSGN not familial - summer

22
Q

ARF or PSGN:

  1. Any age
  2. Males>Females
  3. Pharynx only
  4. Recurrance with reinfxn
  5. Relation to ASO titer
A

Any age - PSGN

Males>Females - PSGN

Pharynx only - ARF

Recurrance with reinfxn - ARF

Relation to ASO titer - ARF

23
Q

ARF:
age typically affected
site of infxn

A

any age, but rare in infants and elderly

pharynx only (PSGN can be in pharynx OR skin)

24
Q

Pathogenesis of PSGN

A

Some M types associated with increased risk of PSGN

Small filterable IMMUNE COMPLEXES are formed and trapped beneath the glomerular basement membrane

Complement deposition and neutrophil recruitment results in damage to kidney

25
Q

what % of healthy women have rectum/vagina colonized with GBS?

A

20-25%

  • baby acquires colonization passing through birth canal
  • 1/100 baby who acquire colonization develop serious invasive disease
26
Q

not a spreading factor for GAS (S. pyogenes)

A

streptolysin O
- binds cholesterol in RBC –> polymerize –> inserts into pore and lyse RBC

*exotoxin of S. pyogenes (GAS)

27
Q

ARF typically occurs this long after acute GAS infxn

A

3-6 weeks

28
Q

What type of GBS can be

A

Early onset disease

29
Q

Virulence factors and toxins of GBS

A
  1. Neuraminidase
  2. C protein
  3. B hemolysin
  4. Protease
  5. Hyaluronidase

Lipotechoic acid causes adherence
(M, T, R proteins are absent)

30
Q

How do humans protect against GBS?

A

Antibody against capsular polysaccharides mediates protection
- Ab is serotype specific

31
Q

Enterococci colonize the nl GI tract, Upper resp tract, GU tract, and skin. They have inherent resistance to what?

A
Cephalosporins
PCN
AG
tmp/smx
Clindamycin
  • inducible transferable high level vancomycin resistance (VRE)
  • these are part of nl flora and are opportunistic in nature
32
Q

Strep Veridans are found where?

A

nl flora in pharynx

- cause dental caries and endocarditis

33
Q

Most common cause of bacterial pneumonia

A

Streptococcus pneumoniae

34
Q

Pharyngitis can result in ____ (129)

A

ARF and PSGN

*Pharyngitis can result from general infxn

35
Q

PSGN is more commonly caused by (pick one) Impetigo/Pharyngitis

A

Impetigo

*pharyngitis can result in PSGN but not as much as impetigo

36
Q

ARF and PSGN occurs how many weeks after initial infxn?

A

ARF: 3-6 weeks
(master chef)

PSGN: 2 weeks
(Puffy cola colored guy)