Streptococci

Question 1

How to diff staph and strep

Answer 1

Staph is cat +

Strep is cat -

Question 2

What enhances strep growth?

Answer 2

Blood or serum enhances growth

Question 3

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

Answer 3

a-hemo:

1. S. pneumoniae
2. S. veridans

B-hemo:

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

Question 4

Both S. pneumoniae +

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

Answer 4

1. S. pneumoniae
   - optochin sensitive
2. S. veridans
   - optochin resistant

Question 5

Hemolysis type of E. faecalis

- where are they found

Answer 5

None

-found in intestinal tract of man and animals

Question 6

Major virulence of S. pyogenes

Answer 6

M protein

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

Question 7

How do we kill M protein?

Answer 7

Antibody against Mprotein allows killing

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

Question 8

Streptolysin O

Answer 8

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).

Question 9

Spreading factors of GAS

Answer 9

1. Streptokinase
2. Hyaluronidase
3. DNAse
4. Proteinase

Question 10

Streptolysin S of GAS are virulent how?

Answer 10

Hemolytic

Cytotoxic

Question 11

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

Answer 11

Fever
Rash
Shock

Question 12

Streptokinase of GAS are virulent how?

Answer 12

Activates plasminogen –> plasmin

Plasmin lyses thrombin + fibrin clots

Question 13

Hyaluronidase of GAS are virulent how?

Answer 13

dissolves ground substance of connective tissue

–> facilitate spread through tissue planes

Question 14

DNAase of GAS are virulent how?

Answer 14

Dissolves DNA

Question 15

Proteinase of GAS are virulent how?

Answer 15

proteolytic destruction

Question 16

Well demarcated deep erythema is due to what?

Answer 16

GAS probably

Question 17

GAS infxns manifest as what?

Answer 17

Pus forming infxns
- pneumonia, osteomyelitis, cellulitis

Acute rheumatic fever

Post strep glomerulonephritis

Question 18

Acute rheumatic fever (ARF)

Answer 18

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

Question 19

PSGN

Answer 19

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

Question 20

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

Answer 20

ARF

Cant really prevent PSGN with preventive therapy

Question 21

Which is genetic, ARF or PSGN? What seasons?

Answer 21

ARF is familial- winter/spring

PSGN not familial - summer

Question 22

ARF or PSGN:

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

Answer 22

Any age - PSGN

Males>Females - PSGN

Pharynx only - ARF

Recurrance with reinfxn - ARF

Relation to ASO titer - ARF

Question 23

ARF:
age typically affected
site of infxn

Answer 23

any age, but rare in infants and elderly

pharynx only (PSGN can be in pharynx OR skin)

Question 24

Pathogenesis of PSGN

Answer 24

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

Question 25

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

Answer 25

20-25% - baby acquires colonization passing through birth canal - 1/100 baby who acquire colonization develop serious invasive disease

Question 26

not a spreading factor for GAS (S. pyogenes)

Answer 26

streptolysin O - binds cholesterol in RBC --> polymerize --> inserts into pore and lyse RBC *exotoxin of S. pyogenes (GAS)

Question 27

ARF typically occurs this long after acute GAS infxn

Answer 27

3-6 weeks

Question 28

What type of GBS can be

Answer 28

Early onset disease

Question 29

Virulence factors and toxins of GBS

Answer 29

1. Neuraminidase 2. C protein 3. B hemolysin 4. Protease 5. Hyaluronidase Lipotechoic acid causes adherence (M, T, R proteins are absent)

Question 30

How do humans protect against GBS?

Answer 30

Antibody against capsular polysaccharides mediates protection - Ab is serotype specific

Question 31

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

Answer 31

``` Cephalosporins PCN AG tmp/smx Clindamycin ``` * inducible transferable high level vancomycin resistance (VRE) - these are part of nl flora and are opportunistic in nature

Question 32

Strep Veridans are found where?

Answer 32

nl flora in pharynx | - cause dental caries and endocarditis

Question 33

Most common cause of bacterial pneumonia

Answer 33

Streptococcus pneumoniae

Question 34

Pharyngitis can result in ____ (129)

Answer 34

ARF and PSGN *Pharyngitis can result from general infxn

Question 35

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

Answer 35

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

Question 36

ARF and PSGN occurs how many weeks after initial infxn?

Answer 36

ARF: 3-6 weeks (master chef) PSGN: 2 weeks (Puffy cola colored guy)