Micro of Staph - Cross Flashcards Preview

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Flashcards in Micro of Staph - Cross Deck (47):
1

What do all Staph have that helps you identify them vs. strep?

Catalase (can degrade H2O2)

2

What type of infection(s) does Staph epidermidis normally cause?

Prosthetic hardware/IV catheter infections, endocarditis

3

What type of infection(s) does Staph saprophyticus cause?

UTI; 2nd most common cause

4

People with arthritis or other joint damaging diseases are at increased risk for osteomyelitis. Why?

Joint damage exposes underlying fibronectin/laminin, Staph aureus can easily adhere to the glycoproteins

5

What area of the skeleton is especially vulnerable for osteomyelitis due to arthritis?

The vertebral column (lumbar especially)

6

What is the carrier state?

Individual harbors a potential pathogen and can be a source of infection for others

7

What is colonization?

Acquisition of a new organism and it may cause infection

8

What is colonization resistance?

Nonpathogenic resistant bacteria occupy attachment sites interfering with pathogenic bacterial colonization

9

Gram stain of S. aureus?

Gram positive cocci in clusters (grapelike)

10

Morphology of S. aureus?

Beta hemolytic; catalase(+), coagulase(+), ferments mannitol

11

What gene contains the sequence for the altered PBPs that confers methicillin resistance?

MecA

12

What serum do they use in the lab for the coagulase test?

Rabbit serum (she said to know this)

13

Where is the main site of colonization (on the body) for S. aureus?

The nose

14

Name all the S. aureus virulence factors (there are 10)

1) Staphyloxanthin
2) Coagulase
3) Hemolysins
4) Portein A
5) Teichoic Acid
6) Polysaccharide capsule
7) Peptidoglycan
8) Alpha toxin/Hemolysin
9) Panton Valentine (P-V) leukocidin
10) Gamma toxin/leukotoxin

15

What does staphyloxanthin do? What does it specifically do to the bacteria when on agar?

It inactivates superoxides produced by WBCs; it confers the gold color unique to S. aureus

16

What does coagulase do?

converts prothrombin-->thrombin; this delays neutrophil migration

17

What do hemolysins do?

Hemolyse RBCs and use their Fe2+ to grow

18

What does Protein A do?

Binds to the Fc portion of IgG to prevent complement activation; no C3b is produced so phagocytosis is greatly impaired

19

What do teichoic acids do?

Mediate the adherence of staph to mucosal cells

20

What does peptidoglycan do?

Stimulates macrophages to produce cytokine storm/activate complement; causes the "septic shock" picture seen in S. aureus bacteremia

21

What does P-V leukocidin do?

Pore forming cytotoxin that kills leukocyte by cell membrane disruption and causes tissue necrosis

22

What diseases specifically does P-V leukocidin allow S. aureus to cause?

Necrotizing PNA and severe soft tissue/skin infection

23

What does gamma-toxin/leukotoxin do?

Lyses phagocytes/RBCs

24

What bacteria almost always causes an abscess?

S. aureus

25

What virulence factors cause scalded skin syndrome?

Exfoliative toxins A and B

26

What age group is scalded skin syndrome commonly seen in?

Newborns, 3-7 days of age

27

What do exfoliative toxins A and B do to the body?

Protease that cleaves desmoglein; separates the epidermis at the granular layer

28

What toxin causes S. aureus induced food poisoning? Describe the illness

Enterotoxin A; vomiting and watery, NON-BLOODY diarrhea

29

Why is enterotoxin A so virulent?

It is heat resistant (brief cooking won't destory it) and it is resistant to stomach acids

30

Describe bullous impetigo

Seen in young children; flaccid bullae with clear yellow fluid that later becomes more turbid; rupture will leave behind a thin brown crust, commonly on the TRUNK

31

What is the pathogenesis of Staph toxic shock syndrome?

Toxin mediated/superantigen, elicits large amount of IL-1, IL-2, and TNF-a release

32

Common scenarios causing staph toxic shock syndrome?

Tampon use, nasal packing to stop epistaxis, post-op infection

33

Blood cultures in Staph aureus toxic shock syndrome?

NEGATIVE 95% of the time

34

Lethal complication of toxic shock syndrome, commonly seen in bacteremia (I know this question sucks)?

DIC

35

Resistance seen in MRSA (mechanism of resistance)?

Change in PBPs in the cell membrane

36

Resistance seen in VRSA (mechanism of resistance)?

D-ala replaced with D-lactate; vancomycin can no longer affect it

37

Resistance seen in VISA (mechanism of resistance)?

Synthesis of unusually thickened cell well

38

What is the D-test?

Culture bacteria on a plate with a disk of clindamycin and one of erythromycin. If area around the clinda is "D-shaped" the test is +, indicates inducible resistance (DON'T USE CLINDA)

39

Generalized tx guidelines for Toxic shock syndrome?

Aggressive fluid replacement therapy, vasopressors (can cause distal necrosis). Abx and surgical debridement, if necessary

40

Why do you use clindamycin in the treatment of TSS? What other abx shares the same function?

It suppresses toxin synthesis; can also use Linezolid

41

Morphology of Staph epidermidis?

Catalase(+), Coagulase(-), non-hemolytic, urease(+), does NOT ferment mannitol, Novobiocin sensitive

42

What is the main pathogenic mechanism of staph epidermidis?

It has adhesins for interaction with surface proteins; once it attaches to a catheter or prosthetic device it secretes a polysaccharide biofilm (insulates it from phagocytosis/abx)

43

You get a blood culture positive for Staph epidermidis. The patient is afebrile and in no distress. What do you think?

Contamination; Staph epi is all over the skin and commonly contaminates blood cultures

44

Staph saprophyticus morphology?

Catalase(+), Coagulase(-), non-hemolytic, urease(+), does NOT ferment mannitol, Novobiocin resistant

45

Novobiocin test. Distinguishing between which bacteria?

Staph epidermidis (SENSITIVE) vs. Staph saprophyticus (RESISTANT)

46

What 2 morphologic characteristics distinguish S. aureus form all other staphylococci?

Coagulase (+) and B-hemolysis

47

Pathogenesis of enterotoxin-A mediated food poisoning

Superantigen in the GI tract, causes massive IL-1 and IL-2 release from macrophages/helper T cells