Hdm Test 4: S. Aureus Skin Infections

Front 1

Common areas of Staph aureus

Back 1

anterior nares, skin, pharyngeal cavity, GI tract

(generally hairy, mucosal areas)

Front 2

Most predictive variable for invasive disease

Back 2

nasal colonization

Front 3

3 classes of colonized patients

Back 3

persistent (same and keeps)
Intermittent
Non-carriers

Front 4

Most common location for staph aureus

Back 4

skin

Front 5

Infected pilosebaceous unit, can also get apocrine glands

Back 5

folliculitis (will remain after popping)

Front 6

Boil, folliculitis that gets into subQ layer

Back 6

furuncle

Front 7

Coalescing furuncles; closest to blood supply

Back 7

carbuncle (warm compress and drainage)

Front 8

Which superficial skin infection should be treated with antibiotics?

Back 8

Carbuncles, close to vasculature

Front 9

2 main forms of impetigo

Back 9

non-bullous (honey coated)
bullous (almost completely by staph aureus)

Front 10

2 Key signs for bullous impetigo

Back 10

yellow pus
Nikolsky's skin (rubbing off separate layers)

Front 11

Systemic sloughing off of skin after staph aureus infection

Back 11

Staph Scalded Skin Syndrome aka pemphigus neonatorum (Ritter's)

Front 12

Target of exfoliative toxins in SSSS

Back 12

Desmoglein I (other desmogleins assist as you move further down deeper)

Front 13

10% of breastfeeding mothers have this infection

Back 13

mastitis

Front 14

superficial cellulitis, "peau d'orange" appearance

Back 14

erysipelas (mild cellulitis)

Front 15

Deeper infection, lacks erysipelas presentation, more painful than erisypelas

Back 15

cellulitis

Front 16

Acute febrile illness, hypotensive, organ dysfunction, epithelial desquamation

Back 16

S. aureus Toxic Shock Syndrome

(needs iron availability)

Front 17

Underlying cause of Toxic Shock Syndrome

Back 17

presense of TSST-1 superantigen

bypasses T-cell: antigen specificity, activating up to 20% of T-cell population W/ massive cytokine response

Front 18

Toxins causing Bullous impetigo/Scalded skin syndrome

Back 18

exfoliative toxins (Eta, Etb)

Front 19

3 components of S. aureus bacteremia needed for survival

Back 19

capsule
antimicrobial peptide resistance
survival within neutrophil (key to danger)

Front 20

Colonization of heart valves, chamber septae, and/or vessel walls; Binds to damage mediated by FnbAB and/or ClfAB

Back 20

infective endocarditis

Front 21

Symptoms of endocarditis

Back 21

fever w/ hear murmur
petuchiae (in eyes)
splenomegaly

Front 22

Which sided endocarditis is more common in IV drug users?

Back 22

right-sided (knicks tricuspid valve, leading to pulmonary emboli

Front 23

Which sided endocarditis is more difficult to treat?

Back 23

Left sided

Front 24

Necrotizing pneumonia is often partnered with what?

Back 24

Influenza (70% of superinfections caused by S. aureus)

-PVL also common

Front 25

Differences in small colony varients

Back 25

slow growing, no gold sheen, not B-hemolytic
-tolerant of antibiotics

Front 26

2 common presentations of S. aureus small colony variants

Back 26

osteomyelitis (live intracellularly)
pneumonia/cystic fibrosis

Front 27

Common bones for osteomyelitis

Back 27

long bones in children
vertebrae in adults

Front 28

septic arthritis

Back 28

S. aureus most common cause in children, non-gonococcal septic arthiritis

Front 29

alpha toxin role for staph aureus

Back 29

pore-forming, causes B-hemolysis

Front 30

Key for gamma toxin variant, selective for human PMNs

Back 30

Panton-Valentine leukocidin

Front 31

Role of delta toxin

Back 31

pore forming

Front 32

Why so many toxins?

Back 32

Maintain separation of immune cells and staph aureus

Front 33

General type of staph aureus infections

Back 33

extracellular, produce lots of

Front 34

Role of MSCRAMMs

Back 34

Adherence

Front 35

Role of Protein A, spa

Back 35

binds Fc portion of IgG/B cell receptor

Front 36

Porphyrin acquisition use in staph aureus

Back 36

iron/nutrients

Front 37

S. aureus innate immune response evasions

Back 37

inhibits opsonophagocytosis (blocks complement activation)
resists PMN killing (resists peptides)

Front 38

How are surface structures on Staph anchored?

Back 38

sortase

Front 39

Location of problems within staph aureus

Back 39

pathogenecity islands (probably moved by phages)

Front 40

3 families of S. aureus plasmids

Back 40

rolling circle family
pSK639 family
multiresistance family

Front 41

Alternative transpeptidase gene

Back 41

mecA (from chickens)

Front 42

In general, where did community MRSA develop? Which key one did not?

Back 42

Generally in the community, except for USA300 which is one of the most common forms now in both hospital and community

Front 43

Common presentation of CA-MRSA

Back 43

skin and soft tissue

Front 44

Tx for CA-MRSA

Back 44

trimethoprim-sulfonamide
clindamycin (can have inducible resistance)
Vancomycin

Front 45

What should not be used with a positive D-test?

Back 45

clindamycin

Front 46

Key differentiating test for staph

Back 46

positive coagulase test

Front 47

Normal cause of non-bullous impetigo

Back 47

GAS, increasingly by s. aureus

Front 48

cause of staph food poisoning

Back 48

emetic toxins (SEA-SEU), T-cell over-activation

Front 49

Acute infection, usually painless;
lots of swelling in hip, shoulder, knee, or elbow

Back 49

Bursitis

Front 50

3 purposes of Toxins/hemolysins: HIa, HIb, HIg PVL, HId PSMs

Back 50

cytotoxic to leukocytes/erythrocytes
phagocyte avoidance
nutrient release

Front 51

Purpose of immunomodulation

Back 51

Spa surface structures

Front 52

Isd surface structure purpose

Back 52

Fe2+ acquisition

Front 53

What do CHIPS, SCIN, SAK do for S. aureus?

Back 53

resist opsonophagocytosis

Front 54

What do Dlt and Mpr protect against?

Back 54

antimicrobial peptides

Front 55

Purpose of carotenoid pigment

Back 55

antioxidant