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Block 7 Week 2 > Skin and soft tissue infections- Kozel > Flashcards

Skin and soft tissue infections- Kozel Flashcards

1
Q

(blank) is any skin infection that is pyogenic

A

pyoderma

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2
Q

Primary pyoderma can be (blank) or (blank)

A

purulent or non-purulent

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3
Q

What is this:

-vesicular, later crusted, superificl infection of skin

A

impetigo

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4
Q

What causes non-bullous impetigo?

A
  • streptococcus pyogenes (20-30%)
  • staphylococcus aureus (now most common)
  • mixed infection
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5
Q

What is this:
begins as erythematous papules that evolve into vesicles and pustules that rupture
Dries to form honey-colored crusts on erythematous base
typically heals without scars

A

Impetigo

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6
Q

What causes bullous impetigo?

A

strain of s. aureus producing exfoliating toxin.

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7
Q

What does the toxin of bullous impetigo do?

A

cleaves dermal-epidermal junctions

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8
Q

What is ecthyma?

A

deeper form of impetigo that presents as ulcerative pyoderma of skin

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9
Q

Ecthyma follows (blank) or (blank)

A

insect bits

minor trauma

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10
Q

What bacteria causes ecthyma?

A

S. aureus and/or S. pyogenes

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11
Q

Does ecthyma heal with scars or no scars?

A

scars

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12
Q

What is this:

collections of pus within dermis and deeper tissue

A

Cutaneous abscess

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13
Q

What bacteria causes cutaneous abscesses?

A

S. aureus, can be polymicrobial

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14
Q

What are all the purulent primary pyodermas?

A

-cutaneous abscess
-folliculitis, carbuncles, furuncles
-chancriform leions
-

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15
Q

What is this:

pyoderma located wtihin hair folicle

A

folliculitis

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16
Q

What is this:

inflammatory nodule extending into subcutaneous tissue; follows folliculitis

A

Furuncle (boil)

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17
Q

What is this:

coalescent process involving multiple follicles

A

carbuncle

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18
Q

What is the etiology of folliculitis, carbuncles, and furuncles?

A

S. aureus

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19
Q

What kind of lesions are chancriform lesions?

A

ulcerative lesion

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20
Q

Cutaneous anthrax and venereal infections are forms of (blank) lesions.

A

chancriform

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21
Q

What is this:

  • direct inoculation with bacillus anthracis
  • begins as painless pruiritic papule; enlarges, vesiculates (malignant pustule), becomes necrotic and covered by eschar
A

Cutaneous anthrax

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22
Q

What venereal infections are types of chancriform lesions?

A

treponema pallidum and haemophilus ducreyi

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23
Q

What are other infections that can cause chancriform lesions?

A

Franciscella tularensis
Mycobacterium ulcerans
Mycobacterium marinum

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24
Q

What are these:

diffuse, superficial, spreading skin infections

A

Erysipelas and cellulitis

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25
Q

Is erysipelas and cellulitis associated with collections of pus?

A

No

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26
Q

Purulent lesions (discharging pus) require (blank). (e,g abscess, furuncle, carbuncle)

A

drainage

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27
Q

Cellulitis requires (blank) therapy

A

antimicrobial

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28
Q

(blank) is an infection involving upper dermis and subcutaneous fat

A

cellulitis

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29
Q

When do you get cellulitis?

A

after trauma, or underlying skin lesion (i.e furuncle or ecthyma)

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30
Q

Describe the symptoms of cellulitis

A

Pain, erythema, involved area very red, hot, and swollen

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31
Q

What is the etiology of cellulitis?

A

Streptococci- Group A and others; less often S. aureus

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32
Q

If you see the words trauma, water contact, or animal, insect or human bites?

A

cellulitis

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33
Q

What is this:
superifical cellulitis w/ prominent lymphatic involvement
-painful; sharp demarcation from adjacent normal skin

A

Erysipelas

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34
Q

What is the etiology of Erystipelas?

A

S. pyogenes

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35
Q

What is this:
aggressive subcutaneous infection that tracks along the superficial fascia-all tissues between skin and underlying muscle

A

necrotizing fasciitis

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36
Q

Necrotizing fascitis most often is an extension from a skin (blank)

A

lesion

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37
Q

Necrotizing fasciitis is a (blank) toxicity

A

systemic

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38
Q

What is the etiology of necrotizing fasciitis?

A 
S. pyogenes
S. aureus
Vibrio vulnificus
Aeromonas hydrophila
****often polymicrobic****
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39
Q

What are other clinical forms of subcutaneous tissue infection?

A
  • syngeristic necrotizing cellulitis
  • clostridial anaerobic cellulitis
  • Misc. infections secondary to trauma
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40
Q

What are five systemic bacterial infections that produce rashes or skin lesions

A
  • bacteremia
  • leptospirosis
  • rat-bite fever
  • annular erythema
  • rocky mountain spotted fever
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41
Q

What causes bacteremia?

A

S. aureus
Group A streptococcus
N. meningitidis

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42
Q

What causes leptospirosis (Weils disease)?

A

leptospira interrogans

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43
Q

What causes annular erythema (lyme disease)?

A

Borrelia burgdorferi

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44
Q

What causes rocky mountain spotted fever?

A

rickettsia rickettsii

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45
Q

What is the rash you see in rat bite fever?

A

petechial and purpuric lesion

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46
Q

What is the rash you see in leptospirosis?

A

macropapular rash

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47
Q

What is the rash you see in lyme disease?

A

annular erythema

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48
Q

What is this:

  • follows pharyngitis by group A streptococcus,
  • streptococcal pyogenic exotoxin A (SpeA)
A

Scarlet Fever

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49
Q

What is this:

  • follows local infection by S. aureus
  • Staph exfoliating toxin
A

Scalded skin syndrome

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50
Q

What is this:

  • follows infection by staph aureus
  • staph TSST-1 superantigen
A

Toxic Shock syndrome

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51
Q

What are the infections following animal contact (6)?

A 
Cutaneous anthrax
Cat-Scratch disease
Erysipeloid
Pasteurela multocida
Bubonic plague
Tularemia
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52
Q

What causes cutaneous anthrax?

A

bacillus anthracis

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53
Q

What causes cat-scratch disease?

A

bartonella henselase

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54
Q

What causes erysipeloid?

A

erysipelothrix rhusiopathiae

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55
Q

What animals cause erysipeloid?

A

fish, marine animals, swine or poultry

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56
Q

What causes pasterurella multocida?

A

dog or cat bites

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57
Q

What causes bubonic plague?

A

yersinia pestis

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58
Q

What causes tularemia?

A

francisella tularensis

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59
Q

What is this:
wound-surgical wounds
source- nosocomial, moist environments

A

Serrtia marcesens

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60
Q

What is this:
wound-cuts and abrasions
source-fresh water

A

aeromonas spp.

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61
Q

What is this:
woud-burns
source-environmental

A

pseudomonas aeruginosa

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62
Q

What is this:
wound-cuts and abrasions
source-brackish and salt water

A

vibrio parahemolyticus

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63
Q

What is this:
wound-battlefield injuries
source-nosocomial

A

Acinetobacter baumanii

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64
Q

What is this:
wound-human bite, fistfight
source- human mouth

A

Eikenella corrodens

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65
Q

What is this:
presence of pus within individual muscle groups
usually S. aureus (90%)
most cases in tropics

A

Pyomyositis

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66
Q

What is this:

  • necrotic damage to muscle tissue
  • occurs after muscle injury and contamination with soil or other material containing spores
  • extreme pain, crepitus due to gas formation, yellowish/bronze discoloration
A

Myonecrosis/gas gangrene

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67
Q

What is the etiology of myonecrosis/gas gangrene?

A

Clostridium perfringens (most common) and other clostridial species

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68
Q

What is this:
The patient is a 6-year-old boy who presented with an apparent skin infection that began as small vesicles that rapidly pustulated and developed thick, golden-yellow crusts shown below. Culture on blood agar is also shown below. Gram stain from the culture is also shown. The patient was treated with cephalex, and the infection resolved over several days.
Three weeks after the infection, the patient developed a generalized edema and hematuria with smoky-colored urine. Physical exam found that the patient was hypertensive. A test for anti-DNAse antibodies was positive

A

poststreptococcal glomerulonephritis

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69
Q

What is this:
catalase negative
gram positive cocci in pairs or chains
typicaly require complex media-blood or serum

A

Streptococci

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70
Q

How do you classify strep?

A

hemolytic patterns on blood agar
antigenic-lancefield grouping
biochemical (physiological) properties

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71
Q

How do you classify beta hemolytic strep?

A

lancefiled grouping

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72
Q

How do you classify alpha and gamma hemolytic strep?

A

by biochemical testing

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73
Q

What is this:
Partial hemolysis - greening of agar
Numerous species: S. salivaris, S. mitis
Normal flora of mucous membranes

A

alpha hemolytic strep

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74
Q

What is this:
Complete hemolysis - clear zone
Streptolysins O and S

A

beta hemolytic

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75
Q

What is this:
No hemolysis
Misc. normal flora, opportunists and anaerobes

A

Gamma hemolytic or non-hemolytic

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76
Q

If you see carbohydrate antigen in cell well then what type of strep do you have?

A

beta hemolytic strep

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77
Q

Most human pathogens belong to group (blank) and is called strep (blank)

A

A

pyogenes

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78
Q

What groups of strep are normal flora of mucous membranes, occasional pathogens?

A

B,C,F,G,H,K,L

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79
Q

What groups of strep are in lower animals?

A

E, M, N

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80
Q

What group of strep is enterococcus, now enteroccucus faecalis

A

group D

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81
Q

Some strep with C. carbohydrate antigen may be (blank), (blank), or (blank)

A

alpha, beta or gamma

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82
Q

What diseases does S. pyogenes cause?

A

pharyngitis, pyoderma, rheumatic fever

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83
Q

What is the hemolytic pattern of strep pyogenes and what is the serological classification?

A

beta

A

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84
Q

What is the hemolytic pattern of strep agalactiae and what is the serological classification?

A

Beta

B

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85
Q

What diseases does S. agalactiae cause?

A

neonatal sepsis, meningitis

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86
Q

What is the hemolytic pattern and serological classification of strep agalactiae?

A

beta

B

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87
Q

What diseases does S. anguinosus, S. equi, etc. cause?

A

puerperal sepsis, enocarditis

88
Q

What is the hemolytic pattern and serological classification of s. anginosus, S equi etc?

A

Beta

C

89
Q

What diseases doesE. faecalis, E. faecium, E. durans (enterococci); S. bovis, S. equinus; (nonenterococci) cause?

A

endocarditis, UTI

90
Q

What is the hemolytic pattern and serological classification of E. faecalis, E. faecium, E. durans (enterococci); S. bovis, S. equinus; (nonenterococci)?

A

Alpha, beta, or nonhemolytic

D

91
Q

What diseases does S. pneumoniae cause?

A

pneumonia, otitis media, meningitis

92
Q

What is the hemolytic pattern of S. pneumonia?

A

alpha

93
Q

What diseases does S. mutans group, S. salivaris group, S. mitis group, etc cause?

A

subacute endocarditis

94
Q

What is the serological classification and hemolytic patterns of S. mutans group S. salivaris group, S. mitis group?

A

none or viridans group

Alpha or nonhemolytic

95
Q

What is the lancefield carbohydrate?

A

C carbohydrate

96
Q

What does the lancefied carb show you?

A

S. pyogenes (since all are group A)

polymer of rhamnose and N-acetyl-glucosamine

97
Q

Where in the cell do you find Lancefield carb (c carb)?

A

in matrix of cell wal

98
Q

What is this:

  • type specific
  • subdivides group A into > 100 types
  • induces type-specific protective immunity
A

M protein (found in S. pyogenes)

99
Q

What are the extracellular enzymes found in S. pyogenes?

A

streptolysin O, DNAse, hyaluronidase

100
Q

What are these caused by:

  • pharyngitis
  • skin and wound infections
  • bacteremia
  • toxemia
  • non-suppurative disease (post strep sequelae)
A

Group A strep infections

101
Q

What are the skin and wound infections of group a Strep infections?

A

impetigo
erysipelas
cellulitis
myositis and necrotizing fascitis

102
Q

What is this:

colonization of healthy skin; infection via minor trauma

A

impetigo

103
Q

What is this:

dermal infection with spreading erythema and edema

A

erysipelas

104
Q

What is this:

skin infection that involves subcutaneous tissue

A

cellulitis

105
Q

WHat is this:

skin infection that involves deep subcutaneous tissues, destruction of muscle and fat

A

myositis and necrotizing fasciitis

106
Q

What are the two types of toxemia that Group A strep infections cause?

A
  • Scarlet fever

- Toxic shock-like syndrome (TSLS)

107
Q

What are the 2 types of non-suppurative disease -post-strep sequalae caused by Group A strep infections?

A

glomerulonephritis

Rheumatic fever

108
Q

What are the four virulence factors associated with adherence?

A

Lipoteichoic acid
F protein
M protein
Hyaluronic acid capsule

109
Q

What does lipoteichoic acid do?

A

adhesion to epithelial cells

110
Q

What does F protein do?

A

binds fibronectin, adhesions to nasopharyngeal epithelial cells (sfbl -streptococcal fibronection binding protein I)

111
Q

What does M protein do?

A

binds to epithelial cells

112
Q

What does hylauronic acid capsule do?

A

facilitates adhesion to nasal mucosa

essentia for early colonization

113
Q

What are the 2 virulenc factors that avoid phagocytosis?

A

Hylaruonic acid capsule

M protein

114
Q

What is this:

  • antiphagocytic
  • essential for virulence
  • induces solid type-specific immunity; >100 types
  • Candidate for vaccine development
A

M protein

115
Q

Streptococcal pyrogenic exotoxins (Spe) can cause (blank) (blank) and (blank)

A

rash of scarlet fever
Toxic shock like syndrome (TSLS)
Superantigens

116
Q

What are other names for streptococcal pyrogenic exotoxins (Spe)?

A

Erythrogenic toxin, scarlet fever toxin

117
Q

What do superantigens of strep pyrogenes cause?

A

release of IL-1, IL-2, IL-6, TNF-alpha, IFN-gamma

118
Q

Streptococcal pyrogenic exotoxins are coded by (blank)

A

lysogenic bacteriophage

119
Q

What is this:

activates steps in inflammation and septic shock (e.g. complement cascade, cytokine secretion, coagulation cascade)

A

Lipoteichoic acid

120
Q

what are the virulence factors that cause tissue damage and spreading?

A
  • Streptolysin O
  • Streptolysin S
  • Streptokinase
  • Streptodornase
  • Hyaluronidase
121
Q

What is this:

porin; oxygen labile, antigenic, anti-streptolysin O (ASO)

A

streptolysin O

122
Q

What is this:

Oxygen stable; non-antigenic

A

Streptolysin S

123
Q

What is this:

converts plasminogen to plasmin; lyses blood clots

A

Streptokinase

124
Q

What is this:

DNAse; reduces viscosity of abscess material

A

Streptodornase

125
Q

What are these characteristics of:
strawberry tongue-> enlarged fungiform papillae
Red cheeks and pale area around the mouth
-fine, red, and rough-textured, blanches upon pressure

A

Rash of scarlet fever

126
Q

What is the exotoxin that causes fever, rash , systemic effects due to the release of superantigens that stimulate cytokine release of IL-1, IL-2, IL-6, TNF-alpha and INF-gamma

A

SpeA

127
Q

Where is the site of infection for rheumatic fever? Tell me about it

A

pharynx
prior sensitization
repeated attacks are common
need prophylaxis

128
Q

Where is the site of infection for acute glomerulonephritis? Tell me about it

A 
skin
repeated attacks are rare
nephritogenic strains M protein
complement levels decreased
caused by immune complex problem
129
Q

When do you get your specimen and what do you take?

A

before antibiotics

throat swab, pus, blood

130
Q

What are the 2 ways to do direct examination for strep?

A

gram staining

quick strep test

131
Q

Hows does the quick strep test work?

A

lateral flow technology

detects lancefield carbohydrate antigen

132
Q

What kind of isolation do you use for strep?

A

blood agar

133
Q

What are the differential tests for strep?

A 
Gram positive coccus
Beta hemolytic
Catalase negative
Bacitracin sensitive
Tests for Lancefield Group-specific antigen
134
Q

When do you use serological tests?

A

for retrospective diagnosis

135
Q

What are the 2 available assays for serologic testing?

A

Anti-streptolysin O

Anti-DNase

136
Q

What is this:
typically negative in patients with skin infections
useful for diagnosis of rheumatic fever
not helpful with glomerulonephritis

A

Anti-streptolysin O

137
Q

What is this:
antibodies produced after skin infection
particularly useful if glomerulonephritis is suspected

A

Anti-DNase

138
Q

Do serological tests imply immunity to infection?

A

no

139
Q

How do you transmit pharyngitis?

A

via airborne droplets

140
Q

How do you transmit skin infection?

A

by direct contact (hygiene is a major factor)

141
Q

What is immunity to strep like

A

long term (decades) type-specific immunity due to M protein

142
Q

How do you control strep?

A

prompt and complete treatment; eliminate carriers

143
Q

How do you treat strep infection?

A

penicillin (all strains sensitive prompt use reduces antibody response, essential that infection be treated quickly and completely)

144
Q

What are some issues associated with strep infection treatment?

A

possible mixed infection
necrotizing fasciitis
allergy
risk for rheumatic fever

145
Q

If you have mixed infection such as S. aureus presenting with your strep how should you treat this?

A

with oxacillin or vancomycin

146
Q

How do you treat necrotizing fasciitis?

A

high dose penicillin + clindamycin

need for drainage and surgical debridement

147
Q

How should you treat step if you have an allergy to penicillin?

A

clindamycin or a narrow spectrium cephalosporin; perhaps a macrolide-check current AHA recommendations

148
Q

What should you do for rheumatic fever?

A

antibiotic prophylaxis

149
Q

Is it common to have MRSA as a monomicrobial cause of necrotizing fasciitis?

A

no, it is rare

150
Q

What are the 2 species of staph that are important?

A

staph aureus

coagulase negative staph (i.e staph epidermis and other staph species)

151
Q

What are the general features of staph?

A
  • gram positive cocci in grape like clusters
  • aerobic
  • catalase positive
  • may have golden pigment
  • beta or non-hemolytic (depends on hemolysins)
152
Q

Is staph highly susceptible to physical and chemical agents?

A

no it is relatively resistant to these things

153
Q

Staph carries mutiple plasmids and bacteriophages such as (blank and blank)

A 
penicillinase (beta lactamase)
Toxin production (enterotoxin, toxic shock, etc.)
154
Q

(blank) percent of the S. aureus genome is a core genome conserved among all staph species and strains. The reaminder of genome is mobile DNA (mobile genome)

A

80

155
Q

What are the mobile DNA components of staph?

A

bacteriophage
plasmids
transposons
staph chromosomal cassette (much like a transposon)

156
Q

What is the function of mobile DNA?

A

virulence factors

antibiotic resistance

157
Q

How are the mobile DNA components of staph regulated?

A

operon-like

ex, accessory gene regulator (agr) -quorum sensing

158
Q

What are the infections of skin and subcutaneous tissues caused by staph aureus?

A
  • Impetigo-bullous and pustular

- Abscesses, folliculitis, furuncles, and carbuncles

159
Q

S. aureaus accounts for (blank) pecent of impetigo (bullous and pustular type) the reamined is caused by s. pyogenes alone or in combo with s. aureus

A

80%

160
Q

What are the deep infections associated with S. aureus?

A
  • bacteremia
  • osteomyelitis and septic arthritis
  • pneumonia
  • staph enterocolitis (follows upset of normal flora by broad spectrum antibiotics)
161
Q

What diseases are caused by staph toxins?

A
  • food poisoning
  • scalded skin syndrome and bullous impetigo
  • toxic shock syndrome
162
Q

Is staph highly virulent?

A

no, it is weakly virulent

minimal infecting dose large, predisposing conditions

163
Q

What are the lesions like in staph?

A

suppuration, irreversible tissue damage, scarring

164
Q

What are the structural components associated with staph?

A

capsule
peptidoglycan and lipoteichoic acids
Protein A

165
Q

What is the capsule like in staph?

A

antiphagocytic, made up of type 5 or 8

166
Q

The peptidoglycan and lipoteichoic acids in staph contributes to (blank)

A

inflammation

167
Q

Protein A found in staph has a high affinity for (blank)

A

IgG Fc fragment

168
Q

What are the enzymes associated with staph?

A

coagulase
catalase
penicilinase

169
Q

What does this:
converts fibrinogen to fibrin; helps localize lesions
marker for species

A

Coagulase

170
Q

(blank) facilitates intracellular survival in staph

A

catalase

171
Q

What are the cytotoxins associated with staph?

A

alpha, beta delta and gamma toxins, P-V leukocidin

(toxic via various mechanisms for erythrocytes, leukocytes, and platelets

172
Q

Where do you see exfoliatin toxin (ETA and ETB)?

A

scalded skin syndrome

173
Q

What are the three pyrogenic exotoxins for staph?

A

superantigens
staph enterotoxin
toxic shock syndrom toxin (TSST-1)

174
Q

(blank) are encoded by plasmids (enterotoxins) or bacteriophage (TSST)

A

pyrogenic exotoxins

175
Q

(blank) induce release of IL-1, TNF alpha, and other toxins. Related to strep pyrogenic exotoxins. Have specific toxic activities distinct from superantigen effects.

A

Superantigens

176
Q

What are some staph enterotoxins?

A

(SEA SEB SEC SED SEE)

177
Q

What is this;

  • ingestion of preformed staph entertoxin
  • resistant to heat (boiling for 30 min) and gastric enzymes
  • targets sensory nerve endings in SM of intestine
  • nausea, cramps, vomiting, diarrhea
  • recovery in 24 hr
A

Staphylococcal food poisoning

178
Q

What is this:
toxemia, bulous impetigo is local form, toxin is a serine protease, cleaves dermal-epidermal junction to form fragile, thin roofed vesicopustules, usually in children

A

Staph scalded skin syndrome

179
Q

(blank) is an infection at distant site with release of exoliating toxin in staph scalded skin syndrome

A

toxemia

180
Q

What toxin is found in staph scalded skin syndrome?

A

serine protease

181
Q

What is another name for staph scalded skin syndrome?

A

exfolitive skin disease

182
Q

the toxemia in this disease produces fever, vomiting, diarrea, rash and shock

A

staph toxic shock syndrome

183
Q

What is the possible mechanism behind staph toxic shock syndrome?

A

induction of cytokine release IL-1 and TNF alpha
increased susceptibility to endogenous endotoxin
direct effects on vascular endothelial cels

184
Q

TSST-1 production stimulated by poor (blank)

A

growth conditions

185
Q

What are the blood cultures like in staph toxic shock syndrome?

A

negative

186
Q

What are the effects of TSST-1?

A

fever, systemic effects

187
Q

What is the mechanism behind TSST-1?

A

superantigen: cytokine release: IL-1, IL-2, IL-6, TNF-alpha, INF-g

188
Q

What are the specimens you need to get for lab ID of staph ?

A

pus, purulent fluids, throat, nasal and np swabs, urine etc.

189
Q

How can you do directly examine for staph?

A

pus and CSF

190
Q

What should you isolate staph on?

A

blood agar or selective media (mannitol salt agar)

191
Q

What are the differential characteristics of staph?

A

gram positive coccus
catalase positive
coagulase positive
ferments mannitol

192
Q

How can you recognize MRSA?

A
  • chromogenic media with disks of oxacillin or cefoxitin

- PCR for mecA

193
Q

What is essential in staph and MRSA lab studies?

A

antibiotic sensitivity testing

194
Q

T or F

Interpretation of positive culture report depends on source of specimen and clinical judgement.

A

T

195
Q

Why do you do subspecies typing?

A

to identify epidemic strains

196
Q

How do you approach subspecie typing?

A

antibiotic sensitivity patterns (antibiograms)
biochemical profiles (biotyping)
suscpetibility to bacteriophage (phage typing)
nucleic acid analysis

197
Q

(blank) is the primary resevor of staph.

A

Humans

198
Q

Staph is part of the normal flora of lower (blank), (blank) and (blank)

A

large bowel
skin
anterior nares

199
Q

How are staph infections acquired?

A

air (wound infection)
direct contact
endogenous

200
Q

Carrier rate of staph my be (blank) in normal pop and higher in hospital

A

30%

201
Q

Is there immunity to staph?

A

no therfore reinfection is common and there is no vaccine

202
Q

How can you decontaminate skin staph?

A

mupirocin

203
Q

How do you treat staph?

A

drain lesion; remove foreign body if present
contral underlying diease
antibiotics

204
Q

What are some good drugs to use against staph?

A 
Penicillinase-resistant penicillins, e.g., oxacillin
Clindamycin
TMP-SMX
Doxycycline
Linezolid
Vancomycin
Daptomycin
205
Q

What are the common ways you get antibiotic resistance with staph?

A

penicillinase producing S. aureus (very common)
Rsistance to intermediate levesl of vancomycin (VISA)
vancomycin resistan S. aureus (VRSA

206
Q

What is VISA?

A

Thicker, more disorganized cell wall with free ala-ala groups
Acts as a decoy for vancomycin

207
Q

What is VRSA?

A

Due to vanA gene operon – encodes ala-lactate production
Requires rigorous susceptibility testing
Still relatively rare

208
Q

Where does MRSA lie?

A

on a mobile genetic element called SCCmec (staph chromosome cassette)

209
Q

What makes up SCCmec?

A 
regulate genes (negative repressor operon)
-mecA
210
Q

What is MecA?

A

encoded PBP 2a w/ low affinity for beta lactam antibiotics

211
Q

what is this:
Associated with risk factors, e.g., surgery, indwelling catheter, etc.
Multi-resistant

A

Health care-associated MRSA (HCA-MRSA)

212
Q 
What is this:
No/limited risk factors
Most common cause of skin and soft tissue infections in community
Usually carries the PV leukocidin
Pauci-resistant
A

Community-associated MRSA (CA-MRSA)

213
Q

how do you control staph infection?

A

decolonization of colonized patients or carriers – 1 week of body washing with chlorhexidine + nasal mupirocin

214
Q 
The patient is a 6-year-old male who complained of pharyngeal pain and had a temperature of 101°F. The pharyngeal membrane was fiery red, and a thick exudates covered the pharyngeal membrane and tonsillar area. A quick test for Streptococcus pyogenes antigen was positive. The patient will likely develop a protective antibody-based immunity to the specific serotype of the infecting strain. What is the antigen recognized by this protective antibody?
A)	Streptococcal M protein
B)	Lancefield group A carbohydrate
C)	Streptococcal hyaluronic acid capsule
D)	Cell wall peptidoglycan
E)	Streptolysin O
A

A

215
Q

A culture of skin lesions from a patient with pyoderma (impetigo) shows numerous colonies surrounded by a zone of beta-hemolysis on a blood agar plate. A gram-stained smear from the lesion shows gram-positive cocci. A catalase test of a beta-hemolytic colony is positive. Which of the following bacteria is the most likely cause?

A)	Streptococcus pyogenes
B)	Staphylococcus aureus
C)	Staphylococcus epidermidis
D)	Viridans streptococcus
E)	Staphylococcus saprophyticus
A

A) Streptococcus pyogenes

216
Q 
Scarlet fever is a potential complication of streptococcal pharyngitis. The clinical signs of scarlet fever could be blocked by administration of antibody to this bacterial product.
A)	Peptidoglycan
B)	Teichoic acid
C)	Lancefield C carbohydrate
D)	Streptolysin O
E)	Streptococcal pyrogenic exotoxins
A

E

Block 7 Week 2 (10 decks)

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