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MSK Week 1 > Agents of Skin Infections I and II > Flashcards

Agents of Skin Infections I and II Flashcards

1
Q

What strains cause Impetigo?

A

Group A streptococcus and Staphylococcus A

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2
Q

Exogenous vs. endogenous skin infections

A

Exogenous is direct invasion of microbe from external environment and endogenous is invasion of a microbe from an internal source such as the blood or an infected organ.

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3
Q

Erysipelas

A

Tender, superficial erythematous and edematous lesions mostly on the superficial lymphatics of the skin. Red and clearly demarcated, can be lethal.

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4
Q

What layer of the skin is cellulitis predominantly affective in?

A

Subcutaneous fat layer

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5
Q

What is a furuncle?

A

Boil

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6
Q

Carbuncle?

A

Group of Boils

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7
Q

Folliculitis

A

Inflammation in hair follicles. Starts typically as small red bumps or white-headed pimples around the follicles, turning into nonhealing crusty sores.

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8
Q

Nosocomial

A

Hospital acquired

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9
Q

Myonecrosis

A

Muscle necrosis

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10
Q

Gas gangrene

A

Causes myonecrosis, brought on by Clostridium. Dangerous form of necrosis with necrotic bullae (large blisters)

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11
Q

Fasciitis

A

Caused by GAS, commonly known as flesh eating bacteria. Destruction of skin and subcutaneous tissue

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12
Q

What infections are brought on by Streptococci?

A 
Impetigo
Erysipelas
Cellulitis
Synergistic Cellulitis
Necrotizing fasciitis

Think (NICE Strep)

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13
Q

What infections are brought on by Staphylococci?

A

Folliculitis
Carbuncles
Impetigo
Cellulitis

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14
Q

What infections are brought on by Clostridium?

A

Gas Gangrene

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15
Q

Pyogenic

A

Pus forming

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16
Q

What gram stain is streptococci?

A

Positive

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17
Q

What bacteria are catalase positive? Negative?

A

Negative - Streptococci

Positive - Staphylococci

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18
Q

Hemolytic Test

A

Alpha - You can lyse cells but can’t break down hemoglobin (looks green)

Beta - Complete hemolysis including hemoglobulin

Gamma - Can’t break down blood cells at all

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19
Q

Hemolytic results for bacteria

A

Streptococcus Group A - B hemolytic
Staph A - B hemolytic
Staph - Epidermidis - Gamma

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20
Q

VRSA vs. VISA

A

VRSA - Complete Vancomycin resistance

VISA - Incomplete resistance

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21
Q

Strep vs. Staph catalase tests

A

Strep - Negative

Staph - Positive

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22
Q

Lancefield Group A carbohydrate antigen

A

Not a virulence factor, but is a marker on the cell wall on Group A Streptococci

Specificity of test is great, but sensitivity is poor

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23
Q

Describe a GAS culture

A
  • Glistening due to capsules
  • Form clear zones (we can see through them with light)
  • Sensitive to Basitracen
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24
Q

Basitracen

A

Antimicrobial that acts against the cell wall. We can use this to distinguish GAS on an agar plate

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25
Q

PYR Test

A

Make sure that you have streptococcus. If positive, you have Group A

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26
Q

M protein

A

Virulence factor

  1. Antiphagocytic
  2. Important for binding to epidermis
  3. Homologous to many self proteins making it tricky to target (molecular mimicry)
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27
Q

Hyaluronic Acid capsule

A

Antiphagocytic, disguises bacteria due to similarity to our own proteins

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28
Q

Describe Super Antigens

A

Bind MHCII and TCR together nonspecifically. Causes 20% of our T cells to activate instead of the normal 0.01%. Leads to a shit storms of cytokines

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29
Q

Nosocomial transmissions of bacteria

A

P Aeruginosa - On biofilms on medical equipment

S Epidermidis- UTIs and other infections caused by surgeries and implanted medical equipment like catheters

S Aureus - EVERYWHERE

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30
Q

How do bacteria get these resistances?

A

DNA gets inserted into the bacterial DNA by bacterial phages giving them the ability to make toxins

Horizontal gene transfer OR spontaneous mutations

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31
Q

What is the lysonogenic phase

A

Phase when the virus that infected the bacteria (phage) is not doing anything. Advantages are that the bacteria can not be infected by other viruses and can gain virulence factors

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32
Q

Lytic Phase?

A

When the virus inside of the bacteria is replicating like crazy

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33
Q

Streptolysis O

A

Virulence factor that is toxic to a wide variety of cells. Lyses cells around a colony

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34
Q

DNAases?

A

Virulence factor.

Neutrophils have a second attack method, NET (neutrophil extracellular trap) made up of toxic compounds and DNA fragments that trap and kill pathogens. DNAases released by the bacteria can break these NETs

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35
Q

Streptokinase

A

Virulence Factor

Lyses blood clots to help bacteria spread

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36
Q

C5a peptidase

A

Virulence factor - Degrades complement protein C5a which is what attracts PMNs

37
Q

What causes Rheumatic fever?

A

Caused usually after a sore throat from GAS. It causes a cross reaction between antiM antibodies and the heart = autoimmune

38
Q

Acute glomerulonephritis?

A

Renal injury due to deposition of antigen-antibody complexes on glomeruli

39
Q

PANDAS

A 
Pediatric
Autoimmune
Neuropsychiatric
Disorder
Associated with
Streptococci Group A
40
Q

5 PANDAS criteria

A
  1. OCD
  2. Pediatric Onset
  3. Abrupt onset with episodic course
  4. Association with Group A Strep infections
  5. Neurological abnormalities like motoric hyperactivity, tics, etc.
41
Q

Treatment for GAS

A

PCN-G and/or oral cephalosporins

42
Q

What is the treatment if GAS is mixed with Staph Aureus?

A

PCN-ase resistant antibiotic to treat both

43
Q

Are staphylococci gram positive or negative?

44
Q

Blood agar result for S. Aureus

A

Yellow beta hemolytic

45
Q

Blood agar result for S. Epidermidis

A

White non hemolytic (gamma)

46
Q

Coagulase test results

A

Positive = Staph Aureus

Negative - Staph epidermidis and S Saprophyticus

47
Q

Catalase test

A

Bubbling is positive. Take the colony put in H2O2. If it bubbles then you have staphylococci, if there is no bubbling then it is streptococci

48
Q

Coagulase

A

Aureus makes protein coagulase that turns fibrinogen to fibrin causing a clot around the bacteria to mask it and grow in size

49
Q

Impetigo

A

Infection of the epidermis manifested by intraepidermal vesicles that are filled with exudate and eventually become weeping and crusted lesions

50
Q

Treatment for Furuncle

A

Heat and drain it

51
Q

Folliculitis treatment

A

Muciprocin antibiotic treatment to eliminate nasal carriages

52
Q

Vibrio Vulnificus

A

Salt water exposure, causes fluid filled blisters. Can cause sepsis and be lethal

53
Q

Pseudomonas Aureginosa

A

Can cause Ecthyma gangrenosum, a necrotic reaction

54
Q

Lesions caused by Staph A

A

Osteomyelitis
Septic Arthritis
Meningitis
PNA

Remember Staph (janitors) MOPS

55
Q

Bacteremia caused by Staph A

A 
Endocarditis
Meningitis
PNA
Pyelonephritis
Septicemia
56
Q

Risk factors for boils from Staph A

A

DM
Acne
Wet working conditions
Poor Hygiene

57
Q

Risk factors for wound infections being caused by Staph Aureus

A 
Diabetes Mellitus
Steroid Therapy
Obesity
Malnutrition
Prolonged Surgery
Foreign Body
58
Q

Number one host defense against Staph Aureus?

A

Opsonophagocytosis

59
Q

What complement subunit deficiency puts you at high risk for Staph A?

60
Q

What virulence factors help Staph A defend directly against phagocytosis?

A

Protein A
Catalase
Leukocidin

61
Q

Protein A

A

Binds Fc Receptor

62
Q

Catalase

A

Breaks down H2O2 and makes leukocidin

63
Q

Leukocidin

A

Pokes holes in neutrophil membranes

64
Q

Ribotechnoic acid

A

Binds fibronectin in our ECM proteins which help it break into the cell

65
Q

Hyaluronidase

A

Acts on hyaluronic acids in connective tissue which facilitates dissemination through subcutaneous tissues

66
Q

Cytotoxins of Staph Aureus

A

Alpha hemolysis
Beta Toxin
Delta Toxin
Gamma Toxins and PVLs

67
Q

Alpha Hemolysin

A

potent pore-former that is toxic to many types of cells

68
Q

Beta toxin

A

Also called Sphingomyelinase C, kills cells via hydrolysis of membrane phospholipids

69
Q

Delta Toxin

A

Cytolytic for many cells, nonspecific detergent-like action

70
Q

Gamma Toxins and PVLs

A

Panton-Valentine Leukocidin - pore forming toxins that lyse neutrophils and macrophages

71
Q

What Staph do we suspect for dog bites?

A

Staphylococcus Intermedius since this is a normal flora on healthy dogs

72
Q

Bullous Impetigo

A

Caused by Staph A, gets into the skin and causes abscesses. Usually localized. Big fluid filled sacs everywhere

73
Q

Scalded Skin Syndrome

A

Staph A toxin that creates exfoliatin which gets into the bloodstream and causes shedding of the outermost layer of the skin. Looks like a dark red peeling sunburn all over

74
Q

Treatment for Scalded Skin Syndrome

A

Antibiotics and hydration

75
Q

How does Exfoliatin work?

A

Serine protease that causes splitting of desmosomes in the stratum granulosum. We develop antibodies to this toxin later in life

76
Q

TSST-1

A

Super antigen involved with Toxic Shock Syndrome

77
Q

Immediate symptoms of TSS

A

Fever, chills, vomiting, diarrhea, muscle pains, rash

78
Q

Delayed symptoms of TSS

A

Hypotension, involvement of mucous memranes and multiple systems with desquamation (skin peeling)

79
Q

Risk groups for TSS

A
  1. Menstruating women
  2. Women with contraceptive devices
  3. People with nasal surgery
80
Q

What condition do we see strawberry tongue with?

A

Scarlet Fever (sometimes brought on by TSS)

81
Q

Most common cause of pyoderma

A

Staph Aureus

82
Q

Alcohol soaps in hospitals help with what?

A

Staph Aureus spread

83
Q

PFGE

A

Pulse-field gel electrophoresis

Isolates related clones by cutting chromosomes up into large fragments and seeing if there are mutations, which will change gel migration of the fragments

84
Q

Phage Typing

A

When you use phages on different staph colonies to see which ones die. The ones that live already have that phage in them

85
Q

Story of PCN, MRSA and VRSA

A

Started with PCN, but the bacteria developed PCNase, we fought back with methicillin, but then MRSA came about when the bacteria developed mec A gene which altered PCN binding protein.

Now we use Vancomycin, a glycopeptide that inhibits further production of peptidoglycans (PG) by binding to the PG precursors. This is the current treatment for MRSA, although, continuing the trend, VRSA has developed which is full resistance and VISA which is partial resistance. Acquisition of vanA gene which changed the terminus of the PG chain to stop Vancomycin binding

86
Q

What bacteria develops in biofilms?

A

Staph Epidermidis

87
Q

Which bacteria do we mostly associate with UTI?

A

Staph. Saphrophyticus

88
Q

Types of Spread of bacteria and examples that do this

A

Commensual Staph - Colonizers of normal skin and rarely causes deeper infection unless physically introduced there via a catheter or something. S. epidermidis follows this.

Virulent Staph may cause skin infections from which organisms disseminate to almost any organ or tissue. Staph. Aureus is a good example of this.

89
Q

How do Staph survive so well on the skin surface?

A

They make lipases and glycerol ester hydrolases that degrade the skin lipids to help them grow at high lipid and salt concentration environments.

MSK Week 1 (14 decks)

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