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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
PYR Test
Make sure that you have streptococcus. If positive, you have Group A
26
M protein
Virulence factor 1. Antiphagocytic 2. Important for binding to epidermis 3. Homologous to many self proteins making it tricky to target (molecular mimicry)
27
Hyaluronic Acid capsule
Antiphagocytic, disguises bacteria due to similarity to our own proteins
28
Describe Super Antigens
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
29
Nosocomial transmissions of bacteria
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
30
How do bacteria get these resistances?
DNA gets inserted into the bacterial DNA by bacterial phages giving them the ability to make toxins Horizontal gene transfer OR spontaneous mutations
31
What is the lysonogenic phase
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
32
Lytic Phase?
When the virus inside of the bacteria is replicating like crazy
33
Streptolysis O
Virulence factor that is toxic to a wide variety of cells. Lyses cells around a colony
34
DNAases?
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
35
Streptokinase
Virulence Factor Lyses blood clots to help bacteria spread
36
C5a peptidase
Virulence factor - Degrades complement protein C5a which is what attracts PMNs
37
What causes Rheumatic fever?
Caused usually after a sore throat from GAS. It causes a cross reaction between antiM antibodies and the heart = autoimmune
38
Acute glomerulonephritis?
Renal injury due to deposition of antigen-antibody complexes on glomeruli
39
PANDAS
``` Pediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococci Group A ```
40
5 PANDAS criteria
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
Treatment for GAS
PCN-G and/or oral cephalosporins
42
What is the treatment if GAS is mixed with Staph Aureus?
PCN-ase resistant antibiotic to treat both
43
Are staphylococci gram positive or negative?
Positive
44
Blood agar result for S. Aureus
Yellow beta hemolytic
45
Blood agar result for S. Epidermidis
White non hemolytic (gamma)
46
Coagulase test results
Positive = Staph Aureus | Negative - Staph epidermidis and S Saprophyticus
47
Catalase test
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
Coagulase
Aureus makes protein coagulase that turns fibrinogen to fibrin causing a clot around the bacteria to mask it and grow in size
49
Impetigo
Infection of the epidermis manifested by intraepidermal vesicles that are filled with exudate and eventually become weeping and crusted lesions
50
Treatment for Furuncle
Heat and drain it
51
Folliculitis treatment
Muciprocin antibiotic treatment to eliminate nasal carriages
52
Vibrio Vulnificus
Salt water exposure, causes fluid filled blisters. Can cause sepsis and be lethal
53
Pseudomonas Aureginosa
Can cause Ecthyma gangrenosum, a necrotic reaction
54
Lesions caused by Staph A
Osteomyelitis Septic Arthritis Meningitis PNA Remember Staph (janitors) MOPS
55
Bacteremia caused by Staph A
``` Endocarditis Meningitis PNA Pyelonephritis Septicemia ```
56
Risk factors for boils from Staph A
DM Acne Wet working conditions Poor Hygiene
57
Risk factors for wound infections being caused by Staph Aureus
``` Diabetes Mellitus Steroid Therapy Obesity Malnutrition Prolonged Surgery Foreign Body ```
58
Number one host defense against Staph Aureus?
Opsonophagocytosis
59
What complement subunit deficiency puts you at high risk for Staph A?
C3b
60
What virulence factors help Staph A defend directly against phagocytosis?
Protein A Catalase Leukocidin
61
Protein A
Binds Fc Receptor
62
Catalase
Breaks down H2O2 and makes leukocidin
63
Leukocidin
Pokes holes in neutrophil membranes
64
Ribotechnoic acid
Binds fibronectin in our ECM proteins which help it break into the cell
65
Hyaluronidase
Acts on hyaluronic acids in connective tissue which facilitates dissemination through subcutaneous tissues
66
Cytotoxins of Staph Aureus
Alpha hemolysis Beta Toxin Delta Toxin Gamma Toxins and PVLs
67
Alpha Hemolysin
potent pore-former that is toxic to many types of cells
68
Beta toxin
Also called Sphingomyelinase C, kills cells via hydrolysis of membrane phospholipids
69
Delta Toxin
Cytolytic for many cells, nonspecific detergent-like action
70
Gamma Toxins and PVLs
Panton-Valentine Leukocidin - pore forming toxins that lyse neutrophils and macrophages
71
What Staph do we suspect for dog bites?
Staphylococcus Intermedius since this is a normal flora on healthy dogs
72
Bullous Impetigo
Caused by Staph A, gets into the skin and causes abscesses. Usually localized. Big fluid filled sacs everywhere
73
Scalded Skin Syndrome
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
Treatment for Scalded Skin Syndrome
Antibiotics and hydration
75
How does Exfoliatin work?
Serine protease that causes splitting of desmosomes in the stratum granulosum. We develop antibodies to this toxin later in life
76
TSST-1
Super antigen involved with Toxic Shock Syndrome
77
Immediate symptoms of TSS
Fever, chills, vomiting, diarrhea, muscle pains, rash
78
Delayed symptoms of TSS
Hypotension, involvement of mucous memranes and multiple systems with desquamation (skin peeling)
79
Risk groups for TSS
1. Menstruating women 2. Women with contraceptive devices 3. People with nasal surgery
80
What condition do we see strawberry tongue with?
Scarlet Fever (sometimes brought on by TSS)
81
Most common cause of pyoderma
Staph Aureus
82
Alcohol soaps in hospitals help with what?
Staph Aureus spread
83
PFGE
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
Phage Typing
When you use phages on different staph colonies to see which ones die. The ones that live already have that phage in them
85
Story of PCN, MRSA and VRSA
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
What bacteria develops in biofilms?
Staph Epidermidis
87
Which bacteria do we mostly associate with UTI?
Staph. Saphrophyticus
88
Types of Spread of bacteria and examples that do this
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
How do Staph survive so well on the skin surface?
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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