Agents of Skin Infections I and II Flashcards Preview

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Flashcards in Agents of Skin Infections I and II Deck (89):
1

What strains cause Impetigo?

Group A streptococcus and Staphylococcus A

2

Exogenous vs. endogenous skin infections

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.

3

Erysipelas

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

4

What layer of the skin is cellulitis predominantly affective in?

Subcutaneous fat layer

5

What is a furuncle?

Boil

6

Carbuncle?

Group of Boils

7

Folliculitis

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

8

Nosocomial

Hospital acquired

9

Myonecrosis

Muscle necrosis

10

Gas gangrene

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

11

Fasciitis

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

12

What infections are brought on by Streptococci?

Impetigo
Erysipelas
Cellulitis
Synergistic Cellulitis
Necrotizing fasciitis

Think (NICE Strep)

13

What infections are brought on by Staphylococci?

Folliculitis
Carbuncles
Impetigo
Cellulitis

14

What infections are brought on by Clostridium?

Gas Gangrene

15

Pyogenic

Pus forming

16

What gram stain is streptococci?

Positive

17

What bacteria are catalase positive? Negative?

Negative - Streptococci
Positive - Staphylococci

18

Hemolytic Test

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

19

Hemolytic results for bacteria

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

20

VRSA vs. VISA

VRSA - Complete Vancomycin resistance
VISA - Incomplete resistance

21

Strep vs. Staph catalase tests

Strep - Negative
Staph - Positive

22

Lancefield Group A carbohydrate antigen

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

23

Describe a GAS culture

- Glistening due to capsules
- Form clear zones (we can see through them with light)
- Sensitive to Basitracen

24

Basitracen

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

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.