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Unit 3 Microbio > L22: Bacterial Skin Infections > Flashcards

L22: Bacterial Skin Infections Flashcards

1
Q

How do skin infections occur?

A

Staph normally present on skin

Break in skin introduces staph: but could be prevented with disinfection

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2
Q

Infectious dose for infection drops dramatically when

A

Foreign body is present: splinters, stitches

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3
Q

Initial trigger for acne

A

Androgen hormones

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4
Q

Acne vulgaris

A

Noninfectious form of folliculitis:

disease of sebaceous follicles

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5
Q

Acne vulgaris causative agent

A

Propionibacterium acnes

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6
Q

Propionibacterium acnes

A

G+ anaerobic rod

normal flora on skin, especially sebaceous glands

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7
Q

Inflammatory acne vulgaris

A

develops when follicular contents rupture into the dermis

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8
Q

mild, small firm pink bump

A

papule

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9
Q

clearly inflammed, containing visible pus

A

pustule

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10
Q

most severe form of acne, large, painful, inflamed pus filled lesion lodged deep within skin

A

nodule (cystic acne)

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11
Q

Folliculitis

A

mild pain, itching, irritation with pustules or nodules surrounding hair follicles

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12
Q

Folliculitis treatment

A

Topical:
Benzoyl peroxide wash
Clindamycin ointment

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13
Q

If folliculitis doesn’t resolve with topical treatments….

A

Gram stain to rule out G- etiology or MRSA

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14
Q

2 primary pathogens of folliculitis

A
  1. Staph aureus

2. Pseudomonas aeruginosa

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15
Q

Staph aureus

A

abscess-type infections
G+
coagulase positive
cocci in clusters

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16
Q

Pseudomonas aeruginosa

A

G-
ubiquitous opportunistic pathogen
Pyocyanin/pyoverdin

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17
Q

Hot tub folliculitis

A

Pseudomonas

8-48 hours after hot tub with inadequate chlorine

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18
Q

Furuncle aka

A

boil

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19
Q

Furuncles

A

abscess cause by s aureus
hair follicle+surrounding tissue
neck, thighs, buttocks, face

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20
Q

Carbuncle

A

clusters of furuncles with subcutaneous connections
extend into dermis and subcutaneous tissue
+/- fever, prostrations
neck, back, thighs

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21
Q

Who most frequently gets carbuncles/furuncles

A

obese
immunocompromised
diabetic
elderly

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22
Q

Diagnose a carbuncles/furuncles

A

direct exam

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23
Q

Treat a carbuncles/furuncles

A 
Incision and drainage
MRSA-effective abx if:
>5 mm
Do not resolve with drainage
Spreading
Immunocompromised
Risk of endocarditis
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24
Q

When to give rifampin for carbuncles/furuncles?

A

Fever

multiple lesions

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25
Q

Prevent furuncles (recur often):

A

Chlorhexidine/isopropyl alchol soap

maintenance abx

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26
Q

Impetigo aka

A

pyoderma

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27
Q

Impetigo

A

superficial skin infection with crusting or bullae

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28
Q

Ecthyma

A

ulcerative form of impetigo

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29
Q

Causative agent of impetigo/ecthyma

A

Staphylococci, streptococci, or both

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30
Q

impetigo/ecthyma risk factors

A

Moist environment
Poor hygeine
Chronic nasopharyngeal carriage of agents

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31
Q

Nonbullous impetigo

A

Clusters of vesicles that rupture and crust over

S aureus, 20% MRSA +/- streptococci pyogenes

32
Q

Bullous impetigo

A

exfoliative toxin disrupts epidermal cell connections, causing bullae
toxin doesn’t disseminate
specifically s aureus

33
Q

Ritter’s disease aka

A

staphylococcal scalded skin syndrome

34
Q

Ritter’s disease

A

acute and extensive epidermolysis due to exfoliatin (toxin) that splits skin beneath the granule layer
VERY ill, systemic disease manifestations

35
Q

Bullae of ritter’s disease are

A

sterile: no bacteria or leukocytes due to toxin

36
Q

Nikolsky’s sign

A

Skin peels easily, desquamated areas look scalded

Ritter’s disease

37
Q

2 populations who get Ritter’s disease

A

Children >6 years

Infants

38
Q

Therapy for Ritter’s disease

A

Penicillinase resistant anti-staph abx

treat extensive damage like burns

39
Q

Cellulitis

A

acute infection of skin and deeper subcutaneous tissues:
pain, rapidly spreading erythema and edema, fever, lymph node enlargement
most commonly unilateral lower extremities

40
Q

Erysipelas

A

superficial cellulitis with focal dermal lymphatic involvement

41
Q

Erysipelas is usually caused by

A

Group A strep (s pyogenes)

42
Q

Cellulitis is usually caused by (2)

A
  1. S aureus

2. S pyogenes (GAS)

43
Q

Streptococci+cellulitis

A

more likely to create diffuse, swiftly spreading infections due to expression of tissue destructive enzymes

44
Q

How do you get cellulitis?

A

infected skin break
endogenous seeding
wound may not be evident

45
Q

HEET stands for

A

Heat
Erythema
Edema
Tenderness

46
Q

HEET is used to describe

A

cellulitis

47
Q

What causes cellulitis symptoms?

A

bacterial toxins

inflammatory response

48
Q

Cellulitis appearance

A

localized
sun-burn like
borders blend in elevation and color to surrounding tissue

49
Q

Cellulitis tx

A

abx: empirical infections may be mixed

Avoid NSAIDs: mask pain of myonecrosis, interfere with response to agent

50
Q

MRSA carriage rate in general population

A

2%

51
Q

Recognize MRSA infection:

A

Fluctuance: evidence of fluid
Yellow/white center
Central point (head)
Draining pus/pus may be aspirated with syringe

52
Q

Detection of MRSA

A

PCR assay: mecA gene

Latex agglutination: MecA protein

53
Q

major symptom of necrotizing subcutaneous infections

A

pain out of proportion to clinical signs
initial overlying tissues appear unaffected
tissues are red, hot, swollen

54
Q

How does necrotizing fasciitis spread?

A

along muscle fascia (poor blood supply)

RAPIDLY

55
Q

Necrotizing faciitis infects and destroys

A

muscle fascia and overlying subQ tissue

muscles spared due to being blood rich

56
Q

Type 1 Necrotizing fasciitis

A

Polymicrobial

GAS+anaerobes

57
Q

Risk factors for Type 1 Necrotizing fasciitis

A

DM
surgery
immunocompromised

58
Q

Type 2 Necrotizing fasciitis

A

“Flesh-eating bacteria’

Group A streptococcus pyogenes: Monomicrobic

59
Q

How do you get Type 2 Necrotizing fasciitis?

A 
Entry point often not found, risk unclear: 
blunt trauma (crushing wound), but bite, chickenpox, IVDU, surgery, strep throat
60
Q

Later signs of Necrotizing fasciitis

A

skin changes color: red-purple to patches of blue gray

skin breakdown with bullae: thick pink/purple fluid, cutaneous gangrene, no longer tender (cutaneous anesthesia)

61
Q

How do you differentiate necrotizing fasciitis from cellulitis?

A

necrotizing fasciitis won’t response to abx

cellulitis will respond in 24-48 hours

62
Q

Fascia appearance in Necrotizing fasciitis

A

swollen, dull gray
no true pus
thin brownish exudate
undermining of surrounding tissue, necrotic tissue separates along facial planes

63
Q

Gas gangrene aka

A

Myonecrosis

64
Q

Myonecrosis is caused by

A

Clostridium perfingens type A

65
Q

Clostridium perfingens type A

A

spore-forming
G+
anaerobic bacillus

66
Q

Gas gangrene pathogenesis

A

introduction of cells/spore
reduced oxygen tension
production of exotoxins and insoluble H2 gas promotes split and invasion of nearby tissues

67
Q

What might cause reduced oxygen tension?

A 
trauma
other bacteria
circulatory failure
necrotic tissue
foreign bodies
presence of oxygen utilizing bacteria
68
Q

How rapid is gas gangrene?

A

<24 hours

medical emergency

69
Q

Gas gangrene symptoms

A 
sudden onset of pain from toxin-mediated ischemia
bronze skin
tense skin due to edema
*crepitant* due to H2 gas
bullae: clear, red, blue, purple
70
Q

Diagnose gas gangrene?

A

Tissue biopsy gram stain:
muscle necrosis
gram variable rods
tissue destruction

71
Q

Toxic shock syndrome causative agents

A

both staph aureus and strep pyogenes

72
Q

Toxic shock syndrome presents as

A

fever

sunburn-like whole body rash

73
Q

Streptococcal toxic shock syndrome

A

soft tissue inflammation at site of skin infection
pyrogenic exotoxin superantigens: SpeA, SpeC
bacteremic
necrotizing fasciitis

74
Q

Streptococcal toxic shock syndrome risk factors

A 
HIV
Cancer
DM
VZV
Flu
Childbirth
Surgery
Heart/pulmonary disease
75
Q

Staphylococcus aureus toxic shock syndrome risk factors

A

otherwise healthy with no pre-existing skin infections
Enterotoxin type B superantigen
associated with tampons and surgery

Unit 3 Microbio (13 decks)

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