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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
Prevent furuncles (recur often):
Chlorhexidine/isopropyl alchol soap | maintenance abx
26
Impetigo aka
pyoderma
27
Impetigo
superficial skin infection with crusting or bullae
28
Ecthyma
ulcerative form of impetigo
29
Causative agent of impetigo/ecthyma
Staphylococci, streptococci, or both
30
impetigo/ecthyma risk factors
Moist environment Poor hygeine Chronic nasopharyngeal carriage of agents
31
Nonbullous impetigo
Clusters of vesicles that rupture and crust over | S aureus, 20% MRSA +/- streptococci pyogenes
32
Bullous impetigo
exfoliative toxin disrupts epidermal cell connections, causing bullae toxin doesn't disseminate specifically s aureus
33
Ritter's disease aka
staphylococcal scalded skin syndrome
34
Ritter's disease
acute and extensive epidermolysis due to exfoliatin (toxin) that splits skin beneath the granule layer VERY ill, systemic disease manifestations
35
Bullae of ritter's disease are
sterile: no bacteria or leukocytes due to toxin
36
Nikolsky's sign
Skin peels easily, desquamated areas look scalded | Ritter's disease
37
2 populations who get Ritter's disease
Children >6 years | Infants
38
Therapy for Ritter's disease
Penicillinase resistant anti-staph abx | treat extensive damage like burns
39
Cellulitis
acute infection of skin and deeper subcutaneous tissues: pain, rapidly spreading erythema and edema, fever, lymph node enlargement most commonly unilateral lower extremities
40
Erysipelas
superficial cellulitis with focal dermal lymphatic involvement
41
Erysipelas is usually caused by
Group A strep (s pyogenes)
42
Cellulitis is usually caused by (2)
1. S aureus | 2. S pyogenes (GAS)
43
Streptococci+cellulitis
more likely to create diffuse, swiftly spreading infections due to expression of tissue destructive enzymes
44
How do you get cellulitis?
infected skin break endogenous seeding *wound may not be evident*
45
HEET stands for
Heat Erythema Edema Tenderness
46
HEET is used to describe
cellulitis
47
What causes cellulitis symptoms?
bacterial toxins | inflammatory response
48
Cellulitis appearance
localized sun-burn like borders blend in elevation and color to surrounding tissue
49
Cellulitis tx
abx: empirical *infections may be mixed* | Avoid NSAIDs: mask pain of myonecrosis, interfere with response to agent
50
MRSA carriage rate in general population
2%
51
Recognize MRSA infection:
Fluctuance: evidence of fluid Yellow/white center Central point (head) Draining pus/pus may be aspirated with syringe
52
Detection of MRSA
PCR assay: mecA gene | Latex agglutination: MecA protein
53
major symptom of necrotizing subcutaneous infections
*pain out of proportion to clinical signs* initial overlying tissues appear unaffected tissues are red, hot, swollen
54
How does necrotizing fasciitis spread?
along muscle fascia (poor blood supply) | RAPIDLY
55
Necrotizing faciitis infects and destroys
muscle fascia and overlying subQ tissue | muscles spared due to being blood rich
56
Type 1 Necrotizing fasciitis
Polymicrobial | GAS+anaerobes
57
Risk factors for Type 1 Necrotizing fasciitis
*DM* surgery immunocompromised
58
Type 2 Necrotizing fasciitis
"Flesh-eating bacteria' | Group A streptococcus pyogenes: Monomicrobic
59
How do you get Type 2 Necrotizing fasciitis?
``` Entry point often not found, risk unclear: blunt trauma (crushing wound), but bite, chickenpox, IVDU, surgery, strep throat ```
60
Later signs of Necrotizing fasciitis
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
How do you differentiate necrotizing fasciitis from cellulitis?
necrotizing fasciitis won't response to abx | cellulitis will respond in 24-48 hours
62
Fascia appearance in Necrotizing fasciitis
swollen, dull gray no true pus thin brownish exudate undermining of surrounding tissue, necrotic tissue separates along facial planes
63
Gas gangrene aka
Myonecrosis
64
Myonecrosis is caused by
Clostridium perfingens type A
65
Clostridium perfingens type A
spore-forming G+ anaerobic bacillus
66
Gas gangrene pathogenesis
introduction of cells/spore reduced oxygen tension production of exotoxins and insoluble H2 gas promotes split and invasion of nearby tissues
67
What might cause reduced oxygen tension?
``` trauma other bacteria circulatory failure necrotic tissue foreign bodies presence of oxygen utilizing bacteria ```
68
How rapid is gas gangrene?
<24 hours | medical emergency
69
Gas gangrene symptoms
``` 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
Diagnose gas gangrene?
Tissue biopsy gram stain: muscle necrosis gram variable rods tissue destruction
71
Toxic shock syndrome causative agents
both staph aureus and strep pyogenes
72
Toxic shock syndrome presents as
fever | sunburn-like whole body rash
73
Streptococcal toxic shock syndrome
soft tissue inflammation at site of skin infection pyrogenic exotoxin superantigens: SpeA, SpeC bacteremic necrotizing fasciitis
74
Streptococcal toxic shock syndrome risk factors
``` HIV Cancer DM VZV Flu Childbirth Surgery Heart/pulmonary disease ```
75
Staphylococcus aureus toxic shock syndrome risk factors
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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