L 69 Skin and Subcutaneous Bacterial Infections Flashcards

1
Q

Some characteristics of skin that make it a good defense to disease

A

Acidic pH
Lower temperature than body
Low moisture
Excreted sebum, salt, urea, fatty acids
Normal microbiota: Staph. epidermis, Micrococcus luteus, E. coli
Langerhans cells in the skin to capture and present microbes to T-Cells

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2
Q

Name for a flat, non-palpable skin lesion

A

Macule

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3
Q

Name for palpable skin lesions

A

Papules

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4
Q

Name for palpable fluid-filled lesions

A

Vesicle

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5
Q

Name for palpable skin lesions filled with pus

A

Pustules

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6
Q

What are the 5 factors that determine if you will get acne vulgaris?

A

1) Genetics
2) Follicular hyperkeratinization: increased androgen production increases proliferation of keratinocytes
3) Increased sebum production: regulated by hormones
4) Propionibacterium acnes: bacteria lives in follicles and releases pro-inflammatory mediators
5) Inflammation: Proliferation of P. acnes releases enzymes, surface proteins, heat-shock proteins

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7
Q

Characteristics of P. acnes

A

Gram (+)
Pleomorphic bacterium
Aerotolerant anaerobe
Normal skin flora, likes sebaceous glands
Can be an opportunistic infection in patients with prosthetic devices and I.V. lines

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8
Q

Acne Vulgaris treatment

A

Retinoids: comedolytic and anti-inflammatory, adapalene, tretinoin, oral isotretinoin

Antibiotics: erythromycin and clindamycin
doxycyclin and minocycline

Benzoyl peroxide: antimicrobial

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9
Q

Acne vs folliculitis

A

Acne is a type of folliculitis

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10
Q

What is folliculitis?

A

superficial infection of the hair follicles with purulent material in the epidermis

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11
Q

What bacteria are the cause of folliculitis?

A

Staph. aureus

Pseudomonas auruginosa

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12
Q

Characteristics of S. aureus

A

Gram (+) coccus
Catalase positive (distinguishes it from strep)
Beta-hemolytic
Normal flora on much of the skin

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13
Q

Enzymes of S. aureus infection

A

Coagulase: clots the plasma to form a fibrin protective layer around it
Hemolysis: lyses RBC’s
Leukocidin: lyses WBC’s to release tissue damaging enzymes that damage eukaryotic membranes=> necrotic pulmonary disease
Clumping Factor: binds fibrinogen and causes clot formation

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14
Q

Forms of S. aureus folliculitis

A

Folliculitis barbae: areas of shaving, nasal carriers of staph, erythematous follicular papules that rupture and leave a yellow crust

Sty (hordeolum): folliculitis of the eyelid

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15
Q

Characteristics of Pseudomonas aeruginosa

A
Gram (-) bacilli
Opportunistic pathogen
Fruity smell
Pyocyanin–blue pus
Pyocerdin–green fluorescent siderophore
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16
Q

P. auruginosa type of folliculitis

A
Hot Tub folliculitis
8-48 hours after infection
Itchy maculopapular rash, some pustules
Systemic comoponent: fever, headache, sore throat, malaise, GI distress
Usually self-limiting

Ecthyma gangrenosum: cutaneous infection from bacteremia

17
Q

Folliculitis treatment

A

S. aureus: mild resolves, otherwise topical mupirocin or clindamycin, or oral dicloxacillin for MSSA; TMP/SMX, clindamycin, doxycycline for MRSA

P. aeruginosa: self-limited, resolves 7-10 days, severe cases oral ciprofloxacin

18
Q

What is a furuncle?

A

Caused by S. aureus
Folliculitis progresses, purulent material from a single opening, in areas of friction and perspiration (face, neck, axillae, buttocks)
Pururlent material extends through dermis into sub q tissues to form abscesses

19
Q

What is a carbuncle?

A

S. aureus caused

Aggregate of connected furuncles

20
Q

Treatment of furuncles and carbuncles

A

Warm compress
Incision and drainage
Anrimicrobials

Recurrent: Mupirocin topical applied to nares, axillae, perineum for 5 days with or without clindamycin

Treatment is to prevent hematogenous spread => endocarditis, sepsis and osteomyelitis

21
Q

Pyoderma and its forms

A

Pyoderma: bacterial skin inflammation marked by pus-filled lesions

Impetigo (bullous and non-bullous) and ecthyma are variants

Pyoderma and impetigo limited to epidermis
Ecthyma is when it spreads down to the dermis

22
Q

Nonbullous Impetigo

impetigo contagiosa

A

All ages, but mostly kids 2-6 years
S. aureus or GAS
spread by contact with the lesions, self-infection spreads it

23
Q

Strep. pyogenes characteristics

A

Also called GAS or GABHS
Gram (+) cocci
Mostly spreading infections

Virulence factors:

  • SPE–Strep Pyrogenic Exotoxins A-C, these cause rash and can lead to Scarlet fever
  • M protein: fimbriae/pili associated, impede phagocytosis, creates sequelae like rheumatic fever & acute poststreptococcal glomerulonephritis
24
Q

Spreading enzymes for Impetigo Contagiosa

A

DNase: reduces viscosity of lysed cell contents

Hyaluronidase: invasin

Streptokinase: disolves blood clots, invasin

25
Q

Nonbullous inpetigo

(Impetigo contagiosum) description

A

Staph or Strep but usually Staph

Starts as a macule that fills with fluid or pus, ruptures and leaves yellow crusted exudate that spreads easily

26
Q

Bullous impetigo

A

Staph aureus only
Rare, exfoliative toxin-producing strains
Intraepidermal lesion, begin as vesicles, enlarge to form flaccid bullae w/clear yellow fluid, fluid becomes dark, rupture, thin brown crust forms

Bullae containing exfoliatin but it does not disseminate, stays localized

27
Q

Pyoderma Ecthyma

A

GAS
Ulcerative pyoderma down to the dermis
Greenish-yellow crust
Rarely infectious
Untreated impetigo, preexisting tissue damage, immunocompromised, poor hygiene, diabetes
Lower extremities, pigmentation scars from damage to dermis

28
Q

Treatment of impetigo and ecthyma

A

Hygiene
Debridement
Topical antibiotic: mupirocin
Systemic antibiotic: dicloxacillin, cephalexin; MRSA: TMP/SMX, clindamycin, doxycyclin, linezolid

29
Q

General characteristics of Cellulitis and Erysipelas

A

Two types of similar skin infection
Dermis and Sub q tissue
Cellulitis: middle-aged and older adults
Erysipelas: young kids and old adults

30
Q

Cellulitis risk factors and pathogens

A

GAS:
skin lesions (varicella)
Immunocompromise
Chronic steroid use

S aureus:
Frequent pathogen
does not spread as fast as GAS

Acinetobacter baumannii:
g(-) aerobic rods to cocobacilli
Uncommon but specific
Assoc. with trauma, gunshot, venous catheters
Multi-drug resistant and pan-resistant

Pasteurella multocida:
g(-), mouths of dogs and cats
Purulent drainage

Aeromonas hydrophilia:
g(-) fresh water

Vibrio vulnificus:
g(-) salt water

31
Q

Hallmark cellulitis manifestations

A

Uncomplicated, unnecrotizing inflammation, deeper dermis and sub q,
HEET:
Heat, Erythema, Edema, Tenderness (skin becomes hot and swollen)

32
Q

Other manifestations of cellulitis

A

orange peel appearance
Lymphangitis
Possible bullous, petechiae, ecchymoses

33
Q

Cellulitis Diagnosis

A

2 Categories:

1) Small area, minimal pain, no systemic infection, responds well to treatment: no further workup needed
2) Extensive areas of involvement, spreading, underlying comorbidities; Lab workup required–may be more serious necrotizing fasciitis or myonecrosis

34
Q

Cellulitis treatment

A

Avoid NSAIDS–mask indications of worsening disease, inhibit PMN and cytokine release

Elevate and immobilize
Keep skin moist
Antibiotics depending on purulent vs not

Reevaluate within 24-72 hours

35
Q

Erysipelas

A

A type of cellulitis caused by GAS primarily and S. aureus
Distinct borders as compared to cellulitis
Affects young and old

36
Q

Erysipelas symptoms

A

Involves upper dermis and superficial lymphatics
Lesions raised above surrounding tissue
Clear line of demarcation
Involvement of the ear–significant because ear has no deeper sub q tissue so cellulitis doesn’t usually affect the ears
Some systemic signs: fever, chills

37
Q

Erysipelas distribution

A

Most commonly lower extremities

Face-10%–butterfly distribution

38
Q

Erysipelas treatment

A

Elevation and immobilization
Skin kept moist and hydrated
Antibiotics: IV–ceftriaxone (beta-hemolytic strep), cefazolin (BHS and MSSA)
Followed by oral penicilin or amoxicilin
No macrolides (azithromycin, erythromycin, clarithromycin)