L 69 Skin and Subcutaneous Bacterial Infections Flashcards Preview

Micro Exam 6 > L 69 Skin and Subcutaneous Bacterial Infections > Flashcards

Flashcards in L 69 Skin and Subcutaneous Bacterial Infections Deck (38):
1

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

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

2

Name for a flat, non-palpable skin lesion

Macule

3

Name for palpable skin lesions

Papules

4

Name for palpable fluid-filled lesions

Vesicle

5

Name for palpable skin lesions filled with pus

Pustules

6

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

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

7

Characteristics of P. acnes

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

8

Acne Vulgaris treatment

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

Antibiotics: erythromycin and clindamycin
doxycyclin and minocycline

Benzoyl peroxide: antimicrobial

9

Acne vs folliculitis

Acne is a type of folliculitis

10

What is folliculitis?

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

11

What bacteria are the cause of folliculitis?

Staph. aureus
Pseudomonas auruginosa

12

Characteristics of S. aureus

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

13

Enzymes of S. aureus infection

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

14

Forms of S. aureus folliculitis

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

15

Characteristics of Pseudomonas aeruginosa

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

16

P. auruginosa type of folliculitis

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

Folliculitis treatment

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

What is a furuncle?

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

What is a carbuncle?

S. aureus caused
Aggregate of connected furuncles

20

Treatment of furuncles and carbuncles

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

Pyoderma and its forms

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

Nonbullous Impetigo
(impetigo contagiosa)

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

23

Strep. pyogenes characteristics

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

Spreading enzymes for Impetigo Contagiosa

DNase: reduces viscosity of lysed cell contents

Hyaluronidase: invasin

Streptokinase: disolves blood clots, invasin

25

Nonbullous inpetigo
(Impetigo contagiosum) description

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

Bullous impetigo

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

Pyoderma Ecthyma

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

Treatment of impetigo and ecthyma

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

29

General characteristics of Cellulitis and Erysipelas

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

30

Cellulitis risk factors and pathogens

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

Hallmark cellulitis manifestations

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

32

Other manifestations of cellulitis

orange peel appearance
Lymphangitis
Possible bullous, petechiae, ecchymoses

33

Cellulitis Diagnosis

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

Cellulitis treatment

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

Erysipelas

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

36

Erysipelas symptoms

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

Erysipelas distribution

Most commonly lower extremities
Face-10%–butterfly distribution

38

Erysipelas treatment

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)