L 69 Skin and Subcutaneous Bacterial Infections Flashcards
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
Name for a flat, non-palpable skin lesion
Macule
Name for palpable skin lesions
Papules
Name for palpable fluid-filled lesions
Vesicle
Name for palpable skin lesions filled with pus
Pustules
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
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
Acne Vulgaris treatment
Retinoids: comedolytic and anti-inflammatory, adapalene, tretinoin, oral isotretinoin
Antibiotics: erythromycin and clindamycin
doxycyclin and minocycline
Benzoyl peroxide: antimicrobial
Acne vs folliculitis
Acne is a type of folliculitis
What is folliculitis?
superficial infection of the hair follicles with purulent material in the epidermis
What bacteria are the cause of folliculitis?
Staph. aureus
Pseudomonas auruginosa
Characteristics of S. aureus
Gram (+) coccus
Catalase positive (distinguishes it from strep)
Beta-hemolytic
Normal flora on much of the skin
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
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
Characteristics of Pseudomonas aeruginosa
Gram (-) bacilli Opportunistic pathogen Fruity smell Pyocyanin–blue pus Pyocerdin–green fluorescent siderophore
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
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
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
What is a carbuncle?
S. aureus caused
Aggregate of connected furuncles
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
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
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
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
Spreading enzymes for Impetigo Contagiosa
DNase: reduces viscosity of lysed cell contents
Hyaluronidase: invasin
Streptokinase: disolves blood clots, invasin
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
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
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
Treatment of impetigo and ecthyma
Hygiene
Debridement
Topical antibiotic: mupirocin
Systemic antibiotic: dicloxacillin, cephalexin; MRSA: TMP/SMX, clindamycin, doxycyclin, linezolid
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
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
Hallmark cellulitis manifestations
Uncomplicated, unnecrotizing inflammation, deeper dermis and sub q,
HEET:
Heat, Erythema, Edema, Tenderness (skin becomes hot and swollen)
Other manifestations of cellulitis
orange peel appearance
Lymphangitis
Possible bullous, petechiae, ecchymoses
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
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
Erysipelas
A type of cellulitis caused by GAS primarily and S. aureus
Distinct borders as compared to cellulitis
Affects young and old
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
Erysipelas distribution
Most commonly lower extremities
Face-10%–butterfly distribution
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)
