Skin and Soft Tissue Infections Flashcards
Non-Bullous Impetigo
Overview
- Superficial, involves only the epidermis
- Major pathogens:
- Group A Streptococcus
- Staphylococcus aureus
Non-Bullous Impetigo
Pathogenesis
- Skin colonized following minor abrasion or insect bite → infection
- Stays within the epidermis → vesicles and pustules
Non-Bullous Impetigo
Epidemiology
- Children >> adults
- Predisposing factors
- Hot, humid weather
- Poor personal hygiene
- Crowded living
Non-Bullous Impetigo
Clinical Presentation
Vesicle → pustule → rupture → thick golden crust
Pruritis (itching)
Systemic symptoms are rare
Bullous Impetigo
Overview
- Superficial infection involving the epidermis
- Major pathogen: S. Aureus phage group II
- Pathogenesis: skin manifestations are due to the cutaneous response to the toxin
Bullous Impetigo
Clinical Presentation
Vesicle → bullae → rupture → light brown crust
Systemic symptoms are rare
Folliculitis
Overview
- Infection of the hair follicle
- Most common pathogen: S. Aureus
Folliculitis
Clinical Presentation
Erythematous papule with central pustule around an individual hair
Systemic symptoms are absent
Folliculitis
Treatment
Topical anti-bacterials
Occasionally need systemic antibiotic
Furuncles and Carbuncles
Overview
- Deeper infections of the hair follicles
- Furuncle: abscess deep within the hair follicle
- Carbuncle: more extensive involvement with multiple abscesses
- Most common pathogen – S. Aureus
Furuncles and Carbuncles
Clinical Presentation
- Furuncle: abscess deep within the hair follicle
- Carbuncle: more extensive involvement with multiple abscesses
- Systemic symptoms are common
- Complications: Cellulitis, bacteremia, sepsis
Furuncles and Carbuncles
Treatment
- Drainage (warm compresses will often accomplish this)
- ± Abx (especially if systemic signs)
- ± Surgery (if cannot achieve drainage)
Erysipelas
Overview
- Infection of the dermis
- Pathogen: Group A streptococci
- Pathogenesis:
- Organism enter via a break in the skin
- E.g. abrasions, tinea infection, skin ulceration
- Organism enter via a break in the skin
- Predisposing factors include:
- Poor venous drainage
- Chronic edema of other etiologies
- Obstruction
Erysipelas
Clinical Presentation
Skin: Painful erythema, warmth, well-demarcated borders
Systemic symptoms and signs common
Erysipelas
Management
- Diagnosis:
- Classic clinical findings
- Treatment:
-
Systemic antibiotic active against streptococci but also staphylococci
- Practically, we cannot distinguish this from cellulitis where staphylococcus may be involved so we cover staph too
- Sample antibiotic choices: nafcillin, oxacillin, cefazolin
- In the penicillin allergic pt you can use vancomycin, clindamycin or erythromycin
-
Systemic antibiotic active against streptococci but also staphylococci
Cellulitis
Overview
- Deeper infection beginning in the dermis and extending into the subcutaneous fat
-
Pathogens include:
- Group A Streptococci
- Staphylococcus aureus
- Clostridium
- Other pathogens less common
-
Predisposing factors:
- Poor venous drainage
- Chronic edema of other etiologies
- Lymphatic obstruction
Cellulitis
Clinical Presentation/Management
- Skin: erythema, warmth
- Systemic symptoms and signs
- Diagnosis: typical clinical findings
- Treatment: systemic abx active against strep and staph
- Sample abx as outlined above under erysipelas
Scalded Skin Syndrome
Overview
- Toxin-mediated skin disease
- Most common pathogen: S. Aureus
- Neonates and small children
- Pathogenesis: local infection, then subsequent systemic effects due to exfoliative exotoxin
Scalded Skin Syndrome
Clinical Presentation
- Erythematous rash
- Bullae
- Exfoliation
- Fever
Scalded Skin Syndrome
Management
- Diagnosis:
- Clinical findings
- You cannot find the organism in the skin (except at the site of the primary infection)
- Treatment:
- Antibiotic active against S. Aureus
Scarlet Fever
- Pathogen: Group A Streptococci
-
Pathogenesis:
- Erythrogenic toxin
- Capillary fragility
-
Clinical presentation:
- Erythematous rash
- Pastias lines
- Strawberry tongue
- Circumoral pallor
- Exfoliation
- Diagnosis: culture pharynx
- Treatment: penicillin
Toxic Shock Syndrome
Overview
-
Pathogens:
-
S. Aureus (TSST-1)
- Menstrual-related (tampons)
- Non-menstrual (surgical procedures, vaginal colonization)
-
Group A Strep (SPE A)
- Usually associated with skin and soft tissue infection
-
S. Aureus (TSST-1)
Toxic Shock Syndrome
Clinical Presentation
- Fever
- Hypotension
- Diffuse erythematous rash, which eventually exfoliates
- Multi-organ involvement
Toxic Shock Syndrome
Management
-
Diagnosis:
- Clinical syndrome
- Vaginal or cervical cultures
- Blood cultures
- Skin lesion culture
-
Treatment:
- Fluid replacement/resuscitation
- Removal of tampon if present
- Surgical debridement, if necessary
- Systemic (IV) abx active against streptococci and staphylococci
Necrotizing Fasciitis
Overview
- Infection penetrates beneath subcutaneous fat, into the fascial layers
-
Two main syndromes:
-
Group A Streptococcus (“flesh-eating bacteria”)
- Organism gains entry into skin, either spontaneously or from minor trauma, and progresses to deep infection
-
Mixed infection: facultative and anaerobic organisms
- Source of organisms is the gut
- Seen when there is some break in the gut barrier
- E.g. Abdominal surgery, perirectal or periurethral infection or trauma
-
Group A Streptococcus (“flesh-eating bacteria”)
- Increased incidence in diabetics
Necrotizing Fasciitis
Clinical Manifestations
- At first it may look like cellulitis but you need to look for clues to deeper infection
-
Skin - erythema, purplish hue, dusky gray, bullae
- Skin exquisitely tender and as time passes, there are is anesthesia
- Crepitance and foul odor in mixed infection
- Pt extremely ill
- Mortality 25-50%
Fournier’s Gangrene
Perineal gangrene in diabetic men
Necrotizing Fasciitis
Management
-
Diagnosis:
- Must have a high index of suspicion given the high mortality
- You can often take a probe and find that it will easily go down to the fascial layer
- Culture the skin/tissues/wound
- Treatment: systemic abx and surgery
Myonecrosis
Overview
- Infection penetrates to muscle
- Common pathogens:
- Streptococcus pyogenes
- Mixed infection
- Clostridium (perfringens or septicum)
- Pathogenesis:
- Usually infection gets to muscle by local spread
- Occasionally can get there hematogenously
Myonecrosis
Clinical Manifestations
- Muscle pain and edema
- Systemic symptoms
- Crepitance, with clostridium or mixed infection
- Pt usually also has necrotizing fasciitis
- Draining wound with bronze skin discoloration in clostridial infection
Myonecrosis
Management
- Prognosis: mortality 60-100%
- Diagnosis: must have a high index of suspicion given the high mortality
- Treatment: systemic abx and surgery
