Info
🌱 來自: Huppert’s Notes
Common Skin Infections🚧 施工中
Common Skin Infections
Bacterial
Folliculitis
• Pathophysiology: Staph aureus >> Klebsiella, Enterobacter, and Pseudomonas (hot tub exposure). Causes inflammation of the hair follicles
• Clinical features: Perifollicular erythematous papules and pustules on hair-bearing areas
• Treatment: Antimicrobial washes (chlorhexidine), topical antibiotics, or systemic antibiotics if refractory/recurrent
Furuncles/carbuncles
• Pathophysiology: Deeper infections of the hair follicle (i.e., furuncles) may coalesce to form carbuncles
• Treatment: Incision and drainage
Impetigo
• Pathophysiology: Superficial infection of the epidermis, most commonly caused by Staph aureus or group A strep
• Clinical features: Characterized by well-demarcated erythema with papules that progress to vesicles or pustules, which break and form a thick, “honey-colored” crust
• Treatment: Topical or oral antibiotics
Cellulitis
• Pathophysiology: Deeper infection involving the dermis, subcutaneous tissue, and superficial lymphatics (termed erysipelas)
• Clinical features: Characterized by an acute, ill-defined red lesion that is tender, warm to the touch, and associated with edema; typically unilateral and can present with systemic symptoms such as fever, tachycardia, and leukocytosis
• Microbiology:
- Non-purulent cellulitis (~90% Strep spp., ~10% Staph spp.)
- Purulent cellulitis/abscess (~75% Staph aureus but can be polymicrobial)
• Treatment:
- Address underlying risk factors (e.g., lymphedema, tinea) and treat with systemic antibiotics
- Non-purulent cellulitis:
• Outpatient: Cephalexin ×5 days (alternative = clindamycin). If slow resolution or complicated course consider 7–10 day course
• Inpatient: IV cefazolin. Add MRSA coverage (e.g., IV vancomycin) if patient is unstable, the cellulitis is over an indwelling medical device, known MRSA colonization, recent prior MRSA infection, significant health care facility exposure (dialysis, long term care), injection drug use, or progression on an antibiotic regimen that does not cover MRSA
- Purulent cellulitis:
• Drain abscess, if present, and send for culture
• Outpatient: TMP/SMX ×7 days (can consider no antibiotics if abscess drained in low risk patient)
• Inpatient: IV vancomycin
- Recurrent non-MRSA cellulitis:
• Address risk factors/try to break cycle (tinea/lymphedema/venous stasis/obesity → impaired drainage, worsening anatomic issues → infection)
- Animal bite: Wound care + TDAP + prophylactic antibiotics if host risk factors (immunocompromised, e.g., DM, cirrhosis) or bite risk factors (cat bite, severe/deep, high-risk location, e.g., hand, face, joint)
• Pearls:
- Three general rules for cellulitis:
• Most cases are unilateral, acute onset, and respond within 72 hours of starting antibiotics. If these features are not present, consider alternative diagnoses and/or a dermatology consult. 30% of cellulitis cases are misdiagnosed. Most common alternative diagnoses: Stasis dermatitis, contact dermatitis, inflammatory tinea
• Failure of outpatient antibiotics is often due to an unrecognized abscess (need for drainage)
• Blood cultures are usually unnecessary in the work-up for cellulitis. Exceptions: Severe sepsis, immunocompromised hosts, bites, need for debridement
Necrotizing fasciitis
• Pathophysiology: Infection of the subcutaneous fat and fascia, potentially life threatening (mortality up to 40%) due to rapid spread along fascial planes; may be monomicrobial (commonly Staph aureus or Strep pyogenes), polymicrobial (aerobic and anaerobic bacteria), or can cause gas gangrene (caused by Clostridium spp)
• Clinical features: Early lesions may appear similar to cellulitis but with “pain out of proportion to exam”; rapidly evolves with progressive painful, necrotic lesions and septic shock; may develop hemorrhagic bullae, subcutaneous gas (appreciated on imaging or as crepitus on exam)
• Treatment: Source control (early surgical consultation for debridement) + abx for MRSA, GNRs, and anaerobes (IV vancomycin + pip/tazo +/− clindamycin for toxin production) × 48–72 hrs after source control
• Pearl: Although commonly used, LRINEC score is only ~65% sensitive
Erythrasma
• Pathophysiology: Benign superficial bacterial infection due to Corynebacterium minutissimum
• Clinical features: Characterized by mildly pruritic red-brown plaques in the intertriginous areas with a “cigarette paper” appearance
• Treatment: Topical antibiotics
Staphylococcal scalded skin syndrome (SSSS)
• Pathophysiology: Caused by circulating S. aureus exotoxin (cleaves desmoglein). Most common in children (age <2 yr), although can occur in adults if renal insufficiency or immunocompromised
• Clinical features: Characterized by diffuse erythema and large flaccid sterile bullae; ALWAYS spares the mucosa
• Treatment: Repletion of fluid/electrolyte losses, skin care with moisture and non-stick dressings, systemic antibiotics if concerned for superinfection; consider adding clindamycin for inhibition of toxin production; consider IVIG in severe cases
Lyme disease
• Pathophysiology: Tick-borne illness due to the spirochete Borrelia burgdorferi
• Clinical features: Classically presents with erythema migrans, an erythematous patch with central clearing (“bullseye appearance”) that appears 7–14 days after a tick bite
• Treatment: PO doxycycline for primary Lyme disease
Rocky Mountain spotted fever
• Pathophysiology: Tick-borne illness due to Rickettsia rickettsia
• Clinical features: Classically presents with a macular eruption involving the palms and soles; associated with systemic symptoms including headache, myalgias, and gastrointestinal symptoms; labs may show leukopenia, thrombocytopenia, and elevated LFTs
• Treatment: PO doxycycline
Syphilis
• Pathophysiology: Infection caused by the spirochete Treponema pallidum
• Clinical features:
- Primary: Red papule that erodes to form a painless ulcer with raised borders (“chancre”), typically on the genitalia; occurs 10–90 days after exposure
- Secondary: Diffuse “ham-colored” macules on the trunk and extremities, frequently involving the palms and soles; occurs 2–10 weeks after developing the chancre
• Treatment: See Infectious Diseases Chapter 10
Viral
Herpes simplex virus (HSV)
• Pathophysiology: HSV-1 infection is typically above the waist (oral, facial). HSV-2 infection is typically below the waist (genital); can be primary or recurrent. Typically, first infection with HSV-1 is during childhood (0–5 yr), whereas HSV-2 infection may occur with onset of sexual activity.
• Clinical features: Presents as painful clear vesicles on an erythematous base. May be asymptomatic (subclinical) or have fever, malaise, local lymphadenopathy (primary >> recurrence). Widespread infection can occur in immunocompromised patients (e.g., patients with HIV). Can infect established dermatoses (e.g., eczema herpeticum) or involve cranial nerves (Maurice syndrome).
• Treatment: Acyclovir, valacyclovir
Varicella zoster virus (VZV)
• Pathophysiology: Primary varicella (“chickenpox”) → herpes zoster (“shingles”)
• Clinical features: Herpes zoster presents as localized burning, tingling, or stinging followed by a dermatomal eruption of vesicles and pustules on an erythematous base; considered disseminated if there are vesicles outside the primary dermatome or if involving the CNS (meningitis, encephalitis), liver (hepatitis), or lungs (pneumonia). Ophthalmology consult required if involvement occurs near the eye
• Treatment: Acyclovir, valacyclovir, gabapentin and TCAs for post-herpetic neuralgia
Warts
• Pathophysiology: Common warts (Verruca vulgaris) and anogenital warts (Condyloma acuminata) caused by HPV
• Clinical features: Presents as skin-colored papules with thrombosed capillaries
• Treatment: Salicylic acid, cryotherapy
Molluscum contagiosum
• Pathophysiology: Infection caused by a poxvirus; occurs in children, sexually transmitted in adults; can be severe in HIV/AIDS
• Clinical features: Presents as pink-white smooth papules with an umbilicated center
• Treatment: Typically self-resolves but can use cryotherapy, curettage
Fungal
Tinea
• Pathophysiology: Superficial fungal infection classified by body site involved (pedis = feet, manuum = hands, cruris = groin, capitis = scalp, corporis = body)
• Clinical features: Characterized by annular (ring-like) scaly patches with well-demarcated edges and central clearing; may be pruritic
• Diagnosis: +KOH stain
• Treatment: Topical azoles or terbinafine
• Pearl: Use terbinafine (or another allylamine) as first line for tinea pedis, cruris, and corporis. Allylamines are fungicidal whereas topical azoles are fungistatic.
Pityriasis (tinea) versicolor
• Pathophysiology: Caused by Malassezia furfur
• Clinical features: Presents as non-pruritic oval/round hypo- or hyper-pigmented lesions on the trunk and upper extremities
• Diagnosis: KOH prep with “spaghetti and meatball” appearance
• Treatment: Ketoconazole shampoo or selenium sulfide
Candidiasis/intertrigo
• Pathophysiology: Superficial fungal infection due to Candida spp.
• Clinical features: Presents as bright red (often macerated) patches with satellite pustules in areas of moist occluded skin (intertriginous areas, oropharynx, genitals)
• Treatment: Topical azoles, nystatin, drying/absorbent powders or zinc oxide paste. If widespread, can consider oral fluconazole
Ectoparasites
Scabies
• Pathophysiology: Highly contagious infestation caused by the mite Sarcoptes scabiei hominis
• Clinical features: Characterized by intensely pruritic erythematous papules, excoriations and linear burrows in the interdigital spaces, wrists, ankles, breasts, periumbilical area, and genitals
• Treatment: Permethrin 5% cream, decontamination of clothes and bedding
Lice
• Pathophysiology: Infestation caused by the louse Peduculus humanus; can affect the head, body, or pubic area
• Clinical features: Presents with excoriations and crusted papules on the neck, trunk, proximal arms, or groin; may find live lice on the scalp or eggs (nits) in the hair
• Treatment: Permethrin 1% cream, decontamination of clothes and bedding
Bedbugs
• Pathophysiology: Infestation caused by the insect Cimex lectularis
• Clinical features: Presents with linearly arranged pruritic papules (“breakfast, lunch, and dinner”)
• Treatment: Professional extermination