Bacterial and Fungal Skin Infections

Organisms grouped by mechanism of entry

• Barrier breach → pyogenic invasion: Streptococcus pyogenes (non-purulent cellulitis, erysipelas, non-bullous impetigo) and Staphylococcus aureus including community-associated MRSA (abscess, furuncle, bullous impetigo). Toxin-mediated disease (exfoliative toxin A/B, TSST-1) arises from a small nidus with systemic toxin spread.
• Follicular occlusion/water exposure: S. aureus folliculitis; Pseudomonas aeruginosa in inadequately chlorinated hot tubs; Malassezia folliculitis in sebaceous zones.
• Keratin digestion: dermatophytes (Trichophyton rubrum predominant in the US) spread by fomites, locker-room floors, occlusive footwear, and animal contact (Microsporum canis → inflammatory kerion).
• Commensal overgrowth: Candida albicans in warm, macerated, occluded folds after antibiotics disturb bacterial flora.
• Water/soil inoculation: Vibrio vulnificus (saltwater, shellfish, cirrhosis — hemorrhagic bullae), Aeromonas (freshwater), Erysipelothrix (fish/meat handlers), Mycobacterium marinum (aquarium).

Modifiable risk factors (the ones examiners want treated)

• Tinea pedis and interdigital maceration: the classic portal of entry for recurrent lower-extremity cellulitis; treating it prevents recurrence.
• Obesity, hyperglycemia, occlusive clothing/footwear: moisture and fold friction favor Candida and dermatophytes.
• Poor glycemic control in diabetes: neutrophil dysfunction plus neuropathic ulceration.
• Injection drug use, IV catheters, recent surgery, nasal MRSA colonization, contact sports/crowding (wrestlers, military recruits, incarcerated persons).
• Iatrogenic immunosuppression: systemic or potent topical corticosteroids, TNF-α inhibitors, chemotherapy; topical steroids applied to tinea produce tinea incognito.

Non-modifiable / fixed factors

• Chronic lymphedema or prior saphenous vein harvest: impaired lymphatic clearance of bacteria; predicts relapsing cellulitis.
• Venous insufficiency, advanced age, atopic dermatitis or psoriasis (barrier defects and S. aureus colonization).
• HIV with low CD4+ count, transplant, hematologic malignancy, congenital neutrophil defects (chronic granulomatous disease, Job/hyper-IgE syndrome with cold staphylococcal abscesses).
• Male sex and post-pubertal androgen/sebum production for tinea cruris and tinea versicolor.

Bacterial Skin Infections

• Breach of barrier function: Disruption of the stratum corneum through trauma, maceration, or chronic inflammatory conditions (atopic dermatitis, psoriasis) allows bacterial colonization and invasion into deeper dermal and subcutaneous layers
• Virulence factors: Pathogenic bacteria produce toxins (alpha-toxin in Staphylococcus aureus, exotoxins in Streptococcus pyogenes), hyaluronidases, and proteases that facilitate tissue invasion, immune evasion, and spread through tissue planes
• Host immune response: Recruitment of neutrophils and inflammatory mediators causes local erythema, warmth, edema, and purulence; failure of immune containment permits progression to cellulitis, abscess formation, or bacteremia
• Biofilm formation: Chronic colonization organisms create antibiotic-resistant biofilms, particularly in wounds and devices, limiting penetration and efficacy of antimicrobials

Fungal Skin Infections

• Dermatophyte pathogenesis: Trichophyton, Microsporum, and Epidermophyton species produce keratinolytic enzymes that selectively digest keratin in stratum corneum, nails, and hair; host inflammatory response to fungal antigens causes pruritus and scaling
• Candida colonization and invasion: Candida albicans transitions from commensal colonizer to invasive pathogen in settings of altered microbiota (antibiotic use), warm/moist environment, or immunosuppression (low CD4+ count, corticosteroids); secreted aspartyl proteases and phospholipases enable epithelial penetration
• Lipophilic yeast adaptation: Malassezia furfur proliferates in sebaceous areas due to lipid dependence; produces pityriacin (melanin analog) causing hypo- or hyperpigmentation in tinea versicolor
• Impaired clearance: T-cell dysfunction (HIV/AIDS, organ transplant, TNF-α inhibitors) and neutrophil defects dramatically increase susceptibility to opportunistic fungi and severity of infection

Common Bacterial Infections

• Impetigo (superficial streptococcal/staphylococcal infection): Non-bullous form (70%) presents as honey-crusted erosions on exposed areas (face, extremities); bullous form displays flaccid blisters from exfoliative toxins; highly contagious in children; may follow minor trauma or insect bites
• Folliculitis (hair follicle infection): Pustules or nodules centered on follicular orifices, typically on trunk/legs; Staphylococcus aureus and gram-negative rods (Pseudomonas in hot tub exposure) are causative organisms; usually non-purulent but may progress to abscess
• Cellulitis (non-purulent spreading infection): Ill-defined erythema, warmth, edema, and systemic symptoms (fever, malaise); Streptococcus pyogenes and Staphylococcus aureus most common; predisposing factors include lymphedema, venous insufficiency, tinea pedis as portal of entry
• Abscess/Boil (localized collection): Fluctuant nodule with surrounding erythema and induration; often MRSA in healthcare/community settings; painful and tender; may spontaneously drain or require incision and drainage
• Erysipelas (superficial lymphatic infection): Sharply demarcated, bright red, raised plaque with "orange peel" appearance; classically on face in elderly/immunocompromised; caused by Streptococcus pyogenes; associated with systemic toxicity
• Necrotizing fasciitis (surgical emergency): Rapid progression with severe pain out of proportion to examination findings, skin necrosis, crepitus, hemorrhagic bullae, and systemic toxicity; often polymicrobial or Streptococcus pyogenes with Staphylococcus aureus; high mortality if untreated

Common Fungal Infections

• Tinea pedis (athlete's foot): Interdigital maceration with erythema, scaling, and fissuring (most common type); vesicular or moccasin patterns also occur; pruritic and may itch intensely; Trichophyton mentagrophytes or Trichophyton rubrum most common
• Tinea corporis (ringworm): Sharply demarcated erythematous patches with central clearing creating "ring" appearance and trailing scale; non-follicular distribution; pruritic; any body surface may be involved
• Tinea cruris (jock itch): Pruritic, bilateral, well-demarcated plaques in groin, sparing scrotum; more common in males and warm climates; caused by Trichophyton mentagrophytes, T. rubrum, or Epidermophyton floccosum
• Onychomycosis (nail infection): Distal subungual infection most common—yellow/brown discoloration and thickening progressing proximally; may also present as white superficial form or nail dystrophy; slow progression over months to years
• Candida intertrigo (intertriginous infection): Satellite pustules surrounding erythematous maceration in skin folds (axillae, groin, inframammary); white exudate and erosions present; pruritic and painful; risk factors include obesity, diabetes, antibiotic use
• Tinea versicolor (malassezia infection): Hypo- or hyperpigmented macules/patches coalescing on trunk; fine "spaghetti and meatballs" appearance on KOH prep; non-pruritic usually; recurrent and cosmetically bothersome
• Oral candidiasis (thrush): White plaques on tongue, buccae, hard palate that cannot be scraped off (pseudomembranous form); atrophic form presents as erythematous patches; erythematous angular cheilitis at corners of mouth; indicates immunosuppression in adults

Bacterial Infections

• Clinical diagnosis: Most superficial bacterial infections (impetigo, folliculitis, erysipelas) diagnosed clinically based on characteristic morphology and distribution; clinical judgment sufficient for most non-severe cases
• Culture from purulent material: Indicated for recurrent infections, atypical presentations, suspected MRSA, abscess fluid (always send before incision/drainage), or cellulitis with systemic toxicity; obtain before antibiotics if possible; Gram stain shows gram-positive cocci in clusters (Staph) vs. chains (Strep)
• Blood cultures: Obtain in cellulitis with signs of bacteremia (fever, hypotension, severe systemic symptoms) or in immunocompromised patients; often negative but guides therapy
• Wood's lamp and dermoscopy: Helpful adjuncts but unreliable for diagnosis; erysipelas may show orange-peel texture
• Imaging considerations: Ultrasound or MRI for suspected necrotizing fasciitis to assess fascial involvement; CT for deep space infections or abscess localization

Fungal Infections

• KOH (Potassium Hydroxide) preparation: Gold standard for most dermatophyte infections; scrape scale from border of lesion, mount on slide with 10-40% KOH solution, heat gently; look for "spaghetti and meatballs" (Malassezia) or hyphae and spores; sensitivity 60-70%
• Fungal culture: Indicated when KOH negative but clinical suspicion high; send on Sabouraud dextrose agar; identify species to confirm diagnosis and guide treatment duration; slow growth (1-4 weeks); essential for

Immediate stabilization — exclude the emergency first

• Necrotizing fasciitis: pain out of proportion, rapid progression, crepitus, or hemodynamic instability mandates immediate surgical exploration and debridement — this is diagnostic and therapeutic, and imaging must never delay it (IDSA 2014). Give fluid resuscitation plus empiric broad-spectrum therapy: a carbapenem or piperacillin-tazobactam plus vancomycin (or linezolid) plus clindamycin as a ribosomal protein-synthesis inhibitor to shut off streptococcal exotoxin production. Vancomycin is dosed to a 24-hour AUC targeting AUC/MIC 400–600 per the 2020 IDSA/ASHP consensus — the old 15–20 mcg/mL trough goal is retired. IVIG is adjunctive in streptococcal toxic shock.

First-line therapy by syndrome (IDSA 2014)

• Purulent infection (abscess, furuncle, carbuncle): incision and drainage is the definitive treatment; adjunctive oral antibiotics with MRSA activity (trimethoprim-sulfamethoxazole, doxycycline, or clindamycin) for larger lesions, surrounding cellulitis, systemic signs, or immunosuppression.
• Non-purulent cellulitis/erysipelas: streptococcal coverage with a beta-lactam — penicillin VK, amoxicillin, or a first-generation cephalosporin (cephalexin); IV cefazolin if systemically ill. Elevate the limb and treat concurrent tinea pedis.
• Impetigo: topical mupirocin for limited disease; oral cephalexin or dicloxacillin when widespread or in outbreaks.
• Dermatophytosis: topical allylamine (terbinafine) or azole (clotrimazole). Oral therapy is mandatory where topicals cannot penetrate — tinea capitis (griseofulvin, favored for Microsporum, or terbinafine per AAP Red Book) and onychomycosis (oral terbinafine, ~6 weeks fingernails, ~12 weeks toenails).
• Candidiasis: topical nystatin or azole plus drying measures for intertrigo; clotrimazole troches or nystatin suspension for thrush, with oral fluconazole for moderate–severe or esophageal disease (IDSA 2016 candidiasis guideline).
• Tinea versicolor: topical selenium sulfide or ketoconazole shampoo; oral itraconazole for extensive disease.

Contraindicated / avoid

• Topical corticosteroid monotherapy on tinea → tinea incognito.
• Nystatin for dermatophytes — active only against Candida.
• Oral ketoconazole for cutaneous fungal infection (FDA restricted: hepatotoxicity, adrenal suppression).
• Griseofulvin and oral azoles in pregnancy; itraconazole in heart failure (negative inotropy).

Emergencies — recognize immediately

• Necrotizing fasciitis: fascial-plane spread outruns dermal findings; signaled by pain out of proportion, anesthesia over the lesion, dusky/hemorrhagic bullae, crepitus, or rapidly rising creatinine and lactate. Surgical emergency.
• Streptococcal toxic shock syndrome / staphylococcal TSS: superantigen-driven massive T-cell cytokine release → fever, diffuse macular erythroderma, hypotension, multiorgan failure, later desquamation.
• Bacteremia with metastatic seeding: S. aureus bacteremia can produce infective endocarditis, vertebral osteomyelitis, or epidural abscess — persistent fever after appropriate therapy is the clue; obtain repeat blood cultures and echocardiography.
• Periorbital → orbital cellulitis: pain with extraocular movement, proptosis, or diplopia signals post-septal spread; CT orbits and IV antibiotics.

Disease complications

• Post-streptococcal glomerulonephritis: immune-complex deposition weeks after impetigo — cola-colored urine, hypertension, low C3. Treating impetigo does not reliably prevent it; acute rheumatic fever does not follow skin infection.
• Staphylococcal scalded skin syndrome: exfoliative toxin cleaves desmoglein-1 → superficial sloughing with positive Nikolsky sign, mucosa spared; distinguishes it from SJS/TEN.
• Lymphangitis and chronic lymphedema: repeated cellulitis destroys lymphatics, creating a recurrence cycle.
• Kerion and permanent scarring alopecia from untreated inflammatory tinea capitis; Majocchi granuloma when dermatophyte invades follicles, often after steroid use.
• Id reaction (autoeczematization): sterile vesicular hand eruption remote from active tinea pedis.
• Invasive candidiasis/candidemia in neutropenic or catheterized patients.

Treatment complications

• **Clindamycin → Clostridioides difficile colitis**; new watery diarrhea on therapy.
• TMP-SMX: hyperkalemia, rise in creatinine, and severe cutaneous adverse reactions (SJS/TEN).
• Vancomycin: acute kidney injury (higher AUC exposures), infusion reaction from histamine release.
• Terbinafine: hepatotoxicity and taste/smell disturbance; griseofulvin: teratogenicity and disulfiram-like reaction with alcohol; itraconazole: negative inotropy and CYP3A4 interactions.

• Honey-colored crust on a child's face is impetigo; the sequela tested is post-streptococcal glomerulonephritis, not acute rheumatic fever. Rheumatic fever follows pharyngitis only.
• Pain out of proportion to exam with a rapidly spreading erythema: the single best next step is surgical exploration, not CT, not LRINEC scoring, not "observe on IV antibiotics." Imaging that delays the operating room is the classic wrong answer.
• Purulent vs. non-purulent decides the drug (IDSA 2014): abscess → I&D first, MRSA-active oral agent if adjunct needed; non-purulent cellulitis → beta-lactam (cephalexin) for Streptococcus. Adding MRSA coverage to simple non-purulent cellulitis is the common over-treatment distractor.
• Recurrent lower-leg cellulitis — look for tinea pedis interdigitally. Treating the fungal portal of entry is the association examiners test; missing it is why the cellulitis keeps coming back.
• Bilateral, symmetric, non-tender "cellulitis" without fever is stasis dermatitis, not infection. True cellulitis is essentially always unilateral.
• KOH findings sort the fungi: branching septate hyphae → dermatophyte; "spaghetti and meatballs" (short hyphae + spores) → Malassezia / tinea versicolor; pseudohyphae with budding yeast → Candida. Satellite pustules in a moist fold = candidal intertrigo.
• Topicals fail where keratin is thick or hair is invaded: tinea capitis and onychomycosis require oral therapy (griseofulvin or terbinafine). Prescribing topical antifungal alone for scalp or nail disease is a guaranteed distractor.
• **Nystatin covers Candida only** — it has no dermatophyte activity. Likewise, a topical steroid on tinea creates tinea incognito: less scale, blurred border, expanding ring.
• Thrush in a non-infant, non-inhaler-using adult should prompt HIV testing; esophageal candidiasis is an AIDS-defining illness.