6.3 Inflammatory & Infectious Dermatoses

Inflammatory & Infectious Dermatoses

Dermatologic disorders encompass a broad spectrum of autoimmune, inflammatory, and infectious cutaneous pathologies. Accurate evaluation relies on clinical lesion morphology, anatomical distribution, systemic signs, and histopathological features.

Papulosquamous & Autoimmune Inflammatory Dermatoses

Psoriasis Vulgaris is a T-cell-mediated autoimmune papulosquamous disorder characterized by keratinocyte hyperproliferation:

• Clinical Presentation: Well-demarcated, erythematous plaques covered with thick, silvery-white scales located primarily on extensor surfaces (elbows, knees, scalp, lumbosacral region). Classic clinical signs include the Auspitz sign (pinpoint bleeding when scales are scraped, due to thinned epidermis over elongated dermal papillae) and the Koebner phenomenon (development of psoriatic lesions at sites of mechanical skin trauma). Associated nail changes include pitting, subungual hyperkeratosis, and "oil-drop" discoloration.
• Histopathology: Marked epidermal acanthosis (thickening), parakeratosis (retention of nuclei in stratum corneum), elongation of rete ridges, neutrophilic microabscesses in stratum corneum (Munro microabscesses), and absent stratum granulosum.
• Pharmacotherapy: Mild-to-moderate disease (< 10% body surface area [BSA]) is treated with topical high-potency corticosteroids combined with topical vitamin D analogs (calcipotriene). Moderate-to-severe disease (> 10% BSA) or concomitant psoriatic arthritis requires phototherapy (UVB) or systemic biological agents targeting TNF-alpha, IL-17 (secukinumab), or IL-23 (ustekinumab). Systemic oral corticosteroids are strictly contraindicated because taper or withdrawal triggers life-threatening generalized pustular psoriasis rebound.

Atopic Dermatitis (Eczema) is a chronic pruritic inflammatory skin disease driven by epidermal barrier dysfunction (frequently due to filaggrin gene mutations) and Th2 immune activation:

• Clinical Presentation: Intensely pruritic, ill-demarcated erythematous papules and plaques with lichenification. In infants, lesions affect extensor surfaces and face; in adolescents and adults, lesions concentrate on flexor surfaces (antecubital and popliteal fossae). Forms part of the atopic triad (atopic dermatitis, allergic asthma, allergic rhinitis). Elevated serum IgE is common.
• Complications: Eczema herpeticum represents a secondary superinfection with Herpes Simplex Virus (HSV-1), presenting as widespread punched-out monomorphic erosions with hemorrhagic crusting superimposed on eczematous skin; requires immediate IV/oral acyclovir.
• Treatment: Emollients, topical corticosteroids, and topical calcineurin inhibitors (tacrolimus, pimecrolimus).

Contact Dermatitis divides into:

1. Allergic Contact Dermatitis: Type IV delayed-type hypersensitivity reaction (urushiol from poison ivy, nickel, neomycin). Presents with intensely pruritic linear vesicular eruptions appearing 12 to 48 hours post-exposure.
2. Irritant Contact Dermatitis: Non-immunologic direct chemical damage (soaps, frequent hand washing), localized strictly to contact areas.

Lichen Planus presents with the 5 Ps: Pruritic, Polygonal, Planar, Purple Papules and plaques on flexor surfaces of wrists and ankles. Surface evaluation reveals fine reticular white lines (Wickham striae). Mucosal involvement (white lacy mucosal plaques) occurs in > 50%. Lichen planus is strongly associated with underlying Hepatitis C virus (HCV) infection. Histopathology shows a dense, band-like lymphocytic infiltrate at the dermal-epidermal junction with hypergranulosis and "saw-tooth" rete ridges.

Superficial Bacterial & Fungal Infections

Cutaneous bacterial infections are categorized by depth and anatomical involvement:

• Erysipelas: Superficial dermis and prominent lymphatic infection caused almost exclusively by Group A Streptococcus (Streptococcus pyogenes). Features bright red, warm, edematous skin with sharply demarcated, raised borders, predominantly on the face or lower extremities, accompanied by acute high fever and systemic toxicity.
• Cellulitis: Deeper infection involving the deep dermis and subcutaneous fat. Characterized by poorly demarcated, flat erythematous areas with warmth, swelling, and tenderness. Non-purulent cellulitis is caused by S. pyogenes or MSSA and treated with oral cephalexin or dicloxacillin. Purulent cellulitis (associated with abscesses or furuncles) is driven by community-acquired MRSA and requires oral trimethoprim-sulfamethoxazole, doxycycline, or clindamycin.
• Impetigo: Highly contagious superficial infection in young children. Non-bullous impetigo (S. aureus or S. pyogenes) presents with erythematous macules progressing to flaccid vesicles that rupture into classic honey-colored crusts. Bullous impetigo (epidermolytic S. aureus) presents with clear flaccid bullae. Localized lesions are treated with topical mupirocin. Post-streptococcal glomerulonephritis (PSGN) can follow streptococcal pyoderma, but acute rheumatic fever does NOT follow skin infections.
• Staphylococcal Scalded Skin Syndrome (SSSS): Caused by hematogenous dissemination of S. aureus exfoliative toxins A and B, which target and cleave desmoglein-1 in the superficial stratum granulosum. Occurs primarily in neonates and children < 5 years. Features widespread tender erythema, flaccid bullae, and a positive Nikolsky sign (sloughing of top epidermal layer with gentle pressure). Mucous membranes are characteristically spared. Treatment requires IV anti-staphylococcal antibiotics (nafcillin, oxacillin, or vancomycin).
• Tinea Infections (Dermatophytosis): Fungal infections (Trichophyton, Microsporum) diagnosed by KOH preparation showing segmented hyphae. Tinea capitis presents with scaly alopecia and black dots; requires oral antifungal therapy (griseofulvin or terbinafine) because topical agents do not penetrate hair follicles.

Deep & Necrotizing Soft Tissue Infections

Necrotizing Fasciitis is a fulminant surgical emergency involving rapid necrosis of subcutaneous tissue and fascia:

• Clinical Presentation: Severe pain out of proportion to physical exam findings is the key early sign. Rapid progression to cutaneous anesthesia, skin discoloration (dusky purpura), bullae, and palpable crepitus (subcutaneous gas). Severe systemic toxicity, hypotension, and septic shock develop rapidly. Caused by monomicrobial Group A Streptococcus or polymicrobial anaerobes/aerobes (Fournier gangrene of the perineum in diabetics).
• Diagnostic Risk Stratification: Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC score) >= 6 (evaluating CRP, WBC, hemoglobin, sodium, creatinine, glucose) indicates high probability.
• Management Protocol: Suspected necrotizing fasciitis mandates immediate emergent surgical exploration and operative debridement combined with broad-spectrum IV triple therapy: Vancomycin (for MRSA) + Piperacillin-Tazobactam (for Gram-negatives and anaerobes) + Clindamycin (to suppress streptococcal bacterial toxin synthesis).

Diagnostic Algorithm: Acute Erythematous & Necrotizing Lesion Triage

[ Acute Spreading Erythema & Soft Tissue Pain ]
                       │
       ┌───────────────┴───────────────┐
       ▼                               ▼
[ Pain Out of Proportion / Crepitus ]   [ Pain Proportional to Exam ]
[ Dusky Bullae / LRINEC Score >= 6 ]   │
       │                               ├─► Sharply Raised Borders ──► Erysipelas (S. pyogenes)
       ▼                               ├─► Flat, Indistinct Margins ─► Cellulitis (S. pyogenes/S. aureus)
[ NECROTIZING FASCIITIS ]              └──► Honey-Colored Crusts  ──► Impetigo (Topical Mupirocin)
       │
       ├─► Emergency Surgical Debridement
       └─► Broad-Spectrum IV Triple Therapy
           (Vancomycin + Piperacillin-Tazobactam + Clindamycin)

Comparative Clinical Features of Cutaneous Infections