Inflammatory Skin Diseases PDF

Infectious dermatoses-Bacterial infections Numerous bacterial infections occur in skin. These range from superficial infections known as impetigo, to deeper dermal abscesses associated with puncture wounds that are caused by bacteria such as Pseudomonas aeruginosa. Infectious dermatoses-Bacterial...

Infectious dermatoses-Bacterial infections Numerous bacterial infections occur in skin. These range from superficial infections known as impetigo, to deeper dermal abscesses associated with puncture wounds that are caused by bacteria such as Pseudomonas aeruginosa. Infectious dermatoses-Bacterial infections Impetigo: Clinical features: one of the most common bacterial infections of the skin, is seen primarily in children causative organism is usually Staphylococcus aureus or, less commonly, Streptococcus pyogenes Infectious dermatoses-Bacterial infections Impetigo: Clinical features: typically acquired through direct contact with a source often begins as a single small macule, usually on the extremities or the face near the nose or the mouth, which rapidly evolves into a larger often with a honey-colored crust of dried serum Individuals who are colonized by S. aureus or S. pyogenes are more likely to be affected. less common bullous form of childhood impetigo may mimic an autoimmune blistering disorder. Infectious dermatoses-Bacterial infections Impetigo: Morphology: accumulation of neutrophils beneath the stratum corneum, subcorneal pustule nonspecific reactive epidermal alternation superficial dermal inflammation accompany these findings. Bacterial cocci in the superficial epidermis can be demonstrated by Gram stain. Infectious dermatoses-Fungal infections range from superficial infections with Tinea or Candida spp. to life-threatening Aspergillus spp. infections in immunosuppressed individuals can be superficial (stratum corneum, hair, and nails), deep (dermis or subcutis), or systemic, the last type arising through hematogenous spread, often in an immunocompromised patient. Infectious dermatoses-Fungal infections Clinical Features: superficial infections usually produce erythematous macules with superficial scale that can be pruritic superficial fungal infections may have an annular appearance; also may induce lesions that mimic other psoriasiform or eczematous dermatoses, so it is important to consider the possibility of fungal infection when these conditions are in the differential diagnosis Infectious dermatoses-Fungal infections deeper infections such as those seen with Aspergillus spp. are erythematous and often nodular and sometimes associated with local hemorrhage Infectious dermatoses-Fungal infections Morhology: histologic appearance varies depending on the organism, host response, and degree of superinfection. superficial infections are often associated with a neutrophilic infiltrate in the epidermis. Periodic acid–Schiff (PAS) and Gomori methenamine silver stains are helpful in identifying the fungal organisms. Infectious dermatoses-Fungal infections Deep fungal infections produce greater tissue damage and often elicit a granulomatous response. Aspergillus can be angioinvasive. Infectious dermatoses-Verrucae (Warts) proliferative lesions of squamous epithelial cells that are caused by human papillomavirus (HPV). most common in children and adolescents, but may be encountered in any age group. HPV infection usually stems from direct contact with an infected individual or autoinoculation. Verrucae generally are self-limited, most often regressing spontaneously within 6 months to 2 years. Infectious dermatoses-Verrucae (Warts) Pathogenesis: cutaneous warts are mainly caused by low-risk HPV subtypes that lack transforming potential. Different kinds of warts are identified on the basis of their gross appearance and location and generally are caused by distinct HPV subtypes. Infectious dermatoses-Verrucae (Warts) Verruca plantaris and verruca palmaris occur on the soles and palms, respectively. These rough, scaly lesions can reach 1 to 2 cm in diameter and may coalesce to form a surface that can be confused with ordinary calluses. Condyloma acuminatum (venereal wart) occurs on the penis, female genitalia, urethra, and perianal areas. Infectious dermatoses-Verrucae (Warts) Clinical features: Verruca vulgaris: can occur anywhere but is found most frequently on the hands, a gray-white to tan, flat to convex, 0.1- to 1-cm papule with a rough, pebble like surface. Verruca plana (flat wart): common on the face or dorsal surfaces of the hands . Infectious dermatoses-Verrucae (Warts) Pathogenesis: Like high-risk HPV, low-risk viruses express viral E6 and E7 oncoproteins that lead to dysregulated epidermal cell growth and increased survival. Because the growth of warts is normally halted by the immune response, immunodeficiency is associated with more numerous and larger verrucae. Infectious dermatoses-Verrucae (Warts) Morphology: epidermal hyperplasia; verrucous or papillomatous epidermal hyperplasia cytoplasmic vacuolization (koilocytosis) Infected cells also may demonstrate prominent keratohyalin granules and jagged eosinophilic intracytoplasmic protein aggregates as a result of impaired maturation Part IV BLISTERİNG/BULLOUS DISEASES Blistering/Bullous diseases vesicles and bullae (blisters) occur as secondary phenomena in several unrelated conditions (e.g., herpesvirus infection, spongiotic dermatitis), a group of disorders in which blisters are the primary and most distinctive feature, blistering in these diseases tends to occur at specific levels within the skin, a morphologic distinction that is critical for diagnosis Blistering/Bullous diseases-Pemphigus (Vulgaris and Foliaceus) an uncommon autoimmune blistering disorder resulting from loss of normal intercellular attachments within the epidermis and the squamous mucosal epithelium three major variants: • Pemphigus vulgaris (the most common type) • Pemphigus foliaceus • Paraneoplastic pemphigus Blistering/Bullous diseases-Pemphigus (Vulgaris and Foliaceus) Pathogenesis: Pemphigus vulgaris and pemphigus foliaceus are autoimmune diseases caused by antibody-mediated (type II) hypersensitivity reactions. The pathogenic antibodies are IgG autoantibodies that bind to intercellular desmosomal proteins (desmoglein types 1 and 3) found in the skin and mucous membranes. The antibodies disrupt the intercellular adhesive function of desmosomes and may activate intercellular proteases. Blistering/Bullöz hastalıklar -Pemphigus (Vulgaris and Foliaceus) Blistering/Bullous diseases- Pemphigus (Vulgaris and Foliaceus) The distribution of desmoglein proteins within the epidermis determines the location of the lesions. By direct immunofluorescence study, lesional sites show a characteristic fishnet-like pattern of intercellular IgG deposits. As with many other autoimmune diseases, pemphigus is associated with particular HLA alleles. Blistering/Bullous diseases-Pemphigus (Vulgaris and Foliaceus) Morphology: Pemphigus vulgaris involves both mucosa and skin, especially on the scalp, face, axillae, groin, trunk, and points of pressure. The lesions are superficial flaccid vesicles and bullae that rupture easily, leaving deep and often extensive erosions covered with a serum crust. Blistering/Bullous diseases- Pemphigus (Vulgaris and Foliaceus) Pemphigus foliaceus, a rare, milder form of pemphigus, results in bullae that are mainly confined to the skin, with only infrequent involvement of mucous membranes. The blisters in this disorder are superficial, such that more limited zones of erythema and crusting of ruptured blisters are seen Blistering/Bullöz hastalıklar -Pemphigus (Vulgaris and Foliaceus) Acantholysis: lysis of the intercellular adhesive junctions between neighboring squamous epithelial cells that results in the rounding up of detached cells Blistering/Bullöz hastalıklar -Pemphigus (Vulgaris and Foliaceus) Pemphigus vulgaris: acantholysis involves the layer of cells immediately above the basal cell layer= suprabasal acantholytic blister Variable superficial dermal infiltrates composed of lymphocytes, macrophages, and eosinophils accompany all forms of pemphigus. Blistering/Bullöz hastalıklar -Pemphigus (Vulgaris and Foliaceus) In pemphigus foliaceus, acantholysis selectively involves the superficial epidermis at the level of the stratum granulosum. Blistering/Bullöz hastalıklar -Pemphigus (Vulgaris and Foliaceus) Blistering/Bullous diseases-Bullous Pemphigoid Bullous pemphigoid is another distinctive acquired blistering disorder with an autoimmune basis. Bullous pemphigoid and pemphigus vulgaris are caused by similar pathogenic mechanisms, but differ in their clinical presentation and course due to variation in the location of the target antigen (hemidesmosomes in bullous pemphigoid, desmosomes in pemphigus). Blistering/Bullous diseases-Bullous Pemphigoid Clinical features: The lesions of bullous pemphigoid do not rupture as readily as in pemphigus and, if uncomplicated by infection, heal without scarring. The disease tends to follow a remitting and relapsing course and responds to topical or systemic immunosuppressive agents. Gestational pemphigoid (also known as herpes gestationis, a misnomer since there is no viral etiology) is a clinically distinct subtype that appears suddenly during the second or third trimester of pregnancy. It also is caused by autoantibodies against bullous pemphigoid antigen. Gestational pemphigoid typically resolves after childbirth, but may recur with subsequent pregnancies. Blistering/Bullous diseases-Bullous Pemphigoid Pathogenesis: Blistering in bullous pemphigoid is triggered by the linear deposition of autoreactive IgG antibodies and complement in the epidermal basement membrane. Reactivity also occurs in the basement membrane attachment plaques (hemidesmosomes), where most bullous pemphigoid antigen (most commonly type XVII collagen) is located. The proteins that are recognized by the autoantibodies have structural roles in dermoepidermal adhesion. IgG autoantibodies to hemidesmosome components fix complement and cause tissue injury by recruiting neutrophils and eosinophils. Blistering/Bullous diseases-Bullous Pemphigoid Blistering/Bullous diseases-Bullous Pemphigoid Morphology: tense subepidermal bullae filled with clear fluid epidermis characteristically lacks acantholysis blister roof consists of full-thickness epidermis with intact intercellular junctions, a key distinction from the blisters seen in pemphigus. Blistering/Bullous diseases-Bullous Pemphigoid Early lesions show variable numbers of eosinophils at the dermal-epidermal junction, occasional neutrophils, superficial dermal edema, and associated basal cell layer vacuolization. Blistering/Bullous diseases -Dermatitis Herpetiformis Dermatitis herpetiformis is an autoimmune blistering disorder associated with gluten sensitivity that is characterized by extremely pruritic grouped vesicles and papules. The disease affects predominantly males, often in the third and fourth decades of life. Up to 80% of cases are associated with celiac disease; conversely, only a small fraction of patients with celiac disease develop dermatitis herpetiformis. like celiac disease, dermatitis herpetiformis responds to a gluten-free diet. lesions of dermatitis herpetiformis are bilateral, symmetric, and grouped and preferentially involve the extensor surfaces, elbows, knees, upper back, and buttocks . Blistering/Bullous diseases -Dermatitis Herpetiformis Pathogenesis: Genetically predisposed individuals develop IgA antibodies to dietary gluten (derived from the wheat protein gliadin) as well as IgA autoantibodies that cross-react with endomysium and tissue transglutaminases, including epidermal transglutaminase expressed by keratinocytes. Blistering/Bullous diseases -Dermatitis Herpetiformis direct immunofluorescence, the skin shows discontinuous, granular deposits of IgA selectively localized in the tips of dermal papillae. resultant injury and inflammation produce a subepidermal blister. Blistering/Bullous diseases -Dermatitis Herpetiformis Morphology: Initially, neutrophils accumulate selectively at the tips of dermal papillae, forming small microabscesses The basal cells overlying these microabscesses show vacuolization and focal dermoepidermal separation that ultimately coalesce to form a true subepidermal blister.