Autoimmune Bullous Dermatoses
Pemphigus Vulgaris (Pemphigus vulgaris) Characterized by the formation of an intraepidermal blister. Hematoxylin and eosin (H&E) staining reveals suprabasal clefts that even involve the epithelium of hair follicles. Lymphocytes and specific acantholytic cells—round structures with a large vesicular nucleus and pale cytoplasm—accumulate within the blister cavity. The dermis shows infiltration by eosinophils and lymphocytes. Direct immunofluorescence (DIF) demonstrates IgG and C3 deposition in the intercellular spaces.
Other forms of pemphigus:
- Vegetans: pronounced acanthosis, papillomatosis, and intraepidermal eosinophilic microabscesses.
- Foliaceus and seborrheic: acantholysis occurs in the upper layers (stratum granulosum and stratum spinosum). Detachment of the stratum corneum without the formation of a true blister is possible.
Dermatitis Herpetiformis (Duhring's Disease) A chronic relapsing condition predominantly affecting individuals aged 30–40 (familial forms are more common in women). The rash is polymorphic: vesicles, papules, and urticarial plaques on an erythematous background. The elements tend to group in a herpetiform pattern and evolve in a sequence of vesicle $\rightarrow$ pustule $\rightarrow$ rupture $\rightarrow$ erosion $\rightarrow$ crust. Persistent pigmentation remains at the site of resolution. Nikolsky's sign is negative. Histologically, the process begins with an accumulation of neutrophils and eosinophils in the papillary dermis, forming microabscesses and subepidermal clefts. Initially, the blister is multilocular (multichambered), but as the interpapillary connections break down, it becomes unilocular. DIF reveals granular or linear IgA deposits along the basement membrane.
Eczematous Reaction (Eczema)
Forms the basis of a significant portion of skin pathologies. Exposure to external and internal factors damages the epidermis, increases local osmotic pressure, and triggers an immune response (antigen-antibody reaction involving T lymphocytes).
- Acute period: Appearance of an erythematovesicular rash. The primary element is the spongiotic vesicle. Microscopically (with H&E staining), marked dermal edema with sparse lymphocytic infiltrates is visible. As it progresses, acanthosis, focal parakeratosis, and spongiosis develop. Desmosomal rupture leads to the appearance of subcorneal blisters containing eosinophils and exocytosis of lymphocytes.
- Chronic period: Exudation decreases, and crusts, erosions, and papules appear at the site of vesicles. Fibrosis may form in the dermis at the dermal-epidermal junction.
Viral Skin Infections
Herpes Simplex (Herpes simplex) Caused by herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2). Infection occurs via body fluids (saliva, semen) or direct contact with vesicles.
- HSV-1: Infection typically occurs in childhood, affecting the face and mucous membranes. Triggers for reactivation include solar radiation, stress, hypothermia, fever, and immunodeficiency.
- HSV-2: Infection occurs after puberty, localizing to the genitals.
Histological findings: Begins with marked perinuclear vacuolation and edema of keratinocytes. Cells lose contact, leading to acantholysis and the formation of intraepidermal (often multilocular) microvesicles. Remnants of keratinocytes and multinucleated giant cells are visible inside. Eosinophilic intranuclear inclusions are found within the nuclei.
Shingles (Herpes zoster) Caused by herpesvirus varicella zoster (VZV). Peak incidence occurs in late winter and spring; risk groups include individuals over 50 and children (about 5% of cases under age 15). Manifests as a unilateral erythematous-vesicular rash along nerve pathways accompanied by intense pain (especially when the trigeminal nerve is involved). Pathomorphology: Changes are similar to herpes simplex but significantly more pronounced. Massive dermal edema, nerve and vascular involvement, up to thrombosis and hemorrhage, are characteristic.
Parasitic Diseases (Scabies)
The most common contagious skin disease. Caused by the scabies mite (Sarcoptes scabiei), with an incubation period of 1–2 weeks. Areas with thin skin are predominantly affected: interdigital spaces, flexural creases of the wrists, abdomen, groin, and mammary folds. The pathogenesis involves the fertilized female mite burrowing exclusively into the stratum corneum of the epidermis, where it creates tunnels to lay eggs.