Autoimmune bullous dermatoses
Pemphigus vulgaris (Pemphigus vulgaris) Characterized by the formation of an intraepidermal blister. Hematoxylin and eosin staining reveals suprabasal clefts extending even into the hair follicle epithelium. Lymphocytes and specific acantholytic cells—round structures with a large vesicular nucleus and pale cytoplasm—accumulate in the cavity. Infiltration by eosinophils and lymphocytes is observed in the dermis. Direct immunofluorescence (DIF) shows IgG and C3 deposits 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 (granular and spinous). Detachment of the stratum corneum without the formation of a true blister is possible.
Duhring's herpetiform dermatitis A chronic relapsing process affecting primarily individuals aged 30–40 years (familial forms are more common in women). The rash is polymorphic: vesicles, papules, and urticarial elements on an erythematous background. The elements tend to form herpetiform groupings and evolve according to the pattern: 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, where microabscesses and subepidermal clefts form. Initially, the blister is multilocular (multichambered), but as the interpapillary connections are destroyed, it becomes unilocular. DIF reveals granular or linear IgA deposits in 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 hematoxylin and eosin staining), pronounced dermal edema with sparse lymphocytic infiltrates is visible. As it progresses, acanthosis, focal parakeratosis, and spongiosis develop. Rupture of desmosomes leads to the appearance of subcorneal blisters with eosinophils and lymphocytic exocytosis.
- Chronic period: Exudation decreases; crusts, erosions, and papules appear at the site of the vesicles. Fibrosis may form in the dermis at the border with the epidermis.
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 through contact with vesicles.
- HSV-1: Infection in childhood, affects the face and mucous membranes. Triggers for exacerbations: solar radiation, stress, hypothermia, fever, immunodeficiency.
- HSV-2: Infection after puberty, localized on the genitals.
Histological picture: Begins with pronounced perinuclear edema of keratinocytes. The cells lose contact, acantholysis occurs, and intraepidermal (often multichambered) vesicles form. Remnants of keratinocytes and multinucleated cells are visible inside. Eosinophilic inclusions are found in the nuclei.
Shingles (Herpes zoster) Caused by herpesvirus varicella zoster (VZV). The peak incidence occurs in late winter and spring; risk groups include individuals over 50 and children (about 5% of cases under 15 years old). Manifests as a unilateral erythematous-vesicular rash along nerve trunks with 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 damage, up to thrombosis and hemorrhages, are characteristic.
Parasitic diseases (Scabies)
The most frequent contagious skin disease. Caused by the itch mite; the incubation period is 1–2 weeks. Areas with thin skin are primarily affected: interdigital spaces, flexor folds, abdomen, groin, and mammary glands. The pathogenesis lies in the fact that the fertilized female mite burrows exclusively into the stratum corneum of the epidermis, where it creates tunnels for laying eggs.
Briefly: answers to topical questions
What specific intranuclear inclusions are formed upon infection with the herpes simplex virus, and what are they called?
When infected with the herpes simplex virus, intranuclear inclusions—known as Cowdry bodies—are detected in the nuclei of affected, including vacuolated, cells. In sources, they are described as eosinophilic inclusions, as well as intranuclear basophilic inclusions surrounded by a halo; in neuroinfection caused by HSV-1, Cowdry type A bodies are indicated.
For quick determination of the level of the blister: Pemphigus vulgaris — Intraepidermal (above the basal layer); Pemphigus foliaceus — on the Face/upper layers (in the upper granular layer); Duhring's dermatitis — Sub (subepidermally, above the papillae).
Class and exam questions
What is the main histological difference between herpes zoster and herpes simplex?
The pathomorphology is similar, but in herpes zoster the changes are significantly more pronounced: there is more massive dermal edema, involvement of peripheral nerves and blood vessels, and the development of thrombosis and hemorrhages.
How does the blister evolve in Duhring's dermatitis?
Initially, the blister is multilocular due to preserved connections between the dermal papillae and the epidermis. In the late stage, these connections are destroyed, and the blister becomes unilocular.
Where are the changes localized in seborrheic and foliaceus pemphigus?
Acantholysis occurs in the upper layers of the epidermis (the granular layer and the upper part of the spinous layer). Often, only detachment of the stratum corneum is observed without the formation of a classic blister.
What else to study on this topic
- Mechanisms of spongiotic vesicle formation in acute eczema.
- Immunofluorescence diagnostics (DIF) in various forms of pemphigus.
- Clinical manifestations and severe complications of herpetic infection (e.g., meningoencephalitis).
- The paraneoplastic nature and association with celiac disease in Duhring's herpetiform dermatitis.
- Features of the cellular composition of the inflammatory infiltrate in the dermis in autoimmune dermatoses.
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