Herpetic skin lesions: causes, symptoms, diagnosis, treatment

Herpetic skin lesions include herpes simplex and shingles.

Simple vesicular lichen is caused by the herpes simplex virus type I or II, characterized by pronounced dermato-neurotropism. Infection with the type I virus usually occurs in early childhood (the possibility of intrauterine penetration of the virus into the body is allowed), and with type II - after puberty. The type I virus most often causes damage to the face and skin of other areas of the body, the type 11 virus - to the mucous membranes of the genitals. Antibodies against the type I virus are found in most adults, against type II much less often. Infection with the type II virus most often occurs sexually.

At the sites of virus penetration, primary skin or mucous membrane lesions develop of a vesicular, less commonly bullous nature, sometimes occurring as aphthous stomatitis, keratoconjunctivitis, vulvovaginitis. Frambesiform changes have been described. Viremia often results in general reactions in the form of visceral manifestations, of which encephalitis is the most dangerous. When children are infected with the herpes simplex virus type II during childbirth, 5-50% of them develop disseminated infection, which is often fatal. Subsequently, the infection usually progresses latent, the virus persists in the ganglia, and relapses occur, as a rule, under the influence of factors that reduce the body's resistance, especially cold. In the mechanisms of herpes simplex relapse, an important role is given to the suppression of cellular immunity.

Clinically, the disease is characterized by a rash of small grouped vesicles, usually with transparent contents, which dry up or open up to form erosions, less often - erosive-ulcerative lesions. The rash regresses within a few days, usually leaving no scars. Eye damage is more severe and can lead to vision loss. There is evidence of the role of type II virus in the development of cervical cancer. Atypical variants of the disease include zosteriform, abortive, rupioid, and edematous. In case of persistent and unusual course, it is necessary to exclude HIV infection. The herpes simplex virus is considered one of the frequent agents that provoke the development of erythema multiforme exudative. When patients with eczema or diffuse neurodermatitis are infected with herpes, herpetic eczema develops, more often observed in childhood, characterized by a severe course with high temperature.

Pathomorphology. The main morphological element is an intraepidermal vesicle, formed as a result of edema and destructive changes in epidermal cells (ballooning dystrophy), resulting in the formation of multi-chamber vesicles in the upper parts of the epidermis, surrounded by areas of reticular dystrophy. The presence of intranuclear inclusions (eosinophilic bodies) in the ballooning cells is typical for this disease. In the dermis, morphological changes can range from minor inflammatory infiltration to significant ones involving the walls of blood vessels. Infiltrates consist mainly of lymphocytes and neutrophilic granulocytes.

Histogenesis. Replication of viral DNA occurs in the nuclei of infected cells. A characteristic feature is the early migration of the virus, deprived of its outer shell, into the trunks of sensory nerves, through which it enters the ganglia, where it multiplies and migrates again into the skin. The mechanisms of virus reactivation during relapses of the disease have been little studied. This process is affected by weakened immune control, increased susceptibility of epithelial cells to the virus, and reduced synthesis of interferon.

Shingles, like chickenpox, is caused by a neurotropic virus - Herpesvirus varicella zoster. The development of the disease is facilitated by decreased immunity, severe diseases, especially malignant, lymphoproliferative, radiation exposure and other factors that reduce immunity, including HIV infection. It occurs more often in people over 50 years old, infection usually occurs in childhood, which leads to the development of chickenpox. Shingles in adults is considered a consequence of the reactivation of the virus, which remains in the posterior roots of the spinal cord or trigeminal nerve nodes. Clinically, it is characterized by erythematous-vesicular, less often bullous rashes, located, as a rule, on one side, in the area of nerve damage, accompanied by severe pain, especially when the first branch of the trigeminal nerve is involved in the process. Sometimes, with a more severe course, there may be scattered rashes. They are smaller in size compared to the main focus, similar in morphology to chickenpox foci. The contents of the vesicles and blisters are usually transparent, but may be cloudy or hemorrhagic. In weakened patients, especially when localized on the face, necrotic changes with the formation of long-term non-healing ulcers may be observed. Sometimes the facial, auditory and trigeminal nerves are affected simultaneously. If the eyes are affected, which is observed in about 1/3 of patients, vision loss is possible, and meningoencephalitis occasionally develops. Postherpetic neuralgia may persist for a long time in some patients.

Pathomorphology. Morphological changes in the skin are similar to those in simple vesicular lichen, but are more pronounced. In the epithelial cells of the basal layer, ballooning dystrophy is observed, caused by a sharp intracellular edema, and changes in the nuclei. The affected nuclei contain inclusions in the form of eosinophilic bodies. Intracellular edema is combined with intercellular, which leads to the formation of bubbles in the upper parts of the germinal layer. In the dermis, a weak infiltration of neutrophilic granulocytes is detected, then migrating to the epidermis. In addition, nerve trunks and the corresponding roots of sensory ganglia are affected. Eosinophilic bodies are found in the nuclei of affected ganglion cells, and electron microscopy reveals the herpes virus. Particles of the virus are also found in the endothelial cells of skin capillaries and axons.

Histogenesis. The appearance of skin rashes is preceded by viremia. Several days after the formation of blisters, antibodies to the virus are detected in the blood serum of patients, represented by immunoglobulins G, A and M, some of them (IgG) persist for life. For several days from the onset of the disease, cellular immunity remains suppressed.

Contagious molluscum (syn.: epithelial mollusk, contagious mollusk, contagious epithelioma) is a disease caused by a DNA-containing virus of the smallpox group. The introduction of the virus is facilitated by trauma to the skin, its lymphohematogenous spread is allowed. Infection is accompanied by the formation of antibodies, mainly IgG. Clinically manifested by yellowish-white or reddish lenticular papules of rounded outlines, hemispherical in shape with a shiny surface, an umbilical depression in the center, a dense consistency. When pressing on the papule from its lateral surfaces, a cheesy mass is released from the central opening. The rashes are scattered or grouped, mainly on the face, chest, genitals, in homosexuals - perianally. They can be single, but more often - multiple, especially with immunodeficiency, including that caused by the human immunodeficiency virus. If localized on the eyelids, conjunctivitis and punctate keratitis may develop. Children are mostly affected. The course is long, the disease often heals spontaneously, sometimes scars remain.

Pathomorphology. In the area of the element there are pear-shaped growths of the epidermis, the cells of which, especially the upper layers, contain large intracellular inclusions - molluscum bodies. At first they look like ovoid eosinophilic structures, and when enlarged they become basophilic. In the center of the lesion at the level of the horny and granular layers there is a crater-like depression completely filled with molluscum bodies containing many viral particles. With the superficial location of molluscum bodies in the epidermis, changes in the dermis are insignificant, but in cases of spread of destruction of epithelial cells to the basal layer and penetration of the process into the dermis, a pronounced inflammatory reaction develops in it. The infiltrate consists of lymphocytes, neutrophilic granulocytes, macrophages and giant cells of foreign bodies.

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