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Lecture notes, cheat sheets
Dermatovenerology. Viral dermatoses (most important)
Directory / Lecture notes, cheat sheets Table of contents (expand) LECTURE No. 4. Viral dermatoses 1. Herpes virus infections Herpes virus infections are epidemically widespread in the human population, with a variety of clinical forms, and a persistent course. These diseases are chronic, recur and are accompanied by depression of the immune system. Severe course and frequent relapses of herpes virus infections may be markers of increasing immunodeficiency. Typical shapes Herpes simplex, or herpes simplex. Herpes simplex virus (HSV) is a DNA-containing filterable virus. There are HSV-1, the causative agent of predominantly non-genital forms, and HSV-2, the causative agent of genital forms of the disease. Viruses differ in their set of antigen proteins, some biological properties, as well as in the preferred route of transmission of the virus in natural conditions. The source of infection is an infected person, both during the period of clinical manifestations and during the latent course of the infection. The virus can be isolated from various biological secretions (saliva, tears, vesicle contents). HSV-1 infection often occurs in the first 3 years of a child's life, HSV-2 is associated with the onset of sexual activity. However, HSV-1 can cause damage in the anogenital region, and HSV-2 clinically manifests itself in other areas of the skin and mucous membranes. The routes of transmission of HSV are as follows: 1) direct contact (household, sexual); 2) indirect contact (through household items, dishes, toys, medical instruments); 3) airborne; 4) parenteral (transplantation of organs and tissues, artificial insemination with infected donor sperm); 5) from mother to fetus (transplacental and when passing through the birth canal). During primary infection, virions are adsorbed on epitheliocytes and attached to cell receptors. After a series of transformations in the nucleus of epithelial cells, immature capsids are formed, which are transported to the cytoplasm and, acquiring a membrane, leave the cell. Inflammatory phenomena are noted on the skin or mucosa in case of damage: chemotaxis of cellular elements, release of biologically active substances into the tissues, reactive changes in blood vessels, degradation of epitheliocytes. Clinically, this is manifested by limited edema, hyperemia, microvesicles, as well as a sensation of itching, burning. During primary infection, the virus enters the sensory spinal or cerebral ganglia from the entrance gate of infection (spread along the endo- and perineural pathways, intraaxonally or along Schwann cells). In addition, HSV spreads hematogenously. Primary infection is always accompanied by a period of viremia, as a result of which HSV penetrates not only into the sensory ganglia, but also into many cells of the body. The virus has a tropism for blood cells, immunocytes. Penetrating into the genetic apparatus of the cell, HSV causes cell degradation and death or a significant decrease in functional activity and a state of secondary immunodeficiency, which makes it impossible to completely eliminate HSV. The presence of HSV in the human body leads to a decrease in the tension of both cellular and humoral immunity. The functional activity of nonspecific protective factors is impaired. The interferonogenic ability of leukocytes, the activity of natural killers, and the antibody-dependent cellular cytotoxicity of peripheral blood leukocytes are reduced. The absolute number and functional activity of T-lymphocytes may decrease. With a decrease in immunity, secondary relapses of herpes simplex occur, since the virus can spread from the sensory ganglia through the perineural spaces and re-reach the skin or mucous membranes. The weakening of immune control makes it impossible to completely eliminate the virus from the body; in addition, HSV may be involved in the development of neoplastic processes, such as cervical cancer, prostate cancer, and induction of atherosclerosis. Diseases caused by HSV are divided into primary and secondary or recurrent herpes infection. Allocate the usual course of herpetic infection (localized forms) and forms of severe course against the background of immunodeficiency (common and generalized forms). Primary infection occurs when a person first comes into contact with HSV (usually in children). With a primary infection, the incubation period lasts 2-14 days and in 80% of cases the infection occurs in a subclinical, latent form. Only in 20% of cases are clinical manifestations observed, either in the form of an acute respiratory viral disease of unspecified origin, or in the form of acute aphthous herpetic stomatitis. It is the most common clinical form of primary infection, but can occur as gingivitis, glossitis, or herpetic sore throat. In some cases, during a primary infection, rashes may appear on the skin in various locations. The manifest form of primary infection is accompanied by pronounced signs of intoxication. After the end of the incubation period, a rise in temperature to 39-40 ° C, weakness, headache, and loss of appetite are noted. On the oral mucosa (most often on the mucous membrane of the cheeks, gums, tongue, less often on the soft and hard palate, tonsils) foci of pronounced edema and hyperemia appear, against which grouped vesicles appear after a few hours. Then the vesicles are opened, and in their place point erosive or superficial ulcerative defects are formed. Sometimes erosions merge, forming a defect with a polycyclic contour. Damage to the oral mucosa is always accompanied by severe pain, burning, and salivation. The submandibular, lingual, and cervical lymph nodes are moderately enlarged and more painful on the side of the rash. Clinical recovery occurs after 2-3 weeks. Secondary, or recurrent, herpes simplex occurs when the virus is activated in an infected organism. The number of relapses, the severity of the course, localization, prevalence depend on the type of virus and the immune status of the person. Relapses often occur with a moderate intoxication syndrome or without it. Both primary infection and relapse are characterized by typical rashes on the skin and mucous membranes. Rashes do not migrate, have a fixed character and a tendency to recur on the same areas of the skin and mucous membranes. Any areas on the skin and mucous membranes can be affected, but most often rashes occur on the face, oral mucosa, conjunctiva, skin and mucous membranes of the anogenital region. In typical cases, the lesion is represented by an area of limited edema and hyperemia, against which a group of vesicles with clear, serous content appears. After a few hours, the contents of the vesicles become cloudy due to the chemotaxis of cellular elements and the development of inflammation. The vesicles then break open to form small, closely grouped erosions, or they coalesce into a larger defect with a polycyclic outline. Sometimes the exudate of the vesicles shrinks, forming serous crusts. The addition of secondary coccal flora is possible, and then the crusts take on the appearance of honey. Often, simultaneously with the rash, there is a reaction from the regional lymph nodes in the form of enlargement and moderate pain. After 7-10 days, the crusts are removed, the erosions are epithelialized. A stain remains at the site of the former rash. Blistering rashes are preceded by subjective sensations at the site of future rashes, such as pain, itching, burning, the so-called precursor symptoms. Some patients experience prodromal phenomena in the form of low-grade fever, malaise, weakness, and headache. Relapses often occur during the cold season; they can be provoked by foci of chronic infection. According to the localization of herpetic eruptions, there are: 1) herpetic skin lesions. Typical rashes are most often localized in the region of the red border of the lips, periorally, in the region of the wings of the nose, in other places on the face, as well as on the hands, in the buttocks; 2) herpetic lesions of the mucous membranes. Typical rashes can be localized on any part of the oral mucosa. In place of bubble eruptions, surface erosions with polycyclic edges, aphthae, are formed. The expressed morbidity in the centers of defeat, intensive salivation are typical; 3) herpetic eye lesions (ophthalmoherpes). It is more often observed in children aged 6 months to 5-6 years with a primary infection and in adults 16-25 years old with reduced immune reactivity. A poor prognostic sign is eye damage during a primary infection, as this may be a precursor to the generalization of the process. Ophthalmoherpes is prone to frequent relapses and can manifest itself in the form of vesicular and dendritic keratitis, recurrent corneal erosion, and iridocyclitis. Optic neuritis is rarely observed. The result of ophthalmoherpes may be a decrease in visual acuity; 4) damage to the anogenital area (genital herpes). One of the most common clinical forms of herpes infection. Primary infection occurs with the onset of sexual activity. The disease is often asymptomatic, but such a person is a source of infection for a sexual partner. In some cases, primary infection can be severe, with pronounced signs of intoxication. The clinical picture develops after an incubation period, which lasts on average 7 days. Typical vesicular rashes occur against a background of significant swelling and hyperemia. Having existed for a short time, the vesicles open and leave behind weeping, painful erosions, which epithelialize after 10-14 days. In men, the glans penis, the coronal sulcus, the inner leaf of the foreskin, and the body of the penis are affected. In women, rashes are localized on the skin and mucous membranes of the labia majora and labia minora, in the perineum. Localization of rashes is often determined by the nature of sexual contacts. Rashes are accompanied by regional lymphadenitis, severe pain syndrome; pains are sometimes wired, can be shooting, pulling. Patients feel a burning sensation or itching at the site of the rash. In the future, in more than half of the cases, relapses of the disease are noted, clinically proceeding in the same way as the primary infection, but with a less pronounced intoxication syndrome. Herpes simplex therapy is complex and includes the use of antiviral drugs, immunocorrective agents, and symptomatic treatment. The duration, intensity and volume of the course of therapy is determined by the clinical form of the disease and the severity of its course, the frequency of relapses. If relapses occur once every 1 months or less, localized damage to the skin or mucous membranes and the absence of general symptoms, the following methods are indicated: local and general therapy using antiherpetic drugs. External etiotropic therapy - acyclovir in the form of 6% cream, tebrofen 5-2% ointment. At the same time, the use of aqueous and alcoholic solutions of aniline dyes is indicated. In the event of relapses 1 time in 3 months or more, widespread lesions of the skin and mucous membranes, expressed general phenomena, staged therapy is indicated. Stage I - treatment in the acute period of the disease (relapse). The etiotropic link in therapy is antiherpetic drugs (intravenously, orally, topically). Use acyclovir, famciclovir, alpizarin, flacoside. In persons with immunodeficiencies of various origins, it is necessary to increase the dose of the chemotherapy drug and the duration of administration (the course can be extended for several months, the dose is increased by 2 times). Antiviral chemotherapy drugs can be combined with interferon preparations or its inducers. Immunomodulatory agents, natural antioxidants and herbal adaptogens are recommended. In the case of a pronounced exudative component, prostaglandin inhibitors are prescribed. In case of damage to the oral mucosa, along with external antiviral agents, solutions of aniline dyes and other disinfectants are used. Stage II - therapy in remission, after the subsidence of the main clinical manifestations. The goal is to consolidate the positive effect of the therapy carried out in the acute stage and prepare the patient for vaccination. It is necessary to continue or repeat the course of etiotropic therapy. Sanitation of foci of chronic infection is carried out. Stage III - specific prevention of recurrence of herpes infection using herpes vaccines. Live, inactivated or recombinant antiherpetic vaccines are used if stable remission is achieved. Stage IV - clinical observation. They conduct routine clinical and laboratory examinations of patients (once every 1-3 months), treatment of chronic processes, and correction of immunological disorders. Herpes zoster, or shingles. Unlike simple herpes, shingles affects middle-aged and older people who have previously had chickenpox. Caused by the herpes simplex virus type III. In the case of infection with the herpes virus type III, the source of infection is a person with chickenpox or shingles. A person is contagious at the end of the incubation period until the crusts fall off, especially in the first 7 days from the onset of the rash. The main routes of transmission are airborne, contact and parenteral. Transmission of infection from mother to fetus is possible. The clinical picture of herpes zoster has a number of features. The disease begins acutely or with a prodromal period. Then intense burning pain occurs along the sensory nerve. The pain intensifies with movement, cooling, touching the skin and is monolateral in nature. They can simulate myocardial infarction, renal and hepatic colic. Soon, typical herpetic eruptions appear on the skin along the nerve: grouped vesicles filled with serous contents. After the skin manifestations resolve (after 1-3 weeks), neuralgic pain may persist for several months. There are localized, widespread and generalized forms of herpes zoster. Of the localized forms of herpes zoster, the form that occurs with damage to the intervertebral ganglia of the thoracic and lumbar regions is more common, less often - damage to the ganglion of the trigeminal nerve, the so-called ophthalmic form of herpes zoster, and damage to the geniculate node of the facial nerve. Typical for the ophthalmic form is a monolateral lesion of the skin and mucous membranes. The patient is concerned about photophobia, lacrimation, blepharospasm, severe neuralgic pain, which can spread to the entire face, neck, and scalp. In this case, the danger is vesicular rashes on the cornea, resulting in keratitis, followed by scarring and decreased visual acuity. Rashes, which are localized not only along the affected nerve, but also in other areas of the skin and mucous membranes, determine the common form that is noted in immunosuppression. Therapy for herpes zoster depends on the form of the disease and the general condition of the patient. In severe forms of herpetic infection, accompanied by widespread rashes, ulcerative necrotic lesions, generalization of the process, inpatient treatment in the clinic of infectious diseases is necessary. Etiotropic therapy - general and external treatment with antiviral agents. Use the same drugs as for herpes simplex. General therapy with antiviral drugs is started as early as possible and continued until the rash ceases. Pathogenetic therapy includes interferon preparations, immunomodulators. Symptomatic therapy is aimed at eliminating the pain syndrome, secondary purulent complications. Drug therapy can be combined with novocaine blockade, sessions of diathermy of the perivertebral areas. Apply B vitamins, vitamin C, phytoadaptogens. Outwardly, alcohol and aqueous solutions of aniline dyes are used. Atypical forms There are atypical forms of herpes simplex and herpes zoster. 1. Abortive form. It is characterized by slight hyperemia, edema, barely noticeable papular elements, subjective sensations are usually absent, there may be slight itching. Localization - skin areas with a thickened stratum corneum (skin of the palms and soles). The abortive form of herpes zoster proceeds without typical rashes and is characterized by pain syndrome. 2. Edema form. In this case, the rashes are localized in areas of the skin with loose subcutaneous tissue. The leading symptoms are pronounced edema, hyperemia, against which the vesicles remain invisible or absent. 3. Bullous form. In this form, along with typical vesicles, larger cavity formations (confluent vesicles) are noted, which clinically resemble blisters. 4. Hemorrhagic form. It differs in that the contents of the vesicles are hemorrhagic in nature. 5. Ulcerative necrotic form. Occurs with severe immunodeficiency. In place of the opened vesicles, ulcers are formed, which can increase in size, merge into extensive ulcerative surfaces. May be accompanied by severe signs of intoxication. Generalized forms Children and adults suffering from atopic dermatitis and eczematous reactions may develop a generalized form of herpes simplex - Kaposi's varicelliform pustulosis. It is characterized by an acute onset, a rise in body temperature. On the first day, sometimes a little later, against the background of a general severe condition, multiple vesicles appear on the skin with a depression in the center. Mucous membranes may also be affected. The secondary bacterial flora quickly joins, an admixture of blood appears in the serous contents of the vesicles. As a result of the evolution of elements on the skin, extensive foci covered with hemorrhagic crusts appear, pustular elements and erosions are noted. Characterized by enlarged lymph nodes. There are also generalized clinical forms in which the internal organs are affected. Most often the nervous system suffers: serous meningitis, meningoencephalitis, encephalitis develops. Herpetic encephalitis is a serious condition, which is accompanied by pronounced signs of intoxication, proceeds with cerebral and focal symptoms. For the diagnosis of herpes infection, virological, immunological and serological methods are used (for example, isolation of the virus from the lesion using cell cultures and detection of the viral antigen in biosubstrates using the direct immunofluorescence reaction). Measures for the prevention of herpetic infection are similar to the control measures used for other infections transmitted by contact (including sexual) and airborne droplets. Prevention of herpes zoster is reduced to the exclusion of factors that provoke a decrease in the tension of antiviral immunity. 2. Papillomavirus infection Etiology. Papillomaviruses are the cause of various warts. Belongs to the papovavirus family, which includes a group of DNA-containing viruses. The papillomavirus genus is represented by a very large group of human and animal viruses. Several types of human papillomaviruses (HPV) are pathogenic for humans. HPV-1 causes plantar warts, HPV-2 - vulgar warts, HPV-3 - flat warts, HPV-4 - verruciform dysplasia, HPV-5, 6, 11 - genital warts. All papillomaviruses can play the role of oncogenes. Transmission of HPV infection occurs by contact directly from person to person and indirectly through household items, as well as by autoinoculation. The incubation period can range from several months to several years. The activity of the immune system, especially its cellular component, is of great importance in the development of all types of warts. Clinic. Common warts are localized mainly on the back of the hands, fingers, in the periungual area, and rarely on the face. They are round, dense, non-inflammatory nodules of a grayish-yellow color, rising above the surface of the skin, with an uneven, rough surface. Warts are flat, or youthful, localized on the face and back of the hands. They have the appearance of flat, small rounded papules, normal skin color or yellowish brown. Slightly rise above the level of the skin, have a smooth surface. Plantar warts are localized on the plantar surface of the feet. They resemble a dense grayish callus with a central core, which consists of filiform dermal papillae surrounded by a powerful roller of horny layers. Often painful when walking. Genital warts are localized in the area of the external genital organs, inguinal-femoral, intergluteal fold, perianally, they are small papillary papules on a thin stalk of normal skin color. Papillomas of the mucous membranes and skin are localized on the mucous membranes of the oral cavity, pharynx, larynx, paranasal sinuses, on the mucous membranes of the urinary tract, on the skin of the neck, in the axillary regions. These are single or multiple papillary growths on a thin stalk, having a soft texture. On the mucous membranes, the color is pink or whitish. On the skin, the color varies from flesh to red-brown. Verruciform epidermodysplasia Lewandowski-Lutz is a rare chronic disease that develops in childhood due to a congenital defect of the immune system. The rashes are localized on the skin of the hands, forearms, legs, and less often in other places. They are flat, round papules up to 2 cm in diameter, prone to fusion, without a tendency to regress, covered with grayish-black horny masses soaked in sebum. With this variant of warts, malignant transformation often occurs. Treatment. General therapy: 1) antiviral or etiological therapy; 2) pathogenetic therapy aimed at increasing the body's immune defenses (immunomodulatory therapy). Local Therapy: 1) antiviral external therapy; 2) external destructive methods (cryolysis, electrothermocaustics, laser destruction, exposure to acid solutions), curettage; 3) cytotoxic drugs: condilin, podophyllotoxin, phyllotoxin, 5-fluorouracil. 3. Molluscum contagiosum Molluscum contagiosum is a viral disease characterized by the appearance on the skin of white hemispherical nodules with a central depression, visually resembling a mollusk shell. Etiology. Molluscum contagiosum virus belongs to the smallpox group of viruses. The disease occurs in people everywhere. The infection is transmitted through direct contact with a sick person, or indirectly through household items. Children under 1 year of age rarely get sick, possibly due to immunity acquired from the mother and a long incubation period. The disease is most common in underdeveloped countries with a hot climate. Possible sexual transmission. More often, molluscum contagiosum occurs in patients suffering from atopic dermatitis and eczema. This is due to both a decrease in skin reactivity and prolonged use of topical steroids. Unusually widespread rashes have been noted in patients with sarcoidosis, in patients receiving immunosuppressive therapy, and in HIV-infected subjects. Pathogenesis. The virus invades the keratinocytes of the basal layer of the epidermis and significantly increases the rate of cell division. Then the active accumulation of viral DNA occurs in the spinous layer. As a result, a nodule is formed, in the center of which destruction occurs and the cells of the epidermis are destroyed, while the cells of the basal layer are not affected. The central part of the nodule is represented by detritus containing hyaline bodies with a diameter of 25 microns, which contain viral material. Inflammatory changes in the dermis are insignificant or absent, however, in the case of long-term elements, they can be represented by a chronic granulomatous infiltrate. Clinic. The incubation period ranges from 14 days to 6 months. The rashes are represented by shiny pearly white hemispherical papules with an umbilical depression in the center. Slowly increasing in size, the papule can reach a diameter of 5-10 mm in 6-12 weeks. With a single lesion, the diameter of the papule reaches significant sizes. Plaques consisting of multiple fused nodules are rare. After an injury or spontaneously after a few months, papules can fester and ulcerate. Usually, after existing for 6-9 months, the rash resolves spontaneously, but some persist for up to 3-4 years. Rashes are more often localized on the neck, trunk, especially in the armpits, with the exception of a sexually transmitted infection, when the anogenital region is usually affected. There are single rashes in the face, especially on the eyelids. Molluscum contagiosum elements can also be localized on any part of the skin, including atypical localization - the skin of the soles and the mucous membrane of the cheeks. In HIV-infected subjects, rashes are multiple, localized mainly on the face and resistant to conventional therapy. Diagnostics. Diagnosis is based on the characteristic clinical picture. Microscopic examination of the contents of the nodule clarifies the diagnosis. Electron microscopy and histological examination can be used. Treatment. Patients should avoid visiting swimming pools, public baths, and carefully observe the rules of personal hygiene. Treatment consists of cryotherapy every 2-3 weeks until the lesions completely disappear. Diathermocoagulation, squeezing with tweezers, superficial scraping, followed by lubrication of the elements with a solution of silver nitride, phenol or 5-10% iodine solution are used. Author: Sitkalieva E.V. << Back: Atopic dermatitis >> Forward: Pustular skin diseases (Staphylococcal pyoderma. Streptococcal and streptostaphylococcal pyoderma. Atypical chronic pyoderma)
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