herpetic infection- a group of diseases that is expressed by lesions of the skin, mucous membranes, central nervous system, and other organs.

Symptoms

Herpetic infection caused by types 1 and 2 of the virus

Herpetic skin lesions. The source of infection is a sick person. The main route of transmission is contact. The disease is characterized by damage to a specific area of ​​​​the skin. In the case of orofacial herpes, the lesion is localized in the mouth area. This is manifested by itching, burning, the presence of bubbles, which sometimes merge, burst, and a crust forms in their place. Children with dermatitis may develop Kaposi's herpetic eczema, which is manifested by rashes of vesicles located in groups. It usually develops against the background of fever and intoxication phenomena. Herpetic lesions of the eyes. Herpetic eye damage is observed more often in men aged 20-40 years. Manifested by keratitis, conjunctivitis, blepharoconjunctivitis. Sometimes it can be combined with a lesion of the trigeminal nerve.

Acute herpetic stomatitis

Herpetic lesions of the mucous membranes of the oral cavity are manifested in the form of acute herpetic stomatitis. Acute stomatitis is characterized by fever, symptoms of general poisoning. On the mucous membranes of the cheeks, palate, gums, an accumulation of small bubbles appears. Patients complain of itching and tingling at the site of the lesion. The filling of the bubbles is initially transparent, then cloudy. External erosions appear in the area of ​​the opened bubbles. After 1.5-2 weeks, the mucous membranes are normalized.

Herpetic lesion of the CNS

The defeat of the central nervous system usually occurs in the form of encephalitis or meningitis. In adult patients, signs of herpetic infection of the skin and mucous membranes are first detected, and only then do symptoms of encephalitis develop. The manifestations of herpetic encephalitis are: a sharp increase in body temperature, symptoms of general poisoning and focal occurrences in the central nervous system. The course of the disease is severe. After suffering encephalitis, there may be persistent residual effects (paresis, mental disorders). Relapses are rare. Herpetic serous meningitis develops more often in individuals with primary genital herpes. The body temperature rises, there is a headache, fear of bright light, meningeal symptoms. After a week, the symptoms of the disease disappear.

Genital herpes

The defeat of the genitals manifests itself in the form of acute necrotic inflammation of the cervix in women. It is characterized by a moderate increase in body temperature, malaise, muscle pain, urination disorders, pain in the lower abdomen, enlargement and soreness of the inguinal lymph nodes.

Characterized by bilateral spread of the rash on the external genitalia. In men, genital herpes occurs in the form of rashes on the penis, urethritis, and sometimes prostatitis.

Generalized herpes

Generalized herpes infection can occur in newborns and in individuals with congenital or acquired immunodeficiency. The disease is manifested by its severe course and infection of most organs and systems, mucous membranes, the formation of herpetic encephalitis or meningoencephalitis, hepatitis, and in some cases pneumonia. The disease without the use of modern anti-infective agents often ends in death.

Shingles

Shingles is a disease resulting from the activation of a latent herpes virus type 3. It is characterized by inflammation of the posterior roots of the spinal cord, as well as the appearance of fever, general intoxication and a rash along the sensory nerves involved in the process. People who have previously had chickenpox get sick with shingles. The incubation period for shingles lasts many years. The most common form of the disease is gangliocutaneous, it begins acutely with fever, symptoms of general intoxication, and pronounced burning pains at the site of future rashes. After 3-4 days, a characteristic rash appears. Typical clinical symptoms are ocular and ear forms of herpes zoster. In the ophthalmic form, rashes are localized on the mucous membranes of the eye, nose, and on the skin of the face. With the ear form of a rash - on the auricle and around it, it can also be in the external auditory canal. Facial paralysis may develop.

Cytomegalovirus infection

Cytomegalovirus infection is a viral infection characterized by multiple and varied manifestations, ranging from asymptomatic to severe forms with damage to internal organs and the central nervous system. The causative agent belongs to the herpesvirus type 5. The only source of infection is humans. The infection is transmitted by airborne droplets, contact, sexual contact and transplacental from mother to fetus.
Congenital cytomegalovirus infection.

Infection of newborns occurs during childbirth. Jaundice, an enlarged liver and spleen, and progressive anemia are characteristic of congenital cytomegaly. There may be hemorrhages in the mucous membranes, hematemesis, blood in the stool, bleeding from the navel.

Acquired cytomegaly

The duration of the incubation period is quite large (from 20 to 60 days). The disease lasts from 2 to 6 weeks. The disease is manifested by an increase in body temperature and the appearance of signs of general poisoning. The temperature is unstable, a strong chill is replaced by a strong fever, headache and muscle pain appear. Possible enlargement of the spleen.

Cytomegalovirus infection and HIV infection

Cytomegalovirus disease in immunocompromised people begins with prolonged fever, malaise, complete lack of appetite, night sweats, and muscle and joint pain. The respiratory organs are constantly affected, which is manifested by shortness of breath, patients are worried about a dry cough. In weakened individuals, cytomegalovirus causes an upset of the entire gastrointestinal tract, up to the appearance of ulcers.

Cytomegalovirus infection and pregnancy

The circulation of the virus in the bloodstream of a pregnant woman leads to infection of the fetus. Fetal death and miscarriages are likely if the fetus is infected in the early stages of pregnancy. When infected in the first trimester, a child with congenital malformations may be born. When infected at a later date, the newborn may have congenital cytomegaly without malformations.

Epstein-Barr virus infection

Epstein-Barr virus is a type 4 herpes virus. Refers to oncoviruses, that is, it can cause various tumor diseases.
Burkitt's lymphoma.

Mostly older children get sick, the disease is characterized by the occurrence of intraperitoneal tumors. Nasopharyngeal carcinoma is a disease specific to China. It is characterized by the occurrence of a malignant tumor of the nasopharynx.

"Hairy" leukoplakia of the tongue. A malignant disease characterized by the degeneration of the tissue of the mucous membrane of the tongue.

Herpes virus type 6 infection

A rare disease. It is characterized by the fact that against the background of complete health, a skin rash occurs, which also spontaneously disappears. Infection caused by the herpes virus type 7. This virus also has oncological activity and is capable of causing the development of various tumors. It usually occurs in people with immunodeficiencies in the form of Kaposi's sarcoma.

Herpes virus type 8 infection

This virus is now thought to be the cause of chronic fatigue syndrome.

Treatment

Any herpetic infection is treated with antiviral drugs that have antiherpetic activity.

Etiology. The causative agents of herpes simplex - HSV-1 and HSV-2 - have an icosahedral nucleocapsid containing a double-stranded DNA molecule, protein
a fibrous sheath (tegument) and an outer glycoprotein sheath. Type-specific outer envelope glycoproteins responsible for attachment
and intracellular viral entry. They also induce the production of virus-neutralizing antibodies. HSV-1 and HSV-2 differ in
structure of antigens and DNA.

Herpes simplex viruses are thermolabile, inactivated at a temperature of 50-52 "C after 30 minutes, relatively easily destroyed under the influence of
ultraviolet and x-rays. Ethyl alcohol, proteolytic enzymes, bile, ether and other organic solvents quickly inactivate
HSV.

Like other viruses or bacteria, HSV is resistant to low temperatures.

Epidemiology. The source of infection is people infected with the virus, regardless of whether the infection is asymptomatic or
manifestly.

In an infected person, the virus is found in various secrets, depending on the location of the lesion: nasopharyngeal mucus, lacrimal fluid,
contents of vesicles, erosions, ulcers, menstrual blood, vaginal, cervical secrets, amniotic fluid, semen.
During HSV viremia
circulates in the blood and is excreted in the urine. The highest concentration of the virus is noted in the manifest forms of PH, with an asymptomatic course of the pathogen
may be present in biological material, but at lower concentrations. So, for example, in 5% of adults who do not have clinical
symptoms, HSV can be detected in the nasopharynx.

The main mechanisms of PG infection are percutaneous and aspiration (aerobic). The introduction of the pathogen is carried out through the mucous
membranes or skin damaged by a pathological process (neurodermatitis, eczema, maceration, etc.).

The percutaneous mechanism is realized in natural and artificial ways. Natural routes of transmission of the pathogen in PG are dominant.
Infection of a susceptible person occurs through direct contact with the source of infection (oral-oral, sexually transmitted
way) or indirectly through virus-contaminated dishes, towels, toothbrushes, toys.
In addition, the infection can be transmitted
vertically - from mother to fetus. Herpes simplex is one of the most common sexually transmitted infections. In the past
the etiological role in genital herpes was assigned only to HSV-2, but it is now known that HSV-1 causes the same localization
defeats.

Most people become infected with genital herpes when they become sexually active. The risk groups are the same as for viral hepatitis B and HIV infection:
prostitutes, homosexuals, and people who have many casual sexual partners. The spread of infection is promoted by alcoholism and
drug addiction, which lead to promiscuity and extramarital affairs.

The transmission of PG from mother to fetus occurs in various ways. More often the fetus is infected intranatally during passage through the birth canal, if
a woman suffers from genital herpes and, especially, if there are clinical manifestations at the time of delivery.
At the same time, the entrance gate for the virus
are the nasopharynx, skin, conjunctiva of the fetus. The risk of infection of the fetus in the presence of genital herpes during childbirth is about 40%.

It should be noted that only in women suffering from genital herpes, it is accompanied by vesicular rashes.
latent or asymptomatic infection, which can also be a serious threat to the fetus and newborn.

With genital herpes in women, the virus can enter the uterine cavity in an ascending way through the cervical canal, followed by
infection of the placenta and fetus.

Finally, the virus penetrates and transplacentally during the period of viremia in a pregnant woman suffering from any form of PH, including labial
herpes, provided that the infection is caused by such a serovar (or strain) of HSV, to which there are no protective antibodies in the pregnant woman's body (i.e.
e. there is a primary infection). With any type of infection, different types of pathology of the fetus and pregnancy occur.
Yes, before infection.
the fetus is often affected by the fetal membranes, which leads to premature termination of pregnancy.

Recurrent miscarriage may be associated with genital herpes.

Infection in early pregnancy is dangerous due to possible antenatal death of the fetus and the formation of malformations. At
infection of the fetus in late pregnancy, various options for PH are possible - from the birth of a child with an asymptomatic infection to its severe course with
lethal outcome.

It must be remembered that postnatal infection of children is possible in the presence of PG not only in the mother, but also in medical personnel.

The aspiration (aerogenic) mechanism of infection is realized by airborne droplets.

Thus, with natural transmission routes, the virus retains itself in nature as a species. But also, as with hepatitis B, C, D, HIV infection, with PG
There are also artificial ways of transmitting the virus. Since both during the primary infection and during relapses of PG occurs by the II virus, it is possible
parenteral route of infection, which occurs, for example, in drug addicts. Canned blood can also be a factor in the transmission of infection,
transplants of organs, tissues, sperm (with artificial insemination).

Unlike viral hepatitis and HIV infection, viremia in PH is usually short-lived, so the parenteral route of infection occurs.
infrequently.

In medical institutions, infection is possible when using virus-contaminated instruments used in gynecological,
dental, otolaryngological, ophthalmic, dermatological practice.

HSV-1 infection occurs in most people (nearly 80%) under the age of 6 years. The incidence of both children and adults is affected by PG
socio-economic conditions. People with a high socioeconomic standard of living become infected later in life, and some adults
remains uninfected.

The prevalence of HSV-2 in the population ranges from 2 to 30% in different regions.

Pathogenesis. Entrance gates for HSV are the skin and mucous membranes. Active viral replication in epithelial cells
characterized by the development of focal ballooning degeneration of the epithelium and the occurrence of foci of necrosis. Inflammation occurs in the surrounding area,
accompanied by migration of lymphoid elements, macrophages, release of biologically active substances, vascular reaction. Clinically it
manifested by well-known symptoms: burning sensation, hyperemia, papule, vesicle. However, the infectious process is not limited to this. New
virions enter the lymphatic vessels, then into the blood. Viremia is an important link in the pathogenesis of PH. The virus circulates in the blood
in its constituent elements. Apparently, the virus not only mechanically moves with blood cells, but also changes them. Yes, there are changes
the chromosomal apparatus of lymphocytes and their functional activity, which can cause immunosuppression. As a result of viremia, HSV enters various
organs and tissues, but it has a special tropism for the cells of the nerve ganglia. The penetration of the virus into the nerve ganglia from the site of introduction through
nerve endings and axons.

In a normal immune response, the virus is eliminated from organs and tissues, with the exception of the paravertebral sensory ganglia, where it is stored in
latent state throughout the life of the host.

There are two hypotheses explaining the mechanisms of HSV latency. According to the first of them (“static” hypothesis), viruses in the interrecurrent period
are found only in the cells of the nerve ganglia, possibly in an integrative state. The second ("dynamic") hypothesis suggests the existence in the ganglia
low-replicative infection with constant circulation of viruses along the axons and penetration of a small number of them into the epithelial cells of the skin and
mucous membranes. This process is not accompanied by noticeable lesions, as it is under the control of cellular and humoral factors.
immunity.

Surface glycoproteins of HSV induce the formation of antibodies: during primary infection and relapse - IgM class, and after 1-3 weeks they are replaced
antibodies of the IgG class. Antibodies to HSV do not protect against re-infection and relapse, but to a large extent prevent transplacental
transmission of the pathogen from mother to fetus.

Triggers of relapses of PH, which increase the existing immunodeficiency states in patients, are hypothermia, acute and
exacerbation of chronic infection, stress, surgery, excessive insolation, malnutrition, menstruation. With defects in the immune system, especially
T-cell link, macrophages, interferon production, active replication of the virus begins. Viruses exit the nerve ganglia along the axons, affecting
areas of the skin and mucous membranes innervated by the corresponding neuron. Cell damage, virus reproduction, viremia and
its localization in the same nerve ganglia with the transition to an inactive (low replicative) state. As immunosuppression progresses, activation
virus becomes more frequent, new ganglia are involved in the process, localization changes and the prevalence of skin lesions increases and
mucous membranes. In severe immunodeficiency, various organs are affected - the brain, lungs, liver, the process takes a generalized
nature, which is observed with HIV infection, immunosuppressant therapy, radiation therapy.

It should be noted that with the penetration of the virus into the skin and mucous membranes (primary or recurrent), characteristic symptoms do not always occur.
vesicular rash, local changes may be absent. However, HSV is found in tissues, enters the bloodstream and is released into the external environment.
with saliva, lacrimal fluid, vaginal secretions or semen.

Thus, the infection proceeds with periods of relapses and remissions, the duration of which depends on the state of the human immune system,
strain of the virus and its interaction with other viruses, primarily the herpesvirus family. Of particular importance is PG in persons infected with
HIV. It has been established that herpesviruses, when they enter the genome of a cell affected by HIV, activate it, facilitating replication. This makes it possible to count herpesviruses
cofactors in the progression of HIV infection.

Clinic. Clinical manifestations of PH are extremely diverse both in terms of localization and severity of lesions. generally accepted clinical
classification of this infection does not exist. The proposed classification of systems considers various forms and variants of the SG flow. In accordance with
The mechanism of infection distinguishes between acquired and congenital infection.

Acquired infection can be primary and secondary (syn.: recurrent, recurrent, recurrent).

Primary AI occurs when a person first comes into contact with the virus. The incubation period lasts from 2 to 14 days. Primary PG observed
predominantly in children aged 6 months to 5 years and much less frequently in adults. In children in the first 6 months of life, infection is extremely rare,
since the child's blood contains antiherpetic antibodies transmitted trans-placentally from the mother. By the end of the first year, the titers of these antibodies
decrease, making the child susceptible to HSV.

In 80-90% of initially infected children, the disease proceeds in an asymptomatic form, and only 10-20% of infected children have clinical manifestations.
(manifest form). The most common form of primary herpes is an acute respiratory disease, the etiology of which is usually unknown.
is decrypted. Another, also very common, form of the disease is acute aerpetic stomatitis (vinvivostomatitis), which occurs
predominantly in children. Primary herpes can be manifested by various lesions of the skin, conjunctiva or cornea of ​​the eye.

Primary genital herpes occurs at a later age with the onset of sexual life. For any form of primary herpes that occurs with
clinical manifestations, characterized by a pronounced general infectious syndrome, accompanied by fever and signs of intoxication. This
due to the absence of specific antiherpetic antibodies in the patient. The disease is especially severe in newborns and in people with
immunodeficiency of various nature (including HIV / AIDS). Due to hematogenous dissemination of the virus, general and yawning forms develop.
diseases with damage to many organs, which often leads to death.

Secondary (recurrent) PG occurs as a result of reactivation of the virus present in the body. Relapses of PG compared with the primary
infection usually occur with moderate signs of intoxication, fever (sometimes they are absent at all), with less pronounced changes in the focus
lesions in the form of edema, hyperemia.

Despite some differences in pathogenetic mechanisms and clinical manifestations, primary and secondary herpes have the same localization.
lesions and forms of the disease.

Tegmental herpes simplex (from lat. tegmentalis-integumentary) usually has a localized, less common type of lesion of the outer integument and
visible mucous membranes.

The localized type of tegmental PG is characterized by a clearly defined lesion zone, which usually corresponds to the site of virus introduction (with
primary herpes) or the place of its exit from the nerve endings into the integumentary epithelium (with a secondary infection). In the event that the lesion
spreads to nearby tissues, occurs in distant areas of the skin or mucous membranes, is considered to be a common form
tegmental PG. Common PG, depending on the severity, marks a different degree of immunodeficiency.

Herpetic lesions of the skin. Bubble rashes are typical, more often localized in the area of ​​the red border of the lips and wings of the nose.
However, there may be skin lesions of various localization: forehead, neck, trunk, limbs, etc. In many patients, rashes are preceded by a feeling
burning, pruritus, hyperemia, edema. Then papules appear, turning into vesicles filled with serous contents. In a few days
the contents of the bubbles become cloudy, they open, resulting in the formation of weeping erosion, or dry up and turn into crusts, followed by
epithelization underneath. In place of the torn off crusts, gradually disappearing pigmentation remains. Simultaneously with the formation of vesicles,
moderately increase regional lymph nodes. The whole process is resolved within 7-14 days.

Atypical forms of PG have diverse manifestations. In some patients, the main symptom is a sharp swelling of the subcutaneous tissue,
hyperemia, which are so pronounced that the vesicles remain invisible or absent altogether. This can lead to diagnostic
errors and even incorrect diagnosis of "phlegmon" with subsequent surgical intervention. At the same time, instead of the expected purulent discharge
receive scanty serous-suicidal discharge. This atypical form of PG is called edematous.

Sometimes rashes with herpes simplex are localized along the nerve trunks, resembling herpes zoster, but the pain syndrome is characteristic
for the latter, it is completely absent or slightly expressed. This is herpes simplex zosteriformis, which is more common in immunosuppressed individuals.

Eczema herpetiformis (herpetic) eczema occurs in infants or older children, less commonly in adults with eczema, atopic
dermatitis and other skin lesions. For the first time this form of the disease was described by Kaposi in 1887, therefore it is called "Kaposi's eczema" (not to be confused with
Kaposi's sarcoma!). Usually the disease begins acutely and is accompanied by an increase in body temperature up to 40 ° C, with chills and intoxication. For the first time
a day, sometimes later (3-4th day), a lot of single-chamber vesicles with transparent contents appear on the affected areas of the skin,
spreading gradually to neighboring healthy areas of the skin, a secondary bacterial infection joins. The bubbles burst to form
weeping erosive surfaces, which are then covered with crusts. With extensive lesions, the disease is extremely difficult. Lethality in children
under the age of 1 year is 10-40%. Kaposi's eczema is also observed in immunodeficiency states, including HIV infection.

The ulcerative-necrotic form of herpes simplex, which marks severe immunosuppression, also belongs to atypical ones. It occurs in HIV infection
stages of AIDS, as well as in oncological, hematological patients on the background of radiation, corticosteroid, cytostatic therapy. In place of vesicles
gradually increasing ulcers are formed, reaching a diameter of 2 cm or more. Later, these ulcers may merge into extensive ulcerative surfaces with
uneven edges. The bottom of the ulcers has signs of necrosis and is covered with serous-hemorrhagic fluid, and when bacterial microflora is attached, it becomes purulent.
separable. In the future, the ulcers are covered with crusts. Such skin lesions persist for several months, and reverse development with
rejection of crusts, epithelialization of ulcers and subsequent scarring occurs very slowly.

Ulcerative-necrotic lesions of the skin caused by HSV and persisting for more than 3 months are classified as AIDS-indicator diseases. Such patients
should be carefully screened for HIV infection.

There is also a vemorrhagic form of PG, when the vesicles have bloody contents, which is observed in patients with a violation of the system
hemostasis of various origins.

Herpetic lesions of the mucous membranes of the oral cavity. Acute gingivostomatitis can be a manifestation of both primary and recurrent
infections. This form of the disease is the most common clinical form in young children. The disease begins acutely with
temperature increase to 39-40 "C and intoxication phenomena. On hyperemic and edematous mucous membranes of the cheeks, tongue, palate and gums, as well as on
many bubbles appear in the tonsils and pharynx, which open after 2-3 days and superficial erosions (aphthae) form in their place.
There is intense salivation, soreness develops in the lesions. Recovery occurs after 2-3 weeks, but in 40% of patients
relapses occur. During relapses, the general infectious syndrome is absent or mild.

Herpetic lesions of the mucous membranes of the upper respiratory tract. Acute respiratory disease caused by HPV does not have typical
clinical manifestations and is rarely verified. It is assumed that from 5 to 7% of all acute respiratory infections has a herpetic etiology.

Herpetic lesions of the anorectal region in the form of sphincteritis, cryptitis and distal proctitis are usually caused by HSV-2 and are found on the streets,
using the genital-anal variant of sexual relations, more often in homosexual men.

Herpetic lesions spas (oftapmoserpes). Primary ophthalmic herpes develops in people who do not have antiviral immunity.
The disease is more common in children aged 6 months to 5 years and in adults aged 16 to 25 years.

Primary ophthalmic herpes is predominantly severe and has a tendency to a generalized course, since it occurs in people who do not
having specific antibodies to the pathogen. In 40% of patients, there is a combination of keratoconjunctivitis with widespread lesions of the skin, eyelids, and
as well as oral mucosa.

Recurrent ophthalmic herpes occurs in the form of blepharo-conjunctivitis, vesicular and dendritic keratitis, recurrent corneal erosion,
episcleritis or iridocyclitis, and in some cases - in the form of chorioretinitis or uveitis. Sometimes there is optic neuritis.

Herpetic lesions of the genital organs (aenital verpes) is one of the most common clinical forms of herpes infection caused by HSV-2.
However, there are cases of genital herpes caused by HSV-1. They give a significantly lower number of annual relapses than diseases
caused by HSV-2.

Often, genital herpes is asymptomatic. HSV can persist in men in the genitourinary tract, and in women in the cervical canal,
vagina and urethra. Individuals with asymptomatic genital herpes serve as a reservoir of infection.

Clinically pronounced genital herpes is especially severe during primary infection, often accompanied by fever and signs
intoxication. Edema and hyperemia of the external genital organs develop, then vesicular rashes appear on the penis, in the vulva,
vagina and perineum. The rash is usually profuse and is accompanied by regional lymphadenitis. Vesicles open rapidly, forming erosive,
erosive and ulcerative surfaces. All this is accompanied by a burning sensation, itching, weeping, soreness, makes it difficult, often makes it impossible
sexual intercourse, which leads to the development of neurotic conditions.

In 50-75% of people after primary infection, relapses occur with similar clinical symptoms. Damage, in some cases,
restricted to the external genitalia. Involved in the pathological process: in women - the vagina, cervical canal, cervix and uterine cavity,
ovaries, urethra, bladder; in men, the urethra, bladder, prostate, testes. In both men and women with oral-genital
contacts affect the tonsils, oral mucosa, genital-anal area of ​​the anus, rectum.

People with severe immunodeficiency, including those with HIV infection in the AIDS stage, develop severe ulcerative necrotic lesions.
genitals.

At the same time, after recurrence, the severity of local changes subsides somewhat and abortive forms can be observed. With these forms
typical vesicular rashes are absent or single elements appear for a short time.

Patients are concerned about the burning sensation, itching, slight hyperemia, swelling of the skin and mucous membranes of the genital organs.

Often recurrent genital herpes is accompanied by regional lymphadenitis, sometimes lymphostasis develops and, as a result, elephantiasis
genitals.

In women, recurrent herpes caused by HSV-2 can contribute to the development of cervical carcinoma.

Lesions of the skin and mucous membranes usually have not only a localized, but also a fixed character, i.e., with the next recurrence, they appear
in the same place. However, in some patients, rashes migrate and appear on new areas of the skin and mucous membranes, where they are located in
grouped bubbles. Less often, a herpes infection becomes widespread when vesicles appear in different areas.
skin and mucous membranes, are discrete and resemble chickenpox. Migration of rashes and a common form of herpes simplex -
sign of increasing immunodeficiency.

Visceral herpes simplex. In the visceral form, as a rule, there is a lesion of one internal organ or system. Most often in
the pathological process involves the nervous system, resulting in serous meningitis, encephalitis and meningoencephalitis.

Herpetic serous meninitis. In the etiological structure of serous meningitis, diseases caused by HSV account for 1-3%. Typical flow
disease is accompanied by fever, headache, photophobia, meningeal syndrome and moderate cytosis due to lymphocytes in
cerebrospinal fluid. However, often meningitis of herpetic etiology can be asymptomatic, without a pronounced meningeal syndrome.
Therefore, fever and signs of a cerebral syndrome (headache, vomiting) should be an indication for hospitalization, especially if
mild meningeal symptoms.

Herpetic encephalitis and meninaoencephalitis are severe diseases that occur with cerebral and focal symptoms, characterized by
very high mortality (up to 50%). The disease usually begins acutely - with chills, high fever. Within 2-3 days, the condition of patients quickly and
worsens significantly: meningeal symptoms appear, convulsions, focal symptoms increase, consciousness is disturbed (up to the development
cerebral coma, which is the most common cause of death). In encephalitis and meningoencephalitis, typical vesicular lesions occur
rarely.

In some patients, mainly with primary herpes, lesions of the nervous system are preceded by aphthous gingivostomy atitis.

Herpetic senamum. In second place in terms of frequency of visceral lesions is the liver. Developing hepatitis has common clinical and laboratory
signs with hepatitis B, C. However, there are no markers of hepatotropic viruses, and from the features of the clinical course, fever against the background of
jaundice. As a rule, the disease has a mild course. However, cases of fulminant course of herpetic hepatitis, accompanied by
severe necrotic lesions of the liver parenchyma and hemorrhagic syndrome.

Herpes pneumonia usually occurs in people with severe immunodeficiency, including those with HIV/AIDS. Lesions in the lungs
are in the nature of peribronchial-perivascular changes. Bacterial superinfection is quite common.

Disseminated serpes simplex (serpetic sepsis), which occurs only in severely immunocompromised patients and in children under 1 month of age, refers to
AIDS indicator diseases. Its course fits into the clinic of viral sepsis - the defeat of many organs and systems is accompanied by fever,
intoxication, DIC, the clinical manifestations of which are a hemorrhagic rash (from petechiae to large hemorrhages in the skin and mucous
membranes) and bleeding. Mortality is about 80%.

Visceral and disseminated forms of PG are rare and mark an immunodeficiency state.

Congenital HSV infection may be more common than diagnosed. Just like acquired, it can occur in
localized, widespread and generalized forms. Disseminated infection is characterized by the development of hepatitis, encephalitis, pneumonitis with
damage to the skin and mucous membranes or without it. If etiotropic therapy is not carried out, mortality reaches 65%.

Diagnostics. Virological, immunochemical and molecular biological research methods are used.

The virological method for isolating HSV by in vitro cultivation on cell or organ cultures is the most specific and
sensitive method that allows to detect the pathogen within 3 days. It can be used in clinical practice in the presence of
virological laboratory working with cell or organ cultures.

More accessible are express diagnostic methods for detecting viral antigens in biosubstrates - MFA and ELISA.

Recently, molecular biological methods (PCR and hybridization), which have a high
sensitivity and specificity.

Immunochemical method - ELISA in the determination of anti-herpetic antibodies of the IgG class has, like other serological methods, an insignificant
diagnostic value, since even a high level of these antibodies in the blood can only indicate that a person is infected
and does not allow to associate the existing symptom complex with the activity of HSV. Determination of anti-herpetic lgG antibodies in paired sera reveals
their fourfold increase in only 5% of persons with recurrent PH. The detection of lgM antibodies is somewhat more important, which may be
an indicator of an actively ongoing primary or secondary infection. This is also evidenced by a positive result in ELISA for the presence of antibodies to early
non-structural proteins HSV-1 and HSV-2.

Treatment. Therapy of patients with PH is individual and depends on the form of infection, severity, frequency of relapses. It includes etiotropic, pathogenetic
(immune-oriented, anti-inflammatory and detoxifying agents, reparants) and symptomatic (painkillers, antidepressants, etc.)
directions.

In the etiotropic therapy of PG, the following types of antiviral agents are used:

Acyclovir (zovirax, virolex), is available for parenteral use in 250 mg vials as a sodium salt; for oral
use in tablets and capsules of 200 mg, 400 mg, 800 mg and suspensions (in 5 ml of 200 mg of the drug); for external use: cream 5%, eye ointment 3%.

The dose and course of acyclovir depend on the duration of the disease, the frequency of relapses, the prevalence of the lesion and usually range from 200 mg 5 times a day to
for 5 days up to 400 mg 5 times a day for 7-14 days. For children over 2 years old, the tablet preparation is prescribed in the same dosage as for adults, up to
2 years - half dose.

Particularly intensive should be the treatment of patients with various immunodeficiency conditions and persistently recurrent PH, as well as
visceral and disseminated forms of herpes. In such patients (adults and children over 12 years of age), acyclovir is prescribed intravenously at 5-10 mg / kg
body weight every 8 hours for 7-14 days.

In addition to acyclovir, the group of abnormal nucleosides includes:

Valaciclovir (Valtrex) - in tablets of 500 mg 2 times a day for 5-7 days;

Famciclovir (Famvir) - in tablets of 250 mg 3 times a day for 7 days;

Ribavirin (virazole, ribamidil) - in capsules of 200 mg 3-4 times a day for 7-10 days; children - 10 mg / kg of body weight per day for 3-4 doses, 7-10
days;

Ganciclovir (cymeven) - in tablets 1 g 3 times a day or 1-5 mg / kg of body weight intravenously every 12 hours in severe cases caused by
acyclovir-resistant strains of HSV, visceral and disseminated forms of PG, a course of 2-Zned;

Foscarnet (foscavir), refers to analogues of pyrophosphate - is prescribed for severe, caused by acyclovir-resistant strains of HSV, visceral and
disseminated forms of AHPG at a dose of 40-60 mg/kg of body weight intravenously every 8 hours, followed by a transition to a maintenance dose of 90 mg/kg/day in
within 2-3 weeks. Promising agents for the treatment of herpetic infection with high antiviral activity include: penciclovir,
flacitobine, cidofovir, zonavir, lobukavir, sorivudine, brivudine, usevir and adefovir.

Antiviral agents with various mechanisms of inhibitory action include:

Alpizarin is available as tablets of 0.1 g and 2% or 5% ointment; is prescribed individually depending on the form and course of PG in the dose: 0.1-0.3 g 3-4
once a day for 7-10 days;

Arbidol - in tablets of 0.1 g 3 times a day for 5 days;

Khelepin (helpin, brivudine) - tablets of 0.125 g and 1% or 5% ointment, adults - 4 tablets per day for 4-10 days, children 5 mg / kg of body weight 3 times a day 5-7
days;

Tromantadine, oxolin, tebrofen, florenal, pandavir

Used topically (see below). Promising drugs in this group include:

Flacoside (flacoid glycoside) - tablets of 0.1 and 0.5 g, prescribed 3 times a day, a course of 5-7 days;

Polyrem-retarded adamantane derivative, which allows the drug to be used only once a day at a dose of 0.3 g (2 tablets of 0.15 g)
course - 3-6 days and 2.5% gel (virosan).

Among herbal preparations with a noticeable antiviral effect, in the treatment of herpes infection, most often used
derivatives of licorice and St. John's wort. These funds are used mainly locally. Thus, the epigen produced on the basis of salts of glycyrrhizic acid is noticeably
reduces the healing time of mucocutaneous lesions in PG (and herpes zoster).

Preparations for oral and parenteral use must be combined with antiviral agents for topical use.

Ointment and cream begin to be used when the first signs of infection activation appear (burning sensation, itching, etc.) and continue
up to the epithelialization of erosions. Early topical treatment may prevent the development of vesicles. Prescribe one of the following antiviral ointments
or creams (preferring one that is similar to the pills taken):

Acyclovir - cream 5% and 3% eye ointment 5 times a day,

Alpizarin - ointment 2%, 4-6 times a day,

Oksolin - ointment 1% -2%, 2-3 times a day,

Pandavir - ointment 1%, 2-3 times a day,

Tebrofen - ointment 2% -3% -5%, 2-4 times a day,

Trifluridine - ointment 0.5%, 2-3 times a day,

Tromantadin - gel 1%, 3-4 times a day,

Florenal - ointment 0.5%, 2-3 times a day,

Bromuridine - ointment 2% -3%, 2-3 times a day,

Isopropyluracil (gevizosh) - the ointment is applied to the affected areas of the skin 3-5 times a day.

Pathogenetic therapy is aimed at normalizing the function of the body's immune system, including the activation of the interferon protection system.
and is carried out under the control of immunograms.

Attraction of often recurrent herpetic infection (after the study of interferon status) use natural (natural) and
recombinant interferons (IFN).

Natural (natural) IFN include: alfaferon, velferon, egiferon. Recombinant interferons include: IFN a-2a (Reaferon,
Roferon-A), IFN a-2b (Intron A, Real diron, Viferon - rectal suppositories)

IFN preparations are usually administered subcutaneously or intramuscularly at a dose of 1-3 million IU per day. A convenient form for use are rectal suppositories
"Viferon", prescribed in a daily dose of 1-3 million IU. The effectiveness of treatment largely depends on the selected dose of the drug. So, it was found that
high doses of IFN lead not to stimulation, but to suppression of the activity of macrophages and natural killers, a decrease in the expression of IFN receptors and
deterioration in treatment outcomes.

Interferon inducers currently used in the treatment of herpes infections can be divided into 3 large groups:

1. Preparations from cotton: gozalidon, kagocel, megasin, rogasin, savrats.

2. Preparations of double-stranded RNA or containing double-stranded nucleotide sequences: larifan, polyguacil, poludan, ridostin, ampligen.

3. Others: amixin, comedon (neovir), cycloferon. Most IFN inducers are used according to the treatment regimen 2 days a week. The exception is
only recommendations on the use of comedones and cycloferon (intramuscular injections of drugs on the 1st, 2nd, 4th, 6th, 8th days of treatment). Currently
a tablet form of cycloferon is also produced, which is more convenient for outpatient practice.

In the early period of relapse, the introduction of immunoglobulins containing an increased titer of antibodies to herpetic viruses, 3 ml is indicated.
intramuscularly daily for 4 days. Often, polyspecific immunoglobulins are also used for intramuscular use (donor
gammaglobulin). However, in the treatment of visceral and disseminated forms of PH, polyspecific intravenous immunoglobulins are more significant.
(IVIGi) 3rd-4th generations: Octagam, Intraglobin F, Polyglobin N, Sandoglobin, Venimmune, Pentaglobin enriched with IgM. Among domestic VVIGs
the most famous polyspecific IVIG produced in Nizhny Novgorod. Polyspecific IVIGs are prescribed at a dose of 400-500 mg/kg/day for 4
days.

In immunocorrective therapy of often recurrent PH, cytomedines (Imunofan, Thymalin, T-Activin, etc.), interleukins (Roncoleukin,
betaleykin), drugs that increase the activity of non-specific cellular defense factors (onium polyoxide).

Inactivated antiherpetic vaccines are used to treat frequently relapsing PH. There are several course options
vaccine therapy. The first of them includes two cycles of 5 intradermal injections of 0.2 ml of the vaccine, each with an interval of 3-4 days. Break between two
five-day cycles - 10 days. Repeated courses of vaccine therapy, necessary to obtain a stable therapeutic effect, are carried out after 3-6-12
month or every six months, only 6-8 times. Vaccination is carried out in a hospital setting.

The second option involves intradermal administration of 0.2 ml of the vaccine once a week. For a course of 5 injections. Revaccination after 6-8 months. Only 3-5 courses
revaccination.

The third option includes 6 intradermal injections with an interval of 20 days. There are other options for constructing vaccine therapy courses. Should
note that all of them do not differ significantly in the results of treatment, however, the second and third options are much more convenient for patients, since they do not
require a long stay in the hospital.

With severe edema, burning sensation, itching, non-steroidal anti-inflammatory drugs are used as pathogenetic therapy.
(indomethacin, voltaren, etc.). If necessary, symptomatic agents are prescribed.

The criteria for the effectiveness of the treatment of frequently recurrent PH is the following:

Increase in the duration of remission by 2 times or more,

Reducing the area of ​​damage,

Reducing local symptoms of inflammation (swelling, itching, etc.),

Reducing the duration of breakouts

Shortening the time of epithelialization,

Disappearance or reduction of the general infectious syndrome. If there is a positive trend in at least 1-2 parameters, treatment can be considered
successful. It is necessary to inform the patient about the chronic nature of the infection, which does not pose a threat to life, and the criteria for effectiveness.
the therapy being carried out.

Treatment of primary infection (primary episode)
total acyclovir (Ac), which has a high degree of affinity and selectivity for HSV-1 and HSV-2. Generally accepted recommended regimen
primary (tegmental) PG in immunocompetent persons - 200 mg of Ac 5 times a day for 5 days. In the treatment of immunocompromised individuals (patients with various
types of immunodeficiency states - IDS) use doses that are 1.5-2 times higher than the above, and the course of treatment is 10-14 days. At
in the treatment of severe forms (visceral, disseminated) PH, combination therapy is used, including AC at a dose of 5-10 mg/kg intravenously
drip every 8 hours for 7-14 days, hyperimmune or polyspecific IVIGs at 400-500 mg / kg / day for 4 days, detoxification and
symptomatic remedies.

Treatment of recurrent (secondary) PH There are 4 main methods of treatment of recurrent PH:

1) episodic treatment of each relapse (the so-called "on demand" therapy);

2) episodic treatment that stops the initial manifestations of each relapse (preventive therapy that does not allow the full development of relapse);

3) long-term antiviral therapy (to prevent relapses);

4) staged treatment using combined (antiviral and MMU non-oriented) therapy both during relapse and during
inter-relapse period, in order to prevent or significantly reduce subsequent relapses.

With episodic treatment (on-demand therapy) of recurrent PH, there is a slight shortening of the period of virus isolation and
improvement in clinical parameters such as the appearance of new lesions, time to cure, and duration of symptoms.

Episodic treatment that stops the initial manifestations of relapse (preventive therapy), initiated by the patients themselves, and,
therefore, when started early, at the first appearance of prodromal symptoms, significantly improves clinical and virologic outcomes.

It has been established that the treatment of patients with prodromal symptoms with a 5-day course of Ac at a dose of 200 mg 4 times a day or 400 mg twice a day
stops the process or significantly reduces the severity of exacerbations in almost 80% of them. The greatest effect is observed in those cases when, after medical
counseling, the treatment of all subsequent relapses was started by the patients themselves, since going to the doctor with each new relapse delays the onset
therapy with AC for 48 hours or more.

Long-term antiviral therapy (virus suppressive therapy) should be given to patients with 6-8 or more relapses per year. Patients with less
the number of relapses, uncertain that they are constantly exposed to adverse factors, this method of treatment is also indicated. Sick,
who are on virus-suppressive treatment should be regularly examined to determine the effectiveness of therapy, the need
continue the course, as well as to discuss other issues.

Patients should start with a daily dose of 800 mg divided into 2 or 4 doses. Sequential dose reduction is needed to determine
the smallest daily dose and the optimal regimen for taking the drug for each patient. Drug therapy should be stopped annually for
determination of indications for cessation of viral suppression, since the time intervals before the first exacerbation lengthen over the years, and in some cases
drug withdrawal is possible.

However, it is necessary to explain to patients that AC during virus suppressive therapy cannot completely eliminate relapses. Cases are described
asymptomatic virus carrying, in which the possibility of unintentional infection of sexual partners is not excluded.

Staged treatment using combination therapy, both during relapse and in the inter-relapse period, aims to prevent
or lead to a significant decrease in subsequent relapses. The strategy and tactics of the staged treatment of PH are presented below (Table 7).

If it is impossible to extend the interrecurrent period for more than 2 months, the methods indicated in the table are prescribed vaccine therapy.

Treatment of recurrent PH during pregnancy

Until now, the problem of optimal treatment of pregnant women with a history of genital herpes remains controversial. Available
information that the appointment of oral AC at a dose of 200 mg 4 times a day in the last week of pregnancy in women with a history of
recurrent genital herpes, reduces the risk of infection with PG in newborns. In this connection, the question of the use of AC at a later date is being considered.
pregnancy, but so far there is no permission for its use.

Treatment of PH in immunocompromised patients. When prescribing therapy to infectious patients with signs of severe immunodeficiency (ID),
should be guided by four principles that are successfully used by the staff of our department (A.P. Remezov, V.A. Neverov) in the treatment
patients with immunodeficiency states (VAT):

1. In etiotropic therapy, it is necessary to use only those agents to which the absolute majority in this region are highly sensitive
strains of the pathogen that caused the disease.

2. The dose of the etiotropic drug should correspond to the maximum recommended for the corresponding pathology, (exceeding the dose that
would be used to treat a similar form of the disease in a patient without severe ID).

3. In the process of treatment, it is necessary to exclude (or reduce) the impact of pathological factors that led to the development of SDS.

4. It is necessary to use immunoreplacement and/or immunocorrective therapy.

Immunodeficiency caused by HIV or immunosuppressive therapy increases the risk of reactivation of pathogens of various latent pathogens in such patients.
infections, including PG. Relapses in them occur more often, have more prolonged and severe course. In these cases, long-term antiviral treatment
AC should be started orally immediately, but it is necessary to be aware of the possibility of development of HSV resistance to AC in such patients.

Treatment of PH caused by acyclovir-resistant strains

Over the past 10 years, there has been an increase in the number of reports of HSV resistance to Ac, which is often combined with immunosuppression, especially in
HIV infections. Clinically, this can be expressed in a long progressive course of ulceration, followed by tissue deformation, which can
accompanied by a feeling of discomfort. Most of the HSV strains isolated from such patients are deficient in viral thymidine kinase, therefore, for
treatment of HIV-infected patients with ac-resistant herpes infection, it is necessary to use antiviral drugs that do not require activation
by this enzyme.

Promising results have been obtained in the study of the action of foscarnet. Although foscarnet has serious and side effects, causing
impaired renal function, calcium metabolism, and genital ulceration, it is considered to be preferred in AC-resistant herpetic
infections. The efficacy of using uzevir, lobukavir, brivudine, adefovir and cidofovir in these cases is being studied.

Thus, when prescribing therapy to a patient with recurrent PH, it is necessary to study the history of his disease, determine the frequency and severity
relapses, the presence or absence of prodromal symptoms and, most importantly, to explore the daily impact of environmental factors on life
sick.

In addition, the choice of treatment must take into account the experience of the patients themselves. Patients who are confident that topical application of Ac helps them should
continue this type of treatment. For those who can recognize dormant symptoms and prevent or significantly reduce the severity and
duration of exacerbation with a 5-day oral course of Ac, this type of treatment is preferable to long-term viral suppression
Therapy is also cheaper. In cases where the frequency of relapses is at least 6-8 times a year or patients (with fewer relapses)
sure that they are constantly exposed to adverse factors, long-term antiviral or combined
(antiviral and immune-oriented) therapy. In the treatment of patients with frequent relapses of PH, planning to have offspring, should be
combined (antiviral and immuno-oriented) therapy was used, which stopped relapses for a long time and excluded
asymptomatic virus shedding, the so-called "asymptomatic virus shedding". Treatment is carried out in the period preceding the onset of pregnancy.
In the absence of a clear relapse-stopping effect from combined antiviral and immunocorrective therapy, it is necessary to use
vaccine therapy. If it also does not provide a relapse-free course of pregnancy, it is necessary to raise the question of prescribing the course of Ac in the last
week of pregnancy.

The tasks of dispensary observation of patients with recurrent PH are to establish the causes of immunodeficiency, early detection and
prevention of complications and consequences.

The GP should be aware that various acute and chronic, including focal infections, can contribute to the recurrence of PH - carious teeth,
chronic cholecystitis, adnexitis, cystitis and many others. It is necessary to direct efforts to identify and sanitize the source of infection. matter
occupational hazards, work and rest regimen, nutrition, endocrine diseases, stressful situations.

Sudden increase in recurrence rate, spread and migration of lesions sometimes occur before clinical symptoms
developing malignant tumor of any localization. Such patients, especially if there is no other reason for immunodeficiency, should be carefully
examine.

Women with recurrent genital herpes should be examined by a gynecologist using colposcopy for early
diagnosis of cervical cancer.

AI prevention should include prevention of the spread of the disease by airborne droplets, as well as natural and
artificial ways that implement the percutaneous mechanism of infection

Herpes symptoms. Herpes of the face and mouth. Herpetic lesions of the eyes. Genital herpes. Herpes of the newborn. Diagnosis of a herpetic infection

used in our center Treatment program for chronic viral infections give a chance:

• in a short time to suppress the activity of the infectious process
• effectively restore the body's immune defenses
• reduce the doses of antiviral drugs and reduce the toxic effect of these drugs on the patient's body
• increase sensitivity to traditional antiviral drugs
• prevent recurrence of infection

This is achieved through the use of:

• method Cryomodification of autoplasma allowing to remove from the body toxic metabolites of microorganisms, inflammatory mediators, circulating immune complexes
• technologies Incubation of cell mass with antiviral drugs that ensure the delivery of drugs directly to the site of infection
• technologies Extracorporeal immunopharmacotherapy that work directly with the cells of the immune system and allow you to effectively and for a long time increase antiviral immunity

Herpes symptoms

The herpes simplex virus can infect almost all internal organs and mucous membranes, as well as any part of the skin. The symptoms and course of herpes depend on the location of the viral lesion, age, immune status of the patient and the type of herpes virus. Primary herpes (that is, developed in a patient seronegative for the herpes virus) is often accompanied by a violation of the general condition and localization of the viral lesion both on the mucous membranes and outside them.

Regardless of the type of herpes virus that caused the infection, primary herpes differs from relapses:

• longer course
• longer shedding of the virus into the environment
• higher incidence of complications

Both herpes simplex virus type 1 and herpes simplex virus type 2 cause both facial and oral herpes and genital herpes, and it is impossible to determine the type of herpes virus from the clinical picture. In the same time recurrence rate herpes infection depends on type of herpes virus and localization of infection. Genital herpes caused by herpes simplex virus type 2 reactivates 2 times more often and recurs 8-10 times more often than those caused by herpes simplex virus type 1. Conversely, herpes of the face and oral cavity caused by herpes simplex virus type 1, recurs more frequently than that caused by herpes simplex virus type 2.

The spectrum of symptoms of herpes infection is very diverse. Various classifications of herpes infection have been proposed, but there is no generally accepted clinical classification of herpes infection. One of the most successful classification options for herpes simplex is given below.

Clinical classification of infection caused by herpes simplex virus

(V. A. Isakov, D. K. Ermolenko, 1991)

1.	Depending on the duration of the presence of the virus in the body
	1.1.	Short-term circulation of the herpes simplex virus in the body:
		a)	acute form of herpetic infection;
		b)	inapparent (asymptomatic) form of herpetic infection.
	1.2	Long-term persistence of the herpes simplex virus in the body:
		a)	latent form of herpetic infection;
		b)	chronic form (with relapses);
		v)	slow form of herpes infection
2.	Considering the mechanism of infection.
	2.1.	congenital herpes infection
	2.2.	Acquired herpes infection:
		a)	primary;
		b)	secondary (recurrent).
3.	Depending on the clinic and localization of the pathological process
	3.1.	Typical shapes:
		a)	herpetic lesions of the mucous membranes of the gastrointestinal tract (stomatitis, gingivitis, pharyngitis, etc.);
		b)	herpetic eye lesions: ophthalmic herpes (herpetic conjunctivitis, keratitis, iridocyclitis, etc.);
		v)	herpetic lesions of the skin (herpes of the lips, herpes of the wings of the nose, face, hands, buttocks, etc.);
		G)	genital herpes (herpetic lesions of the mucous membranes of the penis, vulva, vagina, cervical canal, etc.);
		e)	herpetic lesions of the nervous system (meningitis, encephalitis, meningoencephalitis, neuritis, etc.);
		e)	generalized herpes simplex:
			- visceral form (pneumonia, hepatitis, esophagitis, etc.);
			- disseminated form of generalized herpes (clinic of viral sepsis)
	3.2.	Atypical forms:
		a)	edematous;
		b)	zosteriform herpes simplex;
		v)	Kaposi's eczema herpetiformis (Kaposi's varicella pustulosis);
		G)	ulcerative necrotic;
		e)	hemorrhagic

It should be noted that atypical forms of herpes are more common in individuals with immunodeficiency states of various origins.

Symptoms of herpes of the face and mouth

Primary herpes, caused by herpes simplex virus type 1, is most often manifested by symptoms such as stomatitis or pharyngitis, and relapses - by herpetic lesions of the lips. Since stomatitis and pharyngitis are inherent in the primary infection, they occur mainly in children and young people. Herpetic stomatitis lasts from 3 to 14 days. The clinical picture includes symptoms such as: fever, malaise, myalgia, inability to eat, irritability, enlarged cervical lymph nodes. Rashes are localized on the hard and soft palate, gums, tongue, lips and facial skin. With herpetic pharyngitis caused by any type of herpes simplex virus, plaque or erosions appear on the back of the pharynx and palatine tonsils. A third of patients later develop herpetic eruptions on the tongue, buccal mucosa and gums. Characteristic symptoms are fever lasting 2-7 days and an increase in cervical lymph nodes. Herpetic pharyngitis may be indistinguishable from bacterial sore throat, pharyngitis caused by Mycoplasma pneumoniae, and mucosal ulceration of a different etiology (eg, Stevens-Johnson syndrome). There is no convincing evidence that relapses of herpes of the face and oral cavity can occur in the form of pharyngitis.

Reactivation of the herpes simplex virus in the trigeminal ganglion may be accompanied by the release of the herpes virus with saliva in the absence of any clinical manifestations, herpetic eruptions on the oral mucosa, the red border of the lips and the skin of the face. After decompression of the trigeminal nerve root, recurrence of herpes of the face and oral cavity occurs in 50-70% of patients seropositive for the herpes virus, after tooth extraction - in 10-15% (in half of the cases this occurs in the first 3 days after the intervention).

With a weakened immune system, a herpes infection spreads to the deep layers of the skin and mucous membranes. There are ulcers, necrosis, bleeding, severe pain. Patients are often unable to eat or drink. Herpetic mucosal lesions are indistinguishable in symptoms from those caused by cytostatics, trauma, fungal or bacterial infection. Chronic ulcerative herpes is one of the most common infections in AIDS patients. In this case, herpes is often accompanied by candidiasis. Taking acyclovir accelerates healing and relieves pain in mucosal lesions in immunocompromised patients. In those suffering from diffuse neurodermatitis, Kaposi's herpetic eczema occurs - a severe form of herpes of the face and oral cavity, quickly covering large areas of the skin and sometimes complicated by damage to internal organs. Kaposi's herpetic eczema resolves rapidly with intravenous acyclovir.

Herpes is often complicated by polymorphic exudative erythema; it was reported that about 75% of cases of this disease are provoked by the herpes virus. At the same time, herpes simplex virus antigens are found in circulating immune complexes and biopsy specimens of the affected skin. Patients with severe polymorphic exudative erythema caused by the herpes virus are shown to take antiviral drugs continuously.

Recently, it has become clear that the herpes simplex virus may play a role in the etiology of Bell's palsy (idiopathic neuropathy of the facial nerve). Whether antiviral therapy can affect its course is unclear.

Symptoms of genital herpes - genital herpes

Primary genital herpes accompanied by symptoms such as: fever, headache, malaise, myalgia. The predominant local symptoms of genital herpes are:

• painful urination
• discharge from the vagina and urethra
• enlargement and soreness of the inguinal lymph nodes

Extensive bilateral damage of external genitals is characteristic; often at the same time there are elements of a rash at different stages of development - vesicles, pustules, painful hyperemic erosions.

At primary genital herpes more than 80% of women affect the cervix and urethra. In individuals previously infected with herpes simplex virus type 1, primary genital herpes resolves faster and is less often accompanied by a violation of the general condition.

Clinical picture primary genital herpes does not depend on the type of virus that caused it, but the type of virus affects the frequency of relapses. If the disease is caused by the herpes simplex virus type 2, during the first 12 months relapses occur in 90% of patients, if the causative agent is the herpes simplex virus type 1 - in 55% (the median number of relapses per year in the first case is 4, in the second it does not reach one). In genital herpes caused by herpes simplex virus type 2, the recurrence rate is not the same in different patients and, in addition, changes over time. In both men and women, the herpes virus is found in the urine and smears from the urethra in the absence of rashes. For herpetic urethritis painful urination and clear mucous discharge from the urethra are characteristic. Herpes simplex virus is found in the urethra in 5% of women with urethral syndrome. Among women genital herpes sometimes complicated by endometritis and salpingitis, in men - by prostatitis.

Both types of herpes simplex virus cause damage to the rectum, anal canal, and perianal area, which may be asymptomatic. Herpetic proctitis usually observed in patients who practice anal intercourse. However, in a number of heterosexual men and women who do not practice anal intercourse, the herpes virus is shed from the anus into the environment in the absence of clinical manifestations. This the phenomenon is due to the persistence of the herpes virus in the sacral ganglia after primary herpes of the genital organs. With reactivation of herpetic infection, which is often asymptomatic, the herpes virus is found in the mucous membrane of the anal canal and the skin of the perianal region. Herpetic proctitis is manifested by pain and discharge from the rectum, tenesmus, constipation. With sigmoidoscopy, herpetic lesions of the rectal mucosa are detected at a depth of up to 10 cm, with a biopsy - ulceration, necrosis, neutrophilic and lymphocytic infiltration of the lamina propria, sometimes - giant cells with intranuclear inclusions. Herpetic lesion of the anal canal and perianal area occurs against the background of weakened immunity, in particular in patients receiving cytostatics. This form of herpes, like herpetic proctitis, is often observed in HIV-infected people and is severe.

Herpetic felon

Herpetic felon develops as a complication of primary herpes of the face and oral cavity or genital organs, or as an independent infection, for example, due to occupational infection. In both cases, the herpes virus is introduced into the skin of the finger through the damaged epidermis. The disease begins suddenly with swelling, redness and pain in the affected finger. The resulting vesicles and pustules are indistinguishable from those that manifest pyoderma. Fever and enlargement of the elbow and axillary lymph nodes are not uncommon. Herpetic felon can recur. It is very important to make an early diagnosis in order to avoid unnecessary and fraught with complications of surgery and to prevent the spread of infection. To speed up healing, antiviral agents are usually prescribed.

herpes gladiatorum

Herpes can affect any area of ​​the skin. Among wrestlers, outbreaks of herpes are noted, in which herpetic lesions of the skin of the chest, auricles, face, and hands are observed. The transmission of herpes infection is facilitated by skin injuries during fights. To stop the spread of infection, it is necessary to diagnose and start treatment in a timely manner.

Symptoms of herpetic eye disease

IN USA herpetic keratitis is the most common cause of corneal clouding s. The disease is manifested by symptoms such as - sudden pain in the eye, blurred vision, chemosis, conjunctivitis and ulceration of the cornea, shaped like a branching tree (dendritic keratitis). Local application of glucocorticoids worsens the condition and leads to damage to the internal structures of the eye. Surgical debridement, topical antivirals, and interferon preparations hasten recovery. However, relapses occur frequently. Possible damage to the internal structures of the eye due to immune mechanisms. Herpetic chorioretinitis usually develops against the background of generalized herpes and occurs in newborns and HIV-infected. The herpes simplex virus, like the varicella-zoster virus, rarely causes acute retinal necrosis.

Damage to the nervous system in herpesvirus infection

IN USA herpes is the most common recognizable cause of acute viral encephalitis; 10-20% of sporadic cases occur in herpetic encephalitis. The incidence of herpes encephalitis is approximately 2.3 per 1 million people per year. Seasonal fluctuations are not characteristic of it. Two peak incidences occur between 5 and 30 years of age and over 50 years of age. In more than 95% of cases, the causative agent of herpes encephalitis is the herpes simplex virus type 1.

Pathogenesis disease is heterogeneous. Primary herpes can occur in children and young people in the form of encephalitis. In this case, the herpes virus, apparently, enters the CNS from the nasal mucosa, being transported along the axons of olfactory neurons to the olfactory bulb.

However, most adult patients with herpes encephalitis either have a history of herpes or are seropositive for herpes simplex virus type 1.

Approximately 25% of patients with herpetic encephalitis in the oropharyngeal mucosa and brain tissue have different strains of the herpes virus. In these cases, encephalitis is caused by re-infection with another strain of herpes simplex virus type 1 with the penetration of the pathogen into the central nervous system. To explain the causes of encephalitis in cases where the same strain of the herpes virus is found in the mucous membrane of the oropharynx and brain tissue, two hypotheses have been proposed. According to the first, the reactivation of the herpes virus in the trigeminal or autonomic ganglia is accompanied by its spread to the central nervous system along the nerves innervating the middle cranial fossa. According to the second, the herpes virus for a long time rests in a latent state directly in the central nervous system, where it is reactivated. In any case, using oligonucleotide probes, herpes simplex virus DNA was found in the brain tissue of adults who did not die from herpes.

For herpetic encephalitis characterized by an acute onset with fever and focal neurological symptoms; symptoms of damage to the temporal lobes are especially characteristic. Distinguishing herpetic encephalitis from other viral encephalitis and other focal infectious and non-infectious diseases of the central nervous system is not easy.

The most sensitive non-invasive method for early diagnosis is the detection of herpes simplex virus DNA in the CSF by PCR. The titer of antibodies to the herpes simplex virus in both CSF and serum in herpetic encephalitis usually increases, but this rarely occurs in the first 10 days of the disease. Therefore, serological methods are only suitable for retrospective confirmation of the diagnosis.

A biopsy allows you to identify antigens and DNA of the herpes simplex virus in brain tissue and isolate the virus from it in cell culture. It is a highly sensitive method with a low complication rate. In addition, a brain biopsy makes it possible to diagnose other treatable encephalitis.

Antiviral drugs administered intravenously can reduce mortality in herpetic encephalitis. Aciclovir is more effective than vidarabine. However, despite treatment, residual neurological defects are not uncommon, especially in patients older than 35 years. Most specialists, if herpes encephalitis is suspected, recommend starting intravenous acyclovir without waiting for laboratory confirmation of the diagnosis.

Herpes simplex virus is isolated from the CSF in 0.5-3% of patients hospitalized for serous meningitis. Herpetic meningitis is often complicated primary genital herpes . This is an acute disease that lasts 2-7 days and resolves on its own. The main symptoms are headache, fever, mild photophobia. The CSF shows lymphocytic cytosis. Residual neurological defects are uncommon.

Herpes simplex virus is the most common recognizable cause meningitis Mollare. In this case, antibodies to the herpes simplex virus or viral DNA are detected in the CSF. Daily intake of antiviral agents reduces the likelihood of virus reactivation.

Like the varicella-zoster virus, the herpes simplex virus can cause autonomic neuropathy, especially when the sacral ganglia are affected. Described paresthesia in the buttocks and perineum, urinary retention, constipation, impotence. The CSF shows cytosis. Symptoms gradually resolve over several days or weeks. In some cases, hypoesthesia or weakness in the legs have been noted for many months. Occasionally herpes leads to the development of transverse myelitis with rapidly progressive paralysis of the legs and Guillain-Barré syndrome. With the reactivation of the herpes simplex virus type 1, apparently, damage to the peripheral nervous system, in particular Bell's palsy and polyneuropathy of the cranial nerves, can also be associated. The leading symptoms of the latter are transient hyperesthesia in the zone of innervation of the trigeminal nerve and vestibular disorders. There are no data on the effect of antiviral therapy on the frequency and severity of these neurological disorders.

Herpetic lesions of internal organs

Visceral forms of herpes usually due to viremia. Multiple organ damage is characteristic, although sometimes only herpetic esophagitis, herpetic pneumonia or herpetic hepatitis.

Herpetic esophagitis occurs with the direct spread of infection from the oropharyngeal mucosa or with the reactivation and migration of the herpes virus into the mucosa of the esophagus along the vagus nerve. The main symptoms are pain when swallowing, dysphagia, chest pain, weight loss. On the mucosa of the esophagus, multiple oval erosions with a hyperemic bottom appear, some of which are covered with fibrinous films. The distal esophagus is predominantly affected, but in severe cases, the esophageal mucosa is affected throughout its entire length. Neither esophagoscopy nor radiography with contrasting barium suspension makes it possible to distinguish herpetic esophagitis from candidal and radiation esophagitis, thermal and chemical burns. However, cytological and virological examination of the material obtained by esophagoscopy is of great help in the diagnosis. Antiviral agents alleviate the patient's condition and accelerate the healing of erosions.

herpetic pneumonia is rare. Only patients with severe immunodeficiency are susceptible to it. Herpetic pneumonia, which occurs when herpetic tracheobronchitis spreads to the lung parenchyma, is in the nature of necrotic bronchopneumonia. With hematogenous dissemination of the herpes virus in patients with herpes of the face and oral cavity or genital organs, bilateral interstitial herpetic pneumonia develops. Herpes pneumonia is often accompanied by bacterial, fungal or protozoal. Among immunocompromised patients, mortality in the absence of antiviral therapy exceeds 80%. Herpes simplex virus is also found in ARDS, but its role in the pathogenesis of this condition is unclear.

Herpetic hepatitis also rarely occurs against the background of normal immunity. The disease is accompanied by fever, a rapid increase in the concentration of bilirubin and serum aminotransferase activity, leukopenia (less than 4000 leukocytes per 1 μl), and sometimes DIC.

Other complications of herpes are also described - herpetic monoarthritis, adrenal necrosis, idiopathic thrombocytopenic purpura, glomerulonephritis. Generalized herpes rarely occurs with normal immunity. In immunocompromised, malnourished, burn victims, herpes sometimes affects the adrenal glands, pancreas, small and large intestines, and bone marrow. In pregnant women, hematogenous dissemination of the herpes virus in primary herpes can result in the death of both the fetus and the mother. Fortunately, this rarely happens, as a rule - when infected with herpes in the third trimester of pregnancy.

Herpes of newborns

Among newborns (more precisely, among infants younger than 6 weeks), the frequency of visceral forms of herpes and herpetic encephalitis is the highest. In the absence of treatment, these forms of herpes infection develop in more than 70% of newborns infected with herpes. Mortality in untreated herpes of newborns is 65%. Among survivors of herpetic encephalitis, less than 10% of children develop normally. Vesicular herpetic rash, which is easy to suspect the diagnosis, in many newborns appears only at the height of the disease.

According to most studies, the causative agent in 70% of cases is the herpes simplex virus type 2. Infection with it almost always occurs during the passage of a child through an infected birth canal, but congenital herpes has also been described - usually in children whose mothers had primary herpes during pregnancy. Infection with herpes simplex virus type 1 is also mostly due to primary herpes of the genital organs in the mother, which developed at the end of pregnancy, and the passage of the child through the infected birth canal. At the same time, a newborn can become infected with this virus even after birth - at home, as a result of contact with a family member suffering from herpes of the face and oral cavity (including during asymptomatic reactivation of the virus), or in a maternity hospital. Antiviral therapy reduces mortality to 25%, but newborns who have had herpes often become disabled. Especially dangerous is herpetic encephalitis caused by the herpes simplex virus type 2.

Diagnosis of a herpetic infection

Diagnosis of herpes infection based on both clinical and laboratory criteria. The clinical diagnosis is accurate if there are grouped vesicles on a hyperemic base. However, there are increasing reports that herpes lesions are atypical and mimic other skin conditions. Herpetic urethritis or pharyngitis is generally not always accompanied by skin rashes. To confirm the diagnosis and select therapy, it is recommended to use laboratory methods. In scrapings from the bottom of the vesicles, stained according to Wright, Giemsa (Zank test) and Papanicolaou, giant cells and intranuclear inclusions characteristic of herpes are visible. These methods are useful for rapidly confirming the diagnosis in outpatients. However, they are relatively insensitive and do not allow to distinguish herpes from herpes zoster. In addition, experience is needed to detect giant cells in smears.

The most accurate methods for confirming the diagnosis of a herpes infection are the isolation of the herpes virus in cell culture, the detection of antigens or DNA of the herpes virus in scrapings from the elements of the rash. The herpes simplex virus has a cytopathic effect on different types of cells. By this action, as a rule, the herpes virus can be identified 48–96 hours after the introduction of the test material into the cell culture. Centrifugation of a single-layer cell culture with the test material significantly accelerates the infection process and makes it possible to detect viral antigens after 24 hours.

The sensitivity of virus isolation in cell culture depends on:

1. stages of development of the elements of the rash (the virus is isolated from vesicles more often than from erosions)
2. forms of the disease (with primary herpes, the virus is isolated more often than with relapses)
3. state of immunity (when the immune system is weakened, the reproduction of the virus is more intense)

With herpes of the face and mouth and genital herpes, the sensitivity of detecting viral antigens is close to the sensitivity of virus isolation in cell culture, but when examining cervical mucus and saliva in individuals with asymptomatic virus reactivation, it is twice as low.

PCR is more sensitive than the isolation of the herpes virus in cell culture, especially with herpetic lesions of the central nervous system, and also if the material is taken from healing erosions. Laboratory methods make it possible to establish the type of herpes virus, which may be important in epidemiological terms. In addition, knowledge of the type of herpes virus can predict the frequency of recurrence of herpes infection.

In primary herpes, the study of paired sera (taken at the acute stage of the disease and during the recovery period) reveals seroconversion. With relapses, an increase in antibody titer by 4 times or more is observed only in 5% of patients. Serological methods, especially the determination of type-specific antibodies of herpes viruses, are used to detect the carriage of herpes simplex virus types 1 and 2.

According to a number of studies, patients who have antibodies to herpes simplex virus type 2 recognize recurrences of infection in themselves if they are informed about how these recurrences manifest themselves. Each of these patients should be warned that the reactivation of the herpes virus can be asymptomatic, accompanied only by the release of the pathogen from the mucous membrane of the cervix, urethra, anus, or from microscopic erosions not visible to the eye. The possibility of transmission of infection with such reactivation of the virus is not in doubt.

herpetic infection- a group of diseases caused by the herpes simplex virus, which are characterized by damage to the skin, mucous membranes, central nervous system, and sometimes other organs.

Etiology. The causative agent belongs to the herpes family (Herpes viridae). This family also includes varicella-zoster viruses, herpes zoster, cytomegaloviruses and the causative agent of infectious mononucleosis. Contains DNA, virion size 100-160 nm. The viral genome is packaged in a regular capsid consisting of 162 capsomeres. The virus is covered with a lipid-containing membrane. It reproduces intracellularly, forming intranuclear inclusions. The penetration of the virus into some cells (for example, neurons) is not accompanied by virus replication and cell death. On the contrary, the cell has a depressing effect and the virus goes into a state of latency. After some time, reactivation may occur, which causes the transition of latent forms of infection into manifest ones. According to the antigenic structure, herpes simplex viruses are divided into two types. The genomes of type 1 and type 2 viruses are 50% homologous. Type 1 virus mainly causes damage to the respiratory organs. The occurrence of genital herpes and generalized infection of newborns is associated with the herpes simplex virus type 2.

Epidemiology. The source of infection is man. The causative agent is transmitted by airborne droplets, by contact, and the genital - sexually. With congenital infection, transplacental transmission of the virus is possible. Herpes infection is widespread. In 80-90% of adults, antibodies to the herpes simplex virus are found.

Pathogenesis. The gateway of infection is the skin or mucous membranes. After infection, viral replication begins in the cells of the epidermis and the skin proper. Regardless of the presence of local clinical manifestations of the disease, virus replication occurs in a volume sufficient to introduce the virus into sensory or autonomic nerve endings. It is believed that the virus or its nucleocapsid propagates along the axon to the nerve cell body in the ganglion. The time it takes for infection to spread from the hilum to the ganglions is not known in humans. During the first phase of the infectious process, the multiplication of viruses occurs in the ganglion and its surrounding tissues. The active virus then migrates along efferent pathways represented by peripheral sensory nerve endings, leading to disseminated skin infection. The spread of viruses to the skin along the peripheral sensory nerves explains the fact of extensive involvement of new surfaces and the high frequency of new rashes located at a considerable distance from the sites of the primary localization of the vesicles. This phenomenon is typical both for individuals with primary genital herpes and for patients with oral herpes. In such patients, the virus can be isolated from the nervous tissue, located far from the neurons innervating the site of the introduction of the virus. The introduction of the virus into the surrounding tissues causes the spread of the virus through the mucous membranes.

After completion of the primary disease, neither the active virus nor the surface viral proteins can be isolated from the nerve ganglion. The mechanism of latent viral infection, as well as the mechanisms underlying the reactivation of the herpes simplex virus, is unknown. Reactivation factors include ultraviolet radiation, skin or ganglion trauma, and immunosuppression. In the study of herpes virus strains isolated from a patient from different lesions, their identity was established, however, in patients with immunodeficiencies, the strains isolated from different sites differed significantly, which indicates the role of an additional infection (superinfection). Factors of both cellular and humoral immunity play a role in the formation of immunity against the herpes virus. In persons with a weakened immune system, a latent infection turns into a manifest one, and the manifest forms are much more severe than in persons with a normal functioning of the immune system.

Symptoms and course. The incubation period lasts from 2 to 12 days (usually 4 days). Primary infection often proceeds subclinically (primary-latent form). In 10-20% of patients, various clinical manifestations are noted. The following clinical forms of herpes infection can be distinguished:

• erpetic skin lesions (localized and widespread);
• herpetic lesions of the mucous membranes of the oral cavity;
• acute respiratory diseases;
• genital herpes;
• herpetic lesions of the eyes (superficial and deep);
• encephalitis and meningoencephalitis;
• visceral forms of herpetic infection (hepatitis, pneumonia, esophagitis, etc.);
• herpes of newborns;
• generalized herpes;
• herpes in HIV-infected people.

Herpetic lesions of the skin. Localized herpes infection usually accompanies some other disease (acute respiratory disease, pneumonia, malaria, meningococcal infection, etc.). Herpetic infection develops at the height of the underlying disease or already in the recovery period. The frequency of herpes in acute respiratory infections ranges from 1.4% (with parainfluenza) to 13% (with mycoplasmosis). General symptoms are absent or masked by manifestations of the underlying disease. Herpetic rash is usually localized around the mouth, on the lips, on the wings of the nose (herpes labialis, herpes nasalis). At the site of the rash, patients feel heat, burning, tension or itching of the skin. On moderately infiltrated skin, a group of small vesicles filled with transparent contents appears. The bubbles are closely spaced and sometimes merge into a continuous multi-chamber element. The contents of the bubbles are initially transparent, then cloudy. The bubbles subsequently open, forming small erosions, or dry up and turn into crusts. A secondary bacterial infection is possible. With relapses, herpes usually affects the same areas of the skin.

A widespread herpetic skin lesion may occur in connection with a massive infection, for example, in wrestlers, with close contact, the herpes virus is rubbed into the skin. Outbreaks of herpetic infection in wrestlers are described, which occurred when one of the wrestlers had even small herpetic eruptions. This form (herpes gladiatorum) is characterized by a large area of ​​skin lesions. At the site of the rash, itching, burning, pain appears. With an extensive rash, an increase in body temperature (up to 38-39 ° C) and symptoms of general intoxication in the form of weakness, weakness, and muscle pain are noted. The rash is usually localized on the right half of the face, as well as on the arms and torso. The elements of the rash can be in different stages of development.

At the same time, vesicles, pustules and crusts can be detected. There may be large elements with an umbilical depression in the center. Sometimes the elements of the rash can merge, forming massive crusts that resemble pyoderma. Such a peculiar way of transmission of herpes infection in athletes allows us to think about the possibility of a similar transmission of other infectious agents, in particular, HIV infection.

Koposi's variceliform rash (eczema herpetiformis, vacciniform pustulosis) develops at the site of eczema, erythroderma, neurodermatitis and other chronic skin diseases. Herpetic elements are numerous, quite large. The vesicles are single-chamber, sink in the center, their contents sometimes have a hemorrhagic character. Then a crust forms, there may be peeling of the skin. In areas of affected skin, patients note itching, burning, skin tension. The regional lymph nodes are enlarged and painful. With this form, fever lasting 8-10 days is often observed, as well as symptoms of general intoxication. In addition to skin lesions, herpetic stomatitis and laryngotracheitis are often observed. There may be eye lesions more often in the form of dendritic keratitis. This form is especially difficult in children. Lethality reaches 40%.

Herpetic lesions mucous membranes of the oral cavity manifest as acute herpetic stomatitis or recurrent aphthous stomatitis. Acute stomatitis is characterized by fever, symptoms of general intoxication. Groups of small bubbles appear on the mucous membranes of the cheeks, palate, and gums. Patients complain of burning and tingling in the affected area. The contents of the bubbles are initially transparent, then cloudy. In place of bursting bubbles, surface erosions form. After 1-2 weeks, the mucous membranes are normalized. The disease may recur. With aphthous stomatitis, the general condition of patients is not disturbed. On the mucous membranes of the oral cavity, single large aphthae (up to 1 cm in diameter) are formed, covered with a yellowish coating.

Acute respiratory diseases. Herpes simplex viruses can cause inflammation of the mucous membranes of the upper respiratory tract. From 5 to 7% of all acute respiratory infections are due to herpes infection. Herpetic lesion of the pharynx manifests itself in the form of exudative or ulcerative changes in the posterior pharyngeal wall, and sometimes tonsils. In many patients (about 30%), in addition, the tongue, buccal mucosa, and gums may also be affected. However, most often, according to clinical manifestations, herpetic acute respiratory infections are difficult to distinguish from those of other etiologies.

Genital herpes is of particular danger in pregnant women, as it causes a severe generalized infection of newborns. May also contribute to cervical cancer. Genital herpes can be caused by the herpes simplex virus, both type 2 and type 1. However, genital herpes caused by type 2 recurs 10 times more often than herpes caused by type 1 virus. Conversely, herpetic lesions of the oral mucosa and facial skin caused by type 1 virus recur more often than with the disease caused by type 2 virus In other respects, diseases caused by the first or second type do not differ in their manifestations. Primary infection sometimes proceeds in the form of acute necrotizing cervicitis. It is characterized by a moderate increase in body temperature, malaise, muscle pain, dysuric phenomena, pain in the lower abdomen, symptoms of vaginitis, enlargement and soreness of the inguinal lymph nodes. Characterized by bilateral spread of the rash on the external genitalia. The elements of the rash are polymorphic - there are vesicles, pustules, superficial painful erosions. The cervix and urethra are involved in the majority of women (80%) with a primary infection. Genital herpes that occurred in people who had previously been infected with the herpes virus type 1 are less often accompanied by systemic lesions, their skin changes heal faster than with a primary infection in the form of genital herpes. The manifestations of the latter, caused by type 1 and type 2 viruses, are very similar. However, the frequency of relapses in the affected genital area varies significantly. With genital herpes caused by type 2 virus, 80% of patients have relapses during the year (about 4 relapses on average), while with a disease caused by type 1 virus, relapses occur only in half of patients and no more than one relapse per year. It should be noted that the herpes simplex virus could be isolated from the urethra and from the urine of men and women even during the period when there were no rashes on the external genitalia. In men, genital herpes occurs in the form of rashes on the penis, urethritis, and sometimes prostatitis.

There are rectal and perianal herpetic eruptions caused by herpes viruses types 1 and 2, in particular in homosexual men. Manifestations of herpetic proctitis are pain in the anorectal region, tenesmus, constipation, discharge from the rectum. With sigmoidoscopy, hyperemia, edema and erosion can be detected on the mucous membrane of the distal intestine (to a depth of about 10 cm). Sometimes these lesions are accompanied by paresthesia in the sacral region, impotence, urinary retention.

Herpetic eye disease observed more often in men aged 20-40 years. This is one of the most common causes of corneal blindness. There are superficial and deep lesions. They can be primary and recurrent. The superficial ones include primary herpetic keratoconjunctivitis, tardive dendritic keratitis, epitheliosis and herpetic marginal corneal ulcer, the deep ones include discoid keratitis, deep keratoiritis, parenchymal uveitis, parenchymal keratitis, deep ulcer with hypopyon. The disease is prone to relapsing course. May cause persistent clouding of the cornea. Ophthalmic herpes is sometimes combined with a lesion of the trigeminal nerve.

Herpetic encephalitis. Herpes infection is the most common cause of sporadic acute viral encephalitis in the United States (up to 20% of encephalitis is due to herpes infection). Most often, people aged 5 to 30 years and older than 50 years get sick. In almost all cases (over 95%), herpetic encephalitis is caused by type 1 virus. In children and young people, a primary infection can already lead to the development of encephalitis. In children, encephalitis can also be an integral part of a generalized herpes infection and be combined with multiple visceral lesions.

In most cases, in adult patients, signs of herpetic lesions of the skin and mucous membranes first appear, and only then do symptoms of encephalitis develop. Often, strains of the herpes virus isolated from the oropharynx and from brain tissues differ from each other, which indicates reinfection, but more often the cause of encephalitis is the reactivation of a latent infection localized in the trigeminal nerve.

Clinical manifestations of herpetic encephalitis are a rapid increase in body temperature, the appearance of symptoms of general intoxication and focal phenomena from the central nervous system. The course of the disease is severe, mortality (without the use of modern etiotropic drugs) reached 30%. After suffering encephalitis, there may be persistent residual phenomena (paresis, mental disorders). Relapses are rare.

Herpetic serous meningitis (0.5-3% of all serous meningitis) develops more often in individuals with primary genital herpes. Body temperature rises, headache, photophobia, meningeal symptoms appear, moderate cytosis in the cerebrospinal fluid with a predominance of lymphocytes. The disease proceeds relatively easily. After a week, the symptoms of the disease disappear. Sometimes there are relapses with the reappearance of meningeal signs.

Visceral forms herpetic infections are more often manifested in the form of acute pneumonia and hepatitis, the mucous membrane of the esophagus may be affected. Visceral forms are a consequence of viremia. Herpetic esophagitis may be due to the spread of the virus from the oropharynx or the penetration of the virus into the mucous membrane along the vagus nerve (with reactivation of the infection). There are chest pains, dysphagia, body weight decreases. Endoscopy reveals inflammation of the mucous membrane with the formation of superficial erosions, mainly in the distal esophagus. However, the same changes can be observed in lesions of the esophagus with chemicals, burns, candidiasis, etc.

herpetic pneumonia is the result of the spread of the virus from the trachea and bronchi to the lung tissue. Pneumonia often occurs when a herpes infection is activated, which is observed with a decrease in immunity (taking immunosuppressants, etc.). In this case, a secondary bacterial infection is almost always superimposed. The disease is severe, mortality reaches 80% (in persons with immunodeficiencies).

Herpetic hepatitis It also develops more often in people with a weakened immune system. The body temperature rises, jaundice appears, the content of bilirubin and the activity of serum aminotransferases increase. Often, signs of hepatitis are combined with manifestations of thrombohemorrhagic syndrome, reaching the development of disseminated intravascular coagulation.

Of the other organs that can be affected by viremia, damage to the pancreas, kidneys, adrenal glands, small and large intestines was observed.

Herpes of newborns occurs as a result of intrauterine infection mainly with the herpes virus type 2. It proceeds severely with widespread lesions of the skin, mucous membranes of the mouth, eyes and central nervous system. Internal organs (liver, lungs) are also affected. In most cases (in 70%), herpetic infection proceeds in a generalized manner with involvement of the brain in the process. Mortality (without etiotropic therapy) is 65%, and only 10% develop normally in the future.

Generalized herpetic infection can be observed not only in newborns, but also in persons with congenital or acquired immunodeficiencies (patients with lymphogranulomatosis, neoplasms, receiving chemotherapy, patients with hematological diseases, persons receiving long-term corticosteroids, immunosuppressants, and also HIV-infected). The disease is characterized by a severe course and damage to many organs and systems. Common lesions of the skin and mucous membranes, the development of herpetic encephalitis or meningoencephalitis, hepatitis, and sometimes pneumonia are characteristic. The disease without the use of modern antiviral drugs often ends in death.

Herpes in HIV-infected usually develops as a result of the activation of an existing latent herpes infection, while the disease quickly becomes generalized. Signs of generalization are the spread of the virus through the mucous membrane from the oral cavity to the mucous membrane of the esophagus, trachea, bronchi, followed by the development of herpes pneumonia. A sign of generalization is also the appearance of chorioretinitis. Encephalitis or meningoencephalitis develops. Skin lesions affect different areas of the skin. Herpetic rash usually does not disappear, skin ulcerations form at the site of herpetic lesions. Herpes infection in HIV-infected people does not tend to spontaneously heal.

Diagnosis and differential diagnosis. Recognition of a herpes infection in typical cases is based on the characteristic clinical symptoms, i.e. when there is a characteristic herpetic rash (a group of small vesicles against the background of infiltrated skin). To confirm the diagnosis, virus isolation (detection) methods and serological tests are used to detect antibodies. The contents of herpetic vesicles, saliva, scrapings from the cornea, fluid from the anterior chamber of the eye, blood, cerebrospinal fluid, pieces of the biopsied cervix, cervical secret can serve as material for isolating the virus from a sick person; at autopsy, they take pieces of the brain and various organs.

Intranuclear viral inclusions can be detected by microscopy of Romanovsky-Giemsa-stained scrapings of the base of the vesicles. However, such inclusions are found only in 60% of patients with herpes infection, in addition, they are difficult to differentiate from similar inclusions in chicken pox (shingles). The most sensitive and reliable method is the isolation of the virus in tissue culture. Serological reactions (RSK, neutralization reaction) have little information content. An increase in antibody titer by 4 times or more can be detected only in acute infection (primary), with relapses, only 5% of patients have an increase in titer. The presence of positive reactions without titer dynamics can be detected in many healthy people (due to latent herpes infection).

»» № 3"98 A.V. Murzich, M.A. Golubev.
State Research Center for Preventive Medicine of the Ministry of Health of the Russian Federation.

According to the WHO, diseases transmitted by the herpes virus rank second (15.8%) after influenza (35.8%) as the cause of death from viral infections.

On the territory of Russia and in the CIS countries, at least 22 million people suffer from chronic herpes infection. Among viral infections that affect the genital organs, herpes infection is the most common. This pathogen plays a predominant role in the etiology of spontaneous abortions and premature births, in violation of embryogenesis and organogenesis, and in congenital pathology of newborns.

Almost a third of the world's population is affected by a herpes infection, and 50% of them experience relapses of the disease every year, since there is no immunity against this viral infection. There is evidence that by the age of 5, about 60% of children are already infected with the herpes virus, and by the age of 15 - almost 90% of children and adolescents. Most people are lifelong virus carriers. Moreover, in 85-99% of cases, the primary infection in them is asymptomatic and only in 1-15% - in the form of a systemic infection.

About 90% of the urban population in all countries of the world is infected with one or more types of the herpes virus, and recurrent herpes infections are observed in 9-12% of the inhabitants of different countries. Infection and morbidity are constantly growing, outpacing the natural increase in the population of the Earth. The number of reported cases of genital herpes is growing especially rapidly (increased by 168% over the past decade).

When examining students from one of the US colleges, antibodies to herpes simplex virus types 1 and 2 were detected in 1-4% of individuals; among university students - 9%; persons visiting the family planning clinic - 22%, among pregnant women (without a history of genital herpes) - 32% and persons visiting the clinic for the treatment of sexually transmitted diseases - in 46% of cases (Frenkel M., 1993) .

Herpes infection is understood as diseases characterized by rashes on the skin and / or mucous membranes in the form of vesicles grouped on an edematous-erythematous base and proceeding with damage to internal organs.

Etiology: herpes viruses are "creeping" DNA containing viruses 150-300 nm in size.

Classification:
The group of herpes viruses includes the following subgroups:

1. Herpes simplex virus (HSV) - herpes simplex:
1.1. HSV type 1 (HSV-1) is clinically manifested in the form of herpes of the lips, mouth, eyes, genital herpes.
1.2. HSV type 2 (HSV-2) - genital herpes and generalized herpes of newborns.

2. V. Varicella Zoster - chickenpox and herpes zoster (shingles).

3. Epstein-Barr virus - infectious mononucleosis and Burket's lymphoma.

4. Cytomegalovirus (CMV) - cytomegalovirus.

Herpes simplex virus.
The gates of infection are the lips, skin, mucous membranes (including the eyes). After infection, HSV infection ascends along the peripheral nerves to the ganglia, where it persists for life. Latent herpes infection HSV-1 persists in the ganglion of the trigeminal nerve, and HSV-2 - in the ganglion of the sacral plexus. When activated, the virus spreads along the nerve to the original lesion.

It is believed that the spread of herpes infection is supported not by a chain of continuous infections, but by periodic activation of a latent infection, which turns into clinically pronounced forms under the influence of factors that reduce the functioning of the immune system (flu, hypothermia, treatment with immunosuppressants, stress, etc.)

HSV-1.
Ways of transmission: from a sick person to a healthy person through direct contact (usually through a kiss), airborne droplets, through household items, transplacental, fecal-oral and sexual. HSV-1 can be isolated from saliva in 2-2.5% of apparently healthy individuals. About 5% of healthy people have herpes simplex virus in the mouth, nasopharynx, lacrimal fluid, and sometimes in the cerebrospinal fluid and are excreted in the feces.

Lip herpes.
Clinically manifested as a group of vesicles 1-3 mm in diameter, located on an edematous hyperemic base. The vesicles are filled with serous contents and are grouped around the mouth, on the lips, and on the wings of the nose. Sometimes there is a widespread herpetic rash on the skin of the hands, buttocks.

The disease is prone to recurrence. The appearance of a rash is often combined with headache, malaise, subfebrile condition, burning sensation, tingling, itching. Regressing, the bubbles shrink with the formation of a crust, or open with the formation of erosion. Recovery occurs in 7-10 days.

Treatment: ointments acyclovir, zovirax, gossypol, tebrofen, and with crusts - tetracycline or erythromycin ointment.

Oral herpes proceeds in the form of herpetic stomatitis and manifests itself as rashes on the oral mucosa in the form of vesicles that open with the formation of erosions with a grayish-white coating (aphthous stomatitis).

Treatment: treatment of the oral mucosa with a 0.1% solution of 5-iodine-deoxyuridine (kericide), acyclovir tablets 200 mg 5 times a day for 5 days.

Herpes eye occurs in the form of keratitis (superficial or deep). The disease is prone to a long relapsing course. The disease often leads to persistent clouding of the cornea and reduced visual acuity. The most dangerous complications are: corneal perforation, endophthalmitis, increased intraocular pressure, cataract development.

Treatment: tablets acyclovir 200 mg 5 times a day for 5 days; instillation of a solution of human leukocyte interferon on the conjunctiva of the eyes, immunostimulants.

HSV-2, genital herpes.
The main route of transmission is sexual. Infection usually occurs when the partner who is the source of the infection has a recurrence of the infection. Along with severe forms of the disease, asymptomatic and undiagnosed genital diseases caused by HSV-2 are more common. Such patients become a reservoir and carriers of a viral infection, infecting others. So, among the adult population of the United States, there are 65-80% of them. Asymptomatic detection of HSV is more defined in women than in men and is more typical of HSV-2 than HSV-1.

Clinic.
1. Primary genital herpes in persons who have not had contact with HSV, it is characterized by genital and extragenital lesions. Most often, the process occurs on the large and small labia, vaginal mucosa and cervix, in the region of the balano-prepuce groove, foreskin, mucosa of the glans penis and urethra. After a latent period lasting from 1 to 5 days, pain, itching appear in the lesions, discharge. In 60% of patients, there is an increase in temperature, headaches and muscle pain, in 23% of cases - an increase in inguinal and femoral lymph nodes. Small, 1-3 mm in diameter serous vesicles appear on the affected areas, sitting on a hyperemic base. Initially transparent, the contents of the vesicles become cloudy, purulent. Vesicles open with the formation of bright red erosion, covered with a thin crust, which disappears as epithelialization progresses. Healing occurs without scarring, but temporary hyperemia or pigmentation remains. The average duration of local manifestations is 10-12 days.

The defeat of the urethra begins suddenly with the release of mucus in the form of a "morning drop", almost colorless. Patients complain of urination disorder, pain, feeling of heat, sometimes itching or burning in the external genital area. After 1-2 weeks, the symptoms disappear, but most patients experience relapses of the disease at intervals of several weeks to several years.

2. Secondary genital herpes is easier and recovery is faster. There are few spilled elements. Relapses in HSV-2 appear earlier and more often than in HSV-1.

Analysis of sera from various population groups showed a very high content of antibodies against HSV-2 in patients with invasive cervical carcinoma (in 83% of cases, versus 20% in the control). Physicians should more closely screen patients with genital herpes infection for both viral and malignant cervical disease.

Secondary genital herpes contributes to the occurrence of cancer of the glans penis.

Treatment: depends on the form and period of the disease.

In primary genital herpes, topical acyclovir 5% ointment or cream, acyclovir tablets 200 mg 5 times a day for 5 days or intravenous acyclovir 5 mg / kg every 8 hours for 5 days, bonofton, tebrofen or oxolinic ointment 6 times a day within 15-20 days, immunostimulants.

In case of damage to the urethra - the introduction of drops of interferon solution.

With erosion - lotions or suppositories with interferon, viferon.

For recurrent genital herpes:

• episodic treatment of each exacerbation: externally 5% acyclovir cream 5 times a day for 10 days, immunostimulants,
• with 6 or more exacerbations per year - long-term therapy with acyclovir 200 mg 4-5 times a day for 3 months, immunostimulants.

Generalized herpes of newborns.
1. Neonatal herpes infection in children is almost always associated with HSV-1, which affects the mouth and face. Transmission of the pathogen most often occurs during childbirth during passage through the birth canal. Most women who give birth to infected children do not have a history of herpetic diseases. The clinical picture is dominated by the phenomena of encephalitis (fever, lethargy, loss of appetite, convulsions), damage to the skin and internal organs (liver, lungs, adrenal glands) is characteristic,

Prevention consists in 100% examination of spouses and pregnant women to detect antibodies to herpes viruses. With obvious clinical manifestations of genital herpes in a pregnant woman - the birth of a child by caesarean section.

The prognosis is doubtful, the mortality rate reaches 90%.

2. Transplacental or by ascending infection, especially after premature rupture of the membranes, as well as by transmission of viruses with sperm through an infected egg, intrauterine infection develops, 50% due to HSV-2. The greatest number of diseases in newborns occurs with primary infection in the mother in late pregnancy. This can lead to fulminant disseminated infection of the fetus and cause disruption of organogenesis and the occurrence of deformities or causes spontaneous premature termination of pregnancy, stillbirth and early infant mortality. Children can be born with underdevelopment of the brain, hepatitis, jaundice, meningitis, calcium deposits in the brain, damage to the eyes, optic nerve, blood cells, adrenal glands, etc. Such children are usually not viable.

Zoster virus.
1. Chicken pox - develops in the absence of previous immunity. The pathogen is transmitted by airborne droplets. Children get sick more often. After the disappearance of clinical manifestations, the virus in the body persists for life.

2. With a sharp decrease in the body's defenses, the virus persists, which manifestly manifests itself in the form of a chicken pox clinic (in persons who have already had it). Then comes (the latent period, characterized by the development of viruses in the ganglia of the peripheral nervous system, and a clinic develops, commonly known as herpes zoster. There is a strong burning sensation, shooting pains, tingling. Pains often simulate the clinic of angina pectoris, appendicitis, etc. at the base, numerous vesicles with serous contents develop.Rashes are localized along the nerves (usually intercostal and trigeminal).Sharp, burning pains of such intensity join that patients scream, are forced to look for a body position in which the pain is less severe.The vesicles merge into bullae, foci appear necrosis The duration of the disease is 3-4 weeks, after which the rash disappears, the pain may remain for several months or years.

Patients with herpes zoster should be most carefully examined for the detection of cancer.

Treatment: locally in the acute period, liquid analgin and flucinar; ointments gossypol, tebrofenovaya, Acyclovir 800 mg 5 times a day for 7-10 days and immunocorrectors. After a single transferred disease does not recur.

Epstein-Barr virus.
The development of infectious mononucleosis is associated with this virus. The disease often gives malignancy to Burket's lymphoma. It occurs more in Africa and Asia, affecting children 2-15 years old. The process takes place in the upper jaw, ovaries, orbits of the eyes, kidneys, spleen, peripheral lymph nodes. Treatment according to the scheme of polychemotherapy of aggressive lymphomas.

Cytomegaly virus.
The infectious process is characterized by damage to the salivary glands with the formation of giant cells with intranuclear inclusions in the tissues, associated with HIV. Transmission of the pathogen requires prolonged and close contact.

The main route of transmission is sexual. The virus is found in saliva, urine, blood, breast milk, semen (very much). It is excreted with saliva up to 4 weeks, with urine - up to 2 years.

The disease is asymptomatic or with a small clinic. With intrauterine infection, children are born with an underdeveloped brain, with massive calcium deposits in it, dropsy of the brain, hepatitis, jaundice, enlargement of the liver and spleen, pneumonia, heart defects, myocardial damage, inguinal hernia, congenital deformities, etc.

Treatment: acyclovir intravenously 5 mg/kg body weight (10 mg/kg) 3 times a day for 10 days in combination with immunostimulating therapy.

Literature.

1. Glazkova L.K., Polkanov B.C. etc. Genital chlamydial infection. Etiology, epidemiology, pathogenesis, diagnostics, clinic and therapy. Yekaterinburg, 1994, p. 90.
2. Grebenyuk V.N., Dmitriev G.A. and other Herpetic urethritis in men.//Vestn. Dermatol. - 1986. - No. 4. p. 52-55.
3. Ilyin I.I. Non-gonococcal urethritis in men. M., 1991, p. 288.
4. Kishchak V.Ya. Herpes simplex virus and carcinogenesis.// Abstract of the thesis. diss. dokt., M., 1984.
5. Kozlova V.I., Pukhner A.F. Viral, chlamydial and mycoplasmal diseases of the genitals. Moscow, 1997, p. 536.
6. Kolomiets N.D., Kolomiets A.G. etc. The study of causal relationships between miscarriage and herpes infection.// Midwife. and gynecol. - 1984. - No. 3, p. 62-64.
7. Posevaya T.A., Tsukerman V.G. et al. The role of herpetic infection in epithelial dysplasia of the cervix and the experience of treatment with antiherpetic drugs.// Vopr. virusol. - 1991. - No. 1. p. 78.
8. Balfour C.L., Balfour H.H. Cytomegalovirus is not an occupational risk for nurses in renal transplant.// J.A.M.A., 1986, vol. 14, p. 256.
9. Brown Z.A. et al. Neonatal herpes simplex virus infection in relation to asymptomatic materinal infection at the time of Labor.// New England J. Med., 1991, vol. 324, p. 1247-1252.
10. Hagay Z.I., Biran G. et al. Congenital cytomegalovirus infection: a long-standing problem still seeking a solution.// Am. J. Obstet. Gynecol., 1996, vol 174 (1), p. 241-245.
11.Gulick R.M. et al. Varicella-zoster virus disease in patients with human immunodeficiency virus infection.// Arch. Dermatol, 1990, vol. 126, p. 1086-1088.
12. Resnick L. et al. Oral hairy leukoplakia.// J. Am. Acad. Dermatol, 1990, vol. 22, p. 1278-1282.