• Herpes symptoms

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    Herpes is an infectious anthroponous viral disease caused by the herpes simplex virus.
    This disease is characterized by polymorphism of clinical symptoms, prolonged latent flow with periodic exacerbations, accompanied by bubble rashes on the skin and mucous membranes, as well as damage to the central nervous system, eyes, internal organs.

    Etiology. The causative agent of herpes simplex infection is the herpes simplex virus( HSV), which belongs to the family. Herpesvindae, by biological properties, is close to the varicella-zoster virus. It has an internal core of linear double-stranded DNA surrounded by a protein shell of icosahedral symmetry. This nucleocapsid is encased in an envelope. The converted shape has a diameter of 120-160 nm, the core - a diameter of 100 nm.

    Virion develops intracellularly, forming intranuclear inclusions. According to their antigenic properties and differences in the nucleotide composition, the pathogens are divided into 2 groups: HSV-1 and HSV-2.The most common HSV-1 - diseases with damage to the skin of the face, mucous membranes of the mouth. With HSV-2, the occurrence of genital herpes, meningoencephalitis, infection of newborns is associated.

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    Epidemiology of .The source is sick and virus carriers. With the primary infection, patients isolate the virus on average for 12 days, with relapse - 4-7 days. Transmission ways - contact, airborne, parenteral, sexual, vertical. The transmission requires close enough contact with the source of the infection, so children become infected, usually when communicating with family members, and it is very important to collect a family history of herpetic anemia. The majority of children are infected with EPG before the age of 5 years. They are more often infected with HSV-1, whereas in adults the incidence of infection caused by HSV-2 increases. Antibodies against HSV-1 and HSV-2 are found in 75% and 11% of adolescents aged 15 years and, respectively, in 90% and 73% of adults. The disease is more common in the autumn-winter period. Sporadic cases of the disease are usually recorded, but outbreaks of IPG in children's groups are possible.

    Pathogenesis of the IPG includes several stages.

    1. Introduction of the pathogen. The entrance gates are the skin and mucous membranes. Once in the cage, the virus begins to multiply rapidly. Change in metabolism and destruction of the cell membrane as a result of budding of mature virions lead to cell death. By spreading a contact, the virus affects neighboring cells.

    2. Viralemia. From the entrance gate the HSV gets first into the regional lymph nodes, and then into the blood. Here it circulates in the composition of the formed elements - erythrocytes, lymphocytes and platelets. Together with the blood flow, as well as lymphogenous and perineural pathways, the virus penetrates the brain and spinal cord. The fixation of the virus in the paravertebral nerve ganglia is of great importance for the further development of the disease. In the process of hematogenous dissemination, especially in patients with IDS, the virus can affect the liver, spleen, adrenal glands, lungs, kidneys and other internal organs.

    3. Development of serous inflammation. At the site of the introduction of HSV, a foci of inflammation arises that is characterized by the appearance of giant cells with intranuclear inclusions, lymphohistiocyte infiltrates and ballooning cell degeneration. Abundant serous exudate exfoliates cells, which leads to the formation of vesicles on the skin, mucous membranes and cysts in internal organs. Along with serous inflammation, foci of necrosis and vasculitis appear in the internal organs, especially in the central nervous system.

    4. Development of complications. HSV has a pronounced immunosuppressive activity, which is associated with the defeat of T-lymphocytes, macrophages, the violation of the reaction of antibody-dependent cytotoxicity, suppression of interferon and complement activity. As a result, a mixed infection is formed, the etiological agents of which, in addition to HSV, are bacteria, intracellular pathogens( chlamydia, mycoplasmas), viruses, protozoa and fungi.

    5. Formation of specific immunity. In response to the introduction of HSV, an immune response develops - protective antibodies and cytotoxic T-lymphocytes are formed that inactivate the virus. At the same time immunity at IPG is non-sterile and does not lead to complete elimination of the pathogen. This is due to the weak immunogenicity of the virus, its immunosuppressive properties, the ability to transfer to L-forms and persist in the nerve ganglia.

    IPG is the representative of opportunistic infections that clinically manifest in conditions of immunodepression. Depending on the state of the immune system, the infectious process can stop at any of the stages listed above, which leads to a significant polymorphism of the clinical symptomatology - from asymptomatic carriage to generalized fatalities. Most often, primary infection with HSV occurs asymptomatically( in 80-90% of patients), and only a small proportion of patients have clinically manifested forms of the disease( 10-20%).However, regardless of the form of primary infection, latent IPG develops in all patients. The virus is preserved for life in the form of an unconfined L-form in the paravertebral nervous ganglia. Under conditions of IDS, HSV reactivation occurs. By axon, the virus re-enters the skin and mucous membranes, where it replicates with the subsequent repetition of all stages of pathogenesis.

    Currently, the working classification proposed by N.I.Nisevich and VFUchaykin in 1990.

    The incubation period is 2-12 days. The main clinical signs: the appearance on the skin and mucous membranes of grouped small strained vesicles on the edematous hyperemia base. The rash is localized mainly around the natural openings - on the red border of the lips and the skin around the mouth( herpes labialis), the wings of the nose, cheeks, eyelids, auricles, less often - on the forehead, buttocks, back and inner thighs, forearms, brushes.

    The mucous membranes of the mouth, larynx, tonsils and conjunctiva can be affected. There is a burning sensation, sometimes malaise, general weakness. The foci disappear on the 7th-9th day.

    There are primary and recurrent simple herpes. Primary simple herpes occurs after primary infection, mainly in children. Characterized by the severity of clinical manifestations, as a result of hematogenous dissemination of the virus may damage the internal organs. One of the most frequent forms is acute stomatitis. After clinical recovery, elimination of the virus from the body does not occur, there is a persistence in the tissues throughout life. Under the influence of unfavorable factors contributing to the emergence of immunodeficiency, there is activation of the virus, which is accompanied by a relapse of clinical symptoms. Recurrent herpes simplex can occur several times a year. In this case, the rash is localized both in the primary lesion sites and in new areas.

    In addition, distinguish atypical forms - edematous, elefantiazopodobnuyu, zosteriformnuyu, hemorrhagic, etc.

    Herpes of the mouth - a viral infection, characterized by the formation of ulcers in the mouth and is known as herpetic fever or blistering. The first time an infection usually occurs in childhood. Although many people are infected with herpes, most of them have no symptoms. Those who get sick from the initial infection develop painful mouth wounds that affect the back of the throat, the sky, the tongue and sometimes the cheeks and the inside of the lips. Usually people feel sick, they have fever, lymph nodes, inflamed throat, and bad breath. Although the symptoms usually subside within 10 to 21 days, the virus remains in the body and is at rest until some factors such as stress, menstruation or exposure to the sun awaken him. Subsequent outbreaks, known as a recurrence of herpes simplex, affect the outer, rather than the inner side of the mouth, usually the edge of one lip. These repeated outbreaks are much more mild and last 8-10 days.

    First described in 1887 by the Hungarian physician M.K.Kaposi. It occurs in children suffering from eczema, dermatoses, neurodermatitis. The duration of the incubation period is 3-5 days. The disease is characterized by a sharp onset - an increase in body temperature to 39-40 ° C, a rapid increase in general infectious symptoms until the development of infectious toxicosis. In the 1-3 days of the disease there is a profuse vesicle rash, located on large areas of the skin. The rash can last for 2-3 weeks. Often, the elements merge, burst, forming a continuous crust, after the rejection of which remains a pink patch or cicatricial changes. The course of the disease can be prolonged. Normalization of body temperature and improvement of general condition occur on the 7-10th day.

    In weakened children, not only the skin and mucous membranes, but also the central nervous system, internal organs, the organ of vision can be involved in the pathological process, which causes an unfavorable outcome of the disease.

    Often occurs with primary infection of HSV in children aged 6 months to 3 years. The development of gingivostomatitis is facilitated by the disappearance of maternal antibodies, lack of local immunity, dentition, etc. The clinic includes manifestations of a general infectious syndrome( fever, symptoms of intoxication), anxiety, salivation and regional lymphadenitis. Thin-walled vesicles appear on the mucous membrane of the oral cavity and gums, which are quickly opened with the formation of painful ulcers. Their surface is covered with a touch of yellowish color. Changes in the oral mucosa persist for 1-5 days.

    Acute respiratory disease caused by HSV.The defeat of the upper respiratory tract is one of the forms of primary IPG in young children. The disease begins sharply with an increase in body temperature and the appearance of symptoms of intoxication. There is a clinic of rhinopharyngitis, pharyn tonsillitis, laryngotraheobronchitis and obstructive bronchitis. On the mucosa of the upper respiratory tract, vesicular rashes are detected, which then turn into erosion. The disease is characterized by a severe prolonged course and frequent attachment of a mixed infection. It was found that HSV is a trigger for the development of bronchial asthma.

    Primary infection is manifested by conjunctivitis or keratoconjunctivitis. Cataracts, uveitis, chorioretinitis can develop in newborns. The defeat of the cornea is superficial, as a tree-like ulcer, or deep( discoid keratitis).The latter proceeds most severely with involvement in the pathological process of the anterior section of the vascular tract, with the outcome in the opacity of the cornea and reduced visual acuity.

    The disease begins acutely and is accompanied by inflammation of the conjunctiva, its ulceration or the appearance of herpetic vesicles on the skin of the eyelid. Involvement in the pathological process of the cornea leads to the formation of surface erosion, lacrimation, photophobia, scleritis, pain syndrome.

    Clinical diagnosis is simplified with a combined eye, skin, mucous membranes of the oral cavity.

    Genital herpes. Genital herpes( herpes genitalis) is characterized by polymorphism of clinical symptoms and a tendency to persistent recurrent course.

    The most common infection occurs during sexual transmission and is usually due to HSV-2, in 5-10% of patients - HSV-1.

    Primary infection is accompanied by deterioration of the general condition, increased body temperature, dysuric phenomena, increased regional lymph nodes, painful sensations in the lesions. Girls develop vesicular or erosive ulcers in the area of ​​the vagina, vulva, labia. Then erosions are formed, the swelling of the genital organs is possible. Further, the body temperature decreases, the rashes dry up, the crusts are rejected with the formation of pigment or depigmented spots. Currently, HSV-2 is not excluded from the development of cervical carcinoma.

    In boys, herpetic vesicles or ulcers are usually formed on the glans penis, less often on its body or foreskin.

    Encephalitis can develop with primary infection( 30% of patients), but more often occurs with reactivation of IPG( 70%).A feature of herpetic encephalitis is the development of deep necrotic changes in the frontotemporal temporal region of the cerebral cortex, which determines the severity of the course of the disease and the high frequency of residual events. In anamnesis, some patients have indications for exacerbations of IPH from their immediate relatives. The disease is often preceded by craniocerebral trauma, severe infectious and somatic diseases. Herpetic rashes on the skin take place only in 20% of patients. There are three stages of herpetic encephalitis.

    The early stage lasts from a few hours to 7 days. In most patients, encephalitis begins acutely and is accompanied by the emergence of general infectious and cerebral syndromes. The body temperature rises, there is a headache, repeated vomiting and hyperesthesia. On the 2nd-4th day the patient's condition deteriorates sharply due to the increase in cerebral symptoms and the addition of focal signs. Rapidly progressing disorder of consciousness in the form of confusion, lack of orientation in place and time, changes the behavior of the patient( aggressiveness, psychomotor agitation).Localized or generalized convulsions, myoclonus, tremor, opercular and autonomic paroxysms occur. There are focal symptoms in the form of mono-and hemiparesis, paresthesia, numbness of the limbs. Often there is a violation of higher nervous functions in the form of aphasia, dysarthria, apraxia, agnosia. In a third of children, neurological symptoms precede the emergence of general infectious and cerebral symptoms, in 10% of patients in the initial period of the disease there is no increase in body temperature. In some patients, the disease develops subacute with the gradual emergence of cerebral and focal symptoms( "pseudotumorous" variant).

    The stage of height is characterized by deepening of consciousness disorders, increased seizures up to epileptic status, disruption of vital functions. The patient has a classical triad of herpetic encephalitis - fever, persistent impairment of consciousness and indigestible convulsions( convulsive-coma syndrome).Progressive focal neurological symptoms. Meningeal symptoms appear in most children on the 3-5th day of the disease, but they are usually mild. In the liquorgram, lymphocytic pleocytosis is detected up to 300-800 cells / mm3 and the protein content is increased to 1.5-2 g / l. The stage of swelling lasts from 1 to 3 weeks.

    The stage of reverse development begins with the 3-4th week of the disease and lasts from 3 to 6 months or more.40-80% of surviving children have gross residual effects in the form of dementia, episyndrome, extrapyramidal disorders, hydrocephalus, and "vegetative state."Herpetic encephalitis in some patients may acquire a recurrent or chronic course.

    The defeat of the nervous system of HSV can also occur in the form of serous meningitis, myelopathy, encephalomyeloradiculoneuropathy.

    HSV can affect the liver, lungs, kidneys, esophagus, etc. Pathology of internal organs is more common in generalized forms of IPH in newborns. Herpetic hepatitis is characterized by an acute onset, marked by symptoms of intoxication. The pre-egg period is short-lived and can be combined with the symptoms of stomatitis. Quickly there is hepato- and splenomegaly, darkening of urine, decolorization of feces and jaundice. In laboratory examination, hyperbilirubinemia is detected by increasing the direct fraction, increasing the activity of transaminases. The disease is characterized by a severe course, frequent development of fulminant forms, and DIC-syndrome, leading to death. Lesions of the lungs( interstitial pneumonia) and kidneys( focal nephritis) do not have specific clinical features and often take the form of a mixed infection.

    The frequency of intrauterine IPG is 1 / 2.5 per 15 thousand newborns. In the antenatal period, 5% of children are infected, in the intranatal period - 95%.Primary genital herpes in a woman at the 32nd week of pregnancy leads to infection of 10% of children, on the eve of childbirth - 40-60%.With recurrence of genital herpes, the risk of infection is much lower - 8%.The child can also become infected with asymptomatic IPG in the mother. In antenatal infection, children are born with clinical manifestations of the disease( congenital infection).With intranatal infection, symptoms appear in the postnatal period( IPH in newborns).

    Clinic of congenital IPG depends on the period of infection. In case of infection in the first two weeks of pregnancy, fetal death occurs or blastopathy occurs - a systemic pathology similar to genetic diseases. Infection in the period of gestation from 2 weeks to 3 months leads to the termination of pregnancy or to the developmental defects at the organ or cell levels - the true malformations. When infecting during the 3rd-6th month of pregnancy, a generalized inflammatory reaction develops with the outcome of fibrosis and the formation of false defects in the development of the central nervous system, the digestive tract, the liver, the organ of vision, lungs, bones, etc. When infected in the third trimester, generalized IPG develops( meningoencephalitis, hepatitis, pneumonia, gastrointestinal lesion), which often ends in a fatal outcome.

    With intrapartum infection, the incubation period is from 3 to 14 days. There are three forms of neonatal IPG - a localized form, a generalized form and meningoencephalitis. Localized form occurs in 20-40% of children and is characterized by the appearance of multiple vesicular rashes on the skin, mucous membranes of the mouth and eyes without signs of a systemic inflammatory reaction. In the absence of specific treatment, generalization of IPH occurs in 50-70% of patients.

    In 20-50% of newborns, the IPG occurs in a generalized form. The symptomatology appears on the 5th-10th day of life and resembles that in sepsis. There is a progressive deterioration in the child's condition( increase or decrease in body temperature, sluggish sucking, vomiting, refusal to eat, shortness of breath, apnea, pale skin, acrocyanosis, anxiety or inhibition).Most children develop a herpetic eruption, but in 20% of patients they are absent. The severity of the condition is determined by the damage to the liver, brain, adrenal glands, lungs, kidneys, etc.

    Encephalitis and meningoencephalitis develop in 30% of patients. Unlike older children, in the newborns, herpetic encephalitis is characterized by a diffuse lesion of the brain substance. In the frontal, parietal and temporal lobes, necrosis and cysts are formed. Clinical symptoms appear more often in the 2-3 weeks of life. The disease begins with a rise in body temperature, lethargy, anxiety, tremor and decreased appetite. Half of the patients have herpetic rashes. In the future, the condition deteriorates sharply due to impaired consciousness and the emergence of poorly controlled local or generalized seizures. There are disorders of thermoregulation, respiration and endocrine function. Mortality in encephalitis is 50%.Half of the surviving children have severe residual phenomena - delay in psychomotor development, microcephaly, paresis, paralysis, etc.

    Diagnosis of IPG is based on the analysis of epidemic history, clinical and laboratory examination. Of great importance is the clarification of the "herpetic anamnesis" concerning the child's immediate surroundings. Clinical diagnosis is greatly facilitated in the presence of typical rashes on the skin and mucous membranes, but it must be remembered that generalized forms of IPG can occur without a vesicle rash. Laboratory diagnosis includes several methods.

    1. The viral method is the "gold standard" of laboratory tests. HSV is isolated from the blood, CSF, the contents of vesicles, biopsies of organs and tissues. The disadvantages are the complexity and duration of the study( 2-3 weeks).Currently, a rapid culture method( shell vial assay) has been introduced into practice, allowing diagnostics within 24-48 hours.

    2. The immunofluorescence method reveals HSV in the contents of vesicles, scraping from the skin and mucous membranes.

    3. Polymerase chain reaction( PCR) allows detecting the DNA of a virus in blood, liquor and other biological materials. Detection of the virus DNA in the blood and CSF is a laboratory marker of the activity of the infectious process. The real-time PCR method allows determining the virus titer in biological fluids, cells, biopsy samples.

    4. The serological method( ELISA) allows the detection of antibodies IgM and IgG, as well as the avidity of IgG antibodies. With the primary acquired IPG, IgM antibodies appear 7 days after infection and persist for 6-8 weeks. IgG antibodies are detected from the 3rd-4th week and reach a maximum at the 6th-8th week. In the first three months, low-like IgG( avidity index less than 30%) is determined, and highly antibodies are subsequently synthesized. If the recurrence of IgM is detected in low titers or absent, and an increase in IgG titer is observed earlier - in the second week. The presence of IgM, low-grade IgG and an increase in the IgG titer by four or more times are laboratory criteria for the activity of the acquired IPG.With a latent form, stably low titers of high-avidity IgG are detected. The criteria for laboratory diagnosis of intrauterine IPG and active replication of the virus include the detection of antibodies of IgM class, low-IgG, the titer of antibodies of IgG class in the umbilical cord blood is four times larger than the maternal, the increase in the titer of antibodies of IgG class by four and more times with a second examination.

    5. The cytological method is based on the detection in giant strokes of giant cells with intranuclear inclusions( Lipshtzyts body).Has an auxiliary value due to low sensitivity.

    The examination complex necessarily includes the study of the immune status. Typical changes include a decrease in the number of T-lymphocytes, T-helpers, natural killer cells, violations of the B-cell link, interferon status, functional activity of neutrophils, macrophages, increased CEC, decreased compliment activity.

    An integrated approach to the treatment of IPG is needed, taking into account the stage of the disease. There are several stages of therapy - treatment in the acute phase, in the stage of reconvalescence and prevention of relapses.

    Hospitalization is carried out taking into account age( children of early age from risk groups), clinical( severe and complicated forms) and socio-epidemiological indications( children from closed collectives, asocial families).For the period of severity of the condition, bed rest is prescribed. Recommended milk-vegetable diet, enriched with vitamins and trace elements. When stomatitis, food should be mechanically, thermally and chemically sparing. Proper care, especially with stomatitis and conjunctivitis, is of great importance for the prevention of complications.

    Etiotropic therapy includes several groups of drugs that are used to take into account the form of the disease.

    1. Virocidal preparations. Anti-herpetic activity is possessed by anomalous nucleosides( acyclovir, valaciclovir, famciclovir) inosine pranobex. Acyclovir is an abnormal guanosine, the integration of which into the DNA molecule of the virus inhibits its further synthesis. The drug accumulates only in cells infected with HSV.The disadvantage of acyclovir is low bioavailability. With the primary localized form of IPG, acyclovir is administered internally during

    for 7-10 days, with relapse - within 5 days. With frequent relapses( six or more times a year), suppressive therapy with acyclovir is recommended. With the common and generalized forms of IPG, acyclovir is administered intravenously drip for 5-10 days, with a subsequent transition to taking the drug inside. The drug is also used topically for dermal-mucous form and ophthalmoherpes. Valaciclovir( valtrex) is well absorbed from the digestive tract and creates a high therapeutic concentration in the blood. The drug is prescribed for children over 12 years of age. Famciclovir( famvir) suppresses the replication of HSV, especially when the virus is resistant to acyclovir. The drug is used to treat adolescents over 17 years of age and adults. Inosine pranobex is active against not only HSV, but also other DNA and RNA-containing viruses, it is an immunomodulator. In recent years, proven antiherpetic activity of arbidol, which is prescribed for children older than 2 years of life.

    2. Interferons. Viferon geneferon light, kipferon, reaferon-EU-lipint are used for localized forms of IPG.In children younger than 7 years for 2 weeks, then 1 candle 2 times a day 2 times a week for 2 weeks, then 1 candle at night 2 times a week for 2 weeks, then 1 candle at night 1 time perweek for 2 weeks. With persistent recurrent IPG, viferon is prescribed 1 candle 2 times a day for 10 days, then 1 candle 2 times a day 3 times a week for 1-12 months under the control of clinical and laboratory indicators. Viferon ointment is applied to the affected areas of the skin. A single dose of genferon light in the form of rectal suppositories in children younger than 7 years is 125 thousand ME, over 7 years - 250 thousand ME.Start therapy - 1 candle 2 times a day for 10 days, supporting treatment - 1 candle per night every other day for 1-3 months. Interferons for intramuscular administration( alpha-interferon, reaferon, realiron, roferon, intron, etc.) are prescribed in the generalized form of IPG and encephalitis for 10-14 days, then, if necessary, the patient is transferred to maintenance therapy with viferon.

    3. Inductors of interferon. They are used only in light and medium-heavy forms of IPG.Interferon inducers include neovir, cycloferon, amixin, kagocel, anaferon, and poludan. Treatment begins in an acute period, then switches to maintenance therapy. Local topical application of hemidan and cycloferon liniment is possible.

    4. Immunoglobulins for intravenous administration. Due to the content of antiherpetic antibodies, these drugs( pentaglobin, intraglobin, intratect, octag, immunonin, etc.) bind extracellular HSV.They are prescribed for generalized, severe and complicated forms.

    5. Antibiotics. With the development of bacterial complications and mixed infection, protected aminopenicillins, third-generation cephalosporins, macrolides, carbapenems are used.

    Pathogenetic therapy includes a set of measures. In light and medium-heavy forms of IPG, detoxification is recommended for drinking, in severe and complicated forms, intravenous drip infusions of glucose-salt solutions are prescribed. A decrease in the level of toxemia is facilitated by the use of enterosorbents( smectic, filter, enterosgel, etc.).In severe, complicated and generalized forms of IPG, methods of extrarenal detoxification-hemosorption and plasmapheresis are shown. An obligatory component of pathogenetic therapy is the appointment of immunomodulators( thymalin, tactivin, timogen, imunofan, polyoxidonium, lycopide, imunorix, derinat, sodium nucleic acid, neupogen, IRS-19, ribomunil, bronchomunal, immunomax, etc.) and cytokine preparations( leukinferon, Roncoleukin)under the control of an immunogram. Anti-edematous therapy using non-steroidal anti-inflammatory drugs( indomethacin, etc.) is used in a pronounced exudative component. Patients are prescribed multivitamins and vitamin-mineral complexes, drugs of metabolic therapy( riboxin, cocarboxylase, cytochrome C, elcar, etc.), probiotics( bifiform, linex, bifidum-bacterium forte, etc.).According to indications, antihistamines, protease inhibitors, antiaggregants, oxygen therapy are used. Glucocorticoids, taking into account their immunosuppressive activity, are used only with herpetic encephalitis short course. Pathogenetic treatment of individual nosological forms of IPG( encephalitis, pneumonia, hepatitis, etc.) is carried out according to general rules.

    Symptomatic therapy includes the appointment of antipyretic drugs, cardiac glycosides, etc. In severe pain syndrome, analgesics are used. Local treatment involves staking the elements of the rash with a 3% solution of hydrogen peroxide, followed by lubrication with a 1% alcohol solution of aniline dyes( brilliant green, methylene blue).For the treatment of erosions, sea buckthorn oil, dog rose, oil solution of vitamin A, salt-koseryl are used. After rejection of the crust, keratoplastic pastes are prescribed( JIaccapa paste, 2-3% naphthalan paste).For the treatment of stomatitis, 1% aqueous solutions of aniline dyes( methylene blue, brilliant green), local antiseptics( borax solution in glycerin, miramistine, hexoral, stopangin, bioparox, strepsils, lysobact, etc.) and lysates of bacteria( imudon) are used.

    Children who suffer from recurrent form of IPG are subject to medical examination. Observation is carried out by a pediatrician and infectious disease doctor with a frequency of examinations once every 3-6 months. The examination includes a clinical examination, according to the indications - a consultation of specialists( neuropathologist, oculist, immunologist, etc.).Assign a laboratory examination - a general blood test, IPG markers using ELISA and PCR, an immunogram;by indications - markers of CMV, VEB, VVZ, toxoplasm, chlamydia, mycoplasma by ELISA and PCR.If necessary, perform an instrumental examination - examination of the fundus, neurosonography, dopplerography, RKT and MRI of the brain, EEG, REG and others.

    Rehabilitation therapy includes a protective regime( prevention of overfatigue, hypothermia, overheating, excessive insolation, psychoemotional stress,).Recommend a balanced diet, enriched with vitamins and trace elements. With frequent relapses, virocidal drugs( acyclovir, valtrex, famvir) are prescribed in suppressive doses, viferon and interferon inducers( cycloferon, neovir, amixin, anaferon) according to prolonged schemes under the control of clinical and laboratory indices of IPG activity. They use multivitamins, vitamin and mineral complexes, probiotics, immunomodulators under the control of the immunogram, carry out the sanation of chronic foci of infection. Teenagers and adults during the inter-recurrence period after immunocorrective therapy are advised to administer a herpetic vaccine followed by a booster every 6-8 months( a total of 3-5 courses).

    Currently, there are no effective herpetic vaccines, so the main importance is attached to non-specific prevention. It is necessary to isolate the patient for the entire period of rashes. An important role is played by timely treatment of family members with manifestations of IPG, the use of gauze masks, the development of hygienic skills in the child. When contacting a patient with IPH, a newborn is recommended to administer an immunoglobulin at a dose of 0.2 ml / kg.

    Great importance is attached to the prevention of intrauterine IPG, which is carried out at the pre-gravity and gravity stages. In the presence of manifestations of genital herpes in the mother and childbirth in a natural way, newborns are subject to laboratory examination and preventive treatment with acyclovir. With negative laboratory tests and the absence of clinical symptoms, preventive therapy is discontinued.