Herpes -infektsionnoe anthroponotic viral disease caused by the herpes simplex virus.
This disease is characterized by polymorphism of clinical symptoms, the long latency over with periodic exacerbations, accompanied by blisters on the skin and mucous membranes, as well as CNS, eyes and internal organs.
etiology. causative agent of herpes simplex infections - herpes simplex virus (HSV), belongs to the family.Herpesvindae, on the biological properties similar to varicella-zoster virus.It has an inner core of a linear double-stranded DNA surrounded by a protein shell icosahedral symmetry.This nucleocapsid encased envelope.The converted form has a diameter of 120-160 nm, the core - diameter of 100 nm.
Virion develops intracellularly, forming intranuclear inclusions.According to its antigenic properties and differences in the nucleotide composition of activators are divided into two groups: HSV-1 and HSV-2.The most common HSV-1 - disease with skin lesions, mucous membranes of the mouth.With HSV-2 is a
Epidemiology .The source are patients and virus carriers.In patients with primary infection excrete the virus for an average of 12 days, with relapses - 4-7 days.Ways of transmission - contact, airborne, parenteral, sexual, vertical.For transmission requires close enough contact with the source of infection, so the children become infected, as a rule, when dealing with members of his family, and therefore it is very important to gather the family "herpes history."Most children are infected with VP T under the age of 5 years.They often are infected with HSV-1, whereas in adults infection rate increases caused by HSV-2.Antibodies against HSV-1 and HSV-2 exhibit 75% and 11% of adolescents aged 15 and respectively, 90% and 73% of adults.The disease is more common in autumn and winter.Usually sporadic cases recorded, but may IPG outbreaks in children's groups.
IPG pathogenesis involves several steps.
1. The introduction of the pathogen.Gateway are the skin and mucous membranes.Once in the cell, the virus begins to multiply rapidly.Changes in the metabolism and destruction of the cell membrane as a result of budding of mature virions lead to cell death.Spreading through contact, the virus infects neighboring cells.
2. viremia.From the input gate of HSV space falls first to the regional lymph nodes and then to the blood.Here, it circulates in the composition of formed elements - erythrocytes, lymphocytes and platelets.Together with the blood flow, as well as lymphogenous and perineural pathways the virus enters the brain and spinal cord.Of great importance for the further development of the disease has a fixation of the virus in the paravertebral nerve ganglia.During hematogenous dissemination, especially in patients with CID, the virus can infect the liver, spleen, adrenals, lungs, kidneys and other internal organs.
3. Development of serous inflammation.In place of the introduction of HSV appears hotbed of inflammation, which is characterized by the appearance of giant cells with intranuclear inclusions, and infiltrates lymphohistiocytic cells ballooning degeneration.Stratifies serous copious exudate cells, which leads to the formation of vesicles on the skin, mucous membranes and internal organs cysts.Along with serous inflammation in the internal organs, especially in the central nervous system, there are foci of necrosis and vasculitis.
4. The development of complications.HSV has expressed immunodepresivnoy activity, which is associated with a lesion of T-lymphocytes, macrophages, violation of antibody-dependent cytotoxicity, inhibition of interferon activity and complement.The result is a mixed infection, etiological agents which, in addition to HSV, are bacteria, intracellular pathogens (Chlamydia, mycoplasma), viruses, protozoa and fungi.
5. Formation of specific immunity.In response to the introduction of HSV develops an immune response - formed protective antibody and cytotoxic T-lymphocytes that inactivate virus.However, when the immune system is a non-sterile IPG and leads to complete elimination of the pathogen.This is due to the poor immunogenicity of the virus, its immunosuppressive properties, ability to move in the L-form and persist in the nerve ganglia.
IPG is representative of opportunistic infections that are clinically manifest in the conditions of immunosuppression.Depending on the immune status of the infectious process can stop at any of the steps listed above, which results in significant clinical symptoms polymorphism - from asymptomatic carrier state to generalized forms fatal.The most common primary HSV infection occurs asymptomatic (in 80-90% of patients), and only a minority of patients have a place to manifest clinical form of the disease (10-20%).However, regardless of the form of primary infection in all patients developing latent IPG.The virus persists for life in the form of shell-less L-shaped in paravertebral nerve ganglia.The CID conditions there is reactivation of HSV.In axons virus re-enters the skin and mucous membranes, where it is replicated to the subsequent repetition of all stages of pathogenesis.
Currently working classification of uses proposed NINisevich and VFUchaikin in 1990
incubation period is -2-12 days.The main clinical signs: the appearance of the skin and mucous membranes of the small grouped vesicles on intense hydropic hyperemic basis.The rash is localized mainly around natural openings - on the red border of the lips and skin around the mouth (herpes labialis), wings of the nose, cheeks, eyelids, ears, at least - on the forehead, buttocks, back and inner thighs, arms, hands.
can be affected mucous membranes of the mouth, larynx, tonsils, and the conjunctiva.There have been a burning sensation, sometimes malaise, general weakness.Outbreaks disappear in 7-9 days.
are primary and recurrent herpes simplex.Primary herpes simplex occurs after primary infection, mostly in children.It is characterized by the severity of clinical manifestations, as a result of hematogenous dissemination of the virus may damage internal organs.One of the most common forms - acute stomatitis.After clinical recovery the elimination of the virus from the body does not take place, there is his persistence in tissues throughout life.Under the influence of adverse factors contributing to immunodeficiency, the activation of the virus, which is accompanied by clinical symptoms of relapse.Recurrent herpes simplex may occur several times a year.Thus eruptions localized areas in the primary lesion, and at new sites.
In addition, distinguish atypical form - swelling, elefantiazopodobnuyu, zosteriformnuyu, hemorrhagic etc.
Herpes mouth -. It is a viral infection characterized by the formation of ulcers in the mouth and known as cold sores or herpes.The first time the infection usually occurs in childhood.Although herpes infected many people, most of them have no symptoms.Those who are sick of the initial infection, painful sores develop in the mouth, which hit the back of the throat, palate, tongue and cheeks and sometimes the inside of the lips.Usually people feel sick, have a fever, swollen lymph nodes, inflamed throat, and there is a bad smell from the mouth.Although the symptoms usually subside in the period from 10 to 21 days, the virus remains in the body and is at rest until it is awaken some type of stress factors, menstruation, or sun exposure.Subsequent outbreaks of disease, known as recurrent herpes simplex, affect the outer and not the inside of the mouth, usually the edge of one lip.These repeated outbreaks much more mild and last for 8-10 days.
first described in 1887 by the Hungarian physician MKSarcoma.It occurs in children suffering from eczema, dermatitis, neurodermatitis.The incubation period is 3 to 5 days.The disease is characterized by acute onset - an increase in body temperature to 39-40 ° C, the rapid increase of obscheinfektsionnyh symptoms until the development of infectious toxicosis.In the 1-3-th day of illness appears abundant vesicular eruption, located on large areas of skin.The rash may last for 2-3 weeks.Often the elements coalesce, burst, forming a solid crust, after which the rejection is pink spot or scarring.The disease can be long.Normalization of body temperature and improvement in general condition occur on 7-10th day.
have impaired children in the pathological process may be involved not only the skin and mucous membranes, but also the central nervous system, internal organs of the body that causes an adverse outcome.
most often occurs when the primary HSV infection in children aged 6 months to 3 years.gingivostomatitis development is promoted by the disappearance of maternal antibodies, the lack of local immunity, teething and others. Clinical manifestations include obscheinfektsionnogo syndrome (fever, symptoms of intoxication), restlessness, drooling and regional lymphadenitis.In the oral mucosa and gums appear walled vesicles that are rapidly opened with the formation of painful sores.Their surface is covered with a touch of yellow 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 primary forms of IPG in infants.The disease begins with acute fever and the appearance of symptoms of intoxication.There is a clinic rhinopharyngitis, farinotonzillita, laringotraheobronhita and obstructive bronchitis.In the upper respiratory tract mucosa reveal vesicular eruptions, which are then converted into erosion.The disease is characterized by severe and prolonged course of frequent addition of mixed infection.It was established that HSV is a trigger for asthma.
Primary infection manifests conjunctivitis and keratoconjunctivitis.Newborns can develop cataracts, uveitis, chorioretinitis.The defeat of the cornea surface is, the type of tree ulcers or deep (discoid keratitis).Last flows most heavily with involvement in the pathological process of the anterior vascular tract, with the outcome of corneal clouding and decreased visual acuity.
Disease begins acutely and is accompanied by inflammation of the conjunctiva, it ulceration, or the appearance of herpetic vesicles on the skin century.The involvement in the pathological process of the cornea leads to the formation of surface erosion, lacrimation, photophobia, scleritis, pain.
Clinical diagnosis is simplified with combined lesions of the eyes, skin, mucous membranes of the oral cavity.
Genital herpes.Genital herpes (herpes genitalis) is characterized by polymorphism of clinical symptoms and the tendency to persistent recurrent course.
Most often infection occurs when the infection through sexual contact and is usually caused by HSV-2, 5-10% of patients - HSV-1.
Primary infection is accompanied by a deterioration of general condition, fever, dysuria, increase in regional lymph nodes, painful sensations in the field of defeat.The girls appear vesicular rash erozivnoyazvennye or in the vagina, vulva, labia.Then formed erosion, possible swelling of the genitals.In the future, the body temperature drops, rashes dry up, crust rejected the formation of pigmented or depigmented spots.Currently, not excluded the involvement of HSV-2 in the development of cervical carcinoma.
Boys herpes blisters or sores usually form on the head of the penis, at least on his body or the foreskin.
Encephalitis may develop during the primary infection (30% of patients), but most often occurs when the reactivation of the HST (70%).A feature of herpes encephalitis is the development of deep necrotic changes in the fronto-parietal-temporal cortex that determines the severity of the disease and the high incidence of sequelae.The medical history of the patients, there are indications of acute IPG in the immediate family.The disease is often preceded by a traumatic brain injury, severe infectious and somatic diseases.Herpetic eruptions occur only in 20% of patients on the skin.There are three stages of herpes encephalitis.
Early stage lasts from several hours up to 7 days.Most patients with acute encephalitis begins and is accompanied by obscheinfektsionnogo and cerebral syndromes.Increased body temperature, there is a headache, repeated vomiting, and hypersensitivity.At 2-4 day the patient's condition is rapidly deteriorating due to increase cerebral focal symptoms and signs of accession.Rapidly progressive impairment of consciousness in the form of confusion, lack of orientation in place and time, change patient behavior (aggression, psychomotor agitation).There are localized or generalized seizures, myoclonus, tremor, opercular and vegetative paroxysms.There are focal symptoms in the form of mono-and hemiparesis, paresthesia, numbness of the extremities.Often there is a violation of the higher nervous functions in the form of aphasia, dysarthria, apraxia, agnosia.One-third of children neurological symptoms precede the appearance obscheinfektsionnyh and brain symptoms, 10% of patients in the initial period of the disease there is no fever.In some patients the disease develops with the gradual appearance of subacute cerebral and focal symptoms ( "pseudotumor" option).
Stage height is characterized by depression disorders of consciousness, seizures, increased frequency of up to status epilepticus, a violation of vital functions.The patient holds the classic triad of herpes encephalitis - fever, persistent disturbance of consciousness and intractable seizures (convulsive-comatose syndrome).Progressing focal neurological symptoms.Meningeal symptoms appear in the majority of children in the 3-5-th day of illness, but they are usually mild.In likvorogramme reveal lymphocytic pleocytosis up to 300-800 cells / mm and increasing the protein content of 1.5 to 2 g / l.Step height extends from 1 to 3 weeks.
reverse development stage begins with 3-4 weeks of illness and lasts from 3 to 6 months or more.In 40-80% of survivors have a gross residual effects in the form of dementia, episindroma, extrapyramidal disorders, hydrocephalus, "vegetative state."Herpetic encephalitis in some patients may become recurrent or chronic.
defeat of the nervous system HSV can occur in the form of serous meningitis, myelopathy, entsefalomieloradikulonevropatii.
HSV can infect the liver, lungs, kidney, esophagus, and others. The pathology of the internal organs is more common in generalized forms of IPG in newborns.Herpetic hepatitis is characterized by acute onset, severe symptoms of intoxication.Predzheltushnogo period is short and may be associated with symptoms of stomatitis.Very soon there hepato- and splenomegaly, dark urine, and jaundice, discoloration of feces.Laboratory tests reveal hyperbilirubinemia by increasing the direct fraction, increased transaminases.The disease is characterized by severe, frequent development of Fulpmes-nantnyh forms of DIC, leading to death.Lesions of the lungs (interstitial pneumonia) and kidneys (focal nephritis) have no specific clinical features, and often occur in the form of mixed infection.
frequency of intrauterine IPG is 1 / 2.5 to 15 thousand. Newborn.The antenatal infected 5% of children in the intrapartum - 95%.Primary genital herpes in women at 32 weeks of gestation leads to the infection of 10% of children before birth - 40-60%.At relapse of genital herpes the risk of infection is much lower - 8%.The child can become infected and asymptomatic IPG his mother.When antenatal infection of children are born with the clinical manifestations of the disease (congenital infection).