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The Anogenitalny herpes infection (genital herpes) represents the chronic recurrent viral disease transferred mainly sexually, which is characterized by damage of skin and mucous membranes of generative organs and an urinogenital path.
According to various researches, genital herpes of the 1st or 2nd type infected 65 — 90% of the population of the globe. According to WHO data, VPG-infection mortality takes the II place after flu. In our country, by some estimates, prevalence of anogenitalny herpes in the general population makes 0,5%.
The greatest value in distribution of genital herpes of the 2nd type has a sexual way of transfer. In most cases infection happens at contact with clinically asymptomatic virusovydelitel. Emergence of a neonatal herpes infection which prevalence at newborns makes 0,003 — 0,05% is also possible, and in 30 — 50% such patients die. Special value has defeat of VPG at HIV infection. It is proved that VPG can activate a HIV genome, and thus, to be risk factor of progressing of AIDS.
• herpes infections of generative organs and urinogenital path;
• herpes infections of perianal integuments and rectum;
• the anogenitalny herpes infection which is not specified.
Forms of genital herpes:
Kliniko-morfologichesky forms of genital herpes:
• first episode of primary infection;
• first display of a nonprime infection;
• first episode of a consecutive herpes infection;
• recuring genital herpes;
• asymptomatic genital herpes.
Depending on localization and severity of defeats:
• The I stage — damage of external genitals;
• The II stage — a herpetic colpitis, a cervicitis and an urethritis;
• The III stage — a herpetic endometritis, a salpingitis or cystitis.
Etiology Both serotypes of a virus of a herpes simplex — VPG-1 and VPG-2 can be causative agents of genital herpes. In family herpes viruses of VPG belongs to group of alpha viruses (in addition to them in family herpes viruses is still beta and gamma viruses). The size of virions averages 120 — 150 nanometers. Virion consists of 3 main components: nucleoid, the capsid covering nucleoid and a lipidosoderzhashchy cover. Virion contains DNA, protein, spermine, spermidine, lipids, glycoproteins. Genomes of VPG-1 and VPG-2 match approximately for 50%. DNA of VPG breeds in a kernel of a host cell, at the same time in a kernel of a cell little bodies inclusions are formed. When moving from a kernel to cytoplasm the virus gets the cover consisting of glycoproteins and lipids.
Pathogeny VPG-2 gets to a human body mainly sexually. As a source of an infection serves the patient with clinical displays of genital herpes or the virus carrier without clinical manifestations, but only on condition of replication of a virus (the subclinical course of an infection). Transfer of a virus can happen at any kinds of contacts: genito-genital, oral and genital, genitalno-oral or oral and proctal. Are among other possible ways of infection transplacental, household, professional and airborne, but at genital herpes they meet extremely seldom.
VPG is implemented into an organism through mucous membranes and skin, and then is quickly taken touch nerve terminations by means of special virus receptors. After implementation the virus gets into a nerve axon in nervous a ganglion where remains in a latent state vaguely long, as a rule, for life.
At the infection caused by VPG-1 usually there is a damage of skin of open parts of a body (a face, extremities), a mucous membrane of eyes, an oral cavity, upper respiratory tracts, and VPG-2 — skin and a mucous membrane of generative organs. At the same time there is no strict specificity on localization of infectious process; in a number of researches it is established that recently VPG-1 share at defeat of generative organs increased from 20 to 40%.
VPG is capable to latent existence with the subsequent reactivation which serves as the reason of development of recurrence of a disease or asymptomatic allocation of the activator. VPG has immunosuppressive effect and can serve as an origin of secondary immunodeficience. The Tropnost of genital herpes to epithelial and nervous cells explains polymorphism of clinical manifestations of a herpes infection.
Clinical signs and symptoms of an illness Genital herpes is characterized by emergence on skin and mucous membranes of the centers of defeat of various degree of manifestation. Emergence of typical herpetic elements — bubbles, erosion, crusts is characteristic of a manifest form. At atypical (edematous and pruritic) the center is provided to a form by deep recurrent cracks of a mucous membrane of generative organs. The abortal form arises at the patients who were earlier receiving antiviral therapy or passed vaccination. It is characterized by emergence of the spots or papules which are followed by an itch and usually disappearing in 1 — 3 days. Treat abortal forms of genital herpes erythematic, papular and prurigo-neurotic; all of them are characterized by lack of vesicular elements. The subclinical form usually comes to light at establishment of sexual contacts of the patients having infections, sexually transmitted or married couples with fertility disturbance. Existence of minimum expressed clinical manifestations or asymptomatic current is characteristic of this form.
The indisposition, headache, sometimes subfebrile body temperature, sleep disorder, nervousness belong to the most frequent symptoms. At women the defeat centers usually are located on a mucous membrane of small and big vulvar lips, a crotch, a clitoris, a vagina and a neck of uterus, on buttocks; at men — on a balanus, a prepuce, a coronal furrow, in the field of an outside opening of an urethra or in it, in a crotch and buttocks.
The first episode of primary genital herpes — true manifestation of primary herpes infection. It arises for lack of antibodies to VPG and can be followed by emergence of characteristic symptoms or proceed latentno (in 65% of cases). Duration of the first episode makes to 3 weeks with gradual increase of expressiveness of clinical manifestations within the first week. The disease is characterized by long allocation of a virus, existence of the centers on generative organs and ekstargenitalny defeats, and also the general symptoms. The sacral radiculopathy, heavy aseptic meningitis or the disseminated infection belong to the complications demanding hospitalization. To the first episode of a nonprime herpes infection
those cases when symptoms of a disease appear at persons at whom earlier antibodies to VPG already came to light belong. Their expressiveness is, as a rule, less intensive, than at the first episode of primary infection, however it is difficult to carry out differential diagnosis between these clinical forms, and in need of specification like genital herpes laboratory tests are required. At the first episode of a consecutive herpes infection of VPG-2 comes to light at persons at whom antibodies to VPG-1, or on the contrary were defined earlier. At recurrent genital herpes latent infection periodically becomes more active. The current can be asymptomatic; in this case statement of the diagnosis is possible only when using cultural or type-specific serological methods of research. Weight and duration of preservation of clinical manifestations at recurrence of genital herpes is less expressed, than at primary form. At 50% of patients antecedent signs are observed: itch, burning, pain, dysuria, increase and morbidity of lymph nodes. The infection caused by VPG-2 is characterized by earlier and frequent development of recurrence, than VPG-1.
Treat the factors promoting emergence or recuring of genital herpes:
• decrease in an immune responsiveness;
• overcooling or overheat of an organism;
• associated diseases;
• some mental and physiological (sexual contacts, periods) states;
• medical manipulations (abortions and introduction of an intrauterine spiral).
Asymptomatic genital herpes is characterized by reactivation of the VPG-infection without development of clinical signs of a disease and observed at patients with defective specific antiherpetic immunity or a system immunodeficiency.
With immunity to VPG-1 infection of VPG-2 occurs less often, the asymptomatic current is more often observed; besides, the risk of development of recurrence and probability of an asymptomatic carriage decreases. At infection with any strain of VPG-2 of reinfection with other strains does not occur.
The diagnosis and the recommended clinical trials The diagnosis is established on the basis of features of a clinical picture and data of laboratory research. As biological material for carrying out researches contents of vesicles, washouts from fabrics and bodies, smears prints, scrapings, biological liquids and secrets of an organism (blood, slime, urine, the lacrimal and spinal liquids) are used.
Treat the main methods of laboratory diagnosis: • virologic: — reproduction and accumulation of virus particles by infection of cellular cultures, 12 — 13-day chicken embryos, experimental animals with the subsequent confirmation and identification like VPG;
• molecular and genetic:
— polimerazny chain reaction;
• identification of antigens of genital herpes:
— radio immune analysis;
— enzyme immunoassay;
— immunofluorescence microscopy;
• registration of an immune response:
— identification circulating in serum or other biological liquids and secrets of an organism of the patient of specific antiherpetic antibodies (IgM, IgG, IgA) by means of reaction of binding complement, reaction of passive hemagglutination, a neutralization test, an enzyme immunoassay;
— assessment of specific cellular immunity to VPG;
— skin tests;
• assessment of the immune status of patients. At the asymptomatic course of recurrence of genital herpes for the first 4 days research on VPG is conducted daily, then — in 7 — 10 days after the end of treatment.
At detection at the patient with genital herpes it is necessary to inspect his sexual partners and at identification of symptoms of an infection at them to begin their treatment. Patients should recommend to abstain from sex life before disappearance of clinical manifestations. For this period use of condoms has to be obligatory at all forms of sexual contacts. Partners should be informed on a possibility of infection with genital herpes at the subclinical course of an infection.
Differential diagnosis of a disease Need for carrying out the differential diagnosis can arise at an atypical or oligosymptomatic current of a herpes infection. Besides, difficulties can arise when the clinical picture of other diseases reminding that at genital herpes is followed by allocation of genital herpes from the centers of rashes.
Clinical displays of genital herpes can remind those at a shankroida, syphilis, and also other diseases which are followed by an ulceration of skin of anogenitalny area (a mange, the fixed erythema, diseases Krone, Bekhcheta, Darya, streptococcal to the impetigo, a pemphigus, pemphigoid, contact dermatitis).
Emergence of roundish, but not polycyclic erosive and ulcer elements, lack of their sgruppirovannost, the expressed reaction of inguinal lymph nodes is characteristic of an initial stage of a shankroid in addition to formation of painful erosion and ulcers. Detection of the activator (Haemophilus ducrey) confirms the diagnosis of a venereal ulcer.
In primary period of syphilis there can be multiple primary affects (hard ulcers) in some cases reminding displays of genital herpes. However existence of the palpated consolidation in the basis of elements, lack of a phase of vesiculation, regional a sclera-demit are inherent to syphilis and are not characteristic of genital herpes. In the secondary period erosive papules can also be similar to herpetic rashes, but data of serological researches confirm the diagnosis of syphilis.
Any of other diseases which are followed by an ulceration of skin of anogenitalny area (a mange, the fixed erythema, diseases Krone, Bekhcheta, Darya, streptococcal the impetigo, a pemphigus, pemphigoid, contact dermatitis) can be complicated by accession of genital herpes or be followed by allocation of VPG. In similar cases carefully collected anamnesis and results of laboratory researches (detection of akantolitichesky cells, scabby zudnya, microscopic examination of the smear painted across Gram, bacteriological research, etc.) promote statement of the correct diagnosis.