HERPES VIRUS INFECTION

The Herpetic infection is caused by the Herpes virus family, which are incorporated by the property to persist in the human organism during all his life and by the ability to cause the various clinical forms in case of immune deficit development.

Herpes simplex is the viral disease caused by Herpes simplex viruses (HSV 1 and HSV 2), that is characterized by the prolonged latent duration with the periodic relapses which are accompanied by appearance of vesicles on a skin and mucus membranes, the CNS and internal organs damage.

Herpes zoster is the viral disease, that is caused by the Varicella-Zoster virus, is characterized by inflammation of intravertebral or cranial nerves nodes and is shown up by a vesicles rash on a skin along the nerves and symptoms of intoxication.

Etiology: DNA-containing virus of HSV 1 and 2 types, the Varicella-Zoster virus, EBV (Epstain Barr virus), CMV (cytomegalovirus), HHV 6, HHV 7, 8 (Human Herpes virus).

Epidemiology:

• The source are patients and virus carriers;

• The way of transmitting is air-droplet, contact (HSV 1), sexual (contact) – HSV 2, transplacental, intranatal (HSV 1), air-droplet (Varicella-Zoster);

• Susceptibility is high on a background of immune deficit, URT viral infections;

• Seasonality: infection more often occurs in winter as sporadic diseases.

Pathogenesis:

·        An entrance gate are the injured mucus membranes and skin.

·        Reproduction of virus.

·        Local changes.

·        Virus by the lymph gets into regional lymph nodes (rarely).

·        Viremia.

·        Organs and systems damage (liver, spleen, lungs, localization in intravertebral ganglia, ganglia of cerebrum).

·        Chronic carrying of the virus (in case of immune deficit).

·        Relapses (on a background of URT viral infections, ultraviolet irradiation, cooling).

Herpes Simplex diagnostic criteria

• Latent period is 2-14 days.

• Acute beginning, toxic signs.

• Mucosa membranes damage (gingivitis, stomatitis (photo 23, 24, 25), tonsillitis) as vesicles, that ruin, forming erosions, are accompanied by the pain.

• Eye damage (conjunctivitis, blepharoconjunctivitis, keratitis, keratoiridocyclitis, choreoretinitis, uveitis, retinal perivasculitis, optic nerve neuritis).

• Skin damage (lips (photo 26), nose (photo 27), eyelids, face, hands, other localization) – painful papules on the red base, than their evolution to small vesicles with the transparent content, they may be connected, clouding of the content, erosions, crusts formation.

• Genital herpes (damage of penis, vulva, vagina, cervical channel, perineum, urethra, endometrium).

• CNS damage (encephalitis, meningoencephalitis, meningitis), peripheral NS damage (neuritis).

• Visceral forms (hepatitis, pneumonia, nephritis and other).

• Relapsed course.

stomatitis

Stomatitis

 

Skin damage

 

Skin damage

 

Herpetic whitlow

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Herpes Zoster diagnostic criteria

• Latent period is 7-21 days, sometimes several months or years (after the chickenpox).

• Acute beginning from high body temperature, toxic signs.

• Burning, itching, pain along the damaged sensory nerve.

• Than skin hyperemia, infiltration in the zone of innervation.

• Firmly grouped papules (in the end of the 1st, on the 2nd day) on the red base, than their evolution to small vesicles with the transparent content, they may be connected, clouding of the content, crusts formation (photo 28), than hyperemied base pales, epithelization ® slight hyperpigmentation (in a week).

Additional investigations

• Virology research of vesicular content, nasopharyngeal smears.

• IF method, PCR.

• Serology: CBR, IEА, PHAR, NR with paired sera (growth of antibodies title in the dynamics).

• CSF investigation (in case of meningoencephalitis signs).

Diagnosis example: Herpes Simplex 1st type local form: stomatitis, severe degree.

Differential diagnostics with herpangina, enterovirus encephalitis, adenoviral keratoconjunctivitis, chicken pox, streptococcus impetigo, erysipelas, eczema, mumps

encephalitis.

Prognosis: The virus of herpes simplex remains in an organism for all the life, severity of relapses is related to the state of the immune system. Lethality makes 80-85 % in case of herpetic encephalitis, in case of recovery severe phenomena remains with the abscense of cork centers function. The defeat of pregnant by the herpes virus results in forming of the inborn defects.

Treatment:

Local damage of the skin and mucous membranes:

• antiviral ointments and creams locally (herpevir, acyclovir, oxolin, tebrophen, bonaphton, cytozar);

• antiseptic fluids (solution of diamond green, methylen blue, peroxide of hydrogen);

• local anesthetics, novocain blockades (in case of Herpes Zoster);

• NSAIDs (paracethamol 10-15 mg/kg or ibuprophen 10mg/kg);

• ultraviolet irradiation.

Keratitis:

• locally 5-iodine-2-desoxyuridin, adenine arabinosid.

In severe forms (encephalitis):

Etiologic therapy:

• Acyclovir 10-20 mg/kg 3 times per day during 14-21 days IV.

Pathogenetic therapy:

• In case of brain edema – dehydration by 25 % MgSO4 IM, lasix 1-3 mg/kg IV or IM, acethazolamid orally;

• Detoxication in moderate case – orally (oral fluids intake corresponds to age norms with including the IV fluids);

• Detoxication in severe cases – IV not more than 1/2 of physiologic age norms during the 1st day, total fluids intake (IV and PO) not more than 2/3 of physiologic age norms in case of normal urination and absense of dehydration.from the 2^nd week correct fluids intake (daily amount of urine not less than 2/3 of all fluids intake;

• In case of seizures – Anticonvulsant therapy: benzodiasepins (seduxenum, sibasonum) 0.3-0.5 mg/kg IV, if they are ineffective – 1 % hexenalum or thiopenthalum sodii in 3-5 mg/kg IV. Dehydration therapy: lasix 2-3 mg/kg IM or IV;

• Glucocrticoids 3-5 mg/kg (by prednisolon), course not more than 10 days.

Base therapy:

• Bed regimen till body temperature normalization, disappearance of general cerebral and considerable improvement of focal neurological signs, not less than 14-16 days;

• A diet (before stable vital functions is due to adequate parenteral infusion therapy);

• Brest feeding or bottle feeding by adopted formulas for infants, in the first day 1/2-1/3 of average volume with a next increase to the complete volume during 2 – 3th days;

• A milk vegetable diet (№5) is appointed for preschoolers or school children, 5-6 times per day with the next passing to the diet №2 whether №15 (depending the age) in the recovery period.

Antibacterial therapy: in case of possible concomitant bacterial infection (by the broadspectrum antibiotic in average therapeutic doses, as cephalosporines 3rd generation or aminoglycosides 3rd generation).

In rehabilitation period:

• Vascular medicine (penthoxyphyllin, nicergolin and others like that);

• In posthypoxia period – nootrops, vitamins group B.

In case of relapsed course:

· adaptogens (eleutherocock, pyrogenal and other);

· vitamins of group B (B1, B2, B12);

· specific antiherpetic immune globulin (in an early period of relapse) 1.5-3 ml IM,

daily during 5-10 days;

·antiherpetic vaccine 0.1-0.2 ml IC in 2-3 days 5 times, twice per year.

At secondary bacterial infection: (penicillins, cefalosporins, aminoglycosides).

Prophylaxis:

•Isolation of patient up to 5 days since the last rashes appear (in case of Herpes Zoster), hospitalization in case of severe and complicated course.

• Contact person younger than 3 years, which have not Herpes Zoster before, are isolated from 11 till 21 day since the contact, for the newborns 0.2 ml/kg normal immunoglobulin IM.

• Carrying of masks by mothers who are breast feeding in case of Herpes simplex 1, observance of hygienic norms.

• To infected pregnant – immunoglobulin IM 0.2 ml/kg.

• Delivery by the caesarean section at Herpes simplex 2 infection.

• Supervision after new-born, whose mothers has herpetic infection, till 2 months.

• Ventilation and moist cleaning up.

Passive immunization (Varicella-Zoster): donor Varicella-Zoster immunoglobulin 0.2-0.5 ml/kg in the first 2 days after the contact (an effect lasts till 21 day), at the secondary contact – immunize again.