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VIRAL INFECTIONS

VIRAL INFECTIONS. Part II. IHAB YOUNIS, MD. Herpes simplex. Etiology. HSV(types 1&2) is a double-stranded DNA virus Characterized by: 1-Neurovirulence:the capacity to invade and replicate in nerves 2-Latency: latent infection in sensory nerve

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VIRAL INFECTIONS

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  1. VIRAL INFECTIONS Part II IHAB YOUNIS, MD

  2. Herpes simplex

  3. Etiology • HSV(types 1&2) is a double-stranded DNA virus • Characterized by: 1-Neurovirulence:the capacity to invade and replicate in nerves 2-Latency: latent infection in sensory nerve ganglia 3-Reactivation:induced by a variety of stimuli (eg, fever, trauma, emotional stress, sunlight, menstruation)

  4. Clinically 1- Acute herpetic gingivostomatitis • Occurs in children aged 6 months to 5 years • Mode of infection: Infected saliva from an adult or another child • The incubation period : 3-6 days

  5. Abrupt onset ,high temperature, anorexia and listlessness • Gingivitis: swollen, erythematous, friable gums • Vesicular lesions: on the oral mucosa, tongue, lips and later rupture and coalesce, leaving ulcerated plaques • Tender regional lymphadenopathy • Perioral skin also may be involved because of contamination with infected saliva

  6. Course • Acute disease lasts 5-7 days • Symptoms subside in 2 weeks • Viral shedding from the saliva may continue for 3 weeks or more

  7. 2-Acute herpetic pharyngotonsillitis • In adults, oropharyngeal HSV-1 causes pharyngitis and tonsillitis more often than gingivostomatitis • Fever, malaise, headache and sore throat • Vesicles rupture to form ulcerative lesions with grayish exudates on the tonsils& posterior pharynx • Less than10% have associated oral & labial lesions • HSV-2 can cause similar symptoms and is associated with orogenital contact or can occur concurrently with genital herpes

  8. 3-Recurrent Herpes labialis • A prodrome of pain, burning & tingling • Followed by the development of erythematous papules that rapidly develop into tiny, thin-walled, intraepidermal vesicles that become pustular and ulcerate • In most patients, fewer than 2 recurrences each year, but some individuals have monthly recurrences • Maximum viral shedding is in the first 24 hours of the acute illness but may last 5 days.

  9. 4-Primary genital herpes • Primary genital herpes can be caused by both HSV-1 and HSV-2 • Recurrences are more common with HSV-2 • Asymptomatic in most patients • Primary genital herpes is characterized by severe and prolonged systemic and local symptoms. The symptoms of persons with a first episode of nonprimary HSV-2 infection are less severe and of shorter duration • Preexisting antibodies to HSV-1 have an ameliorating effect on disease severity caused by HSV-2 • Prior orolabial HSV-1 protects against genital HSV-1 but not HSV-2 • Women's symptoms are more severe and women have a higher rate of complications than men

  10. Clinical features in men • Herpetic vesicles appear in the glans penis, the prepuce, the shaft of the penis, and sometimes on the scrotum, thighs, and buttocks • In dry areas, the lesions progress to pustules and then crust • Herpetic urethritis occurs in 30-40% of patients and is characterized by severe dysuria and mucoid discharge • The perianal area and rectum can be involved in persons who engage in anal intercourse, resulting in herpetic proctitis.

  11. Clinical features in women • Herpetic vesicles appear on the external genitalia, labia majora, labia minora, vaginal vestibule, and introitus • In moist areas, the vesicles rupture, leaving exquisitely tender ulcers • The vaginal mucosa is inflamed and edematous. The cervix may be involved in 70-90% of patients • Dysuria may be very severe and may cause urinary retention

  12. In men and women, the ulcerative lesions persist from 4-15 days until crusting and reepithelialization occur • The median duration of viral shedding is about 12 days.

  13. 5-Recurrent genital herpes • 60% of patients with 1ry genital HSV-2 have recurrences in the 1st year • 38% had 6 recurrences/year and 20% had more than 10 recurrences • Both subclinical and symptomatic reactivation are more common with HSV-2 compared to HSV-1 • Recurrent genital herpes is preceded by a prodrome of tenderness, pain, and burning at the site of eruption that may last from 2 hours to 2 days • Pain is mild, and lesions heal in 7-10 days and constitutional symptoms are uncommon. The lesions heal in 8-10 days and viral shedding lasts an average 5 days • The symptoms are more severe in women than men

  14. Subclinical genital herpes • The majority of primary genital HSV infections are asymptomatic and 70%-80% of seropositive individuals have no history of symptomatic genital herpes Nevertheless, they experience periodic subclinical reactivation with virus shedding, thus making them a source of infection • The rate of viral shedding may be 1-2% . This fact is important in neonatal herpes because most mothers have no signs and symptoms of genital herpes during pregnancy

  15. Histopathology • Epidermal spongiosis • Intraepidermal vesicle formation • Dermal inflammatory infilt

  16. Investigations • HSV infection is best confirmed by isolation of virus in tissue culture • Immunofluorescent staining of the tissue culture cells can quickly identify HSV and can distinguish between types 1 and 2 • Rapid detection of HSV DNA in clinical specimens is now possible with polymerase chain reaction (PCR)

  17. Antibody testing can demonstrate a primary seroconversion, particularly with HSV-1 in childhood • Because of sero–cross-reactivity, HSV-1 and HSV-2 are not generally distinguishable unless a glycoprotein G antibody assay is available • Antibody titer increases generally do not occur during recurrences of HSV.Therefore, the test generally is not used for the diagnosis of mucocutaneous HSV relapse

  18. Tzanck smear is a time-honored procedure to assist in the diagnosis of cutaneous herpesvirusinfections • Typically, an intact vesicle is used from which the vesicular fluid is aspirated • After aspiration, the vesicle should be unroofed aseptically.Using a sterile instrument, the floor of the newly produced ulcer can then be scraped. The obtained material can be spread on a glass microscope slide and then dried and fixed for staining

  19. Staining can be performed with a Papanicolaou stain,Gram or Giemsa • A positive result is the finding of multinucleate giant cells. • Using appropriate immunofluorescent antibody reagents, the smear can distinguish different herpesviruses and nonherpesviruses that may be present (eg, vaccinia, smallpox)

  20. Treatment • 1-Acyclovir (Acyclovir cream, zovirax, Lovir 400 mg tab)) • Inhibits the thymidine kinase of herpes viruses • Evidence from multiple clinical trials shows that topical acyclovir has little or no therapeutic effect

  21. Oral Dose: -First episode mucocutaneous herpes simplex: 400 mg tid for 7-10 d or until clinical resolution - Recurrent genital herpes: 200 mg PO five times daily for 5 d -Chronic suppressive therapy: 400 mg bid or 200 mg 3-5 times daily; reevaluate after 1 y

  22. 2-Valacyclovir (Valtrex): • Prodrug rapidly converted to the active drug acyclovir. More expensive but has a more convenient dosing regimen • Dose: -First episode: 1 g bid for 10 d -Recurrent episode : 500 mg bid for 5 d beginning within 24 h of onset -Suppressive dosing for HSV: 500 mg to 1 g/d

  23. 3-Famciclovir (Famvir) • Prodrug that when biotransformed into active metabolite, penciclovir • Inhibits viral DNA synthesis/replication • Dose: -Recurrent genital HSV: 125 mg bid for 5 d-Suppression of frequent recurrence of genital HSV: 250 mg bid up to 12 mo

  24. Eczema herpeticum

  25. Etiology • It is caused by a disseminated HSV infection in patients with atopic dermatitis • Patients have cell-mediated and humoral defects • A disorder of infants& children of any age • Occurs occasionally in adults

  26. Umbilicated vesiculopustules that progress to punched-out erosions • The eruption is most commonly disseminated in the areas of dermatitis, with a predilection for the head& trunk. Localized forms also exist • The vesicles often become hemorrhagic and crusted and can evolve into extremely painful erosions with a punched-out appearance • These erosions may coalesce to form large, denuded areas that frequently bleed and can become secondarily infected with bacteria

  27. The eruption continues to spread over 7-10 days and may be associated with a high temperature, malaise, and lymphadenopathy • Recurrent episodes may also occur but are milder and not usually associated with systemic symptoms

  28. Eczema herpeticum

  29. Treatment • Acyclovir IV or orally • Eczema treated as usual but steroids are used cautiously • Patients with atopic dermatitis should be aware of herpetic infection

  30. Herpes zoster (Shingles) Zoster=girdle

  31. Etiology • VZV is a double-stranded DNA virus • Infection initially produces chickenpox. Following resolution of the chickenpox, the virus lies dormant in the dorsal root ganglia until focal reactivation along a ganglion's distribution results in herpes zoster • Although the exact precipitants that result in viral reactivation are not known certainly, decreased cellular immunity appears to increase the risk of reactivation.

  32. Regarding primary infection, more than 90% of the population is infected by adolescence, and approximately 100% are infected by 60 years of age • Herpes zoster affects about 10-20% of the population

  33. Clinically • A prodrome (pain,fever, malaise, headache, and dysesthesia) occurs 1-4 days before the development of the cutaneous lesions • Grouped vesicles, usually involving 1, but occasionally up to 3, adjacent dermatomes • Vesicles become pustular, and occasionally hemorrhagic, with evolution to crusts in 7-10 days

  34. Pain may subside in 2-3 w in young patients but may last for 1 m in the elderly • Pain lasting longer than 1-3 months is referred to as postherpetic neuralgia. It affects 10-15% • Its incidence & severity increase with age • Types: -Continuous burnning with allodynia -Spasmodic shooting -Crawling pruritus

  35. Herpes zoster ophthalmicus • Vesicular rashes involving the ophthalmic division of the trigeminal nerve. Crusting begins on the fifth to sixth day • Hutchinson sign: severe ocular complications can occur with a vesicular rash anywhere on the forehead • Herpes zoster oticus • Vesicles involve the external auditory canal, concha, and pinna, postauricular skin, lateral nasal wall, soft palate, and anterolateral tongue • Vertigo and sensorineural hearing loss and/or paralysis of the facial nerve may be noted • Clinically, total loss of the ability to wrinkle the ipsilateral brow differentiates a peripheral seventh nerve lesion from a central seventh nerve lesion, which spares the forehead

  36. Treatment 1-Antivirals:should start within 1-2 d -Acyclovir 800 mg orally 5 times/d. for 7-10 d -Valacyclovir 1gm orally q8h for 7 d - Famciclovir (Famvir) 500 mg PO q8h for 7 d 2-Analgesics 3-?Prednisolone 60 mg/d orally tapered over 3 wk

  37. For postherpetic neuralgia: I- For stabing pain : Anticonvulsants: 1-Gabapentin (Neurontine,Gaptin,Conventine) 400-1200 mg orally 3 tds 2-Phenytoin (Dilantin)100 to 300 mg orally at bedtime; increase dosage until response is adequate 3-Carbamazepine (Tegretol)100-200 mg orally 1-3 times/day

  38. II- For burning pain :Tricyclic antidepressants: 1-Amitriptyline (Tryptizol 10mg Tab ) 25 mg orally tds 2-Imipramine (Tofranil 25 mg tab)25 mg orally 1-6 times/d

  39. Investigations • Tzanck smear • Biopsy is required for definitive diagnosis • PCR

  40. Immunologic tests for viral antigen • Direct immunofluorescence or immunoperoxidase stains • Radioimmunoassay • Enzyme-linked immunosorbent assay • Agar gel immunodiffusion • Immunoelectrophoresis

  41. Serology for VZV antibodies • Neutralizing or complement-fixing antibody tests • Enzyme-linked immunosorbent assay • Radioimmunoassay • Membrane antigen immunofluorescence • Immune adherence hemagglutination

  42. Chickenpox (Varicella)

  43. Etiology • The varicella-zoster virus enters through the respiratory system &by direct contact • The virus replicates in regional lymph nodes • After a week, a secondary viremia disseminates the virus to the viscera and skin • Varicella is highly contagious; secondary attack rates range from 80-90% for household contacts • Varicella's infectious period begins 2 days before skin lesions appear and ends when the lesions crust, usually 5 days later

  44. Clinically • Incubation period: 10-21 days • Prodrome : Low-grade fever, abdominal pain, cough and coryza preced skin manifestations by 1-2 days • Fever usually is low-grade and subsides within 4 days

  45. Rash • The characteristic rash appears in crops • There are 250-500 lesions but can be as few as 10 • Lesion starts as a red macule, rapidly develops into papule, vesicle, pustule and crust • Varicella's hallmark is the simultaneous presence of different stages of the rash • Rash is centripetal starting on the back • New lesions continue to erupt for 3-5 days, crust by 6 days and heal completely by 16 days

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