Human Herpesviruses3-8

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VARICELLA–ZOSTER VIRUS (HHV-3), Varicella –Chickenpox, Herpes zoster – Shingles /EPSTEIN–BARR VIRUS (EBV), CYTOMEGALOVIRUS (CMV) /HHV-5 /HHV-6 /HHV-7 /HHV-8


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Human Herpesviruses3-8

  1. 1. Viral infections Human Herpesviruses Cont.
  2. 2. VARICELLA–ZOSTER VIRUS (HHV-3)
  3. 3. VZV CLINICAL FORMS: • Varicella – Chickenpox • Herpes zoster – Shingles
  4. 4. Varicella (Chickenpox) Highly contagious Mainly Children Generalized Vesicular eruptions on Skin and Mucous membranes Severe manifestations in Adults and Immune compromised. PRODROME: Brief of low-grade fever, URT symptoms, and mild malaise may occur Rapid appearance of pruritic asynchronous exanthem
  5. 5. Varicella (Chickenpox) Pathogenesis
  6. 6. Varicella (Chickenpox) Pathogenesis MODE OF TRANSMISSION: - Airborne droplets and direct contact from varicella patients. - Vesicular fluid of Zoster patients can be the source of Varicella in susceptible individuals. PRIMARY VIREMIA and spread to liver and spleen. SECONDARY VIREMIA follows with viral spread to the skin.
  7. 7. Contagious 1-2 days prior to rash until all lesions are crusted over
  8. 8. Varicella (Chickenpox) Occurs year-round, peaks in late autumn and late winter through early spring INCUBATION PERIOD14-21d. Lesions appear in crops - typically have 3 crops begin in trunk and scalp, then spread peripherally Lesions begin as tiny erythematous papules, that develop central vesicles surrounded by red halos (‘dew drops on a rose petal’) Hallmark - lesions in all stages of evolution Macule Varicella (Chickenpox) C/P
  9. 9. Lesions most numerous centrally.
  10. 10. Varicella (Chickenpox) C/P Lesions began to dry, umbilicated appearance, then surrounding erythema fades and a scab forms. All scabs slough off 10-14 days Scarring not typical unless superinfected Cluster in areas of previous skin irritation Painful lesions along the oral, rectal, and vaginal mucosa, external auditory canal, tympanic membrane
  11. 11. Varicella (Chickenpox) C/P Severe in the immunocompromised host - can be fatal Need to get varicella-zoster immunogloblin 96 hours post-exposure to possible varicella
  12. 12. Varicella (Chickenpox) COMPLICATIONS “6” 1. Secondary bacterial skin infections [M.C.] 2. Varicella Pneumonia, 3. Hepatitis, 4. Encephalitis, 5. Reye syndrome (Aspirin is contraindicated) 6. CVS & neonatal varicella
  13. 13. CONGENITAL VARICELLA SYNDROME (CVS) & NEONATAL VARICELLA • Primary maternal infection during the 1st trimester may lead to spontaneous abortions or CVS (serious) skin lesions, hypoplasia of limbs, chorio-retinitis & CNS defects • Primary maternal infection near the time of birth can lead to widely disseminated infection in the new born with mortality rate of 35% • If rash began a week or more before delivery, maternal Abs transferred via placenta – baby gets the infection but escapes clinical disease
  14. 14. CONGENITAL VARICELLA SYNDROME (CVS) & NEONATAL VARICELLA
  15. 15. Varicella (Chickenpox) DDx “8” 1. Vesicular viral exanthem (e.g. coxsackieviruses) 2. PLEVA 3. Disseminated HSV 4. Drug eruption 5. Insect bites 6. Scabies 7. Rickettsialpox 8. Smallpox
  16. 16. Varicella (Chickenpox) Treatment
  17. 17. IMMUNOCOMPETENT 1. Neonate: Acyclovir, 500 mg/m2 q8h × 10 days 2. Child: Symptomatic treatment alone, or acyclovir, 20 mg/kg PO qid × 5 days 3. Adolescent, adult; Acyclovir, 800 mg PO 5×/day × 7 days IMMUNOCOMPROMISED 1. Mild varicella or mild compromise; Acyclovir, 800 mg PO 5×/day × 7-10 days 2. Severe varicella or severe compromise; Acyclovir, 10 mg/kg IV q8h × 7 days or longer; 3. Acyclovir resistant (advanced acquired immunodeficiency syndrome) Foscarnet, 40 mg/kg IV q8h until healed. Varicella (Chickenpox) Treatment
  18. 18. Varicella (Chickenpox) Prevention VARICELLA ZOSTER IMMUNEGLOBULIN(VZIG) • Postexposure prophylaxis in cases of inadvertent exposure to the virus, • 125 IU/10kg IM; not to exceed 625 IU/dose given within 96 hours of initial contact can  severity of the disease though not prevent it  protection up to 3 wk • VZIG given to neonates whose mothers became infected shortly before birth. VACCINATION • live attenuated varicella vaccine is effective, a two- dose SC in children. • One-time live-attenuated VZV vaccine for eligible persons older than 50 years.
  19. 19. Herpes Zoster
  20. 20. ORDER OF FREQUENCY: 1.Thoracic 50% 2.Lumbar 3.Trigeminal 4.Sacral 5.Cervical 6.Facial
  21. 21. Herpes Zoster (Shingles) Caused by varicella-zoster virus After primary infection, virus lies dormant in genome of sensory nerve root cell Age of Onset; More than 66% are >50 years of age. Reactivation results in a sensory neuritis Incidence, severity and risk of complications increase significantly with age and immunosuppression due to a decline in specific cell- mediated immune response to VZV Occasionally localized dysesthesia but no cutaneous eruption (‘zoster sine herpete’)
  22. 22. Herpes Zoster (Shingles) Postulated triggers include: 1. Mechanical trauma 2. Thermal trauma, 3. Infection, 4. Debilitation 5. Immunosuppression
  23. 23. PRODROME: Pain/pruritis, tingling, hyperesthesia, Pre eruptive pain (pre-herpetic neuralgia), unilateral, dermatomal, precedes the eruption by 4 to 5 ds. Prodromal symptoms may be absent, particularly in children. If cranial nerve involvement - prodrome of severe HA, facial pain, or auricular pain prior to the eruption. Herpes Zoster (Shingles) C/P
  24. 24. ERUPTIVE PHASE: Single dermatome; Does not cross midline red, swollen plaque of varying sizes and spreads to involve part or all of a dermatome The vesicles arise in clusters (grouped) from the erythematous base and become cloudy with purulent fluid by day 3 or 4. Vesicles either umbilicate or rupture before forming a crust, which falls off in 2 to 3 weeks. The elderly or debilitated patients may have a prolonged and difficult course. The major morbidity is post-herpetic neuralgia (PHN). +/- fever or constitutional symptoms. Regional LAD common Herpes Zoster (Shingles) C/P
  25. 25. Herpes Zoster (Shingles) COMPLICATIONS “8” 1. Post-herpetic neuralgia (PHN). The most frequent problem, which is more in elderly 2. Post-herpetic itch (PHI). 3. Local Scarring. 4. Secondary bacterial infection 5. Ramsay-Hunt syndrome (Herpes Zoster Oticus) 6. Disseminated zoster: >20 vesicles Requires intravenous acyclovir 7. Corneal scarring and loss of vision dt. ophthalmic zoster 8. Visceral involvement: pneumonitis; meningoencephalitis; hepatitis
  26. 26. Herpes zoster (ophthalmic zoster). Involvement of the first branch of the fifth nerve. Hutchinson’s sign is the presence of vesicles at the tip, side, or bridge of the nose indicating Involvement of the nasociliary branch of the trigeminal nerve, Which also innervates the cornea.
  27. 27. Shingles When it occurs in a child as young as this 8 month old it is often as a result of primary infection in utero.
  28. 28. Geniculate ganglion of the facial nerve
  29. 29. 1) Zosteriform HSV, 2) Contact dermatitis, 3) Phytophotodermatitis, 4) Bullous impetigo, 5) Cellulitis Herpes Zoster (Shingles) DDx
  30. 30. Systemic antivirals are recommended in all patients over 50 with pain in whom blisters are still present, even if they are not given within the first 72 h of the eruption but within 7 days may also be helpful Herpes Zoster (Shingles) Rx I. ANTIVIRAL THERAPY
  31. 31. Herpes Zoster (Shingles) Rx II. ORAL ANALGESIA 1. Acetaminophen 2. NSAIDs 3. Opiate analgesia Antiviral therapy and analgesics aid acute pain control III. TOPICAL THERAPY 1. Wet dressings with 5% aluminum acetate (Burow solution), applied for 30-60 minutes 4-6 times daily; 2. Lotions (such as calamine). 3. Local anesthetics, such as 10% lidocaine in gel form, or lidocaine patches may acutely  pain IV. CORTICOSTEROIDS Controversial (40-60 mg every morning) typically is administered as early as possible in the course of the disease and is continued for 1 week, followed by a rapid taper over 1-2 weeks.
  32. 32. Herpes Zoster (Shingles) Rx of POST-HERPETIC NEURALGIA 1. Antiviral therapy: The only consistently successful method of treating PHN is to prevent it via prompt treatment of acute zoster and its associated pain. Initiation as early as possible in the course of acute zoster within 72 hours of onset 2. Local anesthetic: (e.g. Lidocaine patch 5 %), 3. Capsaicin: 5 times daily 4. Oral analgesics: Narcotic & nonnarcotic e.g. ibuprofen 5. Anticonvulsants: (Carbamazepine600-800 mg/d. /Gabapentin 900-1800mg/d /Pregabalin). 6. Tricyclic anti-depressants (TCA): (e.g. amitriptyline 10-25 mg PO up to 75 mg/d) 7. Local anesthetic blocking of sympathetic nerves may produce transient relief, their effectiveness in reducing the protracted pain of PHN remains to be determined. 8. Neurosurgery- if necessary helpful in exceptional cases.
  33. 33. EPSTEIN–BARR VIRUS (EBV) /HHV-4
  34. 34. EPSTEIN–BARR VIRUS (EBV) PRIMARY INFECTION:  Infectious mononucleosis (IM) REACTIVATION INFECTION:  EBV lymphoproliferative disorders
  35. 35. (EBV) Infectious Mononucleosis
  36. 36. Infectious Mononucleosis Acute self-limiting illness of children and young adults caused by EBV. Transmission by oral contact, sharing eating utensils, transfusion, or transplantation Incubation period 30-50 days (shorter, 14-20 days, in transfusion-acquired infection) Asymptomatic in children, but symptomatic in adolescents and young adults
  37. 37. Infectious Mononucleosis C/P Latency is established in B lymphocytes ~95% of adults worldwide are seropositive. PRODROME: Fatigue, malaise, anorexia, HA, sweats, chills lasting 3-5 days.
  38. 38. Infectious Mononucleosis C/P 1. Classically, ~80% present with triad of fever, pharyngitis, and lymphadenopathy i. Fever - can have wide daily fluctuations. ii. Pharyngitis, tonsillar and adenoidal enlargement, or s. exudate, halitosis, palatal petechiae. iii. LAD: - anterior cervical and posterior cervical - in classic cases, - generalized LAD toward end of wk 1 2. Splenomegaly: develops in 50% of patients in 2nd-3rd wk 3. Hepatomegaly: in 10% of patients 4. Exanthem: nonspecific erythematous, maculopapular, rash in 5- 10% of patients on trunk and proximal extremities, with spread to face and forearms 5. Ampicillin-induced eruption
  39. 39. Infectious Mononucleosis C/P LESS OFTEN PRESENTATIONS: 1. Genital ulcers 2. Gianotti–Crosti syndrome, 3. Urticaria 4. Erythema multiforme, 5. Erythema nodosum
  40. 40. Infectious Mononucleosis Complications 1. Respiratory tract: Pneumonia, upper airway obstruction from tonsillar and adenoidal enlargement. 2. Blood: Hemolytic anemia and thrombocytopenia. 3. Liver: Icteric hepatitis. 4. CNS: Acute cerebellar ataxia, encephalitis, aseptic meningitis, myelitis, Guillain-Barre syndrome. 5. Spleen: splenic rupture.
  41. 41. Infectious Mononucleosis Dx 1. Lymphocytosis: classic finding (50% or more)/ 10% atypical lymphocytes 2. Elevated liver enzymes: 80% or more 3. Monospot test: - detects heterophile antibodies - specific, not as sensitive - 85% of adolescents + and fewer younger patients 4. Specific EBV antibody titers 5. PCR
  42. 42. CYTOMEGALOVIRUS (CMV) /HHV-5
  43. 43. CYTOMEGALOVIRUS (CMV) PRIMARY INFECTION:  Infectious mononucleosis-like syndrome REACTIVATION INFECTION:  Rare in immunocompetent hosts: Clinical presentations are similar to 1ry CMV infections
  44. 44. CYTOMEGALOVIRUS (CMV) C/P Immunocompetent host Immunocompromised hostMONONUCLEOSIS- LIKE SYNDROME CONGENITAL INFECTIONS 1. Maculopapular/ morbilliform eruption 1. ‘Blueberry muffin’ lesions (extramedullary erythropoiesis) 1. Cutaneous vasculitis 2. Petechiae and purpura 2. Petechiae and purpura 2. Maculopapular/morbilliform eruption 3. Ampicillin-induced eruption 3. Vesicles 3. Petechiae and purpura 4. Urticaria 4. Vesicles 5. Erythema nodosum 5. Ulcers 6. Verrucous plaques 7. Nodules and hyperpigmented plaques
  45. 45. I. Immunocompetent hosts: rarely colitis, encephalitis, myocarditis, and anterior uveitis. II. Congenital and neonates: congenital deafness; mental retardation TORCH infections (toxoplasmosis, rubella, cytomegalovirus and herpes virus). III. AIDS patients: blindness. CYTOMEGALOVIRUS (CMV) Complications
  46. 46. CYTOMEGALOVIRUS (CMV) Dx (1) Serologies (e.g. IgM and IgG antibodies). (2) Molecular amplification techniques (e.g. PCR); (3) Cultures (helpful to determine if drug resistance is present). (4) CMV antigenemia assays (helpful in immunosuppressed hosts). (5) Biopsy of cutaneous lesions (e.g. ulcerations) may show characteristic findings of enlarged endothelial cells with prominent intranuclear inclusions (‘owl’s eyes’).
  47. 47. CYTOMEGALOVIRUS (CMV) Rx • Uncomplicated CMV infection in immunocompetent hosts: primarily supportive. • Immunocompromised hosts or in those with complicated infections: systemic therapy 1. Ganciclovir Intravenous, 2. Valganciclovir Oral, 3. Cidofovir, 4. Foscarnet. • Prevention: is possible by matching CMV serologies between donor and transplant recipients.
  48. 48. HUMAN HERPESVIRUS 6 AND 7 (HHV-6 AND HHV-7)
  49. 49. Human Herpesvirus 6 PRIMARY INFECTION:  Exanthem subitum (roseola, sixth disease)  Febrile syndrome without a cutaneous eruption  Mononucleosis-like syndrome in adults REACTIVATION INFECTION:  Possibly pityriasis rosea  DRESS  Immunocompetent hosts: Fever, cutaneous eruption, hepatitis, pneumonitis, BM suppression, encephalitis, colitis
  50. 50. Exanthem subitum (Roseola infantum, Sixth disease) • 3–5 days of high fever followed by cutaneous eruption as fever fades • Discrete circular ‘rose red,’ 2- to 5-mm macules or maculopapules, often surrounded by a white halo • Enanthem of red papules on soft palate (Nagayama’s spots)
  51. 51. Human Herpesvirus 7 PRIMARY INFECTION:  Usually asymptomatic  Exanthem subitum (roseola, sixth disease) but is less common than HHV-6 REACTIVATION INFECTION:  Possibly pityriasis rosea  DRESS
  52. 52. HUMAN HERPESVIRUS 8 (HHV-8) /KSHV
  53. 53. HUMAN HERPESVIRUS 8 PRIMARY INFECTION:  Children: Fever and morbilliform eruption  Men who have sex with men (MSM): New-onset lymphadenopathy, fatigue, diarrhea & localized cut. eruption  Immunosuppressed hosts: Fever, splenomegaly, lymphoid hyperplasia, pancytopenia, Occasionally rapid-onset KS REACTIVATION INFECTION:  Kaposi’s Sarcoma (KS)  Primary Effusion Lymphoma/B-cell lymphoma  Multicentric Castleman’s Disease: Lymphoproliferative disorder characterized by fever, hepatosplenomegaly, and massive lymphadenopathy
  54. 54. References • Bolognia 3rd ed. • Bolognia Dermatology Essentials. • http://www.dermnetnz.org • http://en.wikipedia.org • http://emedicine.medscape.com • http://www.ijdvl.com
  55. 55. THANK U

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