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VIRAL DISEASES AND SCABIES

VIRAL DISEASES AND SCABIES. Xiaoyan Lyu Department of Dermatology West China Hospital, Sichuan University. Outlines. viral diseases Scabies. Viral Diseases. Herpes Simplex. Synonyms/clinical variants Herpes – herpes simplex

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VIRAL DISEASES AND SCABIES

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  1. VIRAL DISEASES AND SCABIES XiaoyanLyu Department of Dermatology West China Hospital, Sichuan University

  2. Outlines • viral diseases • Scabies

  3. Viral Diseases

  4. Herpes Simplex

  5. Synonyms/clinical variants • Herpes – herpes simplex • Cold sore，fever blister, herpes febrilis, herpes

  6. Definition • a viral dermatosis caused by Herpes simplex virus (HSV)infection • characterized by painful grouped vesicles on the skin and mucous membranes . • Self-limiting ,but recur frequently

  7. Common • One-third of the world’s population has experienced a symptomatic HSV infection

  8. History • Antiquity: Herpetic lesions, Hippocrates and Galen. • 1968 Nahmias and Dowdle HSV-1 was more frequently associated with orolabial HSV-2 with genital infections1

  9. Etiology Pathogen-HSV • alpha subfamily of the Human herpes virus(HHV) • Double-stranded DNA virus affects human only • Sub-classified as HSV-1 & HSV-2

  10. Pathogenesis There are three basic conditions of Infectious diseases： • infection source • transmission route • susceptible population

  11. Pathogenesis HSV-1 • In children ≤10 years of age, most herpetic infections are caused by HSV-1 (>80–90%). • 50–90% of individuals 20 to 40 years old: have HSV-1 antibodies

  12. Pathogenesis HSV-2 is spread primarily by sexual contact • HSV-2 remains the cause of most genital herpes infections (70–90% overall)

  13. Question The herpesvirus infections follows the sequence of primary infection, latency and reactivation. How? What route does HSV take after it enters the body? Where the virus is hiding? What can activate the virus?

  14. Pathogenesis HSV Skin & mucosa Subclinical--asymptmatic Clinical signs retrograde axonal Primary infection reactivation Dorsal root ganglia Latency Remain for life Sunburn,emtional stress depression of immunity 30~50% of cases Less severity Recurrent infection Skin & mucosa

  15. Clinical Manifestations HSV infections have a wide range of clinical presentations Primary infection • Subclinical infections • Herpes gingivostomatitis • Neonatal HSV infection • Kaposi’s varicelliformeruption (Eczema herpeticum) Recurrence Infection 1. Recurrence orolabialHerpes Simplex 2. Cutaneous Herpes Simplex

  16. Clinical Manifestations Primary infection • First HSV infection without pre-existing antibodies to HSV-1 or HSV-2 May be symptomatic or asymptomatic

  17. Primary Infection-Clinical Features 1.Subclinical infections • 90% asymptomatic

  18. Primary Infection-Clinical Features 2. Herpes gingivostomatitis • Most frequently in young children of 1-5 years old • The incubation period is 3 to 12 days. • Prodromal symptoms At the site of inoculation tenderness, pain, mild paresthesias, or burning Systemic symptoms localized pain, tender lymphadenopathy, headache, generalized aching, fever

  19. Primary Infection-Clinical Features 2. Herpes gingivostomatitis • Typical lesions: painful grouped vesicles on an erythematous base on the lips, gingiva, plate, tongue • Mild~severe, Edema and painful oropharyngeal ulcerations can lead to dysphagia and drooling • Course: 1 to 3 weeks

  20. The evolution of lesions Vesicles appear on a red base The center becomes depressed (umbilicated) Crusts form and the lesions heal with or without scarring

  21. Primary Infection-Clinical Features 3. Neonatal HSV infection • 70% are caused by HSV-2 • The infection often appears within the first week of life • Varying degrees of severity

  22. Primary Infection-Clinical Features 4.Kaposi’s varicelliform eruption (Eczema herpeticum) • A HSV-1 infection which can develop in patients with current eczema, atopic dermatitis, burns, or other inflammatory. • Most often in infants/children • Hundreds of umbilicated vesicles; Monomorphic, discrete, 2–3 mm punched-out erosions with hemorrhagic crusts are evident more often than intact vesicles • May have fevers, malaise and lymphadenopathy

  23. Recurrence Infection-Clinical Features • A similar prodrome • lesions fewer in number • decreased severity and duration (1-2weeks)

  24. Stimulus: fever, upper respiratory infections and exposure to ultraviolet • Prodrome: ＜24h, pain, burning, and tingling • Grouped blisters on an erythematous base • Lips, face • Course: 5-7d. 1.Recurrence orolabial Herpes Simplex

  25. Recurrence Infection-Clinical Features 2. Cutaneous Herpes Simplex Herpes simplex may appear on any skin surface .

  26. Recurrence Infection-Clinical Features Frequency of recurrence: • average 2-3 outbreaks annually • varies with anatomic site and virus type. • HSV-1 oral infections recur more often than HSV-2 infections.

  27. Diagnosis • Viral culture: requires 2–5 days • DFA(direct fluorescent antibody assays ) greater sensitivity, ability to distinguish between HSV and VZV, and rapid turnaround time • PCR a rapid, sensitive and specific method to detect HSV DNA in specimens from the skin and other organs. • Serologic assays the mean time to seroconversion following initial infection is 3–4 weeks

  28. DifferentialDiagnosis • Herpes zoster • Impetigo • Fixed drug eruption

  29. Treatment 1. Systemic therapy

  30. Treatment 2. Topical therapy

  31. VericellaHerpes Zoster

  32. Background • Varicella and herpes zoster are two distinct clinical entities caused by the same varicella-zoster virus(VZV) • Varicella(chickenpox) is the primary infection of VZV, characterized by widespread umbilicated vesicles accompanied by fever. • Herpes zoster(shingles). is the manifestation of the reactivation of a latent VZV infection, characterized by grouped vesicles unilaterally distributed along a peripheral nerve with intense neuralgia.

  33. Aetiology & Pathogenesis varicella-zoster virus(VZV) • HHV-3, is the third member of alpha subfamily of human herpes virus. • It is morphologically identical to herpes simplex virus • Affects human only

  34. Vericella-Clinical features • Often occurs in winter and spring • Children between 2 and 10 years • Highly contagious. • The affected individual is infectious from1 to 2 days before skin lesions appear until all of the vesicles havecrusted.

  35. Vericella-Clinical features • Incubation period: 2-3weeks • Prodrome: fever, headache, sore throat, malaise • Typical lesions: Pruritic erythematous macules and papules clear vesicles surrounded by narrow red halos(dew drops on a rose petal) pustules and crusts and heal The presence of lesions in all stages of development is a hallmark of varicella

  36. Vericella-Clinical features • Site: Scalp、face、truck 、extremities、 oral mucosa Number of vesicles ：a few to several hundred • Course：2-3 weeks

  37. VericellaDiagnosis&Differential Diagnosis Diagnosis 1.Distinctive features: • Seasonal prevalence, predilection for children, typical umbilicated vesicles 2.Lab: DFA, PCR Differentiation impetigo

  38. Vericella Treatment • Vaccinatingsusceptible • Isolating infected individuals • Rest & Symptomatic treatment: Topical use of calamine lotion. Oral antihistamines • Antiviral treatment: Acyclovir: 20 mg/kg (800 mg max) po qid×5-10 days

  39. Herpes Zoster Clinical features • Frequency: Prevalent worldwide • Pathogen: varicella zoster virus(VZV) a cutaneous viral infection generally involving the skin of a single dermatome

  40. Dermatome an area of the skin supplied by nerve fibers originating from a single dorsal nerve

  41. Clinical features Prodrome: painand tenderness localized to areas of one or more dermatomes, fever, headache, malaise.

  42. Clinical features • Skin lesions: red papules vesicular pustular closely grouped unilateral distribution in band • Dermatomes infected: thoracic (53%), cervical (20%), trigeminal (15%), lumbosacral (11%)

  43. Clinical Features • Pain: Constant, monotonous, burning or deep aching pain; Shooting, lancination pain; Triggered pain • Local lymph nodes: enlarged and tender • Course: 2-4weeks

  44. Ramsay-Hunt syndrome When the VZV spreads to the geniculate ganglion, the facial and acoustic nerves may be involved, resulting in otalgia, herpetiform vesicles on the external ear canal, and facial paralysis.

  45. Diagnosis&Differential Diagnosis Diagnosis 1.Distinctive features: • Unilateral, grouped vesicles, in band distribution • Pain and tenderness localized to areas of one or more dorsal roots 2.Lab: DFA, PCR Differentiated from Herpes Simplex

  46. Treatment • Rest & Symptomatic treatment: Topical anesthetics Antalgic drugs: amitriptyline 25~75mg Q.n • Antiviral treatment: Aciclovir: 20 mg/kg (800 mg max) po qid×5-10 days Valaciclovir: 20 mg/kg (1 g max) po tid × 5 days

  47. Prognosis • Resolves without sequelae in individuals with intact immune systems. • Postherpetic neuralgia Dysestheticpain (e.g. a burning or stabbing sensation, allodynia) that persists after the skin lesions have healed. This affects 10–20% of all herpes zoster patients and increases in both incidence and severity with age. Last for months or years. tricyclic antidepressants, gabapentin

  48. Molluscum Contagiosum

  49. Molluscum Contagiosum (MC) MC is a contagious dermatosis caused by the Molluscum contagiosum virus(MCV)

  50. Background • Pathogen Molluscumcontagiosum virus(MCV)--poxvirus • Frequency:prevalent worldwide • Age: young children , sexually active adults, immunocompromised persons

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