Herpetic skin infections


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Herpetic skin infections

  1. 1. Herpes simplex &Herpes ZosterBy .Prof.EISHA ABDEL MONIEM
  2. 2. *Human herpes virus includes:1.Herpes simplex virus type 1.2.Herpes simplex virus type 2.3.Varicella Zoster virus4.Epestien – Bar virus.5.Cytomegalovirus.6.HHV 6,7,8
  3. 3.  They are DNA viruses characterizedby tendency to produce : Primary infection----Latency ( neuronsor lymphoid tissue). ----Reactivation(recurrence) It replicate intranuclear ,and oncepatient become infected ,infectionremain for life.
  5. 5. It is the commonest virusinfection of the skin all overthe world.
  6. 6.
  7. 7. Type – 1 HSV1: Found mainly inlesions of the lips ,mouth ,face and nongenital areas(70-90%) ,may also causegenital lesions.Type – 2 HSV2: Found mainly in thegenital lesions (70-90%) ,can also induceoral lesions.
  8. 8. Transmission HSV spread by direct contact, asthe virus is shed in saliva, tears andgenital secretions. Infection results from a kiss given to achild or adult from a person shedding thevirus. The only way to contract HSV 2 is throughdirect sexual contact with an infectedindividual.[
  9. 9. Pathogenesis[ HSV travels through tiny breaks inthe skin or mucous membranes in themouth or genital areas. Evenmicroscopic abrasions on mucousmembranes are sufficient to allow viralentry.
  10. 10. PathogenesisVirus will replicate at the site of infectioninducing primary lesion ,travel byretrograde axonal flow to the dorsal rootganglion, and establish latency (virus existsin a non infectious state) until reactivationwhere the virus particles descend viaperipheral nerves to the skin and inducesrecurrent lesions.
  11. 11. CLINICAL FORMS1.Primary Infection2.Recurrent Infection
  12. 12. 1.The primary infection:-occurs in infants and children who have noimmunity.-Asymptomatic infection(subclinical) is the rule( 90%).-Symptomatic primary infection (clinical)(10%)occur after 3-7 days of exposure usually showsevere clinical picture with prodrome of fever,malais, anorexia and painful tenderlympadenopathy, and cutaneous lesions. Resolutionof symptoms occurs within2-6 weeks.
  13. 13. Morphology of the primary lesionPainful vesicles sometimesumblicated on an erythematous base,that is followed by progression topustules and erosion . Grouped andscattered vesicles typically develop.Crusting of lesions and resolutionoccur within 2 to 6 weeks.
  14. 14. Primary Herpes Simplexclinical types.1. Primary gingivostomatitis (Commonest type).2. Herpetic keratoconjuctivities3. Herpetic whitlow.4. Primary genital herpes.5. Kaposi variclliform eruption.6. Herpes Encephalitis7. Neonatal herpes
  15. 15. • Primary Herpetic gingivostomatitis: .Most cases occur in children between 1-5 years ofage. After an incubation period of 5 days, thestomatitis begins with fever, malaise, restlessnessand excessive dribbling. Drinking and eating arevery painful and the breath is foul. The gums areswollen, inflamed and bleed easily,vesicles on mmthat give white membrane covering erosions on thetongue and oral mucosa. The regional lymph nodesare enlarged and tender. The fever subsides after 3-5days and recovery is usually complete in 2 weeks.
  16. 16. • Keratoconjunctivitis: Primaryherpes infection of the eye causes asevere and often purulentconjunctivitis with superficialulceration of the cornea. The eyelidsare grossly oedematous and there maybe vesicles on the surrounding skin.
  17. 17. Herpetic whitlowA herpetic whitlow is an infection of the herpes virusaround the fingernail. In children, this is often causedby thumbsucking . It is seen in adult healthcareworkers such as dentists because of increasedexposure to the herpes virus. The use of rubber glovesprevents herpes whitlow in healthcare workers
  18. 18. Kaposi varicelliform eruption(Eczema herpeticum( Infants or children with atopic eczemacan develop a potentially fatal HSVinfection in the area of skin that has theeczema .Therefore, people with atopiceczema should avoid being nearanyone with an active herpes infection.
  19. 19. Primary Genital Herpes The Primary genital HSV infection(genital herpes) can be severe andprolonged, with multiple painfulblisters and ulcers in the genital area.Fever and malaise are common, andsome people have burning duringurination, difficulty or pain duringdefecation. HSV2 more than HSV1
  20. 20. Recurrent Herpes Simplex
  21. 21.
  22. 22. RECURRENT HERPES SIMPLEX-Occurs in individuals who have specificantibodies and exposed to activating factors.- Recurrent infections differ from primaryherpes simplex in the smaller size of thevesicles, their grouping, absence ofconstitutional symptoms - usually mild andheals within 7 days
  23. 23. Activating Factors*Spontaneously.*Appropriate stimulus:-Stress and psychic factors-Ultraviolet light.-Fever.-Common cold ,infuenza and otherupper respiratory tract infection.
  24. 24.  * Gastrointestinal disturbance as dyspepsiaand diarrhea. * Tooth extraction and trauma to lips. * immunosuppression * Menestruation*Genital herpes: Trauma of coitus Stress Fatigue.
  25. 25. Recurrent Herpes simplex1.Recurrent herpes libialisCold sore2.Recurrent genital herpes
  26. 26. Recurrent herpes libialisCold sore.Develops on the lips. Starts bytingling sensation , followed byredness and swelling. Usually, fluid-filled blisters form on the erythematousbase and break ,open and leavingsores. The sores quickly form a scab.After about a week, the scab falls offand the episode ends..
  27. 27.
  28. 28. Recurrent Genital HerpesSimplexBurning sensation in the genitalia, buttocks, and thighs Small blisters or open sores on genitals or inner thighs; inwomen, often occur inside the vagina May be painful or not In women, vaginal discharge Fever, muscle aches Headache Painful urination Swollen lymph glands in the groin
  29. 29. If a patient is diagnosed with genitalherpes, testes for other sexuallytransmitted diseases such asChlamydia and gonorrhea should beperformed.
  30. 30. PatologyEpidermisIntraepidermal supra basal vesicle produced byBalooning degenerationReticular degenerationof epidermal cells that show intarnuclear eosinophilicinclusion bodies and multinucleated giant cells (2-15 nuclei)due tofusion of cellsDermiscellular infiltration (neutrophils)vasculities
  31. 31. Prognosis. Usually the number of outbreaks isgreatest in the first year and higher forHSV-2 genital lesions than HSV-1 coldsores. Each year after that, the numberof outbreaks usually goes down andthey become less severe
  32. 32. Complications Herpetic keratitis –scarring within the cornea andpossible blindness Secondary infection Persistent herpes infection, with so close attacks. Encephalitis and/or meningitis. Lung infection.
  33. 33. Special Populations Newborns – herpes infections contracted during delivery fromthe mother can lead to meningitis, herpes infection in theblood, skin infection, and may even be fatalWhen the immune system is suppressed:HIVChemotherapy for cancer Long term use of high doses of corticosteroids
  34. 34. Differential diagnosisHerpes ZosterThrush stomatitisImpetigo contagiosumAcute eczemaErythema multiformis
  35. 35. D.D of genital herpesFolliculitisChancroidgenital soresBehcet’s disease
  36. 36. Diagnosis Tzanc smear: to detect giant cells by openingfresh vesicle and scrape its base.The most rapiddiagnosis is by detection of viral antigen byimmunofluorescence in scrapings from lesions orthe virus seen by electron microscopy in vesiclefluid. Diagnosis by culture of the virus from vesiclefluid requires only 1– 5 days. The detection of HSVDNA in the cerebrospinal fluid( Lumber puncture)
  37. 37. TreatmentAntiviral therapy: . In primaryinfection or troublesome recurrentherpes simplex, antiviral therapy isindicated. Acyclovir interferes with theaction of DNA polymerase. Acyclovir isof proven clinical value against herpessimplex and varicella zoster virus.
  38. 38. Valacyclovir and famcyclovir arechemically related to acyclovir andhave the same mechanism of action
  39. 39. .The usual oral dose ofAcyclovir: is 200mg five times daily .for 5 or more days.Valacyclovir: 500mg three times dailyfor 5 daysFamicyclivir: 125 mg three times dailyfor 5 days.
  40. 40.  Antiviral cream, applied every 2hours during the attack can shortenthe healing time and duration ofsymptoms of a cold sore .
  41. 41.  Severe HSV infections, includingherpes encephalitis and infections innewborns, are treated withintravenous acyclovir. .
  42. 42.  Prophilaxis: Preventing HSV infection is difficult becausepeople can spread the virus even when they dont have any symptomsof an active outbreak. Avoiding direct contact with an open lesion will lower the risk ofinfection. People with genital herpes should avoid sexual contact when theyhave active lesions, the use of condoms, may lower the risk ofinfection. People with active HSV lesions should also avoid contact withnewborns, children with eczema, or people with suppressed immunesystems, because these groups are at higher risk for more severedisease. To decrease the risk of infecting newborns, a cesarean delivery (C-section) is recommended for pregnant women who have an activeHSV infection at the time of delivery.
  43. 43. Varicella (chickenpox) andzoster (shingles)
  44. 44. Aetiology Varicella and Herpes zoster are caused bythe same virus, herpes virus varicellaeor varicella zoster virus (VZV).Varicellais the primary infection , after which thevirus persists in nerve ganglion cells,usually sensory.Herpes Zoster is the resultof reactivation of this residual latent virus
  45. 45. Epidemiology Primary varicella is an endemic disease. Varicella isone of the classic diseases of childhood, with the highestprevalence occurring in the 4 - 10 years old age group. Varicella is highly communicable, with an attack rateof 90% in close contacts. Most people become infected before adulthood but10% of young adults remain susceptible. Herpes zoster, in contrast, occurs sporadically andevenly throughout the year.
  46. 46. TransimissionVaricella is transmitted by dropletinfection from the nasopharynx and dryscales are not infectious. Patients areinfectious to others from 2 days beforeto 5 days after the onset of the rash.Sub clinical infections may occur2..rash…..5--------------
  47. 47. Zoster patients are infectious, from virusin the lesions and, in some instances, thenasopharynx. Chickenpox occurs insusceptible contacts of zoster patients.
  48. 48. Chicken poxVaricella
  49. 49. Clinical features Incubation period of 14-21 days. : After 1-2 days of fever, development of small red papulestakes place which very rapidly become tense clear vesiclesthat may turn to pustules, they are surrounded by red areolae.In 2-4 days a dry crust forms and soon separate, to leave ashallow pink depression which heals without scarring.theselesions are associated with pruritis that may be tense. The vesicles appear in 3-5 crops over 2-4 days. They are mostnumerous on the trunk, then on the face, scalp and limbs. Theirdistribution is centripetal. A characteristic feature is thepresence of lesions at different stages in each site. Lesions arecommon inside the mouth.
  50. 50. Complication Most common complication is secondarybacterial infection of the vesicles. Severe complications which may be lifethreatening include viral pneumonia,encephalititis, and haemorrhagicchickenpox.
  51. 51. Herpes Zoster (Shingles(
  52. 52. Herpes Zoster (Shingles( Herpes Zoster mainly affect a single dermatome of theskin. It may occur at any age but the vast majority ofpatients are more than 50 years of age. The latent virus reactivates in a sensory ganglion andtracks down the sensory nerve to the appropriatesegment Herpes zoster affecting the eye and face may causegreat problems
  53. 53. Triggering factors1.Old age2.Trauma to vertb. Column as fracture spine anddisc prolapse.3.Lymphoma and neoplasm4.Antimitotic drugs.5.X-ray therapy.6.Diabetes.7.Infection.8.Disturbed immunity.
  54. 54. CLINICAL FEATURESSymptomsPain usually precedes, associatesor follows the eruptions .It ranges frommild burning to severe agonizing pain.It may be accompanied by fever,headache, malaise, and tendernesslocalized to areas on one or moredermatom.
  55. 55. Morphology of the lesionThe disease is characterized by suddenappearance of group of vesicles onerythematous base on lineardistribution occuring along thecourse of the affected nerve ornerves,lesions are unilateral..The early lesioncontains a clear serum but after few daysbecome purulent,the wall ruptures and crustforms.
  56. 56.  The pain subsides gradually as theeruption disappears. Recovery iscomplete in 2-4 weeks . Occasionally,the pain is not followed by the eruption(zoster sine eruption).
  57. 57. Clinical TypesLocalization1.Herpes zoster pectoralis (50%)---Inter costal nerves.2.Herpes zoster cranialis ----Trigeminal nerve(15%)a. HZ frontalis ----supraorbital nerveb. HZ Ophtalmicus---eye affected ,vesicles at the side of thenose,conjunctiva red and inflammed,superficial or deep keratitis.c. HZ of the maxillary division—vesicles in the uvula andtonsilar aread.Hz of the mandibular division---vesicles on the posteriorpart of the tongue ,the floor of the mouth and the buccal mm.
  58. 58. e. Ramsy –Hunt syndrome----geniculate ganglion,pain in theear,nausea vomiting nystagmus and lossof hearing, and vesicles on the pinna ofthe ear. Facial palsy is a frequentcomplication.
  59. 59. 3.HZ cervicalis (10%) -----cervical nerves.4.HZ abdominalis ---abdominal nerves.5.Lumbosacral variety (10%):Sacralis-----urinary bladder symptomsdysuria,frequency and even retention ofurine may occur.Femoralis----femoral nerve
  60. 60. Morphological classification1.Abortive type.2.Hemorrhagic type.3.Gangrenous ,necrotic type.4.Generalized or disseminated type.5.Bilateral type
  61. 61. Complications1.Secondary bacterial infection.2.Eczematization.3.Post herpetic neuralgia4.Ocular complications as keratiti,ophthalmitis and blindness.5.Gangrene formation.6.Telengiectasia and skin atrophy.7.Neuralgic complication :menegities ,encephalitis and facialpolsy.8.Urinary complication : cystitis and or urinary retension.
  62. 62. Differential diagnosis1.Herpes simplex.2.Acute eczema.3.Impetigo contagusum.4.Erythema multiformis.
  63. 63. Prevention Preventive measures should be consideredfor individuals at risk of contracting severevaricella infection e.g. leukaemic children,neonates, and pregnant women Where urgent protection is needed, passiveimmunization should be given. Zosterimmunoglobulin (ZIG) is the preparation ofchoice but it is very expensive. A live attenuated vaccine is available .
  64. 64. TreatmentGeneral:Analgesics ,tegretol andvitamineB12Local:Drying agent as gentian violet 1%acyclovir cream 5%.local antibiotic as Na fucidate.
  65. 65. Varicella Vaccineusually is given between the ages of 12 to15 months. The Centers for DiseaseControl and Prevention (CDC) alsorecommends a booster shot at 4 to 6years old for further protection. The CDCalso recommends that people 13 years ofage and older who have never hadchickenpox or received the chickenpoxvaccine get two doses of the vaccine.
  66. 66. Antiviral therapyAcyclovir 400 5 times daily for 7 d. Famcyclovir250mg 3 times daily for 7 d. Valcyclovir 1000 mg 3times daily fo 7 days. Such treatment preventsprogression of the eruption, reduces the systemiccomplications of varicella and zoster, lessens zosterpain during treatment, reduces the risk ofdevelopment of post-herpetic neuralgia and if itdevelops, it decreases its duration. Ophthalmiczoster is treated by antiviral therapy together withophthalmologic supervision.
  67. 67. For post-herpetic neuralgia a tricyclicanti-depressant is useful.