• A 30-year-old male, presented to the Dermatology
OPD with :
Umbilicated pearly white elevated lesions over face
since 01 month
Diagnosis??
Causative organism ??
M/m ??
Viral Infections……DR 8.1, 8..7
Department of Dermatology
GMCH, Sundargarh
Chapter 4
CONTENTS
 Classification
 Etiopathogenesis
 Molluscum contagiosum
 Human papilloma virus infection
 Herpes simplex infection
 Herpes zoster infection
 Epstein Barr virus infection
 Other herpes infection
 Viral exanthem
 Uncommon viral infection of skin
Classification of virus
DNA VIRUS
 Enveloped (double stranded)
• Herpesviridae
• Hepadnaviridae
 Non-enveloped (double stranded)
• Papillomaviridae
• Polyomaviridae
• Adenoviridae
 Single stranded (non-enveloped)
• Parvoviridae
• Poxviridae
RNA Virus
• Flaviviridae
• Togaviridae
• Retroviridae
• Coronaviridae
• Picornaviridae
• Calciviridae
• Orthomyxoviridae
• Paramyxoviridae
• Rhabdoviridae
• Arenaviridae
• Reoviridae
Etiopathogenesis
 Cell lysis (Herpes)
 Cell proliferation (Pox, HPV)
 Carcinogenesis (Cervical Ca, Hepatoma)
 Exanthemata - Viraemia, Type 3 hypersensitivity (Arthus) reaction, virus
lodged in dermal capillaries and replicate in epidermis.
 Persistent infection: Periods of latency and reactivation (HSV, VZV)
 Molluscum contagiosum virus:
 4 types (MCV 1-4) , Type 1 – M/C
 DNA virus, Poxviridae family.
 Children and sexually active adults.
 Direct skin to skin contact, sexual transmission also
 Incubation period: 2 weeks to 6 months
 Typical lesions: discrete, dome shaped, umbilicated pearly white
papules.
 Pseudo- koebner’s phenomenon
Molluscum Contagiosum
 Agminate Molluscum Contagiosum – Plaque form
 Molluscum dermatitis (localized eczematous dermatitis around lesions in
atopic) – Meyerson’s phenomenon
 D/D: Cryptococcosis, Histoplasmosis, Penicillinosis
 Histopathology- Henderson-Paterson bodies (molluscum bodies)-
Intracytoplasmic eosinophilic inclusion
 Treatment:
 Self limiting with in 6-9 months
 1st
line : Phenol or TCA , 10 % KOH, Salicylic acid, Topical retinoids
 2nd
line: Needle Enucleation, Cryotherapy
 Systemic : Levamisole, Cimetidine.
 > 100 types of HPV
 Genome of HPV:
 Early genes (E1-E7) : DNA replications, transformation and translations
 Late genes (L1-L2) : codes structural proteins
 Transmission :
 Direct or indirect contact (nail biters, shaving, occupational, swimming
pool)
 Sexual transmission : genital / perianal wart
 Autoinoculation
Human Papilloma Virus
 Non genital :
• Verruca vulgaris (Common warts)
• Verruca Plana (Plane warts)
• Filiform/ Digitate
• Palmoplantar
• Periungual
 Genital :
• Condyloma Acuminata
Clinical Types
 HPV types- 1,2,4,27 and 57
 Young children and adults.
 Meat butchers, frequent
immersion of hand in water are
risk factors
 Papules or plaques with
verrucous surface.
 Commonest site:
 Hands (Fingers and palms)
 Warts do not have
dermatoglyphics
Common Wart/Verruca vulgaris
 HPV types- 3,10, 28 and 41
 Risk factors:
 sun exposure, swimmers
 Common sites:
 Face, lower legs
 Few milimetres brown or skin
coloured flat topped papules
 Pseudo-Koebnerisation seen
Verruca Plana
 HPV types- 1, 2, 4, 27
 Seen at pressure points
 On paring :
 multiple small black points (dilated
capillary loops)
 Type :
 Mosaic type: painless superficial (HPV-2)
 Myrmecia type: painful deep (HPV-1)
 Differentiate from corn and callosity
Palmo-Plantar warts
 Filiform and digitate warts
• Finger like projection
 Periungual warts
• Seen in nail biters
• Recalcitrant to treatment
Epidermodysplasia verruciformis
• Rare, generalized, persistent inherited
disorders that predisposes children to
widespread HPV infections &
malignancies.
• HPV -5 & 8 – most commonly isolated
• Widespread & persistent skin lesions –
photoexposed sites
• Face & neck – resemble planar warts
• Trunk & limbs – resemble pityriasis
versicolor/seborrheic keratoses.
• Donot resolve spontaneously, recur with
treatment
• Risk of malignant changes - high
 Low risk: HPV types-6 and 11
 High risk : HPV types-16 and 18
 Condyloma acuminata:
• Lobulated papules usually multifocal,
cauliflower like mass may be seen in
moist occluded areas
• Sites- intraurethral in men, mucosal
surface of cervix or vulva, perianal
skin, vulva
• Enhanced visualization by Aceto-
whitening for cervical lesions
Genital Warts
 Giant Condyloma acuminata (Buschke Lowenstein tumor)
• Large exophytic cauliflower like masses
• Well differentiated SCC with only local invasion
• Mutant variant of HPV 6 & 11
 Bowenoid paulosis
• Hyperpigmented papules or flat surface
• HPV types-16,18
• Sites- Penis, Perianal area, vulva
 Diagnosis
• Clinically
• Histopathology- Koilocytosis , Papillomatosis , Acanthosis
• DNA hybridisation, Immunohistochemistry
Histopathology :
Based on type of administration
• Patient administered
Imiquimod 5% cream
Podofilox 0.5% solution
or gel
Sinecatechins 15%
ointment
• Physician administered
Cryotherapy
Podophyllin resin 10-25%
(Not recommended for
pregnant women)
Trichloroacetic acid 80-90%
Surgical removal
• Not recommended generally:
IFNs
5-fluorouracil
Treatment:
Podophyllotoxin (Podofilox)
• Purified extract of the Podophyllum plant
• MOA:
 Binds to cellular microtubules---- inhibits mitotic division at
metaphase
• Dose & Dosage:
 The 0.5% solution or 0.15% cream is applied with a cotton
swab or finger, respectively, over the condylomata (also on
normal appearing skin between the lesions) twice daily for
three days-----followed by four days of no therapy. Similar
three cycles repeated.
• Applications are limited to less than 0.5 ml or 10 cm2 per
treatment session
• The initial application is by the physician to demonstrate proper
application and subsequently by the patients themselves.
Imiquimod
• Imiquimod (imidazoquinolinamine) is a nucleoside-like
compound acts as an immune response modifier
• Induce local production of cytokines including interferon
gamma and tumor necrosis factor alpha
• Has no direct antiviral activity
• Imiquimod cream (5%) is usually supplied in single use
sachets.
• It is applied to the warts with the fingers three times per
week (every other night) ------- the area washed with mild
soap and water the next morning.
• Treatment is continued until wart clearance or for a
maximum of 16 weeks
Podophyllin
• It is a complex resin of podophyllotoxin, alpha peltatum and
beta peltatum
• Podophyllin inhibits mitosis at metaphase
• Dosage: Concentration of 10%–25% dissolved in tincture of
benzoin .
• The surrounding skin is protected with Vaseline, Then it is
applied to the warts by a physician using a cotton tipped swab.
• 1 to 4 hour after application, it is completely washed off.
• Dose : once or twice a week for up to six weeks.
• Applications are limited to less than 0.5 ml or 10 cm2 per
treatment session.
• It is contraindicated in pregnancy as it can lead to fetal death
and abortions
3 types of vaccine :
 Bivalent (16,18)- Cervarix
 Quadrivalent (6,11,16,18)- Gardasil:
9 to 26 years-Male and female
100% effective
Protection at least 5 years
0,2,6 month ; i.m
 Nonavalent (6,11,16,18, 31,33,45,52,58) – Gardasil 9
Male and female - 9 to 26 years
(2 dose schedule-9 to 14 years, 3 dose schedule-15 to 26
years)
Prevention:
 Human Herpes virus 1 (Herpes simplex virus 1 (HSV 1))
 Human Herpes virus 2 (Herpes simplex virus 2 (HSV 2))
 Human Herpes virus 3 (Varicella-Zoster virus (VZV))
 Human Herpes virus 4 (Epstein Barr virus (EBV))
 Human Herpes virus 5 (Cytomegalovirus (CMV))
 Human Herpes virus 6 (HHV 6)
 Human Herpes virus 7 (HHV 7)
 Human Herpes virus 8
( Kaposi’s sarcoma associated Herpes Virus (KSV)(HHV 8))
Human Herpes Virus
 Herpes Simplex Virus I :
 Herpes labialis
 Herpetic gingivostomatitis
 Herpetic whitlow
 Herpetic gladiatorum
 Herpes sycosis
Herpes Virus
 Herpes Simplex Virus II :
 Herpes progenitalis
 Herpetic vulvovaginitis
 Complicated :
 Eczema herpeticum
 Disseminated HSV
 Herpes Simplex Virus in HIV :
 Chronic, recurrent, ulcer,
eschar formation and
dissemination
 Primarily involve skin and mucous surfaces
 Can be disseminated in neonates and immunocompromised hosts
 HSV-1 : >90% of primary infections caused by HSV-1 are subclinical;
more common
 HSV-2- usually the genital pathogen and usual pathogen of neonatal
herpes
 Clinical infections type:
 Primary first episode
 Non-primary first episode
 Recurrent episode
 Asymptomatic infections
Herpes simplex infections
 Fever blisters, cold sore
 Triggers : Fever, UVB, Surgery
 95 % HSV – 1
 Presentation :
 Grouped painful vesicles on an
erythematous base.
 Often prodrome of tingling or
itching, flu like symptoms
 Variable severity of recurrent
lesions.
Orolabial Herpes
Herpetic Gingivostomatitis
• High fever, irritability, anorexia, mouth pain, drooling
• Gingivae becomes intensely erythematous, edematous, friable and tends to
bleed
• Symptoms last 5-14 days, but virus can be shed for weeks following resolution
 Differential diagnosis:
 Aphthous ulcer, Herpangina, Stevens Johnson Syndrome, Syphilis
 Diagnosis :
 Tzanck smear- multinucleated giant cells
 H/P- Ballooning degeneration → Reticular degeneration
 HSV antibody titre : IgG/IgM
 Immunofluoroscence, PCR-most sensitive
 Herpetic Sycosis
• Shaving after facial herpes induces a slowly spreading folliculitis
of the beard with few isolated vesicles.
 Herpes Gladiatorum – in wrestlers & rugby players
 Herpes associated Erythema Multiforme
 Herpetic whitlow
• Herpetic infection of the fingers.
• Children (thumb sucking)
• Adults : 2/3 cases HSV-2, Children nearly 100% HSV-1
 HSV-2 in majority of cases.
 Skin to Skin contact
 Active lesions are infective
 Asymptomatic shedding ( majority of transmission).
 Prior HSV-1 infection does not protect from HSV-2 infection but may
lessen severity of first outbreak.
 Primary infection:
 Grouped vesicles which appear for 7-14 days.
 Fever, Flu like symptoms, inguinal lymphadenopathy, proctitis if rectal
involvement.
 Recurrent (>6 episodes/ year) lesions with typical prodrome of
burning/itching followed by outbreak which is less severe than the
primary infection healing in 6-10 days.
Genital Herpes
Genital Herpes simplex infection
 Symptomatic
 Topical : Acyclovir, Penciclovir, Cidofovir
 Systemic :
Treatment
Antiviral
Primary
(for 7-10 days)
Recurrence
(for 5 days)
Suppressive
(For 1yr)
Acyclovir 200 mg 5
times / day
400 mg TDS 400 mg BD
Valaciclovir 1 gm BD 500 mg BD 1 gm OD
Famciclovir 250 mg TDS 125 mg BD 250 mg BD
 Extent of initial involvement predicts outcome:
• Localized : rarely fatal
• Disseminated disease fatal
 Presentations in newborns
• Majority present with vesicles.
• Disseminated herpes with CNS involvement may occur without skin
involvement.
• Few cases never have vesicles.
• Treatment: Acyclovir 250 mg/(m)2 q8 hours x7 days
Intrauterine and Neonatal Herpes
 Severe disseminated HSV1
 Multiple crops can appear over 7-10 days (like varicella)
 If area of involvement is large, can be lots of fluid loss and potentially fatal
 Onset of high fever, irritability, and discomfort
 In areas of currently or recently affected skin (for those with atopic
eczema or chronic dermatitis)
 Lesions begin as pustules, then rupture and crust over the course of a
couple of days, sometimes hemorrhagic.
 Risk of secondary bacterial infections
 Treatment : IV Acyclovir
Eczema herpeticum
(Kaposi’s varicelliform eruption)
 Primary VZV infection
 IP= 14-17 days
 Polymorphic lesions begins on face, scalp and
spreads to trunk. (Centripetal)
 Macules → Papules → Vesicles → Pustules
and crust.
 Dewdrop over rose petal appearance
 Infectious 4 days before and 5 days after
exanthem appears.
 Crust formation- not contagious
Varicella (chicken pox)
 Secondary bacterial infection may result in scarring.
 Other complications :
• Pneumonia : neonates and adults (1/400)
• Reyes syndrome: encephalitis, hepatitis with aspirin use.
• Thrombocytopenia
• Purpura Fulminans : DIC with low proteins C and S
 Treatment :
• Acyclovir (800mg 5 times a day for 1week) for severe cases, high
risk individuals and adults (>13 years).
• Acyclovir resistant cases- Foscarnet & Cidofovir
• No Aspirin
• Isolation from immunocompromised person.
 Mother: increased risk for varicella pneumonia.
 Baby :
• Spontaneous abortion (3% by 20 wks), Fetal death, Pre-term labor
• Congenital varicella syndrome :
 Hypoplastic limbs, scars, ocular and CNS disease,
 highest between 12 and 20 weeks.
• Neonatal varicella: if maternal infections 5 days before till 2 days after
delivery .
• Treatment : Acyclovir, VZIG to baby
Varicella in Pregnancy
Varicella Vaccine:
 OKA strain of Live attenuated virus
 Children <12 years : 1st
dose- between 12 and 15months of age
: 2nd
dose- Age of 4-6 years
 Adults : 2 doses given 4-8 week apart
VZIG (VZV specific Ig): Post exposure prophylaxis
 Neonates of mother having varicella 7 days before to 7 days after delivery
 Nonimmune pregnant women exposed to VZV
 Immunocompromised/ Organ transplant recipients/ Taking Oral steroid for 14
days in last 3 months
Prevention
 Reactivation of latent herpes zoster
infection from dorsal root ganglia
• Vesciculo- pustular lesions , often
with crusting
• Typically along a dermatome at
times involving adjacent
dermatomes.
• Preceded by pain, itching
Herpes Zoster/Shingles
 Duration of the lesion: Age of pt (Young = 2-3weeks, Elderly = 5-6 weeks)
 Severity of lesions: level of immunosuppression
 Incidence of H.Z. increases with age (>50 yrs) and immunosuppression
 Heals without scaring in young, scarring in elderly and severe eruptions.
Disseminated Zoster
 >20 vesicles outside dermatome, but not adjacent.
 Elderly or Immunocompromised
 Hemorrhagic/gangrenous lesions with outlying vesicles or bullae.
 Involvement of 5th
cranial nerve,
ophthalmic branch
 Lesion location on tip/side of nose:
‘Hutchinson’s sign’ (Nasocilliary branch)
 Ocular complications
• Uveitis , Keratitis
• Glaucoma, optic neuritis
 Encephalitis
Herpes Zoster Ophthalmicus
 Facial and auditory nerve involvement with inflammation of
geniculate ganglion
 Lesions distributed over external auditory meatus, tympanic
membrane, tonsillar fossa and soft palate.
 Facial paralysis with or without tinnitus, vertigo and deafness
Ramsay Hunt syndrome
 Diagnosis : Tzanck (MNG) , direct fluorescent antibody, culture, PCR.
 Symptomatic treatment
 Antivirals :
Acyclovir 800mg x 5times/day for 1 week (may lessen severity of
symptoms in acute outbreak. May lessen incidence of PHN).
Famciclovir 250-500 mg TDS
Valaciclovir 1gm TDS
Duration : 1week (immunocompetent), 2 weeks (immunosuppressed)
Diagnosis and Treatment
 After 4 weeks of herpes zoster .
 Mechanism : irritable nociceptors, spinal deafferentiation
 Constant burning pain, intermittent stabbing/shooting pain, Allodynia.
 Risk factors : prodromal pain, severe pain during acute phase, greater rash
severity, opthalmic zoster.
Treatment
 Topical : Capsaicin, topical lidocaine.
 Oral : Opoid analgesics, amitryptiline, gabapentin, Pregabalin
 Injectable : lidocaine / steroids (Modified Jaipur block- xylocaine+
bupivacaine+methylprednisolone)
Post Herpetic Neuralgia
Infectious mononucleosis
 Incubation period : 3-7 wk
 Bilateral enlargement of cervical and other lymph glands
 High grade fever, malaise, Pharyngitis ,splenomegaly.
 Ampicillin triggers maculopapular eruption.
 Lab findings :
• TLC = 10,000 to 40,000.
• Abnormal large lymphocytes (Downey cells) are 10% of total
leukocyte count.
• Heterophile antibodies 1:160 of higher
Epstein Barr Virus
 Associated with chronic shedding of EBV in the oral cavity.
 Presentation: Poorly demarcated, corrugated, white plaques
on lateral aspect of tongue.
 Unlike thrush, cannot be removed by scraping.
 HIV / AIDS pt.
 Treatment
• Not required
• Podophyllin and tretinoin are used but lesions recur
Oral Hairy Leukoplakia
 HHV 6A causes multiple sclerosis and HHV 6B causes Exanthem
subitum or Roseola Infantum (sixth disease).
Human Herpes virus 6
Human Herpesvirus 7
 HHV 7 has been associated with febrile illness in children, exanthem
subitum and questionably pityriais rosea.
 HHV 7 infection can reactivate HHV6 from latency.
Human Herpesvirus 8
 Three proliferative diseases are associated with HHV 8:
Kaposi sarcoma, Primary effusion lymphoma and Castelman’s
disease.
Pityriasis Rosea
• Etiology: HHV6> HHV7,
May be drug induced (captopril,
imatinib)
• Herald patch/ mother patch
• Christmas tree or fir tree pattern
( along langers line)
• Collarette of scales
• Hanging curtains sign
• Treatment : self resolving in 4-10 weeks
 Macular :
• Rubella
• EBV (infectious
mononucleosis)
• HHV 6 (roseola)
• HHV 7
 Maculopapular :
• Togavirus
• Measles- Koplik spots
• Human parvovirus B19
(erythema infectiosum)-
Slapped cheek appearance
Viral Exanthems
 Maculopapular - vesicular :
• Coxsackie A (5, 9, 10,16)
• Echovirus (4, 9, 11)
 Maculopapular – petechial :
• Togavirus (Chikungunya)-
Centrofacial
hyperpigmentation/Chik sign
• Bunyavirus haemorrhagic fever
(Lassa)
 Urticarial :
• Coxsackie A9 and Hepatitis B
 Pox Viruses :
• Cowpox, Orf, Milker’s nodule
 Epstein Barr Virus :
• Infectious Mononucleousis, OHL, Gianotti Crosti,
• Lymphomas
 Viral insect-borne and haemorrhagic fevers:
(Toga, Flavi, Arena, Filo, Bunya)
• Chikungunya, Dengue ( White island in sea of red), Kyasanur
Forest Disease, Lassa
 Picorna Viruses :
• Herpangina, hand, foot and mouth disease ( Coxackie A16, Entero
Virus 71).
Uncommon Viral Infections of the Skin
Measles
HFMD Erythema infectiosum
DHF Chikungunya
Sample Questions
1) Discuss the clinical features and management of infections caused by
varicella zoster virus. (6+4)
2) Discuss the different treatment modalities and preventions of
anogenital wart. (10)
3) Write in brief about (5 marks each)
a) Management of genital herpes
b) Molluscum contagiosum
c) Pityriasis rosea
d) Post herpetic neuralgia
 What is the likely diagnosis? (1)
 Name the causative agent. (1)
 Name other disease caused by same
agent due to reactivation of latent
Stage in dorsal root ganglion. (1)
 What will be the findings in Tzank
smear from base of vesicles? (1)
 Write the Drugs, Dosage and duration
for it’s treatment. (1)
A 20 year male presented to Skin OPD with history of fever,
malaise and multiple red blisters since 2 days.
OSCE
A) Caused by HHV3
B) Due to primary VZV infection
C) Ramsay hunt syndrome is its
complication
D) Treated by Acyclovir 400mg TDS
A 16 year girl presented to Skin OPD with history of pain and
multiple red blisters over right side of forehead & nose since 2
days. Which of the following is true regards the condition?
Scenario based MCQ
Q.1) Eosinophilic intracytoplasmic inclusions bodies seen in
molluscum contagiosum is termed as
A. Odland bodies
B. Civate bodies
C. Henderson Peterson bodies
D. Cowdery type A
Q.2) The following diseases are associated with Epstein-Barr virus
infection except :
E. Infectious mononucleosis
F. Bowenoid papulosis
G. Nasopharyngeal carcinoma
H. Oral hairy leukoplakia
MCQ’S
Q.3) Kaposi’s Sarcoma is associated with
A. HHV 6
B. HHV 7
C. HHV 8
D. HHV 3
Q.4) Hanging curtain sign & collarete of scales is seen in
E. Pityriasis versicolor
F. Pityriasis rosea
G. Psoriasis
H. Pityriasis lichenoid chronica
Q.5) Which of the following is not a treatment of anogenital wart?
A. Imiquimod
B. Podophyllin
C. Cryosurgery
D. Aceto-whitening
Q 6) Identify the correct match
E. Christmas tree pattern ----------- Parvo B19
F. Slapped cheek appearance --------HHV6
G. White islands in the sea of red -----------Dengue Virus
H. Centro-facial hyperpigmentation -------- EBV
Thank You!

4 Viral Infection - Copy.pptxf#/{\-%<#_=#^$_^$_

  • 1.
    • A 30-year-oldmale, presented to the Dermatology OPD with : Umbilicated pearly white elevated lesions over face since 01 month Diagnosis?? Causative organism ?? M/m ??
  • 2.
    Viral Infections……DR 8.1,8..7 Department of Dermatology GMCH, Sundargarh Chapter 4
  • 3.
    CONTENTS  Classification  Etiopathogenesis Molluscum contagiosum  Human papilloma virus infection  Herpes simplex infection  Herpes zoster infection  Epstein Barr virus infection  Other herpes infection  Viral exanthem  Uncommon viral infection of skin
  • 4.
    Classification of virus DNAVIRUS  Enveloped (double stranded) • Herpesviridae • Hepadnaviridae  Non-enveloped (double stranded) • Papillomaviridae • Polyomaviridae • Adenoviridae  Single stranded (non-enveloped) • Parvoviridae • Poxviridae RNA Virus • Flaviviridae • Togaviridae • Retroviridae • Coronaviridae • Picornaviridae • Calciviridae • Orthomyxoviridae • Paramyxoviridae • Rhabdoviridae • Arenaviridae • Reoviridae
  • 5.
    Etiopathogenesis  Cell lysis(Herpes)  Cell proliferation (Pox, HPV)  Carcinogenesis (Cervical Ca, Hepatoma)  Exanthemata - Viraemia, Type 3 hypersensitivity (Arthus) reaction, virus lodged in dermal capillaries and replicate in epidermis.  Persistent infection: Periods of latency and reactivation (HSV, VZV)
  • 6.
     Molluscum contagiosumvirus:  4 types (MCV 1-4) , Type 1 – M/C  DNA virus, Poxviridae family.  Children and sexually active adults.  Direct skin to skin contact, sexual transmission also  Incubation period: 2 weeks to 6 months  Typical lesions: discrete, dome shaped, umbilicated pearly white papules.  Pseudo- koebner’s phenomenon Molluscum Contagiosum
  • 7.
     Agminate MolluscumContagiosum – Plaque form  Molluscum dermatitis (localized eczematous dermatitis around lesions in atopic) – Meyerson’s phenomenon  D/D: Cryptococcosis, Histoplasmosis, Penicillinosis  Histopathology- Henderson-Paterson bodies (molluscum bodies)- Intracytoplasmic eosinophilic inclusion  Treatment:  Self limiting with in 6-9 months  1st line : Phenol or TCA , 10 % KOH, Salicylic acid, Topical retinoids  2nd line: Needle Enucleation, Cryotherapy  Systemic : Levamisole, Cimetidine.
  • 9.
     > 100types of HPV  Genome of HPV:  Early genes (E1-E7) : DNA replications, transformation and translations  Late genes (L1-L2) : codes structural proteins  Transmission :  Direct or indirect contact (nail biters, shaving, occupational, swimming pool)  Sexual transmission : genital / perianal wart  Autoinoculation Human Papilloma Virus
  • 10.
     Non genital: • Verruca vulgaris (Common warts) • Verruca Plana (Plane warts) • Filiform/ Digitate • Palmoplantar • Periungual  Genital : • Condyloma Acuminata Clinical Types
  • 11.
     HPV types-1,2,4,27 and 57  Young children and adults.  Meat butchers, frequent immersion of hand in water are risk factors  Papules or plaques with verrucous surface.  Commonest site:  Hands (Fingers and palms)  Warts do not have dermatoglyphics Common Wart/Verruca vulgaris
  • 12.
     HPV types-3,10, 28 and 41  Risk factors:  sun exposure, swimmers  Common sites:  Face, lower legs  Few milimetres brown or skin coloured flat topped papules  Pseudo-Koebnerisation seen Verruca Plana
  • 13.
     HPV types-1, 2, 4, 27  Seen at pressure points  On paring :  multiple small black points (dilated capillary loops)  Type :  Mosaic type: painless superficial (HPV-2)  Myrmecia type: painful deep (HPV-1)  Differentiate from corn and callosity Palmo-Plantar warts
  • 14.
     Filiform anddigitate warts • Finger like projection  Periungual warts • Seen in nail biters • Recalcitrant to treatment
  • 15.
    Epidermodysplasia verruciformis • Rare,generalized, persistent inherited disorders that predisposes children to widespread HPV infections & malignancies. • HPV -5 & 8 – most commonly isolated • Widespread & persistent skin lesions – photoexposed sites • Face & neck – resemble planar warts • Trunk & limbs – resemble pityriasis versicolor/seborrheic keratoses. • Donot resolve spontaneously, recur with treatment • Risk of malignant changes - high
  • 16.
     Low risk:HPV types-6 and 11  High risk : HPV types-16 and 18  Condyloma acuminata: • Lobulated papules usually multifocal, cauliflower like mass may be seen in moist occluded areas • Sites- intraurethral in men, mucosal surface of cervix or vulva, perianal skin, vulva • Enhanced visualization by Aceto- whitening for cervical lesions Genital Warts
  • 17.
     Giant Condylomaacuminata (Buschke Lowenstein tumor) • Large exophytic cauliflower like masses • Well differentiated SCC with only local invasion • Mutant variant of HPV 6 & 11  Bowenoid paulosis • Hyperpigmented papules or flat surface • HPV types-16,18 • Sites- Penis, Perianal area, vulva  Diagnosis • Clinically • Histopathology- Koilocytosis , Papillomatosis , Acanthosis • DNA hybridisation, Immunohistochemistry
  • 18.
  • 19.
    Based on typeof administration • Patient administered Imiquimod 5% cream Podofilox 0.5% solution or gel Sinecatechins 15% ointment • Physician administered Cryotherapy Podophyllin resin 10-25% (Not recommended for pregnant women) Trichloroacetic acid 80-90% Surgical removal • Not recommended generally: IFNs 5-fluorouracil Treatment:
  • 20.
    Podophyllotoxin (Podofilox) • Purifiedextract of the Podophyllum plant • MOA:  Binds to cellular microtubules---- inhibits mitotic division at metaphase • Dose & Dosage:  The 0.5% solution or 0.15% cream is applied with a cotton swab or finger, respectively, over the condylomata (also on normal appearing skin between the lesions) twice daily for three days-----followed by four days of no therapy. Similar three cycles repeated. • Applications are limited to less than 0.5 ml or 10 cm2 per treatment session • The initial application is by the physician to demonstrate proper application and subsequently by the patients themselves.
  • 21.
    Imiquimod • Imiquimod (imidazoquinolinamine)is a nucleoside-like compound acts as an immune response modifier • Induce local production of cytokines including interferon gamma and tumor necrosis factor alpha • Has no direct antiviral activity • Imiquimod cream (5%) is usually supplied in single use sachets. • It is applied to the warts with the fingers three times per week (every other night) ------- the area washed with mild soap and water the next morning. • Treatment is continued until wart clearance or for a maximum of 16 weeks
  • 22.
    Podophyllin • It isa complex resin of podophyllotoxin, alpha peltatum and beta peltatum • Podophyllin inhibits mitosis at metaphase • Dosage: Concentration of 10%–25% dissolved in tincture of benzoin . • The surrounding skin is protected with Vaseline, Then it is applied to the warts by a physician using a cotton tipped swab. • 1 to 4 hour after application, it is completely washed off. • Dose : once or twice a week for up to six weeks. • Applications are limited to less than 0.5 ml or 10 cm2 per treatment session. • It is contraindicated in pregnancy as it can lead to fetal death and abortions
  • 23.
    3 types ofvaccine :  Bivalent (16,18)- Cervarix  Quadrivalent (6,11,16,18)- Gardasil: 9 to 26 years-Male and female 100% effective Protection at least 5 years 0,2,6 month ; i.m  Nonavalent (6,11,16,18, 31,33,45,52,58) – Gardasil 9 Male and female - 9 to 26 years (2 dose schedule-9 to 14 years, 3 dose schedule-15 to 26 years) Prevention:
  • 24.
     Human Herpesvirus 1 (Herpes simplex virus 1 (HSV 1))  Human Herpes virus 2 (Herpes simplex virus 2 (HSV 2))  Human Herpes virus 3 (Varicella-Zoster virus (VZV))  Human Herpes virus 4 (Epstein Barr virus (EBV))  Human Herpes virus 5 (Cytomegalovirus (CMV))  Human Herpes virus 6 (HHV 6)  Human Herpes virus 7 (HHV 7)  Human Herpes virus 8 ( Kaposi’s sarcoma associated Herpes Virus (KSV)(HHV 8)) Human Herpes Virus
  • 25.
     Herpes SimplexVirus I :  Herpes labialis  Herpetic gingivostomatitis  Herpetic whitlow  Herpetic gladiatorum  Herpes sycosis Herpes Virus  Herpes Simplex Virus II :  Herpes progenitalis  Herpetic vulvovaginitis  Complicated :  Eczema herpeticum  Disseminated HSV  Herpes Simplex Virus in HIV :  Chronic, recurrent, ulcer, eschar formation and dissemination
  • 26.
     Primarily involveskin and mucous surfaces  Can be disseminated in neonates and immunocompromised hosts  HSV-1 : >90% of primary infections caused by HSV-1 are subclinical; more common  HSV-2- usually the genital pathogen and usual pathogen of neonatal herpes  Clinical infections type:  Primary first episode  Non-primary first episode  Recurrent episode  Asymptomatic infections Herpes simplex infections
  • 27.
     Fever blisters,cold sore  Triggers : Fever, UVB, Surgery  95 % HSV – 1  Presentation :  Grouped painful vesicles on an erythematous base.  Often prodrome of tingling or itching, flu like symptoms  Variable severity of recurrent lesions. Orolabial Herpes
  • 28.
    Herpetic Gingivostomatitis • Highfever, irritability, anorexia, mouth pain, drooling • Gingivae becomes intensely erythematous, edematous, friable and tends to bleed • Symptoms last 5-14 days, but virus can be shed for weeks following resolution  Differential diagnosis:  Aphthous ulcer, Herpangina, Stevens Johnson Syndrome, Syphilis  Diagnosis :  Tzanck smear- multinucleated giant cells  H/P- Ballooning degeneration → Reticular degeneration  HSV antibody titre : IgG/IgM  Immunofluoroscence, PCR-most sensitive
  • 29.
     Herpetic Sycosis •Shaving after facial herpes induces a slowly spreading folliculitis of the beard with few isolated vesicles.  Herpes Gladiatorum – in wrestlers & rugby players  Herpes associated Erythema Multiforme  Herpetic whitlow • Herpetic infection of the fingers. • Children (thumb sucking) • Adults : 2/3 cases HSV-2, Children nearly 100% HSV-1
  • 30.
     HSV-2 inmajority of cases.  Skin to Skin contact  Active lesions are infective  Asymptomatic shedding ( majority of transmission).  Prior HSV-1 infection does not protect from HSV-2 infection but may lessen severity of first outbreak.  Primary infection:  Grouped vesicles which appear for 7-14 days.  Fever, Flu like symptoms, inguinal lymphadenopathy, proctitis if rectal involvement.  Recurrent (>6 episodes/ year) lesions with typical prodrome of burning/itching followed by outbreak which is less severe than the primary infection healing in 6-10 days. Genital Herpes
  • 31.
  • 32.
     Symptomatic  Topical: Acyclovir, Penciclovir, Cidofovir  Systemic : Treatment Antiviral Primary (for 7-10 days) Recurrence (for 5 days) Suppressive (For 1yr) Acyclovir 200 mg 5 times / day 400 mg TDS 400 mg BD Valaciclovir 1 gm BD 500 mg BD 1 gm OD Famciclovir 250 mg TDS 125 mg BD 250 mg BD
  • 33.
     Extent ofinitial involvement predicts outcome: • Localized : rarely fatal • Disseminated disease fatal  Presentations in newborns • Majority present with vesicles. • Disseminated herpes with CNS involvement may occur without skin involvement. • Few cases never have vesicles. • Treatment: Acyclovir 250 mg/(m)2 q8 hours x7 days Intrauterine and Neonatal Herpes
  • 34.
     Severe disseminatedHSV1  Multiple crops can appear over 7-10 days (like varicella)  If area of involvement is large, can be lots of fluid loss and potentially fatal  Onset of high fever, irritability, and discomfort  In areas of currently or recently affected skin (for those with atopic eczema or chronic dermatitis)  Lesions begin as pustules, then rupture and crust over the course of a couple of days, sometimes hemorrhagic.  Risk of secondary bacterial infections  Treatment : IV Acyclovir Eczema herpeticum (Kaposi’s varicelliform eruption)
  • 35.
     Primary VZVinfection  IP= 14-17 days  Polymorphic lesions begins on face, scalp and spreads to trunk. (Centripetal)  Macules → Papules → Vesicles → Pustules and crust.  Dewdrop over rose petal appearance  Infectious 4 days before and 5 days after exanthem appears.  Crust formation- not contagious Varicella (chicken pox)
  • 36.
     Secondary bacterialinfection may result in scarring.  Other complications : • Pneumonia : neonates and adults (1/400) • Reyes syndrome: encephalitis, hepatitis with aspirin use. • Thrombocytopenia • Purpura Fulminans : DIC with low proteins C and S  Treatment : • Acyclovir (800mg 5 times a day for 1week) for severe cases, high risk individuals and adults (>13 years). • Acyclovir resistant cases- Foscarnet & Cidofovir • No Aspirin • Isolation from immunocompromised person.
  • 37.
     Mother: increasedrisk for varicella pneumonia.  Baby : • Spontaneous abortion (3% by 20 wks), Fetal death, Pre-term labor • Congenital varicella syndrome :  Hypoplastic limbs, scars, ocular and CNS disease,  highest between 12 and 20 weeks. • Neonatal varicella: if maternal infections 5 days before till 2 days after delivery . • Treatment : Acyclovir, VZIG to baby Varicella in Pregnancy
  • 38.
    Varicella Vaccine:  OKAstrain of Live attenuated virus  Children <12 years : 1st dose- between 12 and 15months of age : 2nd dose- Age of 4-6 years  Adults : 2 doses given 4-8 week apart VZIG (VZV specific Ig): Post exposure prophylaxis  Neonates of mother having varicella 7 days before to 7 days after delivery  Nonimmune pregnant women exposed to VZV  Immunocompromised/ Organ transplant recipients/ Taking Oral steroid for 14 days in last 3 months Prevention
  • 39.
     Reactivation oflatent herpes zoster infection from dorsal root ganglia • Vesciculo- pustular lesions , often with crusting • Typically along a dermatome at times involving adjacent dermatomes. • Preceded by pain, itching Herpes Zoster/Shingles
  • 40.
     Duration ofthe lesion: Age of pt (Young = 2-3weeks, Elderly = 5-6 weeks)  Severity of lesions: level of immunosuppression  Incidence of H.Z. increases with age (>50 yrs) and immunosuppression  Heals without scaring in young, scarring in elderly and severe eruptions. Disseminated Zoster  >20 vesicles outside dermatome, but not adjacent.  Elderly or Immunocompromised  Hemorrhagic/gangrenous lesions with outlying vesicles or bullae.
  • 41.
     Involvement of5th cranial nerve, ophthalmic branch  Lesion location on tip/side of nose: ‘Hutchinson’s sign’ (Nasocilliary branch)  Ocular complications • Uveitis , Keratitis • Glaucoma, optic neuritis  Encephalitis Herpes Zoster Ophthalmicus
  • 42.
     Facial andauditory nerve involvement with inflammation of geniculate ganglion  Lesions distributed over external auditory meatus, tympanic membrane, tonsillar fossa and soft palate.  Facial paralysis with or without tinnitus, vertigo and deafness Ramsay Hunt syndrome
  • 43.
     Diagnosis :Tzanck (MNG) , direct fluorescent antibody, culture, PCR.  Symptomatic treatment  Antivirals : Acyclovir 800mg x 5times/day for 1 week (may lessen severity of symptoms in acute outbreak. May lessen incidence of PHN). Famciclovir 250-500 mg TDS Valaciclovir 1gm TDS Duration : 1week (immunocompetent), 2 weeks (immunosuppressed) Diagnosis and Treatment
  • 44.
     After 4weeks of herpes zoster .  Mechanism : irritable nociceptors, spinal deafferentiation  Constant burning pain, intermittent stabbing/shooting pain, Allodynia.  Risk factors : prodromal pain, severe pain during acute phase, greater rash severity, opthalmic zoster. Treatment  Topical : Capsaicin, topical lidocaine.  Oral : Opoid analgesics, amitryptiline, gabapentin, Pregabalin  Injectable : lidocaine / steroids (Modified Jaipur block- xylocaine+ bupivacaine+methylprednisolone) Post Herpetic Neuralgia
  • 45.
    Infectious mononucleosis  Incubationperiod : 3-7 wk  Bilateral enlargement of cervical and other lymph glands  High grade fever, malaise, Pharyngitis ,splenomegaly.  Ampicillin triggers maculopapular eruption.  Lab findings : • TLC = 10,000 to 40,000. • Abnormal large lymphocytes (Downey cells) are 10% of total leukocyte count. • Heterophile antibodies 1:160 of higher Epstein Barr Virus
  • 46.
     Associated withchronic shedding of EBV in the oral cavity.  Presentation: Poorly demarcated, corrugated, white plaques on lateral aspect of tongue.  Unlike thrush, cannot be removed by scraping.  HIV / AIDS pt.  Treatment • Not required • Podophyllin and tretinoin are used but lesions recur Oral Hairy Leukoplakia
  • 47.
     HHV 6Acauses multiple sclerosis and HHV 6B causes Exanthem subitum or Roseola Infantum (sixth disease). Human Herpes virus 6 Human Herpesvirus 7  HHV 7 has been associated with febrile illness in children, exanthem subitum and questionably pityriais rosea.  HHV 7 infection can reactivate HHV6 from latency. Human Herpesvirus 8  Three proliferative diseases are associated with HHV 8: Kaposi sarcoma, Primary effusion lymphoma and Castelman’s disease.
  • 48.
    Pityriasis Rosea • Etiology:HHV6> HHV7, May be drug induced (captopril, imatinib) • Herald patch/ mother patch • Christmas tree or fir tree pattern ( along langers line) • Collarette of scales • Hanging curtains sign • Treatment : self resolving in 4-10 weeks
  • 49.
     Macular : •Rubella • EBV (infectious mononucleosis) • HHV 6 (roseola) • HHV 7  Maculopapular : • Togavirus • Measles- Koplik spots • Human parvovirus B19 (erythema infectiosum)- Slapped cheek appearance Viral Exanthems  Maculopapular - vesicular : • Coxsackie A (5, 9, 10,16) • Echovirus (4, 9, 11)  Maculopapular – petechial : • Togavirus (Chikungunya)- Centrofacial hyperpigmentation/Chik sign • Bunyavirus haemorrhagic fever (Lassa)  Urticarial : • Coxsackie A9 and Hepatitis B
  • 50.
     Pox Viruses: • Cowpox, Orf, Milker’s nodule  Epstein Barr Virus : • Infectious Mononucleousis, OHL, Gianotti Crosti, • Lymphomas  Viral insect-borne and haemorrhagic fevers: (Toga, Flavi, Arena, Filo, Bunya) • Chikungunya, Dengue ( White island in sea of red), Kyasanur Forest Disease, Lassa  Picorna Viruses : • Herpangina, hand, foot and mouth disease ( Coxackie A16, Entero Virus 71). Uncommon Viral Infections of the Skin
  • 51.
  • 52.
  • 53.
  • 54.
    Sample Questions 1) Discussthe clinical features and management of infections caused by varicella zoster virus. (6+4) 2) Discuss the different treatment modalities and preventions of anogenital wart. (10) 3) Write in brief about (5 marks each) a) Management of genital herpes b) Molluscum contagiosum c) Pityriasis rosea d) Post herpetic neuralgia
  • 55.
     What isthe likely diagnosis? (1)  Name the causative agent. (1)  Name other disease caused by same agent due to reactivation of latent Stage in dorsal root ganglion. (1)  What will be the findings in Tzank smear from base of vesicles? (1)  Write the Drugs, Dosage and duration for it’s treatment. (1) A 20 year male presented to Skin OPD with history of fever, malaise and multiple red blisters since 2 days. OSCE
  • 56.
    A) Caused byHHV3 B) Due to primary VZV infection C) Ramsay hunt syndrome is its complication D) Treated by Acyclovir 400mg TDS A 16 year girl presented to Skin OPD with history of pain and multiple red blisters over right side of forehead & nose since 2 days. Which of the following is true regards the condition? Scenario based MCQ
  • 57.
    Q.1) Eosinophilic intracytoplasmicinclusions bodies seen in molluscum contagiosum is termed as A. Odland bodies B. Civate bodies C. Henderson Peterson bodies D. Cowdery type A Q.2) The following diseases are associated with Epstein-Barr virus infection except : E. Infectious mononucleosis F. Bowenoid papulosis G. Nasopharyngeal carcinoma H. Oral hairy leukoplakia MCQ’S
  • 58.
    Q.3) Kaposi’s Sarcomais associated with A. HHV 6 B. HHV 7 C. HHV 8 D. HHV 3 Q.4) Hanging curtain sign & collarete of scales is seen in E. Pityriasis versicolor F. Pityriasis rosea G. Psoriasis H. Pityriasis lichenoid chronica
  • 59.
    Q.5) Which ofthe following is not a treatment of anogenital wart? A. Imiquimod B. Podophyllin C. Cryosurgery D. Aceto-whitening Q 6) Identify the correct match E. Christmas tree pattern ----------- Parvo B19 F. Slapped cheek appearance --------HHV6 G. White islands in the sea of red -----------Dengue Virus H. Centro-facial hyperpigmentation -------- EBV
  • 60.

Editor's Notes

  • #57 Answer to MCQ – 1] C 2] B
  • #58 Answer to MCQ – 3] C , 4] D
  • #59 Answer to MCQ – 3] C , 4] D