Viral Diseases

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Course of Dermatology

Viral Diseases

Yin Guang-wen
Dept. of Dermatology The First
Affiliated Hospital of ZhengzhouUniversity
Viral Diseases
 Viruses are obligatory intracellular parasites.
 Two main groups of viruses are distinguished:DNA and RNA.
 viruses can cause some skin diseases,such as:
- Varicella
- Herpes Zoster
- Herpes Simplex
- Cowpox
- Measles
- Warts (verruca) and so on
Varicella & Herpes Zoster
 Varicella & Herpes Zoster are distinct clinical entities caused by
varicella-zoster virus (VZV).
 VZV is a double-stranded DNA virus.
 The differences between these two diseases are due to differences in the
host and in the circumstances of infection.
 Varicella is the result of primary infection of a susceptible individual.
 Herpes zoster represent activation of an endogenous infection that has
persisted in latent form following an earlier attack of varicella.
Varicella & Herpes Zoster

 Difference in clinical manifestations between varicella and


zoster apparently depends on the immune status of
individual patients:
 those with no prior immunologic exposure to varicella
virus, most commonly children, develop the clinical
syndrome of varicella
 while those with circulating varicella antibodies develop a
localized recrudescence, zoster
Varicella
 VZV is the etiologic agent of the clinical syndrome of chickenpox
(varicella).
 Vericella is largely a childhood disease
 more than 90% of cases occurring in children <10 years of
age.
 The disease is quite benign in healthy child.
 In adult and immunocompromised patients, there is increased
morbidity.
Varicella (chickenpox)

-- Vericella usually is acquired by the inhalation of airborne


respiratory droplets from an infected host.
-- Highly contagious nature of VZV :
"epidemics" of vericella spread through schools:
one infected child quickly spread virus to many
classmates.
-- Within the incubation period of 10 to 21 days
vericella (chickenpox)
Clinical feature
rapid sequential progression over 12-14 hours to
papules, clear vesicles, and pustules, with subsequent
central umbilication and crust formation.
Small erythematous macules appear on scalp, face,
trunk, and proximal limbs,
Vesicles also may appear on the palms and soles,
and mucous membranes with painful, shallow
oropharyngeal or urogenital ulcers.
vericella (chickenpox)
 Infectivity
 Typical patient is infectious for 1-2 days prior to the
development of rash and for 4-5 days afterwards, which
usually is the time at which the last crop of vesicles has
crusted over.
Typical skin lesion
Characteristic vesicle:

Active and healing lesions in all stages of development


Lesions characteristically heal without scarring, though
excoriation or secondary bacterial superinfection
predispose to scar formation.

Vesicle on erythematous base, "a dewdrop on a rose


petal"
vericella
Active and healing
lesions in all stages of
development:
Macules,
papules,
clear vesicles, pustules
and crust
vericella
 Active and healing
lesions in all stages of
development:
 Macules,
 papules,
 clear vesicles,
pustules , crust,
central umbilication
vericella in children and
adults
 Childhood
 usually is not heralded by a prodrome, but rather begins with the
onset of an exanthem.
 Adults and adolescents
 may be preceded by a prodrome of nausea, myalgia, anorexia,
and headache.
 have a more complicated course than that seen in children.
 may experience a more widespread rash, prolonged fever, and
increased chance of complications, the most common being
varicella pneumonia.
Treatment
 Primary varicella infection in the healthy child is a rather
benign disease
 Require symptomatic therapy only.
 Acyclovir
 given orally (dosage: 20 mg/kg qid for 5 d)
 shown to decrease the duration and symptoms of primary
varicella infection
Herpes zoster
 Definition
- Herpes zoster ("shingles") is an intraepidermal vesicular
eruption occurring in a dermatomal distribution.
- It is caused by the recrudescence of latent varicella-zoster
virus in persons who have had varicella.
Etiology

 Vericela zoster virus


 nature infection(vericela) or immunization
 virus remains latent in the sensory dorsal root ganglion
cells
 (immunosupression and age,and other unknown factors)
virus replicate, traveling down the sensory nerves into
the skin (herpes zoster)
Incidence

 From 10% to 20% of individuals develop herpes zoster


during their lifetime.
 The attack rate is age dependent.
 Cancer and AIDS patients have a higher incidence than
the general population.
 There may be a 5% frequency of second attacks.
Clinical Manifestation
 Herpes zoster classically occurs unilaterally within the
distribution of a cranial or spinal sensory nerve
 The dermatomes most frequently affected:
 thoracic (55%)
 the cranial (20%, with the trigeminal nerve being the
most common single nerve involved)
 the lumbar (15%)
 the sacral (5%)
Clinical Manifestation
 Pain
- The cutaneous eruption is frequently preceded by several
days of pain in the affected area, although the pain may
appear simultaneously or even following the skin eruption;
or the eruption may be painless.
- There is a correlation with the pain severity and the extent
of the skin lesions, and elderly persons tend to have more
pain
Clinical Manifestation
 Skin lessions
- The eruption initially presents as papules and plaques of
erythema in the dermatome. Within hours the plaques
develop blisters.
- In the typical case, new vesicles appear for 1 to 5 days,
become pustular, crust, and heal.
- Lesions may become hemorrhagic, necrotic, or bullous.
Herpes zoster
 a unilateral, painful eruption of grouped vesicles
 along a dermatome
Herpes zoster
 a unilateral, painful eruption of grouped vesicles
 along a dermatome
Herpes zoster
Lesions may become hemorrhagic, necrotic, or bullous.
Clinical Manifestation

 Symptoms
- Typically include prodromal sensory phenomena
along 1 or more skin dermatomes lasting 1-10 days
(averaging 48 h), which usually are noted as pain or,
rarely, paresthesias.
Complications
 Postherpetic neuralgia
 is uncommon in patients less than 40 years old

 two thirds of patients more than 60 years old develop

this complication
 is very difficult to control

 Scarring
 is uncommon, except in elderly and immuno-suppressed

patients;
 is correlated with the severity of the initial eruption.
Course
 The total duration of the eruption depends on
 patient age
 severity of eruption
 presence of underlying immunosuppression

 The total duration


 in younger patients, is 2 to 3 weeks
 in elderly patients, may require 6 weeks or more to heal
Diagnosis of Zoster
 The clinical appearance is often adequate to suspect the
diagnosis:
 a unilateral, painful eruption of grouped vesicles along a
dermatome
 hyperesthesia
 Regional lymph node enlargment
 Usually, no laboratory tests are necessary
 The Tzanck preparation
 direct immunofluorescence staining of vesicle smears are
confirmatory in unusual cases.
Therapy
 Antivirus
Acyclovir
10 mg/kg every 8 hours intravenously, or 800 mg five times
daily orally for 7 to 10 days
The newer antivirals,valacyclovir(1000 mg ) and
famciclovir (500 mg ) ,may be given only three times
daily.
 Corticosteroids

- Systemic use, 7-10 day course


- may help some otherwise healthy patients to prevent
postherpetic neuralgia
Therapy

 Analgesic(pain killer)
- Amitriptyline at a dosage of 25 to 75 mg in a single nightly
dose may be helpful in managing postherpetic neuralgia
once it occurs.
- opiate analgesia may be effective if these measures fail
 vitamin
- vitB1,B12,help inflammeted nerve cells recover
Therapy
 Topical treatment
- When the vesiculopustules of herpes zoster rupture,
crusting and weeping are reduced with astringent
compresses. eg,calamine lotion
- Capsaicin analgesic cream 0.075% used topically to kill
pain
Viral Diseases

Warts
Definition

 Warts are benign neoplasms caused by infection of


epidermal cells with papilloma viruses.
 Usually involute spontaneously
 The thickening of the epidermis with scaling and an
upward extension of the dermal papillae containing
prominent capillaries give them their "warty" or
verrucous appearance.
Etiologic factors

 Human papillomavirus, HPV


 Double-stranded, naked DNA viruses characterized as slow
growing.
 Include more than 100 types
 replicate in epithelial cells
Human papillomavirus
under electronic microscopy
Etiologic factors
 Most HPV types cause specific types of warts and favor
certain anatomic locations, such as plantar warts, common
warts, genital warts, and so on.
 Infection with HPV may be clinical, subclinical, or latent.
Transmission and latent
period
 Warts are usually spread by direct skin-to-skin inoculation
of the virus from one person to another, although
transmission by fomites also probably occurs.
 The time between inoculation and the appearance of a
lesion is quite variable. It varies from one to a few weeks to
a year or more.
Immunology

 Cell-mediated immune responses to the virus are


probably the most important factor in host
resistance .
 Humoral immunity, on the other hand, does not
appear to play a major role in host responses or in
treatment responses
Classification
 Common warts
 Plantar warts
 Flat warts
 Genital warts
Common WartS (Verruca
Vulgaris)
 HPV type 2,and less frequently,1,4,7,and other HPV types are
most frequently responsible for common warts.
 Common warts are occur largely between the ages of 5 and 20
and only 15% occur after the ages of 35,the prevalence in
children is about 5%.
 The natural history of common warts is for them to
spontaneously resolve ---half by 1year and two thirds by 2
years.
Common WartS (Verruca
Vulgaris)
 Typical lesion

 is an elevated, firm papule or nodule with a rough, grayish


or flesh-colored surface
 It interrupts the normal skin lines and is studded with
black puncta.
 Occur individually, in groups, or in a linear fashion from
autoinoculation
 The hands and fingers are the usual sites
 Involvement around nails frequently results in extension
underneath the nail plate
Common WartS

hands and fingers


are the usual sites.
Common WartS

Periungual warts

elevated, firm papule or nodule


with a rough, flesh-colored
surface
Common warts occur on the lip.
Plantar Warts (Verruca
Plantaris)
 HPV type 1 and, less commonly,2,4, and other HPV types
are cause plantar warts
 A plantar warts occurs as a single, or multiple painful
papule on the plantar aspect of foot
 The greater depth of infected tissue makes these warts more
difficult to treat successfully
Plantar Warts (Verruca
Plantaris)
 It is covered by a thick “callus”.
 When the “callus” is pared down with a scalpel, the
underlying wart is visualized with
 interruption of skin lines
 and black puncta(black dots)
Plantar Warts
 Interruption of skin lines
 black dots
Flat Warts (Verruca
Plana )
 HPV type 3 and, less often, types 10,27,and 41 most often
cause flat warts
 Children and young adults are primarily affected
 A flat wart has a subtle appearance
 It is a flesh-colored or reddish brown, slightly raised,
flat-surfaced, 2 to 5mm in diameter, well-marginated
papule.
 On very close inspection (a hand magnifying lens may be
needed), the surface appears finely verrucous.
Flat Warts (Verruca
Plana )
 Multiple lesions commonly affect the hands ,lower arms and
face.
 Autoinoculation:
 linear arrangement of lesions
 Scratch is the common reason
 Often in patients who shave their beard or shave their legs
Flat Warts
Multiple lesions commonly affect the hands,lower arms and face.
Autoinoculation:
linear arrangement of lesions
Scratch is the common reason
Condyloma Acuminatum

 involves the external genitalia, perineal region, rectum, and,


occasionally, urethra and vagina.
 composed of soft moist papules and plaques
 has a verrucous surface that often is cauliflower-like
 frequantly re-occur
Treatment
 Treatment of warts is nonspecific, destructive, and usually painful

 The goal is destruction of the keratinocytes that are infected with


HPV

 This may be accomplished with a variety of physical or chemical


modalities
The physical modalities include

 Cryotherapy with liquid nitrogen


 The most common initial mode of treatment
 Laser therapy
 Electrodesiccation
 Surgical excision
 does not guarantee the wart will not recur
The chemical modalities include
 salicylic acid paint
 25% podophyllin
 Bleomycin injections
 has high efficacy and is now an important form of
treatment for recalcitrant common wart
 is injected into and immediately beneath the wart
Course and
Complications
 It is estimated that 35% to 65% of warts spontaneously
resolve within 2 years
 Treatment results in cure rates of as high as 80%
 Very rarely it becomes carcinoma

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