VIRAL INFECTIONS OF

SKIN & SOFT TISSUES

APSARA
ARIF
 Warts (Verruca)
Etiology
 Human papilloma virus (HPV) is a DNA virus
which has not been cultured in vitro.

 With polymerase chain reaction techniques,

more than 100 types of HPV identified.

 Association exists between HPV type and the

clinical disease caused which is given in the
table below
 TRANSMISSION

 Nongenital warts: Transmitted through

direct skin-to-skin contact and by auto-
inoculation.

 Anogenital warts:
Sexual transmission: both
heterosexual and homosexual. Vertical
transmission: mother with anogenital
warts can transmit infection to the
newborn, during vaginal delivery. The
infection manifests as laryngeal papillomas
in infant
 CLINICAL FEATURES
Warts present clinically as:
 Verruca vulgaris.
 Palmoplantar warts.
 Verruca plana.
 Filiform warts.
 Epidermodysplasia verruciformis.
Anogenital warts.
 VERRUCA VULGARIS
Also known as COMMON WARTS
Usually asymptomatic.
 Morphology
* Single or multiple, circumscribed, firm
papules with verrucous (hyperkeratotic) dry,
stippled surface .
* About 60% of common warts resolve
spontaneously.
* Sites Can occur anywhere on the body,
but most frequently seen on back of hands,
fingers, knees, and feet
figure
PALMOPLANTAR WARTS

 Palmoplantar warts are of two types:

*Superficial palmoplantar warts.

*Deep palmoplantar warts.

SUPERFICIAL PALMOPLANTAR
WARTS (MOSAIC WARTS)
Usually painless.

 Morphology: Hyperkeratotic papules

and plaques consisting of multiple,
small warts, which are tightly packed .

 Sites: Soles and less often palms

 DEEP PALMOPLANTAR
WARTS (myrmecia)
 Painful (sometimes
excruciatingly so!).
Morphology:
Hyperkeratotic, deep-seated
papules (barely visible above the
skin surface), surrounded by a
horny collar and the wart
actually becomes apparent as a
soft granular brown papule, only
when the collar is pared.
VERRUCA PLANE ( PLANE WARTS)

Morphology ;
 Multiple, slightly elevated, flat smooth

papules .
Skin colored or darker lesions; may have
an erythematous halo.
 Lesions may be arranged linearly
(pseudo Koebner’s phenomenon) due to
auto-inoculation
Site
 Face and on dorsal aspect of hands.
fig
 FILIFORM WARTS

Morphology
 Asymptomatic, thin elongated, firm
projections arising from a horny base
Site
 Most frequently on the face (inoculation by
shaving) and scalp.
fig
 ANOGENITAL WARTS

Sexually transmitted disease.

 A variety of clinical variants, e.g.,
condyloma acuminata, papular
warts, and Bowenoid papulosis.
 Most frequently on the glans,
perianal region, vulva, and cervix
 COURSE OF WARTS

Spontaneous resolution; In healthy

individuals most warts resolve spontaneously
(30% in 6 months and 60% in12 months) as
the host mounts an immune response.

When wart is spontaneously regressing,

punctate areas of blackish discoloration (due
to capillary thrombosis) appear on surface
and the wart resolves with no sequelae
Persistent warts
 Mosaic warts are very recalcitrant.
 In immunocompromised individuals, (on
immunosuppressive therapy, with
lymphoreticular malignancies or with HIV
infection) warts are persistent, extensive,
and have an oncogenic potential
Complications of warts;

• Large genital lesions may obstruct labor in

pregnant women.
• Seen in:
-Cervical infection with high-risk HPVs
-HIV infection
-Epidermodysplasia verruciformis
 DIAGNOSIS

Points for diagnosis

Warts are diagnosed on the basis of:

• Characteristic warty appearance with a rough, dry stippled
surface.
• Presence of pseudo Koebner’s phenomenon, especially in
plane warts.
• Typical histology
 TREATMENT

Treatment of viral warts depends on

 Site.
 Number of lesions.
 Type of lesions.
 Age of patient.
Treatment options
Several methods of treatment are
available:
a) Cryotherapy
b) Topical agents( Salicylic acid (10–
25%), Wart paint, Retinoic acid
(0.05–0.1%), Formalin(22 soaks))
c) Mechanical removal
Treatment table
 MOLLUSCUM CONTAGIOSUM

Etiology Agent;
-Pox virus.
Transmission
-Direct spread.
fig
 COURSE

 Self-limiting.
 Lesions usually clear spontaneously in about
a year usually without any scarring (though
some lesions may resolve with scarring).
 Large solitary lesions may not resolve
spontaneously.
 Lesions are persistent, extensive, and
difficult to treat in immunocompromised
individuals and in patients with atopic
dermatitis
Complications
 Secondary infection.

Investigations
- In children, usually none needed.
- In doubtful cases, cytological examination of
expressed material reveals large eosinophilic
intracytoplasmic inclusion bodies.
- In adult patients with extensive and persistent
lesions, underlying HIV infection should be
ruled out
 DIAGNOSIS

Points for diagnosis

Diagnosis of MC is based on:
- Presence of pearly white umbilicated papules.
- Extrusion of the cheesy core through the central
crater; characteristic cytological appearance of
the expressed material.
- Differential diagnosis MC should be
differentiated from: a. Verruca vulgaris.
b. Cryptococcosis.
Treatment
 VARICELLA ZOSTER INFECTIONS

-Varicella
Synonym: Chicken pox.

Etiology
*Varicella-zoster virus.
*Highly contagious, spread by droplet route.
* Patient infectious for 1–2 days before the exanthem
appears and for 4–5 days thereafter (total
infectious period 5–7 days), i.e., till the last crop of
vesicles has crusted. Incubation period is 2 weeks
Clinical features
- Prodrome Low-grade fever and malaise.
- Morphology ;
*Lesions appear in crops.
* Itchy papules that rapidly turn into
clear superficial vesicles and then
pustules. *Particular time, lesions at
different stages of evolution are present.
 Typical vesicle of varicella is superficial and thin
walled and it looks like a drop of water lying on,
rather than in the skin.

The irregular perivesicular erythema give the

lesions a “dew drop on rose petal” appearance

 Eventually, the lesions crust in a few days and

heal, usually, without scarring. Sometimes,
however, depressed scars or hypopigmentation
may develop.

Oral lesions may be present.

fig
Investigations
- None are usually required.

Diagnosis
Points for diagnosis Diagnosis of CP is based on: -
Prodrome of low-grade fever.
-Eruption of papules, vesicles and pustules in
different stages of evolution appearing in crops.
-Typical “dew drop on a rose petal” appearance
-Characteristic centripetal distribution
Treatment table
 HERPES ZOSTER

Synonym: Shingles
Etiology
Varicella-zoster virus.
- After an attack of chicken pox, the virus lies
dormant in the sensory root ganglion. Reactivation
occurs, causing herpes zoster.
- Predisposing factors for reactivation are:
Old age. Lymphoreticular malignancies
e.g., Hodgkin’s disease and leukemia.
Human immunodeficiency virus infection.
Sometimes without apparent cause
Clinical features
Symptoms Prodrome of segmental pain begins 1–4
days before the eruption.
Morphology
- Erythema and edema are rapidly followed by
appearance of grouped vesicles in a segmental
distribution.
- Vesicles rapidly become pustular and crust.
Crusts fall off in about a fortnight and lesions heal
with no (minimal) scarring.
- Mucous membranes within an affected
dermatome may be involved. Draining lymph
nodes are often enlarged
Sites of predilection

Unilateral segmental distribution, though

lesions may affect more than one adjoining
dermatome.
A few stray lesions may be found outside the
dermatomal distribution of the main lesions.
 Thoracic intercostal nerves and ophthalmic
division of trigeminal nerve most frequently
affected. Other spinal nerves also involved.
fig
 COMPLICATIONS

- Postherpetic neuralgia: Persistent neuralgic

pain in some patients (in elderly, when ophthalmic
division is involved and in immunosuppressed).
- Zoster of the ophthalmic division of trigeminal
nerve may be associated with corneal ulcers and
scarring. Eye involvement is indicated when vesicles
are present on the side of the nose (Hutchison’s sign).
- Secondary bacterial infection may occur.
- Generalized chicken pox-like eruption (often
hemorrhagic) may complicate segmental zoster in
immunocompromised individuals and in those with
internal malignancies. Rarely, motor paralysis
 INVESTIGATIONS

None usually required; in doubtful

cases, presence of giant cells on
cytopathology is confirmatory.
 Rule out an underlying
immunodeficiency (lymphoreticular
malignancies and HIV infection), if
disseminated hemorrhagic lesions
present.
Diagnosis

 Points for diagnosis Diagnosis of zoster is

based on:
*Severe pain.
*Unilateral, segmental distribution.
* Presence of grouped vesicles on
erythematous and edematous skin;
rapidly evolve into pustules and then
crust.
Treatment
-Mild cases
*Treat pain with analgesics (round
the clock).
* Treat secondary bacterial infection
with broadspectrum antibiotics.
 Severe cases
 Symptomatic treatment: NSAIDs.
 Specific treatment: With antiviral drugs.
Indications: antiviral drugs are indicated in:
Severe cases (disseminated lesions, hemorrhagic
lesions and multidermatomal lesions).
Immunocompromised patients. Ophthalmic
zoster.
Antiviral drugs: start within 72 h of an attack.
Following drugs can be used:
Acyclovir: 800 mg, five times a day × 7 days
(adult dose).
Famciclovir: 500 mg, three times a day × 7
days. Valacyclovir: 1 g, three times a day × 7
HERPES SIMPLEX VIRUS INFECTIONS
Etiology
Causative agent HSV hominis; two main
antigenic types:
*Type I: Usually causes herpes labialis and
infections above the waist.
*Type II: Usually causes perigenital
infection. But there is considerable overlap.
 TRANSMISSION

Infection occurs via mucous membranes

or traumatized skin either through:
- Direct contact: Usually occurs in
children from an infected adult who is often
asymptomatic yet shedding virus.
- Sexual contact: Usually in adults,
herpes genitalis being the most common
cause of infective genital ulcer disease.
Again asymptomatic shedding important.
 PATHOGENESIS

-When a person is infected, the disease

may be symptomatic but more often is
asymptomatic.
- After the first episode, the virus lies
dormant in the sensory nerve ganglia but is
capable of causing recurrent episodes of
clinical infection during which the virus is
shed. Viral shedding (though less often and
less severe) also occurs in the absence of
clinical lesions (asymptomatic shedding)
 CLINICAL FEATURES

The severity of clinical disease depends on whether the

infection is primary or recurrent
First episode disease
Primary type I infection
Usually occurs in children.
Manifestations:
May be asymptomatic.
Or may present as acute gingivostomatitis: characterized
by closely grouped vesicles which rapidly form polycyclic
ulcers covered with a yellow pseudomembrane. Heal in
about a fortnight.
Primary type II infection

Usually in sexually active individuals.

Seen on genitalia. Often asymptomatic
especially in females.
When symptomatic:
Manifests as grouped painful vesicles
(appearing as white plaques), which
rapidly erode to form polycyclic ulcers on
erythematous background .
Constitutional symptoms and inguinal
lymphadenopathy seen
Post primary infection

- This is primary infection usually with HSV

type II in a patient who has some degree
of immunity due to previous HSV type I
infection or vice versa, (latter situation
being less frequent).
- Manifestations are less severe than
primary infection
fig
 INVESTIGATIONS

Usually no investigations are needed

for herpes labialis but for herpes
genitalis, following investigations are
helpful: a)Identification of virus
in tissues:
Tzanck smear
Culture
Fluorescent antibody test
b)serology
 DIAGNOSIS

-Points for diagnosis

Diagnosis of HSV infection is based on:
*Presence of grouped vesicles
which rupture to give rise to polycyclic
erosions; primary infection more
symptomatic and severe and lesions
may be covered with white/yellow
pseudomembrane.
* Recurrences at same sites
Differential diagnosis
HSV infection needs to be
differentiated from:
a. Herpes zoster
TREATMENT
 Maculopapular Viral Exanthems
Measles (Rubeola)

- Incubation period: 10 days.

- Prodrome: 2–4 days ;Fever, photophobia,
conjunctival injection, and upper respiratory
catarrh.
- Mucosal involvement: Koplik’s spots in buccal
mucosa.
- Cutaneous lesions: Maculopapular confluent rash
(deep red to brown) which evolves in a cranio-
caudal fashion and fades with scaling.
- Treatment: Symptomatic. Watch for pneumonitis.
- Prophylaxis: Measles vaccine.
German Measles
- Very mild disease.
- Risk of congenital malformations in
fetus, if pregnant woman is infected.
- Lymphadenopathy, followed by a
transient, faint, erythematous,
discrete macular rash
 Hand, Foot, and Mouth Disease
 Etiology:
Picorna virus infection of animals, which sometimes
affects humans.

Age: Occurs both in adults and children.

Clinical features: Incubation period: 2–18 days.

Prodrome: malaise, headache and fever, with burning in
oral mucous. Mucocutaneous lesions: painful vesicles in
oral mucosa, and occasionally on palms, soles and
interdigital skin. Vesicles are typically oblong (Figs. 14.58A
and B). Disease more severe in infants and children.
Treatment: Symptomatic.
fig
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