VIRAL SKIN INFECTIONS

Viral skin diseases are classified by clinical features into three types:

- 1 Degeneration of epidermal cells and blistering (e.g., in herpes

simplex and herpes zoster),
2
- Tumorous changes in epidermal cells (e.g., in verruca vulgaris),
- 3 Allergic eruptions on the whole body (e.g., in measles and rubella).
The first two types are caused by viral infection in epidermal
keratinocytes; the last type is caused by systemic viral infection (viremia).

Viral warts

Warts (verrucae) are common and benign cutaneous tumors due to

infection of epidermal cells with human papilloma virus (HPV). Over 100 150

subtypes of DNA human papilloma virus have been identified. The virus
most commonly infects children and young adult by direct inoculation and
is transmitted by touch, sexual contact or at the swimming baths. They
commonly appear at sites of trauma. A line of warts may appear as a result
of scratching (Koebner phenomenon).

Clinical presentation
Certain clinical patterns are well recognized:
verrucae valgarus
1. Common warts. These present as dome-shaped papules or nodules with
a rough keratotic surface. They are usually multiple, and are commonest
on the hands or feet in children but also affect the face and genitalia. Their
surface interrupts skin lines. Thrombosed capillaries appear as black dots
on the surface of warts, an important diagnostic sign.
‫الفالول الخيطي‬

2. Filliform (digitate) warts: Consist of finger like projections,

commonly around the mouth, eyes, ala nasi, beard area and scalp.

3. Plane warts. These are smooth flat-topped papules, often slightly

brown in colour, and commonest on the face and dorsal aspects of the
hands. They are usually multiple and resist treatment, but eventually
resolve spontaneously, often after becoming inflamed. They can show the
Koebner phenomenon.

4. Plantar warts. These are seen in children and adolescents on the soles
of the feet; pressure causes them to grow into the dermis. They are painful The only
type
and covered by callus, which, when pared, reveals dark punctate spots because
(thrombosed capillaries). A cluster of fused planter warts is referred to as itinward
grows

(mosaic warts). They should be differentiated from corns, as planter warts

lack skin lines crossing their surface, and have central black dots that bleed
with additional paring. Lateral pressure on a wart causes pain, while the
corn is more painful on direct pressure.

5. Subungual and periungual warts:

They occur next to the nails, at the tips of fingers and toes.

6. Genital warts. In males these affect the penis, and in homosexuals, the
perianal area. In females, the vulva, perineum and vagina may be involved.
The warts may be small, or may coalesce into large cauliflower-like
'condylomata acuminata'. Genital warts may be associated with an
increased risk of cervical and anal carcinoma.

7. Epidermodysplasia verruciformis:

Inherited as autosomal recessive disorder in which there is widespread

and persistent infection with HPV, giving rise to a characteristic
combination of plane warts, pityriasis versicolor – like lesions and reddish
plaques. Malignant change (squamous cell carcinoma) is very common,
but metastasis is rare.

Management
In children, 30-50% of common warts disappear spontaneously within 6
months. Otherwise treatment will depend on the type of wart. Generally
any destructive non scarring method could be used, such as:

- Chemical cautery (salicylic acid "S.A.", trichloroacetic acid

"T.C.A."…).
Imiquimod is immune stimulater excellent but expensive 80K iraqi dinar

- Electrocautery.
- CO2 laser.
- Cryotherapy.
- Curettage.
- Contact immunotherapy by using dinitrochlorobenzene "D.N.C.B."
- Topical tretinoin or 5- fluorouracil "5FU" for plane warts.
- Podophyllum resin especially for genital warts.
- Intralesional Bleomycin sulphate.
- Intralesional interferon alpha- 2b recombinant.
- Oral zinc sulphate, levamisole or cimitedine for widespread warts.
 ‫الفالول اللؤلؤي‬

Molluscum contagiosum

They are discrete pearly-pink umbilicated papules which are caused by a

DNA pox virus. Mollusca mainly affect children or young adults. Spread
is by contact, including sexual transmission or on towels. The dome-shaped
papule, a few mm in diameter, has a punctum and if squeezed, releases a
cheesy material. The areas commonly involved are the face, trunk, axillae
and extremities in children; and pubic and genital areas in adults.
Treatment: Curettage, chemical cautery, topical tretinoin. Just pricking of
Without scaring
the lesions with or without use of irritant materials may be enough.
Pulse die laser is the best

ORF:

Orf is an exanthemous zoonotic disease caused by a parapox virus and

occurring primarily in sheep and goats but it can also infect humans
through direct contact with infected animals. The incubation period is 5–6
days. Lesions, which may be single or multiple, start as small firm papules
that change into flat-topped apparently pustular nodules with a violaceous
and erythematous ring.The condition clears up spontaneously in about a
month. Infected locations can include the finger, hand, arm and face. Some
cases may trigger the appearance of erythema multiforme.

Herpes simplex ‫لطمة الحمه‬

Herpes simplex is a very common acute self-limiting vesicular eruption

due to infection with Herpesvirus hominis.
Acyclovir cream used before the skin lesions appears to
Aetiopathogenesis and pathology shorten the duration

Herpes simplex virus is highly contagious and is spread by direct contact

with infected individuals. The virus penetrates the epidermis or mucous
membrane epithelium and replicates within the epithelial cells.
After the primary infection, the latent non-replicating virus resides
mainly within the dorsal root ganglion, from which it can reactivate, invade
the skin and cause recrudescent lesions.
There are two types of herpes simplex virus. Type 1 disease is usually
facial or non-genital, and type 2 lesions are commonly genital, although
this distinction is not absolute. The pathological changes of epidermal cell
destruction by the herpes virus result in intraepidermal vesicles and
multinucleate giant cells. Infected cells may show intranuclear inclusions.
Clinical presentation
-Primary infection
1
Type 1 primary infection usually occurs in childhood and is often
subclinical in about 80 % of the cases.
Acute gingivostomatitis is a common presentation of primary infection
in those with symptoms. Multiple and discrete vesicles appear on the lips
and mucous membranes that quickly erode and are painful. Sometimes the
cornea is involved. The illness is often accompanied by fever, malaise and
local lymphadenopathy and lasts about 2 weeks.
2
Primary type II virus infections, usually transmitted sexually, cause
multiple and painful genital or perianal blisters which rapidly ulcerate.
- Recurrent (recrudescent) infections
It mean recurrence of skin lesion in the same place at each time. They
may be precipitated by respiratory tract infections (cold sores), ultraviolet
radiation, menstruation or even stress. Common sites include the face and
lips (type I), and the genitals (type II), but lesions can occur anywhere.
Vesicles differ from those in primary infections by their smaller size, less
number, closer grouping and the usual absence of constitutional symptoms
or lymphadenopathy, unless there is secondary infection. The outbreak is
often preceded for a few hours, by tingling or burning. Crusts form within
24-48 hours, and the infection fades after a week. Attacks may be
precipitated by respiratory infection or fever (hence 'cold' sore), sunlight or
local trauma.

Diagnosis:
Geimsa stain
1. Tzanck smear: a cytological smear from the base of viral vesicles,
stained to show the multinucleated giant cells, characteristic of herpes
infections.
2. Serological tests: seroconversion or a rise in Ab – titer can be detected
by complement fixation test (C.F.T.), especially in the primary infections,
or by ELISA test.
3. Culturing the virus from vesicular fluid.
 Management
Mild herpetic lesions may not require any medication. The treatment of
choice for recurrent mild facial or genital herpes simplex is acyclovir
(Zovirax) cream (applied 5 times a day for 5 days), in severe primary or
extensive recurrent cases, antiviral drugs should be tried:
 "Acyclovir": inhibits viral DNA polymerase. It is active against HSV
and HZV.
 "Famcyclovir": similar action to acyclovir with longer half life.
 "Valcyclovir": it is an acyclovir pro – drug, with better oral
bioavailability.

VARICELLA ZOSTER INFECTIONS:

1 Varicella (chickenpox)
Cause
The herpes virus varicella-zoster is a highly contagious viral infection,
commonly afffects children, transmitted by airborne droplets or vesicular
fluid. The severity of the disease and the complications are greater in
adults.

Presentation and course papules > vesicles > pustules > crusts > healed
The incubation period ranges from 9 – 21 days, averages 14 days,
Example of
polymorphi followed by the prodromal symptoms of slight malaise, fever or headache
c rash 1
followed by the development of papules, which
3
turn rapidly into clear
2
vesicles, the contents
4
of which soon become pustular. Over the next few
5
days the lesions crust and then clear, Lesions of different stages are present
at the same time in any body area, giving the characteristic "polymorphic
rash". Lesions appear in crops, are often itchy, and are most profuse on the
trunk and least profuse on the periphery of the limbs (centripetal). Patients
are contagious from 2 days before onset of the rash until all lesions have
crusted. An attack of chicken pox usually confers lifelong immunity.

Complications
• Pneumonitis, with pulmonary opacities on X-ray.
• Secondary infection of skin lesions.
• Haemorrhagic or lethal chickenpox in the immunocompromised.
 Acute cerebellar ataxia and Reye's syndrome (if the patient had took
salicylates during the infection).
 Systemic involvement (myocarditis, hepatitis, arthritis…).

Treatment
2
HERPES ZOSTER (SHINGLES):

Herpes zoster (shingles) is an acute, self-limiting, vesicular eruption

occurring in a dermatomal distribution; it is caused by a reactivation of
Varicella zoster virus.

Aetiopathogenesis and pathology

Herpes zoster nearly always occurs in subjects who have previously had
varicella (chickenpox). The virus lies dormant in the sensory root ganglion
of the spinal cord, but when reactivated, the virus replicates and migrates
along the nerve to the skin, producing pain and ultimately inducing the
cutaneous lesions of shingles.

Clinical presentation

Pain (pre herpetic neuralgia), tenderness, itching or paraesthesia in the

dermatome may precede the eruption by 3-5 days. Erythema and grouped
vesicles follow, scattered within the dermatomal area. The vesicles become
pustular and then form crusts which separate in 2-3 weeks to leave scarring.
Secondary bacterial infection may occur. Herpes zoster is normally
unilateral and may involve adjacent dermatomes. The thoracic dermatomes
are affected in 50% of cases and, in the elderly, involvement of the
ophthalmic division of the trigeminal nerve is particularly common. Two-
thirds of patients with herpes zoster are over 50 years of age, and it is
uncommon in children. The lesions shed virus, and contacts with no
previous exposure may develop chickenpox. Local lymphadenopathy is
usual.

Special types of herpes zoster:

 HERPES ZOSTER OPHTHALMICUS:

Due to involvement of any branch of the ophthalmic nerve. The rash
extends from eye level to the vertex, but does not cross the midline. The
commonest ocular complications are anterior uveitis and keratitis.

 RAMSAY – HUNT'S SYNDROM:

Involvement of the geniculate ganglion, manifested clinically as herpes
2
zoster oticus (eruption on the 1pinna of the ear and in external auditory
meatus), facial nerve paralysis and auditory symptoms. Both sensory and
motor portions of the seventh cranial nerve are involved.
  DISSIMINATED HERPES ZOSTER:
Widespread herpes zoster involving skin, lungs and brain may occur in
patients with immunocompromization, especially those with Hodgkin's
disease.

Complications

Serious complications may occur in herpes zoster. These include:

- Necrosis, secondary infection and scarring.
- Ocular and auditory complications. Corneal ulcers and scarring may
result from
- shingles of the first trigeminal division.
- Neurogenic bladder and urinary retention in cases of sacral zoster
(S2, S3, S4).
- Encephalitis.
- Post herpetic neuralgia: is the persistence of severe pain in a
dermatome for more than one month, after lesions of herpes zoster have
disappeared. It is more common in elderly and in cases of trigeminal nerve
involvement. The pain subsides in the majority within 12 months.

Management

1. In mild shingles, treatment is symptomatic, with rest, analgesia and

bland drying preparations such as calamine lotion. Secondary bacterial
infection may require a topical antiseptic or antibiotic. More severe
cases may be treated, if seen within 48 hours of onset, with oral
aciclovir (800 mg 5 times per day for 7 days) or famciclovir (750 mg
once daily for 7 days) which promote resolution, reduce the viral
shedding time and may reduce postherpetic neuralgia.
Immunosuppressed patients often require intravenous aciclovir.

2. Treatment of post herpetic neuralgia:

 Heavy analgesia.
 Tricycles antidepressants and carbamazine.
 Systemic steroids.
 Topical "capsaicin" (substance P depletor).
 Intralesional xylocain with or without steroids.
 Nerve block in resistant cases.
german measles‫الحصبة االملانية او الـ‬ ‫الحصبة العادية‬

Rubella & Measles

These types are caused by systemic viral infection (viremia).
Rubella
Froschheimer spots
Runny nose
More numbers Less severe

The rash appears after 1-2 days

For any question, please sent it for the following email:

muhammad.k.albakaa@jmu.edu.iq