Viral Skin Infections

Presented by: Laith Sorour

Herpes Simplex Virus

• Herpesvirus hominis is the cause. The virus is ubiquitous and carriers continue to shed virus particles in their saliva or tears.

Two types: 1. Type I Virus (HSV-1) : usually extragenital. 2. Type II virus (HSV-2): mainly on the genitals.

*however, this distinction is not absolute.

• Route of infection: 1. mucous membranes 2. abraded skin.

• After the episode associated with the primary infection, the virus may become latent, possibly within nerve ganglia, but still capable of giving rise to recurrent bouts of vesication (recrudescences).

Presentation Primary infection :

• most common manifestation of a primary type I infection in children is an acute gingivostomatitis

• Malaise, headache, fever and enlarged cervical nodes.

• Vesicles, soon turning into ulcers, seen scattered over the:

• Lips • Mucous membranes.

• The illness lasts about 2 weeks.

Herpetic whitlow

• Direct inoculation (eg. During wrestling)

• Pus-filled blisters on a fingertip.

Primary type II

• Transmitted sexually

• Multiple

• Painful

• Genital or perianal blisters which rapidly ulcerate.

Recurrent (recrudescent) infections

• Same place each time.

• Precipitated by

• RTI (cold sores)

• Ultraviolet radiation

• Menstruation

• Stress.

• Common sites

• Face

• Lips (type I)

• Genitals (type II)

• Lesions can occur anywhere.

• Tingling, burning or pain is followed within a few hours by Erythema and clusters of tense vesicles.

• Crusting occurs within 24–48 h .

• The whole episode lasts about 12 days.

Complications • Herpes encephalitis or meningitis

• Disseminated herpes simplex

• Eczema herpeticum: patients with atopic eczema are particularly susceptible to widespread cutaneous herpes simplex infections. Those looking after patients with atopic eczema should stay away if they have cold sores.

• Recurrent dendritic ulcers leading to corneal scarring.

• Recurrent herpes simplex infections are regularly followed by Erythema multiforme.

Investigations: • Culture

• Antibody titres rise with primary, but not with recurrent infections.

Treatment: • Sunblock

• Dabbing with the surgical spirit

• Topical bacitracin, mupirocin, framycetin or fusidic acid (20 infection)

• Aciclovir cream ( applied 5-6X a day for the first 4 days of the episode)

• More effective still is oral aciclovir 200 mg five times daily for 5 days

• Recurrences in the immunocompromised can usually be prevented by long-term treatment at a lower dosage.

ECZEMA HERPETICUM erythma multiform

HPV • Warts are caused by the human papilloma virus.

• Their prevalence is highest in childhood.

HPV-1, 2 and 4 are found in common warts.

HPV-3 is found in plane warts.

HPV-6, 11, 16 and 18 are most common in genital warts.

• Warts adopt a variety of patterns :

1. Common warts: The first sign is a smooth skin- coloured papule , often more easily felt than seen. usually occur on the hands ,face and genitals . They are more often multiple than single . Pain is rare.

2. Plantar warts: These have a rough surface, which protrudes only slightly from the skin and is surrounded by a horny collar . On paring, the presence of bleeding capillary loops allows plantar warts to be distinguished from corns . Often multiple , plantar warts can be painful.

3. Mosaic warts : These rough marginated plaques are made up of many small tightly packed but distinct individual warts. They are most common on the soles but are also seen on palms and around fingernails. Usually , they are not painful.

4. Plane warts :These smooth flat-topped papules are most common on the face and brow, on the backs of the hands , and on the shaven legs of women. Usually skin-coloured or light brown, they become inflamed as a result of an immunological reaction, just before they resolve spontaneously . Lesions are multiple and painless

5. Facial warts: These are most common in the beard area of adult males and are spread by shaving. They are painless.

6. Anogenital warts : Papillomatous cauliflower-like lesions,with a moist macerated vascular surface

• Complications : • Some plantar warts are very

painful

• Epidermodysplasia verruciformis (treeman syndrome) AR

• Malignant change is otherwise rare although infection with HPV types 16 and 18 predisposes to cervical carcinoma. HPV infections in immunocompromised patients have also been linked with skin cancer.

Treatment : Many warts give no trouble, need no treatment and go away by themselves. Otherwise, treatment will depend on the type of wart. • Palmoplantar warts : home treatment is best, with one of the

many wart paints or plasters now available, Most contain salicylic acid

• No progress after regular correct use of salicylic acid Cryotherapy with liquid nitrogen , however its painful.

• Anogenital warts : self-treatment using podophyllotoxin or imiquimod , Two vaccines against HPV-6 and 11 are now available.

• Facial common warts : These are best treated with electrocautery .

• Plane warts : On the face these are best left untreated and spontaneous resolution will occur.

• Solitary , stubborn or painful warts : These can be removed under local anesthetic with a curette or Bleomycin can also be injected into such warts .

Varicella (Chickenpox)

Cause

• The herpes virus varicella-zoster is spread by the respiratory route; its incubation period is about 14 days.

Presentation and course

• Slight malaise then papules, which turn rapidly into clear vesicles on a pink base (‘dew drops on a rose petal’).Vesicles soon become pustules and then umbilicate.

• Over the next few days the lesions crust and then clear, sometimes leaving white depressed scars. Lesions appear in crops, are often itchy and are most profuse on the trunk and least profuse on the periphery of the limbs (centripetal).

• Second attacks are rare. Varicella can be fatal in those who are immunologically compromised.

Complications • Pneumonitis, with pulmonary opacities on X-ray.

• Secondary infection of skin lesions.

• Haemorrhagic or lethal chickenpox in patients with leukaemia and other immunocompromised children and adults.

• Scarring.

Differential diagnosis • Smallpox, mainly centrifugal anyway, has been universally

eradicated in 1980, and the diagnosis of chickenpox is seldom in doubt.

Investigations • None are usually needed. The Tzanck smear is positive.

Treatment • In mild attacks, calamine lotion topically is all that is required.

• Aciclovir, famciclovir and valaciclovir should be reserved for severe attacks and for immunocompromised patients; for the latter.

• Prophylactic aciclovir can also be used to prevent disease if given within a day or two of exposure.

• Alive attenuated vaccine is now available, and being more widely used. It is not universally effective and should not be given to patients with immunodeficiencies, therapeutic immunosuppression, or blood dyscrasias who might not be able to resist even the attenuated organism.

Herpes zoster (Shingles) • Caused by the herpes virus varicella-

zoster/HHV-3 (reactivation)

• The incidence is high, when weaken normal defence mechanisms in:

• Old age • Hodgkin’s disease • AIDS • Leukaemia

• Shingles does not occur in epidemics

• Patients with zoster can transmit the virus to others in whom it will cause chickenpox.

Presentation and course

• Start with a burning pain, Soon followed by erythema and grouped.

• Sometimes blood-filled vesicles scattered over a dermatome.

• The clear vesicles quickly become purulent

• Over the space of a few days burst and crust.

• Scabs usually separate in 2–3 weeks, sometimes leaving depressed depigmented scars.

• Unilateral

• It may affect more than one adjacent dermatome.

• The thoracic segments and the ophthalmic division of the trigeminal nerve are involved disproportionoften.

• Generalized chickenpox-like eruption accompanying segmental zoster, particularly if the lesions are unusually haemorrhagic or necrotic, should raise suspicionsately of:

• Immunocompromised state

• Malignancy`

Complications:

• Secondary bacterial infection is common.

• Motor nerve involvement is uncommon, but has led to paralysis of ocular, facial muscles, diaphragm & bladder.

• Corneal ulcers and scarring (zoster of the ophthalmic division of the trigeminal nerve). A good clinical clue here is involvement of the nasociliary branch (vesicles grouped on the side of the nose).

• Persistent neuralgic pain, after the acute episodeis over, is most common in the elderly.

DDx:

• Pain (before the rash has appeared) • Acute appendicitis • Myocardial infarction

• An early painful red plaque may suggest • cellulitis • Herpes simplex • Eczema • Impetigo

NOTE: THE DERMATOMAL DISTRIBUTION AND THE PAIN ALLOW ZOSTER TO BE DISTINGUISHED EASILY FROM HERPES SIMPLEX, ECZEMA AND IMPETIGO.

Investigations:

• Cultures (only positive in 70%)

• Biopsy or Tzanck smears • Multinucleated giant cells • Ballooning degeneration of keratinocytes

Treatment:

• Systemic treatment (within the first 5 days)

• Early: Famciclovir and valaciclovir

• Late: (supportive) • Systemic treatment is not likely • Rest • Analgesics • Calamine • Prevention (|vaccine) better than treatment

Orf • Contagious pustular dermatitis is common in lambs. Its cause is a parapox virus that can be

transmitted to those handling infected animals.

• The incubation period is 5–6 days.

• Lesions, which maybe single or multiple, start as small firm papules that change into flat-topped apparently pustular nodules with a violaceous and erythematous surround

• The condition clears up spontaneously in a bout a month

Complications 1. Lymphadenitis and malaise are common.

2. Erythema multiforme

3. ‘Giant’ lesions can appear in the immunosuppressed

Investigations

• None are usually needed.

• If there is any doubt, the diagnosis can be confirmed by the distinctive electron microscopic appearance of the virus obtained from crusts.

Treatment • Topical antibiotic helps to prevents secondary infection; otherwise no active therapy is

needed.

Molluscum contagiosum Cause • common pox virus infection which can be spread by

direct contact (e.g. sexually or by sharing a towel at the swimming bath).

Presentation and course • The incubation period ranges from 2 to 6 weeks.

• Individual lesions are shiny, white or pink, and hemispherical they grow slowly up to 0.5 cm in diameter. A central punctum which may contain a cheesy core that gives the lesions their umbilicated look.

• On close inspection a mosaic appearance may be seen.

• Multiple lesions are common and their distribution depends on the mode of infection. Atopic individuals and the immunocompromised are prone to especially extensive infections.

• spread by scratching and the use of topical steroids.

• Untreated lesions usually clear in 6–9 months, often after a brief local inflammation. Large solitary lesions may take longer. Some leave depressed scars.

Complications Eczematous patches secondarily infected

Investigations • None are usually needed, but the diagnosis can be

confirmed by looking under the microscope for large swollen epidermal cells, easily seen in unstained preparations of the lesion.

Treatment • Treatment Many simple destructive measures

cause inflammation and then resolution. They include squeezing out the and curettage.

• doing nothing is often the best option in children.

• Sometimes a local anaesthetic for an hour, will help children to tolerate more attacking treatment

• Sparse eyelid lesions can be left alone but patients with numerous lesions may need to be referred to an ophthalmologist for curettage.

Thank you

• Resources:

• Clinical dermatology 5th edition

• PUBMED