2. Warts (Verruca):
Etiology: Human papilloma virus (HPV)
Epidemiology:
==Age
Nongenital warts: Most frequent in children and young adults,
Anogenital warts: In adolescents and adults, though occasionally may be seen in children.
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 anogenitalwarts can transmit infection to the
newborn,during vaginal delivery.
3. Clinical Features
Verruca vulgaris: Verrucous papules; on hands and feet.
Superficial palmoplantar warts: Superficial, confluent,painless warts; on palms, soles.
Deep palmoplantar warts: Deeper, discrete, painfulwarts; on palms, soles.
Verruca plana: Flat, smooth papules; on face.
Filiform warts: Elongated warts; on face and scalp.
Anogenital warts: Sexually transmitted, genital warts.
6. Plane warts: multiple, skin-colored
papules.
Filiform warts: thin, firm projections in
the beard region.
7. Treatment:
Cryotherapy:
Cryogens: Liquid nitrogen, carbon dioxide, and nitrous oxide.
Technique: A cotton-tipped applicator dipped in cryogen is applied firmly to
the wart.
Electric cautery and radiofrequency ablation (RFA)
8. Topical agents:
Salicylic acid (10–25%):Keratolytic, so reduces thickness of
wart and induces an inflammatory response.
Wart paint: Contains salicylic acid and lactic acid.
Retinoic acid (0.05–0.1%):
Formalin soaks: Ideal for multiple small plantar warts. Feet
are soaked in 4% formalin solution for about 10 min.
9. Mechanical removal:
Mechanical removal using a curette followed by
cauterization of the bleeding base using
trichloroacetic acid (TCA) 50% is a frequently
method when other facilities are not available.
10. Molluscum Contagiosum (MC)
Etiology: Pox virus.
Transmission:
- Direct spread.
- Fomites (clothes and towels).
- Sexual transmission.
Morphology: Usually multiple. Pearly white, dome-shaped papules which are umbilicated.
Treatment: Mechanical destruction, chemical cauterization or cryotherapy. Wart paint, if
several lesions.
13. Varicella-Zoster Infections: chicken
pox
Etiology: Varicella-zoster virus.
Highly contagious, spread by droplet route.
Patient infectious for 1–2 days before the exanthema 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.
Prodrome: Fever and malaise.
Site: Centripetal distribution.
14. Morphology:
Lesions appear in crops.
Itchy papules that rapidly turn into clear superficial vesicles
and then pustules with erythematous halo
dew drops on rose petal appearance.
Heal with minimal scarring unless complicated by
secondary infection or hemorrhagic lesions (as seen in
immunocompromised).
15.
16. Sites of predilection :
Lesions most profuse on the trunk (covered parts) and least on face and limbs (centripetal
distribution).
18. Herpes Zoster: Shingles
Etiology: Varicella-zoster virus. After an attack of chicken pox, virus lies
dormant in sensory root ganglia. Zoster is a manifestation of its reactivation.
Morphology: Very painful, segmental eruption of grouped papules and vesicles on an
erythematous, slightly edematous base. Self-limiting. Crust in a week.
Sites of predilection:
Unilateral segmental distribution, though lesions may affect more than one adjoining
dermatome.
Thoracic intercostal nerves, ophthalmic division of trigeminal nerve.
20. Treatment:
Mild cases
Treat pain with analgesics (round the clock).
Treat secondary bacterial infection with broad spectrum antibiotics.
Severe cases:
Symptomatic treatment: NSAIDs.
Specific treatment: With antiviral drugs
Antiviral drugs: start within 72 h of an attack.
Acyclovir: 800 mg, five times a day × 7days (adult dose).
Famciclovir: 500 mg, three times a day × 7days.
Valacyclovir: 1 g, three times a day × 7 days
21. Complications:
Postherpetic neuralgia: Persistent neuralgic pain in some
patients.
Hutchison’s sign: is a clinical sign which may refer to:
Hutchinson's pupil, a unresponsive and enlarged pupil on the side
of an intracranial mass;
Vesicles on the tip of the nose, or vesicles on the side of the nose,
precedes the development of ophthalmic herpes zoster.
Secondary bacterial infection may occur.
22. Herpes Simplex Virus (HSV) infections
Etiology: HSV HOMINIS (type I and type II).
Type I generally causes lesions above the waist,
while type II causes genital infection.
After primary infection (first infection),the virus lies
dormant in sensory ganglion and gets activated from
time to time.
24. Clinical Features
First episode disease:
Primary type I infection: Usually occurs in children.
Manifestations: asymptomatic.
Or may present as acute gingivostomatitis: characterized by
grouped vesicles which rapidly form ulcers covered with a yellow
pseudomembrane.
Heal in about a fortnight.
Malaise, fever, and lymphadenopathy are frequent.
25. Primary type II infection
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.
28. Recurrent infections
Occur due to reactivation of virus from sensory
nerve ganglia.
Manifestations are precipitated by:
Upper respiratory infections associated with
fever
Ultraviolet radiation.
Stress.
Menstrual periods.
29. Investigations
Usually no investigations are needed for herpes
labialis but for herpes genitalis, following
investigations are helpful.
Identification of virus in tissues: Tzanck smear:
Fluorescent antibody test:
Polymerase chain reaction:
