Cutaneous Viral Infections Alisha Plotner, MD Assistant Professor Division of Dermatology.

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Presentation transcript:

Cutaneous Viral Infections Alisha Plotner, MD Assistant Professor Division of Dermatology

Learning Objectives  Diagnose viral infections of the skin based on their clinical findings.  Plan treatment approaches for viral infections of the skin.

VERRUCA/CONDYLOMA Cutaneous Viral Infections

Warts  Due to human papilloma virus (HPV), which is a double stranded DNA virus  Can infect epithelial keratinocytes (skin, genital, mucosa)  Well over 70 different HPV viral strains  Can present anywhere in body, including fingers, hands, feet, genitals

HPV Types  Plantar warts – HPV 1  Periungual warts – HPV 2  Flat warts – HPV 3  Benign genital warts HPV 6 or 11  Genital warts with malignant potential HPV 16, 18, 31, 33

Genital Warts  Most common sexually transmitted disease  HPV types 6 and 11 are most common  HPV types 16, 18, 31, 33 can induce squamous cell cancer  Can appear as verrucous papules in genital surface or genital area  Are potentially contagious even after treatment has produced visible resolution  Can be associated with cervical cancer and anal cancer  Individuals with suppressed cell mediated immunity are at particular risk for developing genital and anal cancer, including HIV and organ transplant patients

Wart Treatment  Destructive  Scalpel or curette  Salicylic Acid  Liquid nitrogen  Laser  Inhibit HPV proliferation  5-fluorouracil  Podophylotoxin  Immune modulating  Imiquimod  Interferon

MOLLUSCUM CONTAGIOSUM Cutaneous Viral Infections

Molluscum Contagiosum  Due to a large DNA virus classified as a pox virus  More common in children, especially with atopic dermatitis or immunosuppressed adults, especially with advanced HIV  Often presents with a small (1-3mm) shiny, skin colored papule with a central dimple  Patients with advanced HIV may exhibit extremely large molluscum  May resolve spontaneously or be treated, if symptomatic

Molluscum treatment  Spontaneous resolution  Curettage  Salicylic acid  Liquid nitrogen  Cantharidin  Imiquimod

HERPES VIRUS INFECTIONS Cutaneous Viral Infections

Oral & Genital Herpes Simplex Virus (HSV)  Are double-stranded DNA virus and generally spread by direct skin to skin contact  HSV-1 – cause 80% oral-labial, 20% genital herpes cases  HSV-2 – cause 80% genital, 20% oral-labial herpes cases  In the U.S. population, prevalence of HSV-1 antibodies (indicating infection) is 80-90% and prevalence of HSV-2 antibodies is 20%

HSV Cutaneous Manifestation  Manifest as pain, burning, tingling prior to the appearance of the lesions  Lesions are localized groups of vesicles on an erythematous base  Vesicles rupture producing a painful superficial ulcer  After initial contact, virus replicates in mucocutaneous tissue, travels down axon, establishes latency in dorsal root ganglion

HSV-1 and HSV-2 Treatment  Oral or IV antiviral agents  Acyclovir or valacyclovir  Episodic or prophylactic dosing  Prophylactic dosing decreases asymptomatic viral shedding

Neonatal Herpes  Acquired from exposure to HSV shed by mother into birth canal at time of delivery  Most common in mothers with a primary genital HSV infection, but can occur with recurrent genital HSV  Skin lesions are groups vesicles on an erythematous base  Approximately 75% of affected infants will have skin lesions  Neonatal HSV can be a severe multi system fatal infection  If neonatal HSV is suspected, cultures should be obtained and treatment started immediately.

Varicella (Chicken Pox)  Caused by varicella zoster virus (VZV)  Prodrome of low grade fever and generalized malaise  Lesions manifest as small vesicles on an erythematous base (dew drops on a rose petal)

Varicella (chicken pox, cont.)  Individual lesions present as vesicles that rupture and produce superficial ulcers that scab and heal over  Crops of lesions erupt that produce lesions in many different stages  Eruption is prominent on face and extremities

Varicella Zoster  Caused by varicella zoster virus  After an episode of varicella, virus remains latent in dorsal root ganglia and trigeminal ganglion  Reactivation leads to viral proliferation and retrograde axonal transport to skin  Most common in elderly and immunosuppressed patients

Varicella Zoster Manifestations  Presents initially as erythematous plaque along a dermatomal distribution with sharp cut off at midline  Pain, burning, tingling often precedes the eruption  Vesicles soon develop in the plaque, which rupture and scab

Varicella Zoster Complications  V1 dermatomal involvement can lead to visual impairment  Post herpetic involvement can lead to persistent pain for months after the eruption resolves  Disseminated lesions can occur

Varicella Zoster Treatment  Zoster is treated with antiviral medications  Valacyclovir, acyclovir, famciclovir can be given orally, if initiated within 48 hours  Post-herpetic neuralgia is treated with gabapentin, tricyclic antidepressants, nerve blocks

Summary  Warts are caused by the human papilloma virus (HPV)  Different types of warts are caused by differing HPV subtypes  Molluscum contagiosum is a cutaneous pox virus infection seen commonly in children and immunosuppressed adults  HSV 1 and 2 cause both orolabial and genital herpes infections  Varicella zoster virus causes chicken pox (varicella) upon initial infection. Later in life the dormant virus can reactivate causing shingles (zoster).

References  Bolognia, Jorizzo, and Schaffer. Dermatology, 3rd Edition. Saunders, 2012.

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