VIRAL DISEASES part II Andrews’ p501-525 Molluscum contagiosum Poxvirus MCV-1 to -4 and variants MCV-2 in HIV Worldwide Children, sexually active adults and immunosuppressed Direct contact Lesions are smooth surfaced, firm and dome shaped pearly papules A central umbilication is characteristic Clinical pattern depends on the group affected When restricted to only the genital area in a child the possibility of sexual abuse must be considered Secondary infections may occur Seen in 10-30 % of AIDS pts Helper T-cell count of less than 100 Giant lesion may be confused with BCC Henderson-Patterson bodies – basophilic inclusion bodies treatment Topical tretinoin or imiquimod Extraction Light cryotherapy Cantharadin Curettage podophyllotoxin Human monkeypox Rare More than 90% of cases occur in children under 15 Fatality rate of 11% Disease is clinically similar to smallpox Fever followed by vesiculopustular eruption Develop following contact with wildlife sources Human to human transmission may occur Picornavirus group RNA Only coxsackieviruses, the echoviruses, and enterovirus type 71 are significant causes of skin disease Enterovirus infections Person to person transmission occurs by the intestinal-oral route and less commonly the oral route Usually the diagnosis is by clinical characteristics herpangina Disease of children worldwide Coxsackievirus and echovirus Acute onset of fever, ha, sore throat, dysphagia, anorexia, and sometimes a stiff neck Yellowish white, vesicles in the throat, surrounded by an intense areola Most frequently on the anterior faucial pillars, tonsils, uvula, or soft palate Lesions coalesce and ulcerate leaving a shallow crater Lesions disappear in 5-10 days Treatment is supportive Topical anesthetics or allopurinol mouthwash Hand-Foot-and-Mouth Disease Infection begins with a fever and sore mouth 90% have oral involvement Lesions are small rapidly ulcerating vesicles surrounded by a red areola Buccal mucosa, tongue, soft palate, and gingiva Lesions on hands and feet Red papules that quickly turn to gray vesicles With a red halo Typically lasts less than a week Treatment is again supportive Topical anesthetics Coxsackievirus A-16 Distribution and presence of skin lesions differentiates this from herpangina Boston Exanthem Disease Occurred as an epidemic in Boston Caused by echovirus 16 Consisted of sparsely scattered pale red macules and papules Chiefly on the face chest and back Now an uncommon cause of viral exanthems Eruptive pseudoangiomatosis Young children during or immediately following a viral illness develop red papules that resemble angiomas Face trunk and extremities Resolve spontaneously within 10 days Echoviruses 25 and 32 have been implicated PARAMYXOVIRUS GROUP RNA viruses Measles Rubella Measles (rubeola, morbilli) Worldwide disease Commonly affects children under age of 15 months Respiratory spread with an incubation of 912 days Immunizations are highly effective Prodrome- fever, malaise, conjunctivitis and prominent upper respiratory symptoms A macular or maculopapular eruption appears after 1-7 days Anterior scalp line and behind the ears Quickly spreads over the face and involves the entire body by day 3 Purpura may be present Koplik’s spots are pathognomonic, appear during the prodrome Erythematous lesions of the measles exanthem Pink macules with minimally elevated papules with confluence Koplik’s Spots cluster of tiny bluish white papules with an erythematous areola on buccal mucosa opposite premolar teeth complications OM Pneumonia Encephalitis Thrombocytopenic purpura Infection in pregnant patients is associated with fetal death DX Clinical- high fever, Koplik’s spots, conjunctivitis, upper respiratory symptoms, rash course and prognosis maximum intensity of rash reached in 3 days rash fades 5-10 days self limited death 1 in 3000 chronic complication, subacute sclerosing panencephalitis RUBEOLA management Acute Vitamin A decreases morbidity and mortality given to severe measles even if no nutritional deficit is suspected vaccine MMR given at 12-15 months, and 4-6 years measles Rubella German measles, 3-day measles benign contagious viral disease etiology transmission Togavirus inhalation of aerosolized respiratory droplets incubation 12-23 days Vaccination gives lifelong immunity RUBELLA clinical manifestations Prodrome- 1-5 days mild symptoms of malaise, headache, sore throat, eye pain, and moderate temperature elevation Pain on lateral and upward eye movement is characteristic precedes eruption by a few hours to a day children are usually asymptomatic RUBELLA clinical manifestations Eruptive phase begins on neck or face spreads to trunk and extremities in hours lesions are pinpoint to 1 cm, round or oval, pinkish or rosy red, macules or maculopapules (purplish lesions of measles and fine punctate yellow-red lesions of scarlet fever) discrete, grouped or coalesced arthritis of phalangeal joints may be seen in women RUBELLA Diagnosis course and prognosis Clinical, posterior cervical, suboccipital, and postauricular lymphadenitis occurs in more than half can be confirmed with serology typically mild, requiring only symptomatic treatment lesions last 24 -48 hours, followed by desquamation prevention MMR given at 12-15 months, and 4-6 years rubella RUBELLA Forchheimer Spots red palatal lesions start with onset of rash Congenital Rubella Syndrome Infants born to mothers who have had rubella during the first trimester of pregnancy transplacental transmission as high as 80% in the first trimester Typical anomalies include IUGR, deafness, mental retardation, cataracts, retinopathy, cardiac defects, and “blueberry muffin” rash. Prior to pregnancy antibody titer should be verified. Immunization is contraindicated in pregnancy. Asymmetric Periflexural Exanthem of Childhood (APEC) AKA unilateral laterothoracic exanthem Children 8 mo to 10 yrs Cause is unknown Viral origin has been proposed Symptoms of mild upper respiratory or gastrointestinal infection usually precede the eruption Erythematous macules and papules involving the axilla, lateral trunk and flank. In this patient the exanthem progressed to bilateral distribution but maintained leftsided predominance Erythematous papules coalesce to form poorly marginated morbilliform plaques Mild pruritis Lesions begin unilaterally, close to a flexural area, usually the axilla Centrifugal spread to adjacent trunk and extremity The contralateral side is involved in 70% of cases, asymmetrical nature is maintained Lymphadenopathy is seen in 70% Last 2-6 weeks on average Resolves spontaneously Topical steroids or oral antibiotic are of no benefit Oral antihistamines PARVOVIRUS GROUP Erythema Infectiosum (Fifth Disease) Worldwide benign infectious exanthem Parvovirus B19 Spread by respiratory droplets Viral shedding has stopped by the time the exanthem has appeared Incubation 4-14 days prodrome pruritus, low-grade fever, sore throat, malaise seen in 10% of cases Three distinct overlapping stages facial erythema. Red papules on the cheeks that rapidly coalesce. Resembles erysipelas. “slapped cheek.” net pattern erythema. Fishnet like pattern, begins on extremities then extends to trunk recurrent phase. Eruption may reappear following emotional upset or sunlight exposure over next 2-3 weeks. Lacy, reticulated skin eruption over the arm during the second stage of the exanthem Papular Purpuric Stocking and Glove Syndrome Occurs in teenagers and young adults Pruritis, edema, and erythema of the hands and feet, and a fever is present Lesions are sharply cut off at the wrists and ankles Mild erythema of the cheeks, elbows, knees and groin Syndrome resolves within 2 weeks Erythematous patches with petechiae on the palms Serovonversion for parvovirus B19 has been found Complications are uncommon and age dependent Arthritis and arthralgias occur in 60% of adult women Aplastic crises may result in the sickle cell pt In primarily infected pregnant women, fetal death can result from hydrops fetalis as a result of intrauterine anemia, esp. first 20 weeks ARBOVIRUS GROUP Comprise the numerous arthropod-borne RNA viruses West Nile Fever A maculopapular eruption accompanied by lymphadenopathy and fever characterize this disease The Culex mosquito is the vector Disease seen in the Middle East Sandfly Fever AKA phlebotomus fever and pappataci fever Small pruritic papules appear after the bite of a sandfly Fever, ha, malaise, nausea, conjunctival injection, stiff neck, and abdominal pains suddenly develop Recovery is slow, with recurring bouts of fever No specific treatment is available Dengue (break-bone fever) A common disease of tropical regions throughout the world Spread by Aedes aegypti mosquito Disease begins with a sudden high fever, ha, back ache, retroorbital pain, bone and joint pain, weakness, depression and malaise A scarlatiniform or morbilliform exanthem, especially on the thorax and joint flexors may be seen Patient may recover fully at this stage In 1-7% of cases dengue hemorrhagic fever develops, bleeding, thrombocytopenia, and hemoconcentration develop Mortality 1-15% Alphavirus Sindbis virus infection Seen in Finland Transmitted by the mosquito Multiple erythematous papules with a surrounding halo associated with a fever and prominent arthralgias Symptoms resolve over a few weeks PAPOVAVIRUS GROUP DS, DNA viruses Slow growing Replicate within the nucleus Verruca Human papillomaviruses include more than 80 types Most types cause specific types of warts and favor certain anatomic locations Infections are described as clinical, subclinical and latent Verruca vulgaris Commonly HPV 2 5% prevalence in children Frequent emersion of hands in water is a risk factor Natural history is for spontaneous resolution, half by 1 year and two thirds by 2 years Usually located on the hands Present as elevated, rough, grayish papules Verruca vulgaris. Note the characteristic features of ‘church spire’ papillomatosis heaped with orthoand parakeratosis, acanthosis and koilocytosis. Diagnostic clue- warts do not have dermatoglyphics Occur anywhere on skin Spread by autoinnoculation Digitate or filiform warts on the face and scalp Verruca plana HPV 3 Children and young adults Flat-topped papules that are slightly erythematous or brown Generally multiple and grouped Face, neck, dorsa of hands, wrists and knees Men who shave and women who shave their legs Koebnerization Highest rate of spontaneous remission Verruca plantaris HPV type 1 Appear at pressure points on the ball of the foot Frequently several lesions are seen Mosaic wart May be confused with callous, no black dots Myrmecia type- occurs as smooth surfaced, deep, often inflamed and tender papules or plaques- may be confused with mucinous cyst Myrmecial wart Verrucae plantares Photo after the shaving of the hyperkeratotic surface HPV-60 Ridged wart Persistence of dermatoglyphics This type also causes plantar verrucous cysts treatment Depends on the type of wart and the age of the patient Allow 2-3 months of therapy Do not abandon any treatment too quickly TX-flat warts Frequently undergo spontaneous remission Cryotherapy Topical salicylic acid preparations topical tretinoin 5-FU anthralin TX-common warts Two basic approaches Destruction and Induction of local immune reactions Cryotherapy, salicylic acid preparations, canthrone, bleomycin, surgical ablation, laser, high dose cimetidine, heat treatment, isotretinoin, hypnotic suggestion, DNCB TX-plantar warts Salicylic acid preparations Cryotherapy Cantharadin Bleomycin, laser, and DNCB Genital warts The most common sexually transmitted disease Lifetime risk in sexually active young adults may be as high as 80% A large portion of genital HPV is either subclinical or latent Infection is closely linked with cancer of the cervix, glans penis, anus, vulvovaginal area, and periungal skin Transition zones of cervix and anus Numerous HPV types are associated with genital warts Those producing benign lesions- low risk Those associated with cancer- high risk or oncogenic type Most common are HPV-6 and HPV-11 most common HPV-16 and HPV-18 Virtually all condylomata are caused by types –6 and –11 Condylomata acuminata Appear as lobulated papules that are frequently multifocal Intraurethral condylomata may present with terminal hematuria, altered urinary stream, or urethral bleeding Numerous genital warts may appear during pregnancy Other sexually transmitted disease may be present Bowenoid papulosis and HPVinduced genital dysplasias Characterized by flat, often hyperpigmented papules Singly or in multiples HPV-16may behave similar to other genital warts May progress to invasive SCC Bowenoid papulosis of the anus positive for high-risk HPV in a homosexual male Erythroplasia of Queyrat. A well demarcated velvety plaque of the prepuce positive for high-risk HPV Giant condyloma acuminatum (Buschke-Löwenstein tumor) A rare, aggressive wart-like growth that is a verrucous carcinoma HPV-6 Most often occurs on the glans penis or prepuce of an uncircumcised male May invade deeply, and uncommonly metastases Complete surgical excision Buschke- Löwenstein Tumor Cauliflower-like deeply infiltrating giant condyloma acuminata Diagnosis of genital warts Inspection Acetowhitening may help in the differentiation of certain genital papules Bowenoid papulosis may require Bx Treatment of genital warts Recurrence is frequent Not proven to reduce transmission to sexual partners nor to prevent progression to dysplasia or cancer Subclinical of the external genitalia should not be sought or treated Bleeding genital warts may increase the sexual transmission of HIV and hepatitis B and C Treatment of genital warts Podophyllin 4-8 hrs, weekly application Purified podophyllotoxin 0.5% sln Aldara, 3 alternate days per week TCA (safe in pregnancy) Cryotherapy (also safe in pregnancy) Electrofulgeration or electrocauterization CO2 laser Any surgical method that generates a smoke plume is potentially infectious to the surgeon 5-FU 5% cream, esp. bowenoid papulosis Systemic and intralesional interferon alfa CDC no longer recommends Genital warts in children Children can acquire genital warts through vertical transmission perinatally, digital inoculation or autoinoculation, fomite or social nonsexual contact, or through sexual abuse HPV typing has demonstrated that most warts in the genital area of children are “genital” HPV type And most children with them have family members with them as well Finding of a nongenital type does not exclude abuse The risk for sexual abuse is highest for children older than 3 yrs of age Case-by-case management Should screen for other STDs Podophyllotoxin, imiquimod, light cryotherapy Recurrent respiratory (laryngeal) papillomatosis HPV associated papillomas may occur throughout the respiratory tract, from the nose to the lungs Bimodal distribution- children under 5 and after 15 Affected young children were born to mothers with genital condylomata and present with hoarseness HPV-6 HPV-11 Carcinoma that is often fatal develops in 14% Heck’s disease Linked to HPV-13 AKA focal epithelia hyperplasia Small white to pinkish papules occur diffusely in the oral cavity Epidermodysplasia verruciformis A rare inherited disorder characterized by widespread HPV infection and cutaneous SCCs Most commonly inherited as and AR trait HPV-3, HPV-10 and many other “unique” types Pathogenesis is unknown Presents in childhood and continues throughout life Skin lesions include flat, wartlike lesions of the dorsal hands, extremities, and face SCCs develop in 30-60% of pts, most often on sun exposed areas,-5,-8,-47 Actinic background Surgery, radiation is contraindicated Strict sun avoidance Warts in immunosuppressed patients Predisposing conditions include organ transplantation, immunosuppressive medication, congenital immunodeficiency diseases, lymphoma and HIV infection By 5 yrs posttransplant 90% of pts have warts Regular dermatologic examinations Standard methods of treatment, efficacy is reduced RETROVIRUSES Contain RNA which is converted by a virally coded reverse transcriptase to DNA in the host cell The target cell population is primarily CD4+ lymphocytes Transmission by sexual intercourse, blood products/intravenous drug use, and from mother to child during childbirth or breastfeeding HTLV-1 Endemic in Japan, subSaharan Africa and southeastern US Responsible for several clinical syndromes 1% will develop adult T-cell leukemialymphoma Four forms: smoldering, chronic, acute, and lymphomatous, usually progressing in that order Skin lesions in ATLL include erythematous papules or nodules Infected patients may develop various forms of dermatitis mimicking other skin diseases Infective dermatitis, children present with a chronic eczema of the scalp, axilla, groin, external auditory canal, retroauricular area, eyelid margins, paranasal areas and neck Chronic nasal discharge Cultures positive for S. aureus Human Immunodeficiency Virus (HIV, HTLV III) Cutaneous manifestations are prominent Affecting up to 90% of HIV-infected persons Many have multiple skin lesions of different types Skin lesions can be classified into three broad categories: infections, inflammatory dermatoses, and neoplasms Skin lesions tend to appear at a specific stage of disease, making them useful markers Seborrheic dermatitis , pruritis ani, psoriasis, Reiter’s syndrome, atopic dermatitis, herpes zoster, acne rosacea, oral hairy leukoplakia, onychomycosis, warts, recurrent S. aureus folliculitis and mucocutaneous candidiasis- helper T-cell counts 200-500 With counts < 200, pt defined as AIDS Opportunistic infections: chronic herpes simplex, MC, bacillary angiomatosis, systemic fungal infections and mycobacterial infections Hyperreactive skin is also seen: eosinophilic folliculitis, GA, drug reactions, photodermatitis Eosinophilic folliculitis (right) Bacillary angiomatosis (below) T-cell count < 50 = advanced AIDS Unusual presentations of opportunistic infection Treatment is difficult Combination cocktails, (HAART), highly active antiretroviral therapy About half of HIV patients respond Opportunistic infections no longer occur and mortality decreases Eosinophilic folliculitis and drug eruptions may become more frequent and severe Primary HIV infection (Acute seroconversion syndrome) An acute illness develops several weeks after infection Clinical syndrome resembles Ebstein-Barr infection Fever, sore throat, cervical adenopathy, rash, and oral and genital and rectal ulceration Dysphagia may be prominent Oral candidiasis or Pneumocystis carinii may develop Suspect DX in at risk individuals Direct measurement if HIV load will confirm Prompt combination antiviral therapy HIV-Associated pruritis Not caused by HIV disease itself but related to its associated inflammatory dermatoses “papular pruritic eruption”- a wastebasket diagnosis Follicular eruptions are more common Eosinophilic folliculitis is the most common pruritic follicular eruption, helper T-cell <200 Urticarial follicular papules on the upper trunk, face, scalp, and neck 90% of lesions occur above the nipple line Disease wanes and wanes and may spontaneously clear, only to flare unpredictably Peripheral eosinophilia may be present Topical steroids and antihistamines Phototherapy or itraconazole isotretinoin HIV-Associated Neoplasia Kaposi’s sarcoma Superficial BCC SCC Genital HPV-induced SCC Extranodal B-cell and T-cell lymphoma BCC’s behave in the same manner, receive standard management SCC’s, standard management, excision is recommended SCC in sun-exposed skin can be very aggressive Genital SCC, associated with “high-risk” HPV types (-16, -18) Extranodal B-cell and T-cell lymphoma Associated with advanced immunosuppression of AIDS Present as violaceous or plum-colored papules, nodules or tumors MF can also be seen in patients with HIV infection Melanoma Occasionally seen in HIV patients Prognosis is unknown It has been suggested that the risk of metastasis is increased AIDS and Kaposi’s Sarcoma HHV-8 Patients with AIDS present with symmetrical widespread lesions, that are often numerous Any mucocutaneous surface may be involved Favors hard palate, trunk, penis, lower legs and soles DX by biopsy Red-violet papules on the palate in addition to oral candidiasis Treatment depends on the extent and aggressiveness of the disease Effective HAART after about 6 months is associated with involution of KS lesions Initial treatment for fewer than 50 lesions Intralesional vinblastine Cryotherapy Irradiation therapy Systemic therapy in aggressive disease Interferon alfa Vinca alkaloids Bleomycin Liposomal doxyrubicin
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