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Pediatric Molluscum: an Update

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Pediatric Molluscum: an Update CLINICAL REVIEW Pediatric Molluscum: An Update Nanette B. Silverberg, MD 30 years. Deciding the best course of therapy requires PRACTICE POINTS some fundamental understanding about how MCV • Molluscum appears as pearly papules with a central relates to the following factors: epidemiology, childhood dell (ie, umbilicated). immunity and vaccination, clinical features, comorbidities, • Caused by a poxvirus, the disease is very contagious and quality of life. Treatment depends on many factors, and transferred via skin-to-skin contact or fomites. including presence or absence of atopic dermatitis (AD) • One-third of children with molluscum will develop and/or pruritus, other symptoms, cosmetic location, and symptoms of local erythema, swelling, or pruritus. the child’s concern about the lesions. Therapeutics include • Diagnosis usually is clinical. destructive and immunologic therapies, the latter geared • Children are primarily managed through observation; toward increasingcopy immune response. however, cantharidin, cryotherapy, or curettage can be used for symptomatic or cosmetically con- Epidemiology cerning lesions. Molluscum contagiosum virus is the solo member of the Molluscipoxvirus genus. Infection with MCV causes benignnot growth or tumors in the skin (ie, molluscum). Molluscum contagiosum virus (MCV) is a poxvirus that causes The infection is slow to clear because the virus reduces 1,2 infection in humans that is limited to the cutis and subcuta- the host’s immunity. Molluscum contagiosum virus is neous levels of the skin. The virus is transmitted from Doclose a double-stranded DNA virus that affects keratinocytes associates in settings such as pools, day care, and bathtubs. and genetically carries the tools for its own replication Pediatric molluscum is common in school-aged children and (ie, DNA-dependent RNA polymerase). The virus has a resolves spontaneously in healthy children. Widespread lesions, few subtypes—I/Ia, II, III, and IV—with MCV-I predomi- complicated by comorbid dermatitis, are expected in children with atopic dermatitis (AD); however, even children without AD nating in children and healthy humans and MCV-II in 1,2 can develop dermatitis or signs of inflammation or pruritus. patients with human immunodeficiency virus. Typing is Molluscum is the great mimicker in pediatric dermatology; the experimental and is not standardly performed in clinical morphology of the lesions and overlying rash can make mol- practice. Molluscum contagiosum virus produces a variety luscum look polymorphous and similar to other skin illnesses. of factors that block the host’s immune response, pro- This article addresses the issue CUTISof transmission, course of dis- longing infection and preventing erythema and inflam- ease, comorbidities, and therapeutic options, including the gold matory response.3 standard—nonintervention. The decision to intervene is a joint decision among children, parents/guardians, and the practitioner. Molluscum contagiosum virus is transmitted through The first priority should be reduction of symptoms, followed by skin-to-skin contact and fomites, including shared towels, reduction of spread and then disease remission. bathtubs, spas, bath sponges, and pool equipment.2,4,5 Cutis. 2019;104:301-305. Transmission from household contact and bathing together has been noted in pediatric patients with MCV. Based on the data it can be posited that the lesions are softer when wet and more readily release viral particles olluscum contagiosum virus (MCV) infection or fomites, and fomites may be left on surfaces, especially causes the cutaneous lesions we call molluscum. when a child is wet.6,7 Propensity for infection occurs MMolluscum has become common in the last in patients with AD and in immunosuppressed hosts, From the Departments of Dermatology and Pediatrics, Icahn School of Medicine at Mount Sinai, New York, New York. The author reports no conflict of interest. The eTable is available in the Appendix online at www.mdedge.com/dermatology. Correspondence: Nanette B. Silverberg, MD, Mount Sinai Health Systems, Mount Sinai Hospital, Department of Dermatology, 5 E 98th St, 5th Floor, New York, NY 10029 ([email protected]). WWW.MDEDGE.COM/DERMATOLOGY VOL. 104 NO. 5 I NOVEMBER 2019 301 Copyright Cutis 2019. No part of this publication may be reproduced, stored, or transmitted without the prior written permission of the Publisher. PEDIATRIC MOLLUSCUM including children with human immunodeficiency virus after the smallpox vaccine was discontinued, the factors and iatrogenic immunosuppression caused by chemo- appear related; however, the scientific data do not support therapy.1,2,8 Contact sports can increase the risk of trans- the theory of a relationship. Mitchell24 has shown that a mission, and outbreaks have occurred in pools,5,9 day-care patient can develop antibodies in response to ground facilities,10 and sports settings.11 Cases of congenital molluscum bodies inoculated into the skin; however, and vertically transmitted molluscum have been docu- vaccination against molluscum and natural infection do mented.12,13 Sexual transmission of MCV may be seen not appear to produce antibodies that would cross-react in adolescents who are sexually active. Although child- and protect against other poxviruses, including vaccinia to-child transmission can occur in the groin area from or fowl pox infections.25 Cell-mediated immunity also is shared equipment, transmission via sexual abuse also is required to clear MCV and may account for the inflam- possible.14 Bargman15 has mentioned the isolated genital matory appearance of lesions as they resolve.26 location and lack of contact with other infected children Demonstrated factors that account for the rise in MCV as concerning features. Latency of new lesion appearance incidence, aside from alterations in vaccination practices, is anywhere from 1 to 50 days from the date of inocula- include spread through sports,9 swimming,11 and AD,7 tion; therefore, new lesions are possible and expected which have become more commonplace in the United even after therapy has been effective in eradicating States in the last few decades, supporting the theory that visible lesions.10 Although clearance has been reported they may be the cause of the increase in childhood MCV in 6 to 12 months, one pediatric study demonstrated infections. Another cause may be the ability of MCV to 70% clearance by 1.5 years, suggesting the disease often create factors that stem host immune response.1 is more prolonged.16 One-third of children will experi- ence signs of inflammation, such as pruritus and/or ery- Clinical Features thema. Rare side effects include bacterial superinfection Molluscum lesions have a typical appearance of pearly and hypersensitivity.2 papules with a centralcopy dell. These lesions are lighter to One Dutch study from 1994, the largest database sur- flesh colored and measure 1 to 3 mm.2,4,5 The lesions vey of children to date, cited a 17% cumulative incidence cluster in the axillae and extremities and average from of molluscum in children by reviewing the data from 10 to 20 per child.6 Lesions clear spontaneously, but new 103 general practices.17 In a survey and review of mol- ones will continue to form until immunity is developed. luscum by Braue et al,18 annual rates in populations Specificnot clinical appearances of lesions that are not pearly vary but seem to maximize at approximately 6% to 7%. papules are not infrequent. Table 1 contains a short list of Sturt et al19 reviewed the prevalence in the indigenous the manifold clinical appearances of molluscum lesions in West Sepik section of New Guinea and noted annualDo children. 1,2,7,27-35 In particular, certain clinical appearances incidence rates of 6% in children younger than 10 years should be considered. In small children, head and neck (range, 1.8%–10.9%). Epidemics occur and can pro- lesions resembling milia are not uncommon. Giant or duce large numbers of cases in a short time period.18 wartlike lesions can appear on the head, neck, or gluteal The cumulative prevalence in early childhood may be as high as 22%, as Sturt et al19 observed in children younger than 10 years. TABLE 1. Possible Morphologies of Rising incidence and therefore rising lifetime preva- lence appear to have been an issue in the last few MCV/Molluscum Dermatitis decades. Data from the IndianCUTIS Health Service have dem- Pearly papules with a central dell1,2 onstrated increases in MCV in Native American children between 2001 and 2005.20 In adults, the data support a Milialike lesions on the face steady increase of molluscum from 1988-2007, with a Giant molluscum mimicking condylomalike lesions28,29 3-fold increase from 1988-1997 to 1998-2007 in a Spanish Giant molluscum can mimic cysts, abscesses, or 21 study. Better population-based data are needed. growths27,30,31 Warty lesions Childhood Immunity and Vaccination Sequence homology between MC133L, a protein of Viral exanthema–like process: Gianotti Crosti or unilateral laterothoracic exanthema–like32 MCV, with vaccinia virus suggests overlapping genes.22 Therefore, it is conceptually possible that the rise in Erosive lesions mimicking eczema vaccinatum incidence of MCV since the 1980s relates to the loss of Erythema multiforme–like appearance33 vs erythema herd immunity to variola due to lack of vaccination for multiforme triggered by MCV34 smallpox, which has not been offered in the United States Erythema annulare centrifugum–like reaction35 23 since 1972. Childhood immunity to MCV
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