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EPIDEMIOLOGI
MC virus (MCV) infection occurs worldwide and appears specific to humans. The prevalence
of MCV infection has risen significantly in the past several decades, with an 11-fold increase
noted in one US study of patient visits for this disorder over a twodecade span.75 This rise
appears to parallel the overall increase in sexually transmitted diseases. Although a
prevalence rate of less than 5% in US children is often cited,76 the rate varies by location,
and it is thought that subclinical infection may be more common than overt disease. A
representative Australian study documented an overall seropositivity rate of 23%, which
supports the view that subclinical or mild unrecognized disease exists in the population.
HIVinfected individuals are at higher risk for extensive prolonged disease, and individuals
with atopic conditions appear more likely to have increased numbers of lesions and
experience a more prolonged disease course. Transmission may occur via direct skin or
mucous membrane contact, or via fomites. Bath towels, swimming pools, and Turkish baths
have all been reported as sources of infection, and individuals involved in close contact sports
(e.g., wrestling) also appear at higher risk.77,78 Autoinoculation and koebnerization also play
a role in the spread of lesions. Recent reports also document the possibility of vertical
transmission from mother to neonate during the intrapartum period.
GEJALA KLINIS
CUTANEOUS LESIONS. MC often presents with extremely small pink, pearly, or flesh-
colored papules that then enlarge, occasionally reaching sizes of up to 3 cm (giant
molluscum). As they enlarge, a dome-shaped, opalescent morphology may become more
apparent. The lesions may have a central dell or umbilication (Fig. 195-12), within which a
white curdlike substance can be seen that can be expressed with pressure. Most patients
develop multiple papules, often in intertriginous sites, such as the axillae, popliteal fossae,
and groin. Genital and perianal lesions can develop in children and are only rarely associated
with sexual transmission in this population. Lesions may be grouped in clusters or appear in a
linear array. The latter often results from koebnerization or development of lesions at sites of
trauma. Erythema and eczematous changes may occur around lesions; this is termed
molluscum dermatitis. Papules may become erythematous (Fig. 195-12B), which is believed
to be an immune response to the infection. Patients with acquired immunodeficiency
syndrome may develop large and extensive lesions involving both genital and extragenital
sites.82 (see Chapter 198
TES SPESIAL
Diagnosis is usually straightforward. Evaluation of the central contents using a crush
preparation and Giemsa staining can be carried out when necessary (eFig. 195- 12.1 in online
edition), and histopathologic evaluation can be performed as needed. Some clinicians
recommend that an adult with new-onset MC infection undergo evaluation for HIV infection
and/or other causes of an immunocompromised state.84 Histopathologic examination reveals
a hypertrophied and hyperplastic epidermis. Above the basal layer, enlarged cells containing
large intracytoplasmic inclusions (Henderson-Paterson bodies) can be seen (Fig. 195-13).
These increase in size as the cells reach the horny layer.
DIAGNOSIS BANDING
The differential diagnosis includes verrucae, pyogenic granulomas, amelanotic melanoma,
basal cell carcinomas, and appendageal tumors. Fungal infections caused by Cryptococcus,
histoplasmosis, and Penicillium must be considered in immunocompromised hosts (Box 195-
5).
KOMPLIKASI
Although many patients are asymptomatic, pruritus is sometimes a significant problem,
particularly in those patients with underlying atopic dermatitis. Chronic conjunctivitis and
punctate keratitis may develop in patients with eyelid lesions. Secondary bacterial infection
can occur, particularly if patients scratch their lesions.
TATALAKSANA
It is important to discuss the risks and benefits of individual therapies with families before
embarking on treatment for this essentially benign condition, which will generally resolve
without complication in the immunocompetent individual (Table 195-3). For some children,
no treatment is the best option as the childs native immune response may clear the MC
without additional intervention. Many experts use cantharidin 0.7% or 0.9% liquid for
treatment of MC. This extract of the blister beetle, Cantharis vesicatoria, induces
vesiculation at the dermoepidermal junction when applied topically to the skin. It must be
applied with care and washed off 26 hours later. Use on the face or genital areas is not
recommended, and families must be counseled regarding the small risk of extreme reaction or
scarring. Other traditional therapies have included curettage and cryotherapy; however, both
of these treatments are painful. The use of topical anesthetic agents may ameliorate some of
the associated pain, but patients generally find topical cantharidin treatment the most efficient
and least painful. Other topical therapeutic modalities include retinoid creams, imiquimod
cream, salicylic acid, trichloroacetic acid, cidofovir, and silver nitrate paste and tape
stripping. Oral cimetidine has also been used with some success.85 However, a 2009
Cochrane Database analysis of treatments for MC, which identified only 11 therapeutic
studies of high quality, found that no single intervention is convincingly effective for the
treatment of MC.
PENCEGAHAN
Prevention of spread may be enhanced by avoiding trauma to the sites of involvement as well
as avoiding scratching, with the use of antipruritics as necessary. Autoinoculation may be
decreased by treating all existing lesions.GY