MOLLUSCIPOXVIRUS INFECTION: MOLLUSCUM CONTAGIOSUM

Sources
1) Fitzpatrick’s Dermatology in General Medicine 8, 2012
2) Andrew’s Diseases of the Skin : Clinical Dermatology, 12, 2015
3) Lookingbill & Markman’s Principles of Dermatology 6, 2018
4) Dermatology, 4th edition, 2017
5) Rook’s Textbook of Dermatology, 9th edition, 2016

A. Introduction
 Molluscum contagiosum (MC) is a benign but nonetheless frequently troublesome viral infection that most often
affects young children.[1]
 It is characterized by smooth, dome-shaped, discrete, opalescent papules with a central core that occasionally
develops
surrounding areas of scale and erythema (molluscum dermatitis). [1]
 Patients and families are bothered by this infection because of its often prolonged course, as it may persist for
months to years. [1]
 MC is a greater concern in immunocompromised individuals and those with atopic dermatitis, in whom the extent
and duration of infection may be more extreme. [1]
 Sexually transmitted disease occurs in adults but is extremely unlikely in children.[1]
 Molluscum contagiosum (MC) is caused by up to four closely related types of poxvirus, MCV-1 to
MCV-4, and their variants. [2]
 Although the proportion of infection caused by the various types varies geographically, MCV-1
infections are most common worldwide. [2]
 In small children, virtually all infections are caused by MCV-1. There is no difference in the anatomic
region of isolation with regard to infecting type, in contrast to HSV, for example. [2]
 In patients infected with HIV, however, MCV-2 causes the majority of infections (60%), suggesting
that HIV-associated molluscum does not represent recrudescence of childhood molluscum.[2]

B. DEFINITION
 Molluscum contagiosum is caused by a DNA poxvirus that infects epidermal cells. [3]
 Clinically, the lesions appear as smooth, dome-shaped papules that often are umbilicated (Fig. 5.7).[3]
C. EPIDEMIOLOGY
a. Incidence and prevalence
 MC virus (MCV) infection occurs worldwide and appears specific to humans.[1]
 The prevalence of MCV infection has risen signifiantly in the past several decades, with an 11-fold increase noted
in one US study of patient visits for this disorder over a two-decade span. [1]
 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.[1]
 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.[1]
 HIV-infected 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. [1]
 Transmission may occur via direct skin or mucous membrane contact, or via fomites.[1] 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.[1] Autoinoculation and koebnerization also play a role in the
spread of lesions. [1] Recent reports also document the possibility of vertical transmission from mother to neonate
during the intrapartum
period.[1]
 The virus occurs throughout the world, most commonly causing disease in childhood. [5]
o Type 1 molluscum contagiosum virus (MCV‐1) is found in the majority of infections (76–
97%), and whilst there is no relationship between virus type and lesional morphology or
anatomical distribution [66,67] there is some evidence to support a relatively higher incidence
of MCV‐2 type in adults and HIV infection compared to that in children [68].[5]
o The disease is common, with an estimated prevalence of 5–11% [69]. [5]
o The incidence is thought to have increased over the last few decades [70].[5]
 o Viral DNA can be detected on the normal skin of people with molluscum and from objects in
their environment so it is assumed that infection follows contact with infected persons or
contaminated objects [71]. [5]
o It is not known if epidermal injury is important for establishment of infection.[5]

 Infection with MCV is worldwide and increasing. Three groups are primarily affected: young children
(highest in ages 1–4 years), sexually active young adults (ages 20–29), and immunosuppressed persons,
especially those with HIV infection. MC is most easily transmitted by direct skin-to-skin
contact, especially if the skin is wet. Bathing with affected siblings may be a risk factor. Swimming
pools have been associated with infection, sometimes even plantar lesions.(Andrew)
 MC is a common, self-limited condition in children. It also occurs in adults, usually as a sexually transmitted
disease, and in immunocompromised hosts, most notably HIV-infected individuals. Transmission is via skin-to-
skin contact and, less commonly, fomites. (dermatology 4)
 Molluscum contagiosum is a common childhood disease.[1] Spread among family members occurs, but
is uncommon.[1]

b) Age
 The disease is rare under the age of 1 year, perhaps due to maternally transmitted immunity and a long
incubation period.[5]
 There are rare reports of lesions detected in the first few days or weeks of life, suggesting that vertical
transmission can occur [5].
 In hot countries where children are lightly dressed and in close contact with one another, spread within
households is not uncommon.[5]
 The age of peak incidence is reported as between 2 and 5 years [73,74].[5]
 In cooler climates, however, spread within households is rare and infection may occur at a later age
[73,75], perhaps correlated with the use of swimming pools and shared bathing facilities [69,76].[5]
 A later incidence peak in young adults is attributable to sexual transmission with lesions more
common in the genital area. [5]

D. Causative organisms (Rook)

 Molluscum contagiosum virus is classified within the poxvirus family in a specific genus, the
Molluscipox [97] (see Table 25.3), and has features intermediate between the orthopox and parapox
groups. [5]
 It cannot be grown in tissue culture or eggs, and, although it seems to infect only humans and is not
readily transmissible to laboratory animals, has been shown to produce typical changes on human skin
cultured on immuno‐incompetentmice [98]. [5]
 Restriction endonuclease and PCR analyses of molluscum contagiosum virus DNA have identified as
two main types, MCV‐1 and MCV‐2, with two much rarer types, MCV‐3 and MCV‐4 [99,100].[5]

E. Pathophysiology
a) Predisposing factors
 Infection of children through sexual abuse is presumably possible.[5]
 However, to a greater extent than warts, molluscum contagiosum is seen quite commonly on the
genital, perineal and surrounding skin of children, and abuse should not be regarded as likely unless
there are other suspicious features.
 There is a clinical impression that molluscum contagiosum is commoner in patients with atopic eczema
[69,77] but this is not always supported by cohort studies [78]. Topical steroids and also topical
calcineurin inhibitors have been suspected as a contributing factor in eczema and other patients [79–
81].
 Unusually widespread lesions have been reported in patients with immune compromise, such as HIV
disease (see Chapter 31), haematological malignancy [82], sarcoidosis [83], idiopathic CD4
 lymphocytopaenia [84], hyper‐IgE syndrome [85], DOCK8 deficiency [86] and in those receiving
immunosuppressive therapy [87–90] suggesting that cell‐mediated immunity is significant
in the control and elimination of the infection.
 In spite of profound immunosuppression following organ transplantation, the incidence of molluscum
contagiosum infection is not greatly increased in this group and is not as common as other infections
such as warts and herpes simplex [91].
 When MC is restricted to the genital area in a child, sexual abuse must be considered. [2]
 Children with atopic dermatitis (AD), either active or inactive, are four times more likely than
nonatopic children to have more than 50 lesions.[2]
 Transmission from the mother’s skin can occur during vaginal delivery and may be associated with
presentation in the first few months of life.[2]

b) Pathology
 The virus seems first to enter the basal epidermis where an early increase in cell division extends into
the suprabasal layer.[5]
 The cellular proliferation produces lobulated epidermal growths which compress the papillae until they
appear as fibrous septa between the lobules, which are pear shaped with the apex upwards. The basal
layer remains intact. [5]
 Cells at the core of the lesion show the greatest distortion and are ultimately destroyed, and appear as
large hyaline bodies (molluscum bodies) some 25 μm in diameter, containing cytoplasmic masses of
virus material.[5] These bodies are present in large numbers in the cavity, which appears near the
surface at the centre of the fully developed lesion.[5]
 Inflammatory changes in the dermis are absent or slight, but in lesions of long duration there may be a
chronic granulomatous infiltrate.[5] It has been suggested that the inflammatory reaction may be
induced by the discharge into the dermis of the contents of a papule [93] rather than by secondary
infection.[5] In spontaneous regression, the lesions are surrounded by an infiltrate of
interferon‐producing plasmacytoid dendritic cells [94].[5]
 Specific antibodies have been found in about 58–73% of patients with molluscum contagiosum, and,
perhaps due to unrecognized infection, in about 6–16% of controls [95,96], but these have not been
demonstrated to have a role in disease clearance.[5]

D. PATHOGENESIS
 Although it is difficult to produce lesions after experimental inoculation, molluscum contagiosum is
certainly contagious.[3] Intimate physical contact, such as occurs in Turkish baths, wrestling, and
sexual intercourse, has resulted in transmission of the disease.[3]
 The molluscum contagiosum virus replicates in the cytoplasm of the keratinocyte, with resulting large
intracytoplasmic inclusion bodies (molluscum bodies) and proliferation of the epidermis. [3]
 The center of the papule ultimately disintegrates, forming a crater and releasing molluscum bodies.[3]
 Spontaneous involution results from a host immune response that is presumed to be cell mediated. The
stimulus that provokes this response after many months of inactivity is unknown, as with warts.[3]

E. CLINICAL FEATURES

1.) CLINICAL FINDINGS / PRESENTATION

a). CUTANEOUS LESIONS.
 The incubation period is variously estimated at 14 days to 6 months.[5]
 The individual lesion is a shiny, pearly white, hemispherical, umbilicated papule which may show a
central pore (Figure 25.8a). [5]
 It may be identified with a hand lens or dermoscope when less than 1 mm in diameter. [5]
 Enlarging slowly it may reach a diameter of 5–10 mm in 6–12 weeks. Rarely, and usually when
one or very few are present, a lesion may become considerably larger.[5]
 Plaques composed of many small lesions (‘agminate’ form or giant molluscum) occur rarely. Lesions
frequently spread and the number of lesions ultimately present is sometimes very large.[5]
 After trauma, or spontaneously after several months, inflmmatory changes result in suppuration,
crusting and eventual destruction of the lesion.[5]
 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”).[1]
 As they enlarge, a dome-shaped, opalescent morphology may become more apparent. [1]
 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.75[1]
 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.[1]
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.[1]
Patients with acquired immunodeficiency syndrome may develop large and extensive lesions involving both
genital and extragenital sites.82 (see Chapter 198)[1]

 MC lesions are firm, umbilicated, pearly papules with a waxy surface.[4]

They can occur anywhere on the skin surface but are most common in skin folds (e.g. axillae, neck); on the lateral
trunk, thighs, and buttocks; and in the genital region (Fig. 81.13A). [4]
 Facial lesions can also occur and are often especially distressing to the patient (Fig. 81.13B).[4]
Widespread, large, and occasionally deforming lesions may be seen in the setting of immunosuppression,
particularly AIDS (see Ch. 78).[4]
 An associated molluscum dermatitis is common (Fig. 81.13C), especially in children with atopic dermatitis.[4]
Inflammation of MC lesions can occur, often with a pustular or furuncle-like component (Fig. 81.13D); this signals
the development of a host immune response.[4]
 As noted above, an id reaction-like eruption of pruritic erythematous papules that favor the elbows and knees
occasionally develops in conjunction with an inflammatory response to MC.[4]
 Histologic evaluation of an MC lesion reveals large, intracytoplasmic inclusion bodies (molluscum bodies,
Henderson–Patterson bodies) within epidermal keratinocytes, which increase in size as they move toward the skin
surface (Fig. 81.13E).[4] A variably dense dermal infiltrate may occasionally have pseudolymphomatous features.
[4]
 In all forms of MC infection, the lesions are relatively similar. Individual lesions are smooth-surfaced,
fim, dome-shaped, pearly papules, averaging 3–5 mm in diameter (Fig. 19-32).[2]
 “Giant” lesions may be up to several centimeters in diameter.[2]
 A central umbilication is characteristic. Irritated lesions may become crusted and even pustular,
simulating secondary bacterial infection. [2] This may precede spontaneous resolution.[2]
Lesions that rupture into the dermis may elicit a marked suppurative inflmmatory reaction that
resembles an abscess.[2]
 The clinical pattern depends on the risk group affected. [2] In young children, the lesions are usually
generalized and number from a few to more than 100.[2] Lesions tend to be on the face, trunk, and
extremities.[2] Genital lesions, as part of a wider distribution, occur in 10% of childhood cases. [2]
 Several forms of inflammation occur in children with MC.[2]
 The most common inflammatory response, seen in 40% of affected children, is “molluscum
dermatitis.” [2]
 More common in atopic children, it is a mild, eczematous eruption surrounding the individual
lesions.[2] This is not associated with more rapid resolution of the MC, and treatment of this dermatitis
with topical corticosteroids does not appear to lead to increased MC.[2]
 Inflamed MC is characterized by erythema and swelling of the individual lesions, sometimes with
pustulation or fluctuance. [2]
 It occurs in 20% of children with MC and usually heralds the resolution of disease. [2]
 The rarest inflammatory response is a GCS-like reaction, occurring in 5% of children with MC. [2]
 It presents as numerous edematous, erythematous papules or papulovesicles distant from the MC
lesions and favors the elbows and knees, but also affects the buttocks and face. [2]
 Pruritus is prominent.[2]
 In adults, MC is sexually transmitted, and other STDs may coexist. There are usually fewer than 20
lesions; these favor the lower abdomen, upper thighs, and penile shaft in men (Fig. 19-33).[2]
  Pubic hair removal by shaving, clipping, or waxing is a risk factor for acquiring MC by sexual contact.
Mucosal involvement is very uncommon.
 Immunosuppression, either systemic T-cell immunosuppression (usually HIV, but also sarcoidosis,
immunosuppressive medications, and malignancies) or abnormal cutaneous immunity (as in atopic
dermatitis or topical steroid use), predisposes the individual to infection.[2] In AD patients, lesions
tend to be confined to dermatitic skin (Fig. 19-34).[2]
 Secondary infection may occur, but most inflamed MC are not infected, but rather undergoing
spontaneous involution by the immune response. Rarely, erythema annulare centrifugum may be
associated with MC.[2]
 Lesions on the eyelid margin or conjunctiva may be associated with a conjunctivitis or keratitis. Rarely,
the molluscum lesions may present as a cutaneous horn.[2]
 Between 10% and 30% of AIDS patients not receiving antiretroviral therapy (ART) have MC.[2]
 Virtually all HIV-infected patients with MC already have an AIDS diagnosis and a helper T-cell (Th)
count of less than 100. [2]
 In untreated HIV disease, lesions favor the face (especially the cheeks, neck, and eyelids) and genitalia.
 Lesions may be few or numerous, forming confluent plaques. [2]
 Giant lesions can occur and may be confused with a skin cancer.[2]
 Involvement of the oral and genital mucosa may occur, virtually always indicative of advanced AIDS
(Th count <50).[2]
 Facial disfigurement with numerous lesions can occur. Recurrence or new appearance of MC may be
seen in AIDS patients starting ART as a part of IRIS. [2]

Clinical variants
 The distribution of the lesions is influenced by the mode of infection, and by the type of clothing worn,
and hence by the climate.[5]
 In temperate regions, they are commonly seen on the neck or on the trunk, particularly around the
axillae. In children in the tropics, lesions are more common on the limbs.[5]
 In teenagers and young adults, where sexual transmission is the likely mode of spread, lesions in the
ano‐genital area are most common.[5]
 In otherwise healthy subjects, occasional facial lesions are seen, particularly on the eyelids.[5]
 Molluscum may affect the scalp, and indeed any part of the body surface, including the soles where the
appearance is atypical.[5]
 Widespread and refractory mollusca on the face are seen most commonly in HIV disease [102] and
also with iatrogenic immunosuppression. [5]
 Oral lesions on the lips, tongue or buccal mucous membranes are rare but can occur, usually in adults
with a background of immunosuppression, and can be in the absence of associated cutaneous lesions
[104]. Giant or widespread molluscum contagiosum lesions are more common in immunosuppression
but can occur in immune competence [105,106].
 Molluscum can occur in scars and in tattoos [107]. Follicular molluscum contagiosum has been
reported, producing atypical, less protuberant pale papules [108].

DIAGNOSIS
 The diagnosis of MC is easily established in most cases because of the distinctive central umbilication
of the dome-shaped lesion.[2]
 This may be enhanced by light cryotherapy, which leaves the umbilication appearing clear against a
white (frozen) background.[2]
 For confirmation, the pasty core of a lesion is expressed, squashed between two microscope slides
(or slide and coverslip), and stained with Wright, Giemsa, or Gram.[2]
 Firm compression between the slides is required.[2]
HISTORY
In adults, venereal transmission is suggested by a history
of sexual exposure and the location of lesions in the genital region.
PHYSICAL EXAMINATION
The papules of molluscum contagiosum are 2 to 5 mm
wide, hard, smooth, domeshaped, and flesh colored or
translucent. The papules have a central umbilication from
which a “cheesy” core can be expressed. They occur singly
or in groups, most often on the trunk, face, and extremities
of children and on the genitals of sexually active adults.
Uncommonly, they become disseminated, resulting
in hundreds of lesions. If inflamed, they are difficult to
recognize because of secondary erythema and crusting.

SPECIAL TESTS
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 (Fitz)

LABORATORY AND BIOPSY

The diagnosis usually is clinically obvious. When doubt
exists, a simple office procedure is confirmatory. The molluscum papule is removed by curettage and crushed
onto
a slide. This unstained material readily reveals numerous
oval molluscum bodies when examined with a microscope.
A biopsy usually is not necessary unless the typical features
are masked by secondary inflammation (Fig. 5.7B). (Principles)

Investigations
The diagnosis of molluscum contagiosum is usually obvious when
multiple lesions at different stages of evolution are present and
the typical umbilicated papule is evident. The distinctive umbilication can be seen more easily with a
dermoscope or after freezing.
The diagnosis can be confimed by direct microscopy or electron
microscopy of the papule contents, by histopathology or by molecular analysis [99,118–120]. (Rook)
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. (Fitz)
Molluscum contagiosum has a characteristic histopathology.
Lesions primarily affect the follicular epithelium. The lesion is
acanthotic and cup shaped. In the cytoplasm of the prickle
cells, numerous small, eosinophilic and later basophilic inclusion bodies form, called molluscum bodies or
HendersonPaterson bodies. Eventually, their bulk compresses the nucleus
to the side of the cell. In the fully developed lesion, each lobule
empties into a central crater. Inflmmatory changes are slight
or absent. Characteristic brick-shaped poxvirus particles are
seen on electron microscopy in the epidermis. Latent infection
has not been found, except in untreated AIDS patients, in
whom even normal-appearing skin may contain viral particles. Resolving and inflmed lesions may contain a
dense
inflmmatory infitrate of lymphocytes and neutrophils. Some
of the lymphocytes may be large and CD30 positive. MCV
contains an IL-18–binding protein gene that it apparently
acquired from humans. This blocks the host’s initial effective
Th1 immune response against the virus by reducing local
IFN- γ production. (Andrew)

DIFFERENTIAL DIAGNOSIS
 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). [1]
  The differential diagnosis of MC may include adnexal tumors, verrucae, condylomata acuminata, basal cell
carcinoma, juvenile xanthogranuloma, melanocytic nevi (especially Spitz nevi), papular granuloma annulare, and
pyogenic granuloma.[4]
 In immunocompromised hosts, infectious processes such as cryptococcosis or histoplasmosis can mimic MC.[4]
 Inflammatory reactions to mollusca may resemble nummular dermatitis, staphylococcal furunculosis, Gianotti–
Crosti syndrome, or ULTE. [4]
 The translucent papule of molluscum contagiosum can resemble nodular basal cell carcinoma or a
comedo.[3]
 Nodular basal cell carcinomas usually have telangiectasia and occur in sunexposed skin of older
patients.[3]
 Comedones lack umbilication. [3]
 An inflamed molluscum contagiosum may appear to be a bacterial infection of the skin. [3]

 The solitary molluscum may resemble a pyogenic granuloma, a keratoacanthoma or a squamous cell
carcinoma and may be difficult to identify.[5]
 Multiple small lesions can be confused with plane warts.[5]
 In HIV disease, molluscum contagiosum may resemble cutaneous cryptococcosis (see Chapter 32).[5]

Complications and co‐morbidities

In at least 10% of cases, particularly in atopic subjects, a patchy
eczema, often very irritable, develops around one or more of
the lesions a month or more after their onset [109] and erythema
annulare centrifugum and erythema multiforme have also been
reported in association with the infection [110–112]. Chronic conjunctivitis and superfiial punctate keratitis may
similarly complicate lesions on or near the eyelids [113]. The eczema and the
conjunctivitis subside spontaneously when the lesion resolves or
is removed.
Disease course and prognosis
The duration both of the individual lesion and of the attack is
very variable and although most cases are self‐limiting within
6–9 months, it is not unusual for some to persist for 3 or 4 years [77]. Individual lesions are unlikely to persist
for more than 2 months,
but some lesions, particularly if solitary, may persist for up to 5
years [114].
Inflmmatory responses around lesions may indicate that immunological resolution is likely to occur within a few
months [114].
Depressed scars or anetoderma‐like lesions can remain when
mollusca clear [116,117] (Figure 25.8b).

COURSE AND COMPLICATIONS

Spontaneous remission often occurs within 6 to 9 months,
although lesions have been known to persist for many
years, and more lesions may develop by autoinoculation.
Individual lesions can become secondarily inflamed
and may resemble furuncles. Involvement of the eyelids
is uncommon but may result in chronic conjunctivitis.
The development of hundreds of lesions with little tendency for involution should alert the clinician to consider
immunocompromise. Molluscum contagiosum is
one of the most common cutaneous findings in acquired
immune deficiency syndrome (AIDS) and AIDSrelated
complex, infecting 9% of these individuals. In the patient
with AIDS, molluscum contagiosum is often recalcitrant to treatment and causes significant morbidity and
disfigurement. (Principles)
PROGNOSIS AND CLINICAL COURSE
Spontaneous clearance occurs, but often over a prolonged period of months to years. Most families prefer
treatment if lesions persist more than a month or two. In patients with HIV, MC infection is usually indicative
of a more advanced state of HIV, with higher viral load
and lower CD4 T-cell count.84 (Fitz)’
MC resolves spontaneously in immunocompetent children, with the
time interval between onset and clearance of the lesions ranging from
several months to several years. However, treatment may be requested
when there are numerous or cosmetically signifiant lesions. (Dermatology 4)

COMPLICATIONS
Although many patients are asymptomatic, pruritus is
sometimes a signifiant 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. (Fitz)

TREATMENT
It is important to discuss the risks and benefis 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 child’s
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 2–6 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 fid topical cantharidin treatment the most
effiient 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 identifid only 11 therapeutic studies of high
quality, found that no single intervention is convincingly effective for the treatment of MC.86
(Fitz_
Treatment is determined by the clinical setting. In young
immunocompetent children, especially those with numerous
lesions, the most practical course may be not to treat or to use
only topical tretinoin. Aggressive treatment may be emotionally traumatic and can cause scarring. Spontaneous
resolution
is virtually a certainty in this setting, avoiding these sequelae.
Individual lesions last 2–4 months each; duration of infection
is about 2 years. Continuous application of surgical tape to
each lesion daily after bathing for 16 weeks led to cure in 90%
of children. Topical cantharidin, applied for 4–6 h to approximately 20 lesions per setting, led to resolution in
90% of
patients, and 8% of patients improved. This therapy is well
tolerated, has a very high satisfaction rate for patients and
their parents, and complications are rare. If lesions are limited
and the child is cooperative, nicking the lesions with a blade
to express the core (with or without comedo extractor), squeezing the lesion with a tissue forceps, light
cryotherapy, application of trichloroacetic acid (TCA, 35–100%), and removal by
curettage are all alternatives. The application of lidocaineprilocaine (EMLA) cream for 1 h before any painful
treatments
has made the management of MC in children much easier. No
controlled trials have confimed the effiacy of imiquimod,
and two large trials have shown that it is no more effective
than placebo; it cannot be recommended for MC treatment.
Intralesional immunotherapy with candidal antigen injections in up to three lesions led to complete resolution of
all lesions
in 55% of children. Oral cimetidine has been similarly used for
its immunomodulatory effects. Hydrogen peroxide 1% cream,
ingenol mebutate, pulse dye laser, and potassium hydroxide
10% are other reported therapies.
In adults with genital molluscum, removal by cryotherapy
or curettage is very effective. Neither imiquimod nor podophyllotoxin has been demonstrated to be effective. In
fact, the
failure of these agents to improve “genital warts” suggests the
diagnosis of genital MC. Sexual partners should be examined;
screening for coexistent STDs is mandatory.
In patients with AD, application of EMLA followed by curettage or cryotherapy is most practical. Caustic
chemicals should
not be used on atopic skin. Topical corticosteroid application
to the area should be reduced to the minimum strength possible. In immunosuppressed patients, especially those
with
AIDS, management of MC can be diffiult. Aggressive treatment of the HIV infection with ART, if it leads to
improvement
of the Th count, is predictably associated with a dramatic resolution of the lesions. This response is delayed 6–8
months from
the institution of treatment, so reports of resolution with
certain agents in the HIV patient is confounded by the coexistent ART therapy, which is probably the active
component of
the treatment cocktail. MC occurs frequently in the beard area,
so shaving with a blade razor should be discontinued to
prevent its spread. If lesions are few, curettage or core removal
with a blade and comedo extractor is most effective. EMLA
application may permit treatment without local anesthesia.
Cantharone or TCA may be applied to individual lesions.
Temporary dyspigmentation and slight surface irregularities
may occur. Cryotherapy may be effective but must be used
with caution in persons of color. When lesions are numerous
or conflent, treatment of the whole affected area may be
required because of possible latent infection. TCA peels above
35% concentration (medium depth) or daily applications of
5-florouracil (5-FU) to the point of skin erosion may eradicate
lesions, at least temporarily. At times, removal by curette is
required. In patients with HIV infection, continuous application of tretinoin cream once nightly at the highest
concentration tolerated seems to reduce the rate of appearance of new
lesions. Topical 1–3% cidofovir application and systemic infusion of this agent have been reported to lead to
dramatic resolution of molluscum in patients with AIDS. (Andrew)
THERAPY
Treatment may deferred awaiting spontaneous resolution.
However, treatment is usually cryotherapy with liquid
nitrogen or curettage. For children who will not tolerate
the pain of curettage or cryotherapy, the careful application of the blistering chemical cantharidin can be used in
the office, or topical salicylic acid preparations or tretinoin
can be used at home, similar to the treatment of warts.
The most reliable means of eradication is by curettage.
The molluscum papule, composed of many molluscum
bodies, is scraped off, with some discomfort and bleeding. The topical immune response modifier, imiquimod
(Aldara) cream 5% applied daily has also been successful. (Principles)
Therapeutic options include curettage, manual expression, cryotherapy,
topical chemovesicants, keratolytics, and cidofovir (Table 81.6).
Although imiquimod has been used anecdotally for MC, effiacy was
not demonstrated in large controlled studies50. In children, application
of cantharidin is a safe and reasonably effective treatment that has the
benefi of non-traumatic in-offie application (see Ch. 129). However,
it may require more visits than curettage; in addition, it does not have
FDA approval and can be challenging to obtain51. Treatment of molluscum dermatitis with a topical corticosteroid may help
to reduce
associated pruritus and prevent autoinoculation from scratching. (Dermatology 4)

Management [121]
In many instances, therapy is not necessary and natural resolution
can be awaited. The risk of dissemination of the infection can be
minimized by reducing scratching, which can both damage adjacent skin and spread virus from mature papules.
Associated dry
skin or eczema should be treated with emollients and possibly a
weak topical steroid. Transfer of infection to another individual
may be reduced by avoidance of shared towels, contact sports and
communal bathing.
If spontaneous clearance is slow, lesions are symptomatic, or
associated eczema is troublesome, treatment may be desirable.
The choice of treatment will depend on the age of the patient, and
the number and position of the lesions. Treatments aim to destroy
the infected epidermal cells, stimulate an immunological response
or act directly against the virus.
First line
Stimulation of the immune response may occur after destructive
or inflmmatory therapies. Many topical agents can be used to
produce mild to moderate inflmmation and hence potentially
stimulate the development of an immune response against the
virus. Cantharidin, trichloroacetic acid and diluted liquefid phenol are strong irritants which can both cause pain,
blistering and
scarring but with careful application and appropriate dilution
can increase lesion clearance [116,122,123]. Topical salicylic acid
preparations [77,124], tretinoin [125], adapalene [126], nitric oxide
cream [127] and 5–10% potassium hydroxide solution [128,129]
and benzoyl peroxide cream [130] all lead to an irritant reaction
but if the strength of preparation and the frequency of application
are adjusted, individuals can tolerate repeated treatments until
resolution occurs.
Lemon myrtle oil [131] and tea tree oil [132] have been used, the
former with apparent effiacy when compared with placebo.
Damage to the lesions by squeezing the contents or insertion of a pointed cocktail stick may stimulate
inflmmation and
clearance.
Other treatments have been used for molluscum contagiosum with the explicit aim of enhancing the immune
response
although trials are not always randomized or controlled. Effiacy
has been reported with topical diphencyprone [133], imiquimod
cream [134], intralesional or systemic interferon [135,136], systemic cimetidine [137] and intralesional
immunotherapy [138].
Compared to cryotherapy, lesions clear more slowly with
imiquimod, but the treatment is painless and well tolerated in children [139]. In two large unpublished
randomized trials, imiquimod was of no benefi when compared to placebo [140].
Second line
Cryotherapy is effective and commonly used in older children
and adults, but needs to be repeated at 3–4 weekly intervals. The
carbon dioxide or pulsed dye lasers have produced useful effects
[141,142] but like curettage, can cause scars. Photodynamic therapy has also been used with effect [143].
Surgical removal of molluscum contagiosum by curettage has
been used for many years [124] but the rate of successful clearance is reduced if there are many lesions [144].
Children will usually need prior application of topical anaesthetic cream with strict
observance of the maximum safe dose [145].
Third line
The antiviral agent cidofovir has been shown to effectively resolve
molluscum lesions [146,147] (used either intravenously or topically as a 1–3% ointment or cream). It should be
considered for
treating extensive lesions in, for example, immuno‐incompetent
patients where eradication has proved diffiult with standard
treatment regimens.
A recent report has also suggested effiacy of intravenous paclitaxel in severe disease in immunocompromise
[148].(Rook)
PREVENTION
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.