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Molluscum contagiosum

Molluscum contagiosum is caused by up to four closely related types of poxvirus, MCV-1 to 4 and their
variants. Although the proportion of infection caused by the various types varies geographically, throughout the
world MCV-1 infections are most common. 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 (as opposed to HSV, for
example). In patients infected with HIV, however, MCV-2 causes the majority of infections (60%), suggesting
that HIV infection-associated molluscum does not represent recrudescence of childhood molluscum.

Infection with MCV is worldwide. Three groups are primarily affected: young children, sexually active adults,
and immunosuppressed persons, especially those with HIV infection.

Molluscum is most easily transmitted by direct skin-toskin contact, especially if the skin is wet. Swimming pools
have been associated with infection.
In all forms of infection, the lesions are relatively similar.

Individual lesions are smooth-surfaced,
pearly papules,
averaging 3–5 mm in diameter
“Giant” lesions may be up to 1.5 cm in diameter.
A central umbilication is characteristic.
Irritated lesions may become crusted and even pustular,
simulating secondary bacterial infection.
This may precede spontaneous resolution. Lesions
that rupture into the dermis may elicit a marked suppurative
inflammatory reaction that resembles an abscess.

The clinical pattern depends on the risk group affected. In young children the lesions are usually generalized
and number from a few to more than 100. Dermatitis surrounding a lesion usually heralds the resolution of that
lesion. Lesions tend to be on the face, trunk, and extremities. Genital lesions occurring as part of a wider
distribution occur in 10% of childhood cases.

When molluscum is restricted to the genital area in a child, the possibility of sexual abuse must be considered.
In adults, molluscum is sexually transmitted and other STDs may coexist. There are usually fewer than 20
lesions; these favor the lower abdomen, upper thighs, and the penile shaft in men (Fig. 19-33).

Mucosal involvement is very uncommon. Immunosuppression, either systemic T-cell immunosuppression
(usually HIV, but also sarcoidosis and malignancies) or abnormal cutaneous immunity (as in atopic dermatitis
or topical steroid use), predisposes the individual to infection. In atopic dermatitis, lesions tend to be confined to
dermatitic skin
(Fig. 19-34).
Secondary infection may occur. In addition, in about 10% of lesions, a surrounding eczematous reaction is
present (molluscum dermatitis). Rarely, erythema annulare centrifugum
may be associated. 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 (molluscum
contagiosum cornuatum).
Between 10 and 30% of AIDS patients not receiving antiretroviral
therapy have molluscum contagiosum. Virtually all
Fig. 19-33 Molluscum contagiosum of the penis.
Fig. 19-34 Molluscum contagiosum, child with atopic dermatitis.
HIV-infected patients with molluscum contagiosum already
have an AIDS diagnosis and a helper T-cell count of less than
100. In untreated HIV disease, lesions favor the face (especially
the cheeks, neck, and eyelids) and genitalia. They may be few
or numerous, forming confluent plaques. Giant lesions are not
uncommon and may be confused with a basal cell carcinoma.
Involvement of the oral and genital mucosa may occur, virtually
always indicative of advanced AIDS (helper T-cell count
less than 50). Facial disfigurement with numerous lesions can
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, called molluscum bodies or Henderson–Paterson
bodies, are formed. Eventually, their bulk compresses the
nucleus to the side of the cell. In the fully developed lesion
each lobule empties into a central crater. Inflammatory 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. Molluscum contagiosum virus contains an
IL-18 binding protein gene it apparently acquired from
humans. This blocks the host’s initial effective Th1 immune
response against the virus by reducing local IFN-
The diagnosis is easily established in most instances because
of the distinctive central umbilication of the dome-shaped
lesion. This may be enhanced by light cryotherapy that leaves
the umbilication appearing clear against a white (frozen) background.
For confirmation, express the pasty core of a lesion,
squash it between two microscope slides (or a slide and a cover
glass) and stain it with Wright, Giemsa, or Gram stains. Firm
compression between the slides is required.
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;
the 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 so treated. Topical
cantharidin, applied for 4–6 h to approximately 20 lesions per
setting, led to resolution in 90% of patients and 8% of patients
Picornavirus group
improved. This therapy is well tolerated, has a very high
satisfaction rate for patients and their parents, and has rare
complications. If lesions are limited and the child is cooperative,
nicking the lesions with a blade to express the core (with
or without the use of a comedo extractor), light cryotherapy,
application of trichloroacetic acid (35–100%), or removal by
curettage are all alternatives. The application of EMLA cream
for 1 h before any painful treatments has made the management
of molluscum in children much easier. Topical 5%
sodium nitrite with 5% salicylic acid cures about 75% of
patients. No controlled trials have confirmed the efficacy of
imiquimod and it cannot be recommended for the treatment
of molluscum.
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 molluscum contagiosum. Sexual partners
should be examined; screening for other coexistent STDs is
In patients with atopic dermatitis, application of EMLA followed
by curettage or cryotherapy is most practical. Caustic
chemicals should not be used on atopic skin. Topical steroid
application to the area should be reduced to the minimum
strength possible. A brief course of antibiotic therapy should
be considered after initial treatment, since dermatitic skin is
frequently colonized with S. aureus.
In immunosuppressed patients, especially those with AIDS,
management of molluscum can be very difficult. Aggressive
treatment of the HIV infection with HAART, if it leads to
improvement of the helper T-cell count, is predictably associated
with a dramatic resolution of the lesions. This response
is delayed 6–8 months from the institution of the treatment.
Molluscum 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 100% trichloroacetic acid 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 pigment. When lesions are
numerous or confluent, treatment of the whole affected area
may be required because of the possibility of latent infection.
Trichloroacetic acid peels above 35% concentration (medium
depth) or daily applications of 5-fluorouracil (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.
Au WY, et al: Fulminant molluscum contagiosum infection and
concomitant leukaemia cutis after bone marrow transplantation for
chronic myeloid leukaemia. Br J Dermatol 2000; 143:1097.
Charteris DG, et al: Ophthalmic molluscum contagiosum. Br J
Ophthalmol 1995; 79:476.
Diven DG: An overview of poxviruses. J Am Acad Dermatol 2001; 44:1.
Fornatora ML, et al: Intraoral molluscum contagiosum: a report of a
case and a review of the literature. Oral Surg Oral Med Oral Pathol
Oral Radiol Endod 2001; 92:318.
Meadows KP, et al: Resolution of recalcitrant molluscum contagiosum in
HIV-infected patients treated with cidofovir. Arch Dermatol 1997;
Silverberg NB, et al: Childhood molluscum contagiosum: experience
with cantharidin therapy in 300 patients. J Am Acad Dermatol 2000;
Toro JR, et al: Topical cidofovir: a novel treatment for recalcitrant
molluscum contagiosum in children infected with human
immunodeficiency virus 1. Arch Dermatol 2000; 136:983.
Watanabe T, et al: Antibodies to molluscum contagiosum virus in the
general population and susceptible patients. Arch Dermatol 2000;
Xiang Y, Moss B: Molluscum contagiosum virus interleukin-18 (IL-18)
binding protein is secreted as a full-length form that binds cell surface
glycosaminoglycans through the C-terminal tail and a furin-cleaved
form with only IL-18 binding domain. J Virol 2003; 77:2623.

_ Molluscum contagiosum
Molluscum contagiosum
Water wart; molluscum; molluscum sebaceum;
epithelioma contagiosum
Viral skin infection that produces papules
and nodules
Caused by large DNA poxvirus, Molluscipoxvirus;
replicate in the cytoplasm of
epithelial cells and produce cytoplasmic
inclusions and enlargement of infected cells
Clinical manifestation
Solitary or grouped, asymptomatic, firm,
smooth, umbilicated papules, on the skin
and mucosal surfaces; may coalesce into
Molluscum contagiosum. Crystalline papules
with central dell on the face
392 Molluscum sebaceum
plaques; self-limited, but sometimes persists
for months to years; multiple, widespread,
persistent lesions occurring in
immunocompromised patients, particularly
those with HIV disease
Differential diagnosis
Wart; nevocellular nevus; varicella; fibrous
papule of the face; basal cell carcinoma;
sebaceous gland hyperplasia; xanthoma;
milia; syringoma; juvenile xanthogranuloma;
epidermoid cyst; granuloma annulare;
cryptococcosis; histoplasmosis
Cryotherapy; curettage; tretinoin; benzoyl
peroxide; disseminated disease in immunocompromised
patients: cidofovir 0.3% gel
applied twice daily for 7–14 days
Smith KJ, Skelton H (2002) Molluscum contagiosum:
recent advances in pathogenic mechanisms,
and new therapies. American Journal of
Clinical Dermatology 3(8):535–545
Molluscum sebaceum
_ Molluscum contagiosum