What is that? a mollusk? noooo…its a rash. Wait what?
Molluscum Contagiosum is a benign superficial skin disease caused by the Molluscum contagiosum virus, which is a large double stranded DNA virus in the poxvirus family. The poxvirus replicates in the cytoplasm of host keratinocytes producing discrete, small (2-5mm), pearly flesh colored or pink dome shaped papules with a central umbilication or depression. The core of these lesions can occasionally be expressed and consists of a white cheesy material. The lesions are generally painless, but may become inflamed, red, scaly and swollen secondary to scratching or a hypersensitivity reaction. They most commonly occur in the intertriginous regions such as the axillae, groin and neck. They rarely occur on the face or periocular region, but can occur anywhere on the body except the palms and soles. In adults, they are most common in the pubic and genital areas, whereas genital manifestations in children could be an indication of abuse.
The infection is found worldwide, but is more common in developing countries. It has also mainly been considered a pediatric disease, typically occurring in toddlers or younger children over 1 year of age.
The virus is spread by direct contact with an infected individual or by contact with infected fomites, but the virus does not develop latency like the herpes virus. It is unclear as to whether the disease may be spread by simple contact with intact lesions or if breaking the lesion and the subsequent transfer of the lesion’s core material is necessary for transmission. Secondary spread of lesions may occur by autoinoculation by excoriation (especially in patients with atopic dermatitis) as well as by shaving and electrolysis. Swimming pools, steam baths, saunas, and communal spray baths have also been considered as modes of transmission likely because the warm and wet environment facilitates the spread of the virus by fomites. Vaccination against smallpox in infancy had not been found to be protective. The virus is completely contained in this protective sac allowing it to avoid triggering the host immune response. The incubation period of the virus has been estimated to be between 2 weeks and 6 months, with the lesions usually resolving spontaneously in 6-12 months; however some can take up to 4 years to resolve. Atopic dermatitis may be a risk factor for contracting the molluscum contagiosum virus due to barrier breaks and immune cell dysfunction in atopic skin. Patients with atopic dermatitis are also more likely to autoinoculate because of the underlying pruritis from their atopic dermatitis. Immunocompromised patients often have larger (over 15 mm) and more widespread lesions that could be disfiguring and are more resistant to standard therapy.
Diagnosis is generally made merely by appearance of the lesions. Skin biopsy may be necessary in immunocompromised individuals to rule out malignancy or fungal infections. Skin biopsy will reveal “molluscum bodies” which are large, eosinophilic, round, intracytoplasmic inclusions in the epidermis. A microscopic evaluation of a potassium chloride preparation of the soft material obtained from the umbilicated part of the lesion shows inclusion bodies within the keratinocytes as well. The infected cells appear dark and round and disperse easily with slight pressure, whereas normal epithelial cells are flat and rectangular and tend to remain stuck together in sheets. Virions can be seen streaming out of the amorphous mass if a Sedi-Stain or toluidine blue stain is used. Click here for examples.
Complications of molluscum include are minimal and include scarring from excoriation during the healing process and secondary infections.
Treatment of the lesions is usually not necessary in healthy individuals. However, genital lesions should be definitively treated to prevent spread through sexual contact. There are treatment options available for individuals who desire therapy for cosmetic reasons, or if they have underlying atopic dermatitis or are concerned about spreading the lesions to others. These options include removal by cryotherapy with topical liquid nitrogen, curretage or laser therapy. Curettage can be performed with or without anesthetic (EMLA cream) and bleeding after the removal can be controlled with direct pressure or Monsel’s solution. Curettage is useful when there are only a few lesions because it is quick and reliable. It may cause scarring, so should be avoided in cosmetic areas. Cryosurgery is the treatment of choice, as long as the patient is not bothered by pain. The papule is sprayed or touched lightly with a nitrogen-bathed cotton swab until the white frozen border forms an approximately 1 mm halo on the surrounding skin, which should only take approximately 5 seconds. Most lesions can be destroyed in 1-3 treatment sessions at 1-2 week intervals. Excessive freezing can produce hyper or hypopigmentation, so care must be used to not over-expose the skin to liquid nitrogen. A 585 nm pulsed dye laser may be used for laser excision of lesions and is an effective, well-tolerated and quick treatment.
There are also several less painful and invasive techniques available to remove the lesions. These techniques are often more desirable for pediatric patients because they are generally less painful, produce less scarring and may be performed by parents at home in a less threatening environment. The options include: oral cimetidine, topical podophyllotoxin cream, iodine and salicylic acid, potassium hydroxide, tretinoin, cantharidin, Verrusol, trichloroacetic acid peels, imiquimod (a T cell modifier) and hypoallergenic surgical adhesive tape. Topical steroids can also be used to treat nearby dermatitis. A trial of imiquimod 5% cream (Aldara), an immunomodulator, used three times a day for 5 days in males aged 9-27 found a cure rate of over 80%. Children may respond better and with less irritation if treated only once daily. Imiquimod was found to be most efficacious in patients with HIV-1 disease and in the genital area in immune-competent adults. Cantharidin 0.7%, a chemovesicant extract from blister beedle, is very effective and well tolerated in children. It is applied over the surface of the lesion, penetrates the epidermis and induces vesiculation of the lesions through acantholysis. It cannot be used on facial lesions and contact with the surrounding skin should be avoided. The treated areas must be washed with soap and water 4-6 hours after treatment or even sooner if any burning or discomfort occurs. Therapy is repeated at 2-4 week intervals as needed. However, new lesions do occasionally appear at the site treated by cantharidin. Another option similar to cantharidin is Verrusol (1%cantharidin, 30% salicylic acid, 5% podophyllin). Application of podophyllotoxin 0.5% may be tried for cases resistant to other therapies. Another alternative, 5% Potassium hydroxide applied twice daily to each lesion for 30 days results in inflammation and superficial ulceration of each lesion and clinical cure in the majority of patients in just 4 weeks. Hypertrophic scarring and pigment changes may occur. Hypoallergenic surgical adhesive tape applied once each day after showering until the lesion ruptures and the core is discharged have also been shown to be beneficial.
In HIV patients with low CD4 cell counts widespread facial mollusca are more common and therefore have become a marker for severe HIV disease. Therapies targeted at boosting the immune system have proven to be the most effective therapy for molluscum contagiosum in immunocompromised persons. Trichloroacetic acid peels with 25-50% solution repeated every 2 weeks as needed have also shown good success in the treatment of extensive molluscum in HIV patients with no scarring, spreading, or secondary infections. In extreme cases, intralesional interferon has been used to treat facial lesions in HIV patients. The severe and unpleasant side effects of interferon, such as influenza-like symptoms, site tenderness, depression, and lethargy, make it a less-than-desirable treatment.