Molluscum Contagiosum

The full story for those who want to really understand the virus

Molluscum Contagiosum

Molluscum contagiosum is caused by a virus that is a member of the poxvirus family. Poxviruses are notorious for their ability to evade the host’s immune system by both acitve and passive mechanisms. Since the eradication of smallpox, the only poxvirus that naturally infects humans is molluscum contagiosum virus (MCV). MCV causes benign proliferative lesions of the skin in normal individuals. There are at least four types of MCV based on DNA restriction analysis. There does not appear to be any predilection for one virus type to infect certain groups of people, certain ages, or certain body areas, and all virus sub-types seem to infect equally. A recent study demonstrated that one of the proteins coded by the MCV genome inhibits the body’s lymphocytes (white blood cells or WBCs) and prevents inflammation. This may explain why it can take so long for the body to rid itself of MCV.

Molluscum contagiosum is 1% of all U.S. diagnosed of skin disorders.

Molluscum contagiosum is a common infection throughout the United States. It accounts for approximately 1% of all diagnoses of skin disorders by some estimates. The exact incidence in the United States is unknown. Higher incidence in children with eczema as well as in immunocompromised individuals has been documented. An Australian study found anti-MCV antibodies in 39% of adults older than 50 years, demonstrating exposure to be very common. There is no well documented predilection for infection among any racial group. Studies do not demonstrate any definite difference in incidence between the sexes. Cell-mediated immunity is thought to be important in modulating and controlling the infection.

Molluscum contagiosum is very common in children and can persist for years

This is a common infection in children. It is frequently seen on the face, neck, armpit, arms, and hands but may occur anywhere on the body except the palms and soles. Molluscum contagiosum is a chronic infection and lesions may persist from a few months to a few years. These lesions ultimately disappear without scarring. (Unless there is excessive scratching, which may leave marks.)

Typically, the lesion of molluscum begins as a small papule which may become raised up to a pearly, flesh-colored nodule. The papule often has a dimple in the center (umbilication). These papules may occur in lines, where the person has scratched. Scratching or other irritation causes the virus to spread in a line or in groups (crops).

The papules are approximately 2 – 5 millimeters in diameter and painless. There is usually no inflammation and subsequently no redness unless the person has been digging or scratching at the lesions. In the mature molluscum, the top of the nodule may be opened with a sterile needle and a small waxy core can be seen and squeezed out of the lesion.

The molluscum skin lesion commonly has the following qualities:

  • Small (2 – 5 millimeter diameter)
  • Dimple in center
  • Initially firm, flesh-colored, pearl-like, dome-shaped
  • Later lesions become softer, gray, and may drain
  • Central core or plug of white, cheesy or waxy material
  • Painless
  • Single or multiple (usually multiple)
  • Common locations in children: face, trunk, limbs
  • Common locations in adults: genitals, abdomen, inner thigh

mc4Figure 1: Typical appearance of molluscum on the abdomen of a 7 year old girl. Copyright CBR,Inc. 2002 All Rights reserved. May not be reproduced.
Diagnosis is based on the appearance of the lesion and can be confirmed by a skin biopsy. The health care provider should examine the lesion to rule out other disorders and to determine other underlying disorders.

Within months or years molluscum disappears for normal immune systems

In people with normal immune systems, the disorder usually disappears spontaneously over a period of months to years. The lesions may be extensive in people with AIDS or other conditions that affect the immune system. Individual lesions may be removed surgically, by scraping, de-coring, freezing, or through needle electrosurgery. Surgical removal of individual lesions may result in scarring. Medications, such as those used to remove warts, may be helpful in removal of lesions.

Individual lesions of molluscum contagiosum usually disappear within about 2 – 3 months. Complete disappearance of all lesions generally occurs within about 6 – 18 months. The disorder may persist in immunosuppressed people.

  • Persistence, spread, or recurrence of lesions
  • Secondary bacterial skin infections

You may want to call for an appointment with your healthcare provider if you have symptoms suggestive of molluscum contagiosum. You may also want to call for an appointment with your healthcare provider if lesions persist or spread, or if new symptoms appear.

Molluscum is also a sexually transmitted disease (STD).

As seen in children, the virus is highly contagious through direct contact. It may also spread by sexual contact. Molluscum is generally seen on the genitals as a sexually-transmitted disease. Early lesions on the genitalia may be mistaken for herpes or warts but, unlike herpes, these lesions are painless. Because molluscum produces no serious illness and is not of long-term public health significance, it has not been treated as other sexually-transmitted diseases. The importance is significant in the growing population of immunocompromised people with AIDS, who may have rapidly worse case of molluscum contagiosum.

So avoid direct contact with the molluscum skin lesions. Total abstinence is a foolproof way to avoid the molluscum virus and other STDs. You can also avoid STDs by having a monogamous sexual relationship with a partner known to be disease-free.

Neither male and female condoms will fully protect you, as the virus can be on areas not covered by the condom. Nonetheless, condoms should still be used every time the disease status of a sexual partner is unknown. They reduce your chances of getting or spreading STDs. Use them with spermicide with nonoxynol 9.

New molluscum treatment Options

Essential oils from plants in the Myrtle family have demonstrated anti-viral activity, both in cell culture and in some limited clinical studies. The essential oil of Melaleuca alternifolia is one such species with documented antibacterial, anti-fungal, and anti-viral actions. A recent published clinical study demonstrated the effectiveness of an essential oil preparation in the treatment of molluscum in children (Burke BE, Baille JE, Olson R. Treatment of molluscum contagiosum in children with essential oil of Australian lemon myrtle. Biomedicine & Pharmacotherapy, 2004; vol 58).

A product based on this study utilizing essential oil of Melaleuca (tea tree oil) in conjunction with iodine and other essential oils is marketed as ZymaDerm™. The data presented by the company reports better than a 85% success rate after 4-6 weeks. This represents a significant advancement in as much as the treatment is painless, making it a viable alternative to currently painful, invasive treatments, or worse yet, useless hucksterism often promoted on the internet.

References

Cohen J, Powderly WG. Infectious Diseases. 2nd ed. New York, NY: Elsevier; 2004:2053-2056.

Kauffman CL. Molluscum contagiosum. eMedicine. January 6, 2005. Available online at http://www.emedicine.com/derm/topic270.htm Accessed October 31, 2005.

Update Date: 10/31/2005

Updated by: Thomas A. Owens, M.D., Departments of Internal Medicine and Pediatrics, Duke University Medical Center, Durham, NC. Review provided by VeriMed Healthcare Network.

 

How Poxviruses Can Be Eradicated Worldwide — The Smallpox Example

The global eradication of smallpox through the WHO campaign is the most outstanding example of what could be achieved through international cooperation. As a result, poxviruses have been relegated to the position of relatively unimportant human pathogens.

The Global Eradication of Smallpox

The global eradication of smallpox through the WHO (United Nations World Health Organization) campaign is the most outstanding example of what could be achieved through international cooperation. As a result, poxviruses have been relegated to the position of relatively unimportant human pathogens.

A. Properties

The family of poxviridae is divided into 6 genera, with species within each genera closely related.
Poxviruses are the largest viruses known
dsDNA enveloped virus, bricked shaped virions 200-250 * 250-300 nm in diameter. 2 morphological forms are seen: M (mulberry) and C (capsule) forms that are interconvertable. Internally, poxviruses have a biconcave “nucleoid” and 2 lateral bodies.
Inside the cell, the virion often has a double membrane. The lateral bodies contain various enzymes essential for virus replication.
>100 polypeptides have been demonstrated in vaccinia.
Poxviruses are very easy to isolate and will grow in a variety of cell cultures and will produce pocks on the chick chorioallantoic membrane (CAM)

cropped-leaf_site_icon_01.pngElectronmicrograph of molluscum contagiosum particles. (Courtesy of Linda M. Stannard, University of Cape Town)

B. Smallpox

Smallpox was transmitted by respiratory route from lesions in the respiratory tract of patients in the early stage of the disease. During the 12 day incubation period, the virus was distributed initially to the internal organs and then to the skin. Variola major caused severe infections with 20-50% mortality, variola minor with less than 1% mortality. Management of outbreaks depended on the isolation of infected individuals and the vaccination of close contacts. The vaccine was highly effective. If given during the incubation period. It either prevented or reduced the severity of clinical symptoms. The origin of the vaccine strain is not known, it is thought that it may have been horsepox which is now an extinct disease.

The eradication of smallpox

Smallpox was eradicated from most countries in Europe and the US by 1940s. By the 1960s, smallpox remained a serious problem in the Indian subcontinent, Indonesia and much of Africa. The WHO listed smallpox as the top on the list for eradication in 1967. There were certain features of smallpox which made it a highly eradicable disease. (see table below). The WHO smallpox eradication unit was set up in 1967. The initial strategy was separated into 3 phases;

1. Attack phase – This applied to areas where the incidence of smallpox exceeded 5 cases per 100,000 and where vaccination coverage was less than 80%. Attention was given to mass vaccination and improvement in case surveillance and reporting. This phase lasted from 1967-1973. A large amount of financial resoureces were provided for setting up surveillance centres and reference centres. Priority was given to Brazil, sub-saharan African, S.Asia and Africa. Brazil and Indonesis were thought to be the easiest countries to eradicate the virus from. In fact by 1973, smallpox had been eradicated from Braziland Indonesia. It was decided it was time to go on to the consolidation phase.

2. Consolidation Phase – In areas where the incidence was less than 5 cases per 100,000 and vaccination coverage exceeded 80%, the objective was the elimination of smallpox. Vaccination uptake was to be maintained and surveillance improved. Facilities should be made available for isolation.

3. Maintenance Phase – once smallpox had been eliminated, it was essential it was not reintroduced. This phase was entered in 1978. In 1980, the world was declared to be free of smallpox.

It became clear smallpox could not be eradicated with mass vaccination alone.

It soon became clear that smallpox could not be eradicated with mass vaccination alone. In some countries, it was not possible to achieve a smallpox vaccination uptake rate of 80%. More attention was therefore paid to case tracing and isolation procedures.

Experience in West Africa and Indonesia had shown that smallpox can be eliminated without mass vaccination, provided that a high rate of case detection was achieved. The Indian subcontinent was a special problem because of its large size and population. It provided a reservoir for variola major infection. Extra attention was paid to search out unnotified cases that proved to be highly effective. The last cases of variola major occurred in the Indian subcontinent in 1975. The last case of variola minor occurred in Somalia in 1977. The last cases of smallpox occurred in a Birmingham laboratory in 1979.

It was estimated that the smallpox eradication campaign costed US $312 million. If smallpox had not been eradicated, routine efforts to control smallpox would have costed US $1 billion. The success of smallpox eradication was due to the involvement of an international agency which was able to cross national barriers. The following were features that made smallpox an eradicable disease;

  1. A severe disease with morbidity and mortality
  2. Considerable savings to developed non-endemic countries
  3. Eradication from developed countries demonstrated its feasibility
  4. No cultural or social barriers to case tracing and control
  5. Long incubation period
  6. Infectious only after incubation period
  7. Low communicability
  8. No carrier state
  9. Subclinical infections not a source of infection
  10. Easily diagnosed
  11. No animal reservoir
  12. Infection confers long-term immunity
  13. One stable serotype
  14. Effective vaccine available

Other Poxviruses

Monkeypox

Monkeypox was first isolated from monkeys in 1958, but it was not until 1970 that it was associated with human disease. To date, over 400 cases have been investigated, mainly from Zaire. The pathogenesis and clinical features for monkeypox is the same as for smallpox. The main differences are a greater degree of lymphadenopathy and a lower capacity for case-to-case spread. Most cases occur in unvaccinated children. The mortality in human monkeypox is appreciable, being in the order of 10%. The management of human monkeypox is the same as for smallpox. Human monkeypox has not been detected outside West Africa. Although monkeypox was first isolated from monkeys, there is no evidence that African monkeys act as the reservoir. The most likely candidate for reservoir is the African squirrel. One important difference between human monkeypox and smallpox is the lower capacity for human spread. The attack rate among unvaccinated contacts is 9% in contrast to >37% for smallpox. Laboratory workers studying monkeypox should be vaccinated.

Vaccinia

Vaccination with vaccinia (an attenuated and greatly weakened form of the small pox virus) was associated with certain risks. Complications ranged from mild reactions and fatal encephalitis. The overall incidence of complications was around 1/800 although the more severe forms occurred only in 15 per million vaccinees. Recent interest has focused on the possible usage of vaccinia as a vector for immunization against other viruses. It is possible that certain changes can be made to the vaccinia genome which makes it less likely to develop side effects.

Cowpox

Cowpox is a relatively unimportant zoonosis which has only been isolated in Britain and Europe. Infection has been described in humans, cows and cats. Infection in humans usually remain localized, often producing a lesion which is similar to that caused by vaccination, although the inflammatory response is greater and general constitutional symptoms such as fever and myalgia may be present in some cases. In humans, lesions are usually restricted to the hands, but may also be transferred to the face. EM is generally used for the diagnosis of infection. The virus will also grow well on CAM. Human cowpox usually respond to treatment with antivaccinia immunoglobulin, but its use should be restricted to the most severe cases. Although cowpox was first isolated form cattle and farm workers. There is no evidence that cattle serve as the reservoir. In fact, cowpox is very rare in cattle. It has been suggested that the reservoir is actually a small rodent but this is not proven.

Parapoxviruses

Parapoxvirus infections are widespread in sheep, goats and cattle and relatively unimportant but common human infections occur. Infections in cattle and humans are usually referred to as pseudocowpox, paravaccinia or milker’s nodes. Those in sheep and goats as orf. The viruses are closely related and the nomenclature of the human disease is based on the identity of the host form which the infection was acquired. (orf from sheep and pseudocowpox from cattle). Infection occurs via small cuts and abrasions in all hosts and is usually localized. Although the lesions are similar to the early lesions of cowpox and vaccinia, true macrovesicles do not form. In humans, lesions usually occur on the hand but may be transferred to the face.

The laboratory diagnosis is usually made by EM. The virus may also be isolated in human, bovine and ovine cells but such investigations are not part of routine diagnostic virology. Parapoxvirus infections occur worldwide, and are of considerable importance. A survey carried out in New Zealand showed that 1.4% of workers in the meat industry became infected in 1 year. The lesions are surprisingly painless and thus there is probably substantial under-reporting. Idoxuridine had occasionally been prescribed for treatment but no trials have been carried out to prove the efficacy of treatment. Prevention of human infection is difficult. Reasonable precautions should be undertaken when handling infected animals.

Molluscum Contagiosum

Molluscum contagiosum is a specifically human disease of worldwide distribution. The incubation period varies from 1 week to 6 months. The lesion begins as a small papule and gradually grows into a discrete, waxy, smooth, dome-shaped, pearly or flesh-colored nodule. Usually 1-20 lesions but occasionally they may be present in hundreds. In children, the lesions are found on the trunk and the proximal extremities. In adults they tend to occur on the trunk, pubic area and thighs. Individual lesions persist for about 2 months, but the disease usually lasts 18 to 30 months. Constitutional disturbance is rare.

The disease occurs worldwide and is spread by direct contact or fomites. In general it tends to occur in children. The disease may be transmitted from skin to skin after sexual intercourse. A diagnosis can usually be made on clinical appearance alone. The diagnosis can be supported by EM. Unlike other poxviruses, molluscum have not been demonstrated to grow in cell culture. Infection is usually benign and painless, with spontaneous recovery in most cases. Where treatment is desired, various procedures are available.

Tanapox

Tanapox is a poxvirus infection first recognized in 1957 in the Tana River area of Kenya. It is a zoonosis, human cases have only been seen in the Tana valley and Zaire. The distribution of the virus and the real extent of the human infection is not known, as is the method of transmission of infection. The virus produces a mild febrile illness with one or two skin lesions. The virus does not grow in CAM but will grow in a variety of cell lines.

http://virology-online.com/viruses/Poxviruses.htm

New Mollsucum Treatment Options

Essential oils from plants in the Myrtle family have demonstrated anti-viral activity, both in cell culture and in some limited clinical studies. The essential oil of Melaleuca alternifolia is one such species with documented antibacterial, anti-fungal, and anti-viral actions. A recent published clinical study demonstrated the effectiveness of an essential oil preparation in the treatment of molluscum in children ( Burke BE, Baille JE, Olson R. Treatment of molluscum contagiosum in children with essential oil of Australian lemon myrtle. Biomedicine & Pharmacotherapy, 2004; vol 58).

A product based on this study utilizing essential oil of Melaleuca (tea tree oil) in conjunction with iodine and other essential oils is marketed as ZymaDerm™. The data presented by the company reports better than a 85% success rate after 4-6 weeks. This represents a significant advancement in as much as the treatment is painless, making it a viable alternative to currently painful, invasive treatments, or worse yet, useless hucksterism often promoted on the internet.

 

Excerpts from the article 
Molluscum Contagiosum

By Daniel Hanson and Dayna G. Diven
 Dermatology Online Journal 9(2): 2

Abstract: Molluscum contagiosum is a disease caused by a poxvirus of the Molluscipox virus genus that produces a benign self-limited papular eruption of multiple umbilicated cutaneous tumors. This common viral disease is confined to the skin and mucous membranes. Transmission requires direct contact with infected hosts or contaminated fomites. It is generally thought to infect humans exclusively, but there are a few isolated reports of Molluscum contagiosum occurring in chickens, sparrows, pigeons, chimpanzees, kangaroos, a dog, and a horse. The infection is found worldwide and has a higher incidence in children, sexually active adults, and those who are immunodeficent.

Introduction

Molluscum contagiosum, a cutaneous and mucosal eruption caused by a Molluscipox virus, was first described and later assigned its name by Bateman in the beginning of the nineteenth century.[1] In 1841 Henderson and Paterson described the intracytoplasmic inclusion bodies now known as molluscum or Henderson-Paterson bodies.[2] In the early twentieth century, Juliusberg, Wile, and Kingery were able to extract filterable virus from lesions and show transmissibility.[3,4] Goodpasture later described the similarities of molluscum and vaccinia.[5] Though generally thought to infect only humans, case reports of the virus occurring in other animals have been published. [6,7,8,9]

Incidence

Molluscum contagiosum virus (MCV) can be found worldwide with a higher distribution in the tropical areas. The disease is more prevalent in children with the lesions involving the face, trunk, and extremities. In adults the lesions are most often found near the genital region. The disease is endemic with a higher incidence within institutions and communities where overcrowding, poor hygiene, and poverty potentiate its spread.[10] Over the last 30 years its incidence has been increasing, mainly as a sexually transmitted disease, and it is particularly rampant as a result of concurrent human immunodeficiency virus (HIV) infection.[11] The worldwide incidence is estimated to be between 2% and 8%.[12] Less then 5% of the children in the United States are believed to be infected. Between 5% and 20% of patients with HIV have symptomatic MCV.[13,14] There are four main subtypes of molluscum contagiosum: MCV I, MCV II, MCV III, and MCV IV.[15,16] All subtypes cause similar clinical lesions in genital and nongenital regions. Studies show MCV I to be more prevalent (75%–90%) than MCV II, MCV III, and MCV IV, except in immunocompromised individuals.[17,18] There are, however, regional variations in the predominance of a given subtype and differences between individual subtypes in different countries.[19]

Pathogenesis

This disease is transmitted primarily through direct skin contact with an infected individual. Fomites have been suggested as another source of infection, with molluscum contagiosum reportedly acquired from bath towels, tattoo instruments, and in beauty parlors and Turkish baths.[10] The average incubation time is between 2 and 7 weeks with a range extending out to 6 months. Infection with the virus causes hyperplasia and hypertrophy of the epidermis.[12] Free virus cores have been found in all layers of the epidermis. So-called viral factories are located in the malpighian and granular cell layers.[12] The molluscum bodies contain large numbers of maturing virions. These are contained intracellularly in a collagen-lipid-rich saclike structure that is thought to deter immunological recognition by the host.[20] Rupture and discharge of the infectious virus-packed cells occur in the center of the lesion. MCV induces a benign tumor instead of the usual necrotic pox lesion associated with other poxviruses.[21]

Clinical manifestations

MCV produces a papular eruption of multiple umbilicated lesions. The individual lesions are discrete, smooth, and dome shaped. They are generally skin colored with an opalescent character. The central depression or umbilication contains a white, waxy curdlike core. The size of the papule is variable, depending upon the stage of development, usually averaging 2–6 mm. Papules may exceed 1 cm in size in immunosuppressed hosts. The papules may become inflamed spontaneously or after trauma and present atypically in size, shape, and color. The lesions are often grouped in small areas but may also become widely disseminated.

Any cutaneous surface may be involved, but favored sites include the axillae, the antecubital and popliteal fossae, and the crural folds. Rarely, MCV lesions occur in the mouth or conjunctivae.[22,23,24] Autoinoculation is common. Children usually acquire molluscum nonsexually at both genital and nongenital areas. MCV in adults affects the groin, genital area, thighs, and lower abdomen and is often acquired sexually. Around 10% of cases develop an eczematous dermatitis around the lesions, but this disappears as the infection resolves.[25] Patients with atopic dermatitis can have a disseminated eruption. Eruptions in immunocompromised indiviuals are very resistant to treatment.[13,26]

Dermatopathology

Histologically, molluscum contagiosum exhibits intraepidermal lobules with central cellular and viral debris. In the basal layer, enlarged basophilic nuclei and mitotic figures are seen. Progressing upward, the cells show cytoplasmic vacuolization and then eosinophilic globules. The nucleus becomes compressed at the level of the granular cell layer, and the molluscum bodies lose their internal structural markings. Undisrupted lesions show an absence of inflammation, but dermal changes can include an infiltrate that is lymphohistiocytic, neutrophilic, or granulomatous. The latter has been seen in solitary lesions. Antibody to MCV by indirect immunofluorescence has been found in 69% of patients with visible lesions.[27] Polymerase chain reaction can detect MCV in skin lesions.[28] Currently, there is no in-vitro or animal model for MCV. MCV can undergo an abortive infection in some cell lines, which can cause confusion with herpes simplex virus by laboratories.[29] Two sets of investigators have infected human skin with molluscum contagiosum and grafted it onto athymic mice, although there was no continued viral replication.[30,31]

Diagnosis

The clinical appearance of molluscum contagiosum is in most cases diagnostic. Though molluscum cannot be cultured in the laboratory, histological examination of a curetted or biopsied lesion can also aid in the diagnosis in cases that are not clinically obvious. The thick white central core can be expressed and smeared on a slide and left unstained or stained to demonstrate the large brick-shaped inclusion bodies. Electron microscopy has also been used to demonstrate the poxivirus structures. Immunohistochemical methods using a polyclonal antibody allows recognition of molluscum contagiosum in fixed tissue.[32] In-situ hybridization for MCV DNA has also been utilized.[33] Molluscum contagiosum lesions must be differentiated from verruca vulgaris, condyloma accuminata, varicella, herpes simplex, papillomas, epitheliomas, pyoderma, cutaneuos cyptococcosis, epidermal inclusion cyst, basal cell carcinoma, papular granuloma annulare, keratoacanthoma, lichen planus, and syringoma or other adenexal tumors.

 

Common Molluscm Treatments Offered by the Physician

Molluscum contagiosum is a self-limited disease, which, left untreated, will eventually resolve in immunocompetent hosts but may be protracted in atopic and immunocompromised individuals. Some patients pick and scratch at the lesions, a habit that may lead to scarring. In addition, some schools and daycare centers will not admit children with visible molluscum papules. When patients seek medical attention and desire to rid themselves of the papules, there are several means of therapeutic destruction to help speed resolution.

The decision whether treatment is necessary depends on the needs of the patient, the recalcitrance of their disease, and the likelihood of treatments to leave pigmentary alteration or scarring. Most of the common treatments consist of various means to traumatize the lesions. Antiviral and immune-modulating treatments have recently been added to the options, but with limited success. The following is a brief summary of some of the more common treatments.

Cryosurgery

One of the most common, quick, efficient methods of treatment is cryotherapy. Liquid nitrogen, dry ice, or Frigiderm are applied to each individual lesion for a few seconds. Repeat treatments in 2–3-week intervals may be required.[34] Hyper- or hypopigmentation and scarring may be caused by this treatment.

Evisceration

An easy method to remove the lesions is eviscerating the core with an instrument such as a scalpel, sharp tooth pick, edge of a glass slide, or any other instrument capable of removing the umbilicated core. Because of its simplicity, patients, parents, and caregivers may be taught this method so new lesions can be treated at home.[35,36] This method is simple but may not be tolerated by small children.

Curettage

Curettage is another method of removal. It can be used with and without light electrodessication. This method is more painful, and it is recommended that a topical anesthetic cream be applied to the lesions before the procedure to decrease the pain. This method has the advantage of providing a reliable tissue sample to confirm the diagnosis.[35,37]

Tape stripping

Another reported treatment involves the use of adhesive tape. The adhesive side of the tape is repeatedly applied to and removed from the lesion for 10–20 cycles. This action effectively removes the superficial epidermis from the top of the lesion.[38] However, repeated use of the same strip has the potential to spread the virus to adjacent, uninvolved skin.

Podophyllin and podofilox

A 25% suspension in a tincture of benzoin or alcohol may be applied once a week. This treatment requires some precautions. It contains two mutagens, quercetin and kaempherol. Some of the listed side effects include severe erosive damage in adjacent normal skin that may cause scarring and systemic effects such as peripheral neuropathy, renal damage, adynamic illeus, leucopenia, and thrombocytopenia, especially if used generously on mucosal surfaces. Podofilox is a safer alternative to podophyllin and may be used by the patient at home. The recommended use usually consists of application of 0.05 ml of 5% podofilox in lactate buffered ethanol twice a day for 3 days.[35,38] The active agent is absolutely contraindicated in pregnancy.

Cantharidin

Cantharidin (0.9% solution of collodian and acetone) has been used with success in the treatment of MCV. This blister-inducing agent is applied carefully and sparingly to the dome of the lesion with or without occlusion and left in place for at least 4 hours before being washed off. Cantharidin can cause severe blistering. It should be tested on individual lesions before treating large numbers of lesions. It should not be used on the face. When tolerated, this treatment is repeated every week until the lesions clear. Usually 1–3 treatments are necessary.[39]

Tretinoin

Tretinion 0.1% cream has been used in the treatment of MCV. It is applied twice daily to the lesions. Resolution was reported by day 11. Trace erythema at the site of prior lesions was a noted side effect.[41] Tretinion 0.05% cream has also been used with success and decreased irritation.[35]

Cimetdine

Oral cimetidine has successfully been used in extensive infections.[42] The histamine 2-receptor antagonist stimulates delayed-type hypersensivity. One uncontrolled study showed resolution in 9 of 13 patients. In this study, the dosage was 40 mg/kg/day in two divided doses for 2 months.[43] The authors recommended further placebo-controlled, double-blind studies be completed to determine the efficacy of cimetidine in treating MCV. Because cimetadine interacts with many systemic medications, a review of the patient’s other medications is recommended.

Potassium hydroxide

Another treatment option is the use of potassium hydroxide. In one study, an aqueous solution of 10% KOH was applied topically twice daily to all lesions with a swab. The treatment was discontinued when an inflammatory response or superficial ulcer became evident. Resolution occurred in a mean of 30 days.[44] This treatment had some complications including hypertrophic scar formation and persistent or transitory hyper- and hypopigmentation. A subsequent study in pediatric patients recommended the use of 5% KOH and found it equally effective with many fewer side effects.[45]

Pulsed dye laser

The use of pulsed dye laser for the treatment of MC has also been documented with excellent results. The therapy was well tolerated, without scars or pigment anomalies. The lesions resolved without scarring at 2 weeks. Studies show 96%–99% of the lesions resolved with one treatment.[46,47] The pulsed dye laser is quick and efficient, but its expense makes it less cost effective than other options.

Imiquimod

Imiquimod 5% cream has been used topically to treat MCV by inducing high levels of IFN-a and other cytokines locally.[48,49] This potent immunomodulatory agent is well tolerated, although application site irritation is common. It has had no known systemic or toxic effects in children.[50] It is applied to the area nightly for 4 weeks. Clearing can take up to 3 months.

Conclusion

Molluscum Contagiosum is a common, generally benign, viral infection of the skin. It is common in children, sexually active adults, and immunodeficient patients. It is caused by the molluscipox virus, a member of the poxviridae family. This virus differs from other poxviruses in that it causes spontaneously regressing, umbilicated tumors of the skin rather than poxlike vesicular lesions. In immunocompetent, nonatopic patients molluscum contagiosum is usually a self-limited disease for which treatment is not mandatory. However, when treatment is deemed appropriate, multiple local therapeutic options are available. For patients with impaired immune functions with widespread and potentially disfiguring eruptions, the usual local destructive therapies are ineffective; antiviral and immunomodulatory medications have been more successful.

New Molluscum Treatment Options

Essential oils from plants in the Myrtle family have demonstrated anti-viral activity, both in cell culture and in some limited clinical studies. The essential oil of Melaleuca alternifolia is one such species with documented antibacterial, anti-fungal, and anti-viral actions. A recent published clinical study demonstrated the effectiveness of an essential oil preparation in the treatment of molluscum in children (53). A product based on this study utilizing essential oil of Melaleuca (tea tree oil) in conjunction with iodine and other essential oils is marketed as ZymaDerm™. The data presented by the company reports better than a 85% success rate after 4-6 weeks. This represents a significant advancement in as much as the treatment is painless, making it a viable alternative to currently painful, invasive treatments, or worse yet, useless hucksterism often promoted on the internet.

References

1. Bateman F. Molluscum contagiosum. In: Shelley WB, Crissey JT, eds. Classics in Dermatology. Springfield IL; Charles C Thomas, 1953, p20.
2. Brown ST, Nalley JF, Kraus SJ. Molluscum contagiosum Sex Transm Dis 1981;8:227-234.
3. Juliusberg M. Zur Kenntnis des virus des Molluscum contagiosum. Dtsch Med Wochenschr 1905;31:1598-1599.
4. Wile and Kingery, J Cutan Dis., 1917 XXVII, p.431.
5. Bretz S. Molluscum Contagiosum. Emedicine Juournal April 25,2001;2(4).
6. Pusey WA. Moluscum contagiosum In: The Principals and Practice of Dermatology, 4th ed. Appleton, 1924, pp 989-990.
7. Douglas JD, Tanner KN, Prine JR, Van Riper DC, Derwelis SK. Molluscum contagiosum in chimpanzees. J Am Vet Med Assoc 1967;151:901-904.
8. Dangall BG, Witson GR: Molluscum contagiosum in a red kangaroo. Australas J Dermatol 1974;15:115.
9. IB Van Resburg, MG Collett, N Ronen, T Gerdes. Molluscum contagiosum in a horse. J S Afr Vet Assoc 1991;62:72-74.
10. Postlethwaite R. Molluscum contagiosum: A review. Arch Environ Health 1970; 21: 432-452.
11. Becker TM, Blout JH, Douglas J, Judson FM. Trends in molluscum cantagiosum in the United States, 1966-1983. Sex Transm Dis 1986;13:88-92.
12. Billstein SA. Mattaliano VJ Jr. The “nuisance” sexually transmitted diseases: Molluscum contagiosum, scabies, and crab lice. Med Clin North Am 1990; 74: 1487-1505.
13. Schwartz JJ. Myskowski PL: Molluscum contagiosum in patients with human immunodefificiency virus infection. J Am Acad Dermatol 1992;27:583.
14. Lombardo PC. Molluscum contagiosum and the acquired immunodeficiency syndrome. Arch Dermatol 1985; 121: 834-835.
15. Scholz J, Rosen-Wolff A, Burgert K et al. Epidemiology of molluscum contagiosum using genetic analysis of the viral DNA. J Med Virol 1989; 27: 87-90.
16. Porter CD, Archard LC: Characterization by restriction mapping of three subtypes of molluscum contagiosum virus. J Med Virol 1992;38:1.
17. Gottlieb SL, Myskowki PL. Molluscum contagiosum. Int J Dermatol 33: 453-461,1994.
18. Yamashita H, Uemura T, Kawashima M. Molecular epidemiologic analysis of Japanese patients with molluscum contagiosum. Int J Dermatol 1996;35:99-105.
19. Nakamura J, Muraki Y, Yamada M, Hatano Y, Nii S. J Med Virol 1995;46(4):339-48.
20. Burgert JJ, Darai G. Recent advances in molluscum contagiosum virus research. Arch Virol Suppl 1997;13:35-47.
21. Diven DG, An overview of poxviruses, J AM Acad Dermatol 2001;44:1-14.
22. Whitaker SB, Wiefand SE, Budnick SD. Inraoral molluscum contagiosum. Oral Surg Oral Med Oral Pathol. 1991;72: 334-336.
23. Ingraham HJ, Schoenleber DB. Epibulbar molluscum contagiousm. Am J ophthalmol 1998;125:394-396.
24. Vannas S, Lapinleimu K. Molluscum contagiosum of the skin, caruncle, and conjunctiva. Acta Ophthalmol 1967;45:314-321.
25. De Oreo GA, Johnson HH, Binkley GW. An eczematous reaction associated with molluscum contagiosum. Arch Dermatol 1956; 74: 344-8.
26. Cotton DW, Cooper C, Barrett DF, Leppard BJ. Severe atypical molluscum contagiosum infection in an immunocommpromised host. Br J Dermatol 1987;116:871-876.
27. Shirodaria PV, Mattews RS. Observations on the antibody responses in molluscum contagiosum. Br J Dermatol 1997;96:29-34.
28. Thompson CH. Identification and typing of molluscum contagiosum virus in clinical specimens by polymerase chain reaction. J Med Virol 1997;53:205-211.
29. Hovenden JL, Bushhell TE. Molluscum contagiosum: possible culture misdiagnosis as herpes simplex[letter]. Genitourin Med 1991;67:270.
30. Fife KH, Whitfield M, Faust H, Goheen MP, Bryan J, Brown DR. Growth of molluscum contagiosum virus in a human foreskin xenograft model. Virology 1996;226:95-101.
31. Buller RM, Burnett J Chen W, Kreider J. Replication of molluscum contagiosum virus. Virology 1995;213:655-659.
32. Penneys NJ, Matsuo S, Mogollon R. The identification of molluscum infection of immunohistochemical means. J Cutan Pathol 1986;13:97-101.
33. Thompson CH, Biggs IM, DeZwart-Steffe RT. Detection of molluscum contagiosum virus DNA by in-situ hybridization. Pathology 1990;22:181-186.
34. Janniger CK, Schwartz RA. Molluscum Contagiosum in children. Cutis 1993;52: 194-196.
35. Valentine CL, Diven DG, Treatment modalities for molluscum contagiosum. Dermatologic Therapy 2000;13: 285-289.
36. Epstein WL. Molluscum contagiosum. Semin Dermatol 1992;11: 184-189.
37. Janniger CK, Schwartz RA. Molluscum Contagiosum in children. Cutis 1993; 52: 194-196.
38. Arndt KA. Manualof dermatologic therapeutics, 5th ed. Boston: Little Brown, 339-340, 1995.
39. Silverburg NB, Sidbury R, Mancini AJ. Childhood molluscum contagiosum: Experience with cantharidin therapy in 300 patients. J Am Acad Dermatol 2000;43: 503-507.
40. Ohkuma M. Molluscum contagiosum treated with iodine solution and salicylic acid plaster. Int J Dermatol 1990;29:443-445.
41. Papa CM, Berger RS. Venereal herpes-like molluscum contagiosum: treatment with tretinoin. Curis 1976;18:537-540.
42. Avella J, Binder H, Madsen J, Ashkenase P. Effect of histamine H2 receptor antagonists on delayed hypersensitivity. Lancet 1978:1:624-626.
43. Dohil M, Prendiville JS. Treatment of Molluscum contagiosum with oral cimetidine: clinical experience on 13 patients. Pediatric Dermatol 13:310-312.
44. Romiti R, Ribeiro AP, Grinblat BM. Treatment of molluscum contagiosum with potassium hydroxide: A clinical approach in 35 children. Pediatr Dermatol 1999;16: 228-231.
45. Romiti R, Ribeiro AP, Romiti N. Evaluation of the effectiveness of 5% potassium hydroxide for the treatment of molluscum contagiosum. Pediatr Dermatol 2000;17(6):495.
46. Hammes S, Greve B, Raulin C. [Molluscum contagiosum: treatment with pulsed dye laser] Hautarzt 2001;52;38-42.
47. Hughes PS. Treatment of molluscum contagiosem with the 585-nm pulsed dye laser. Dermatol Surg 1998;24: 229-230.
48. Hengge UR, Esser S, Schultewolter T, Behrendt C, Meyer T, Stockfleth E. Goos M. Self administered topical 5% imiquimod for the treatment of common warts and molluscum contagiosum. British Journal of Dermatology 2000;143: 1026-1031.
49. Tyring SK, Arany I, Stanley MA et al. A randomized, controlled, molecular study of condylomata acuminate clearance during treatment with imiquimod. J Infec Dis 1998;178:551-5.
50. Barba Ar, Kapoor S, Berman B. An open label safety study of topical imiquimod 5% cream in the treatment of Molluscum contagiosum in children. Dermatol Online J 2001; Vol 7(1), 20.
51. Zabawski EJ Jr. A review of topical and intralesional cidofovir. Dermatology Online J 2000;6(1):3
52. Zabawaski EJ Jr, Cockerell CJ. Topical cidofovir for molluscum contagiosum in children[letter] Pediatr Dermatol 1999;16(5):414-415.© 2003 Dermatology Online Journal
53) Burke BE, Baille JE, Olson R. Treatment of molluscum contagiosum in children with essential oil of Australian lemon myrtle. Biomedicine & Pharmacotherapy, 2004; vol 58.