Molluscum Contagiosum

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Background

In 1817, long before the recent increased incidence of molluscum contagiosum (MC), Bateman first described milky fluids that could be expressed from characteristic lesions. Henderson and Paterson, 2 researchers studying molluscum contagiosum independently 25 years later, described the milky fluid to be cellular. Only later did the 2 researchers realize they had discovered the hallmark intracytoplasmic inclusion body, appropriately named the Henderson-Paterson body (molluscum body).

Until the early 20th century, the medical community remained unsure of the etiology of molluscum contagiosum. Certain authorities believed the papules to be enlarged sebaceous glands, while others postulated that a parasitic infestation caused the lesions. A breakthrough in the study of molluscum contagiosum occurred in 1905 when Juliusburg discovered and documented the viral nature of molluscum contagiosum.

Pathophysiology

The molluscum contagiosum virus, which contains linear double-stranded DNA, causes molluscum contagiosum. Restriction endonucleases have elucidated 4 discrete viral subtypes: molluscum contagiosum virus subtypes I, II, III, and IV. All subtypes are classified as members of the Orthopoxvirus genus or as unspecified poxviruses. When human infection occurs, the epidermal keratinocytes are targeted. Viral replication occurs within the cytoplasm of the infected cell, generating the characteristic cytoplasmic inclusion bodies. Histologically, these inclusion bodies are most evident within the stratum granulosum and stratum corneum layers of the epidermis. Hyperproliferation of the epidermis also occurs because of a doubling in the rate of cellular division of the epidermal basal layer.

The molluscum contagiosum virus causes 3 distinct disease patterns in 3 different patient populations: children, immunocompetent adults, and immunocompromised patients (children or adults). Children acquire the molluscum contagiosum virus through either direct skin-to-skin contact or indirect skin contact via fomites such as gymnasium equipment and public baths. Lesions typically occur on the chest, arms, trunk, legs, and face. In adults, molluscum contagiosum is considered a sexually transmitted disease (STD). In almost all cases involving healthy adults, patients exhibit few lesions, which are limited to the perineum, genitalia, lower abdomen, or buttocks. Generally, in immunocompetent populations, molluscum contagiosum is a self-limited disease.

Patients infected with human immunodeficiency virus (HIV) or patients who are otherwise severely immunologically compromised may experience a longer course with more extensive and atypical lesions. In patients infected with HIV, lesions generally are distributed more widely, frequently occur on the face, and may number in the hundreds. The cutaneous manifestations of other opportunistic infections, such as cutaneous cryptococcosis, histoplasmosis, and aspergillosis, may mimic molluscum contagiosum and must be ruled out in immunocompromised hosts.

For additional information on HIV, see Medscape’s HIV Transmission & Prevention Resource Center.

Epidemiology

Frequency

United States

The incidence of molluscum contagiosum rose from 1960-1980. It is less common than other STDs, occurring in about 1% of the general population. In a 1984 paper published in the Urologic Clinics of North America, Margolis of the Centers for Disease Control and Prevention reportedthat 1 case of molluscum contagiosum occurs for every 42-60 cases of gonorrhea infection.[22]

The prevalence rate in the population infected with HIV is reported to be 5-18%. In patients who are infected with HIV and who have CD4 cell counts of less than 100 cells/μL, the prevalence of molluscum contagiosum is reported to be as high as 33%.

Mortality/Morbidity

Race

No racial predilection has been reported.

Sex

The incidence in men reportedly is greater than that in women.

Age

Molluscum contagiosum has been reported in all age groups but is observed most commonly in children and adults who are sexually active. Molluscum contagiosum may occur at any age in immunocompromised patients.

History

Physical

Individual lesions are typically discrete, waxy, flesh-colored, dome-shaped, umbilicated papules with a smooth surface. Lesions may be few or numerous, depending on the immunological status of the host. In all patients, lesions generally are asymptomatic, but pruritus and/or perilesional eczematous reactions may develop.

Causes

Risk factors include the following:

Laboratory Studies

Procedures

Histologic Findings

The prototypical hematoxylin and eosin (H&E)–stained histological section of molluscum contagiosum reveals a cup-shaped indentation of the epidermis into the dermis (as seen in the image below).


View Image

This low-power view of a molluscum contagiosum (MC) lesion shows the classic cup-shaped invagination of the epidermis into dermis. The Henderson-Pater....

Within the region of the indentation, the epidermis appears thickened (acanthosis) compared to the surrounding uninvolved skin, and the cornified layer typically is disintegrated. The striking feature is the presence of intracytoplasmic, eosinophilic, granular inclusions within the keratinocytes of the basal, spinous, and granular layers of the epidermis (as seen in the image below).


View Image

This is a medium-power view of a molluscum contagiosum (MC) lesion. Magnification allows better demonstration of the intracytoplasmic molluscum bodies....

These inclusions, termed molluscum bodies or Henderson-Paterson bodies, can measure 35 µm in diameter and tend to displace the nucleus to the periphery of the cell. Ultrastructural studies have shown that the molluscum bodies are membrane-bound sacs that contain numerous molluscum contagiosum virions. The surrounding dermis is relatively unremarkable.

In nonprototypical cases, in which intradermal rupture of molluscum bodies occurs, an intense dermal inflammatory infiltrate consisting of lymphocytes, histiocytes, and occasional foreign body–type multinucleated giant cells may be observed. Rarely, metaplastic ossification may occur. Exceptionally, the dermal inflammatory infiltrate may be intense enough to simulate a cutaneous lymphoma (pseudolymphoma).

Medical Care

The course of molluscum contagiosum usually is self-limited, and lesions generally heal without scarring.

Intervention may be indicated if lesions persist. Therapeutic modalities include topical application of various medications, radiation therapy, and/or surgery. Each technique might result in scarring or postinflammatory pigmentary changes. Frequently, multiple treatment sessions are necessary because of the recurrence of treated lesions and/or the appearance of new lesions by autoinoculation. The benefit of therapy must exceed the risk.

The Food and Drug Administration (FDA) has approved none of the topical or intralesional agents for treatment of molluscum contagiosum.

Surgical Care

Frequently, multiple treatment sessions are necessary because of recurrence of treated lesions and/or the appearance of new lesions by autoinoculation. Each technique may result in scarring or postinflammatory pigment changes.

Medication Summary

Topical medications usually are the first category used in treating active disease. Use acid and intralesional therapies when topical therapy fails.

Imiquimod (Aldara)

Clinical Context:  Induces secretion of IFN-alfa and other cytokines. Mechanisms of action are unknown. May be more effective in women than in men.

Class Summary

These agents are one of the first-line topical treatments for molluscum contagiosum, although not FDA approved for the indication.

Cantharidin (Verr-Canth)

Clinical Context:  Lytic action does not affect basal layer and has minimal effect on the corium. Scarring does not occur.

Class Summary

These are first-line topical agents, although they are not FDA approved for molluscum contagiosum. Effectiveness against warts may result from exfoliation.

Tretinoin topical (Avita, Retin-A)

Clinical Context:  Inhibits microcomedo formation and eliminates lesions. Makes keratinocytes in sebaceous follicles less adherent and easier to remove. Available as 0.025%, 0.05%, and 0.1% creams. Available also as 0.01% and 0.025% gels.

Begin with lowest tretinoin formulation and increase as tolerated.

Trichloroacetic acid (Tri-Chlor)

Clinical Context:  Cauterizes skin, keratin, and other tissues. Although caustic, causes less local irritation and systemic toxicity than other medications in the same class. Response often is incomplete, and recurrence is frequent.

Must be applied by physician in office setting.

Silver nitrate (AgNO3)

Clinical Context:  Second-line therapy after failure with first-line agents. Coagulates cellular protein and removes granulation tissue.

Must be applied by physician in office setting.

Class Summary

The agents are used to aid in the removal of keratin in hyperkeratotic skin disorders, including corns, ichthyoses, common warts, flat warts, and other benign verrucae.

Interferon alfa 2a and 2b (Roferon-A [alfa-2a], Intron A [alfa-2b])

Clinical Context:  Protein product manufactured by recombinant DNA technology. Mechanism of antitumor activity is not understood clearly; however, direct antiproliferative effects against malignant cells and modulation of host immune response may play important roles.

Class Summary

These are second-line agents for use in immunocompromised children.

Australian lemon myrtle (Backhousia citriodora)

Clinical Context:  10% solution of essential oil of Australian lemon myrtle.

Class Summary

These agents are over-the-counter, herbal alternatives.

Warning: Herbal formulations are not regulated by the FDA.

Further Outpatient Care

Deterrence/Prevention

Complications

Prognosis

Author

Ashish C Bhatia, MD, FAAD, Assistant Professor, Department of Dermatology, Northwestern University, Feinberg School of Medicine; Director of Clinical Research, Department of Dermatology and Dermatologic Surgery; Director of Dermatologic Surgery and Dermatology, The Dermatology Institute of DuPage Medical Group

Disclosure: Nothing to disclose.

Coauthor(s)

David Rowe, MD, Pathologist, Laboratory Medicine, Martha Jefferson Hospital

Disclosure: Nothing to disclose.

Julia R Nunley, MD, Professor, Program Director, Dermatology Residency, Department of Dermatology, Virginia Commonwealth University Medical Center

Disclosure: Novartis Grant/research funds Consulting; Biolex Grant/research funds sub-investigator

Robert Orenstein, DO, Associate Professor, Department of Medicine, Medical College of Virginia, Virginia Commonwealth University; Medical Director, Infectious Disease Clinic, Medical College of Virginia Hospitals

Disclosure: Nothing to disclose.

Seth Forman, MD, Private Practice, Tampa, Florida

Disclosure: Abbott Laboratories Honoraria Speaking and teaching

Tracy Campbell, MD, Staff Physician, Department of Dermatology, Rush Medical Center

Disclosure: Nothing to disclose.

Specialty Editors

Daniel R Lucey, MD, MPH, Chief, Fellowship Program Director, Department of Internal Medicine, Division of Infectious Diseases, Washington Hospital Center; Professor, Department of Internal Medicine, Uniformed Services University of the Health Sciences

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

John W King, MD, Professor of Medicine, Chief, Section of Infectious Diseases, Director, Viral Therapeutics Clinics for Hepatitis, Louisiana State University Health Sciences Center; Consultant in Infectious Diseases, Overton Brooks Veterans Affairs Medical Center

Disclosure: emedicine $50.00 author of chapter; MERCK None Other

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital

Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Disclosure: Nothing to disclose.

References

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This low-power view of a molluscum contagiosum (MC) lesion shows the classic cup-shaped invagination of the epidermis into dermis. The Henderson-Paterson bodies are identified readily and stain purple-to-red in this image.

This is a medium-power view of a molluscum contagiosum (MC) lesion. Magnification allows better demonstration of the intracytoplasmic molluscum bodies (staining purple-pink) within the keratinocytes.

Presented here are the classic umbilicated papules of molluscum contagiosum (MC) lesions on the cheek of a child. Facial lesions occur frequently in children, although lesions generally are few.

Molluscum contagiosum (MC) rarely occurs on the face in an adult unless the patient is infected with HIV. When MC occurs in individuals infected with HIV, facial lesions are common and frequently numerous.

Molluscum contagiosum (MC) lesions in individuals infected with HIV may number in the hundreds. In addition, they may become quite large and prominent.

This low-power view of a molluscum contagiosum (MC) lesion shows the classic cup-shaped invagination of the epidermis into dermis. The Henderson-Paterson bodies are identified readily and stain purple-to-red in this image.

This is a medium-power view of a molluscum contagiosum (MC) lesion. Magnification allows better demonstration of the intracytoplasmic molluscum bodies (staining purple-pink) within the keratinocytes.

This molluscum contagiosum body is an intracytoplasmic inclusion body. Notice in the image that the keratinocyte nuclei are displaced to the periphery of the cell and the intracytoplasmic inclusions have a granular quality.