eMedicine Specialties > Pediatrics: General Medicine > Dermatology

Molluscum Contagiosum

Author: Mark A Crowe, MD, Assistant Clinical Instructor, Department of Medicine, Division of Dermatology, University of Washington School of Medicine
Contributor Information and Disclosures

Updated: Dec 3, 2007

Introduction

Background

Molluscum contagiosum virus (MCV) causes a benign viral infection that is largely (if not exclusively) a disease of humans.

MCV causes characteristic skin lesions consisting of single or, more often, multiple, rounded, dome-shaped, pink, waxy papules 2-5 mm (rarely up to 1 cm) in diameter. The papules are umbilicated and contain a caseous plug. MCV is an unclassified member of the Poxviridae family, with features intermediately between the Orthopoxvirus and Parapoxvirus genera. It cannot be grown in tissue culture or eggs. It has been grown in human foreskin grafted to athymic mice but has not been transmitted to other laboratory animals.

By restrictive endonuclease analysis of the genomes of isolates, the following 4 types have been identified: MCV I, II, III, and IV. In one study of 147 patients, MCV I caused 96.6% of infections, and MCV II caused 3.4%; however, no relationship was observed between virus type and lesional morphology or anatomical distribution.1 MCV III and IV are rare. In patients with human immunodeficiency virus (HIV) infection, MCV II causes most infections (60%).

Bateman first described the disease in 1817, and Paterson demonstrated its infectious nature in 1841. In 1905, Juliusburg proved its viral nature. Infection follows contact with infected persons or contaminated objects, but the extent of epidermal injury necessary is unknown. Lesions may spread by autoinoculation. MCV may be inoculated along a line of minor skin trauma, resulting in lesions arranged in a linear pattern. This process, termed autoinoculation, is different from the Koebner phenomenon, which is also called an isomorphic response. In the Koebner phenomenon, new lesions develop along a line of trauma and the etiology of the underlying condition is unknown. Psoriasis and lichen planus are examples of skin conditions that commonly koebnerize.

Methods of MCV transmission between patients have been reported with direct skin contact by children sharing a bath and by athletes sharing gymnasium equipment and benches. An association between school swimming pool use and MC infection is also reported.

Three distinct disease patterns are observed in 3 different patient populations: children, adults who are immunocompetent, and patients who are immunocompromised (children or adults). The prognosis and therapy are different for each situation.

MC is most common in children who become infected through direct skin-to-skin contact or indirect skin contact with fomites, such as bath towels, sponges, and gymnasium equipment. Lesions typically occur on the chest, arms, trunk, legs, and face. Hundreds of lesions may develop in intertriginous areas, such as the axillae and intercrural region. Lesions may rarely occur on the mucous membranes of the lip, tongue, and buccal mucosa. The palms are spared. Patients with atopic dermatitis may develop large numbers of lesions.

In adults, MC most commonly is a sexually transmitted disease (STD). Healthy adults tend to have few lesions, which are limited to the perineum, genitalia, lower abdomen, or buttocks. MC in healthy children and adults is usually a self-limited disease.

Widespread, persistent, and atypical MC may occur in patients who are significantly immunocompromised or have acquired immunodeficiency syndrome (AIDS) with low CD4 T-lymphocyte counts. MC may be the presenting complaint in patients with AIDS. MCV infection in immunocompromised patients may be particularly resistant to therapy. Other opportunistic infections in these patients may closely resemble MC.

Pathophysiology

The virus replicates in the cytoplasm of epithelial cells, producing cytoplasmic inclusions and enlargement of infected cells. This virus only infects the epidermis. Infection follows contact with infected persons or contaminated objects, but the extent of necessary epidermal injury is unknown. The initial infection seems to occur in the basal layer, and the incubation period is usually 2-7 weeks. This is suggested by the fact that, although viral particles are noted in the basal layer, viral DNA replication and the formation of new viral particles do not occur until the spindle and granular layers of the epidermis are involved. Infection may be accompanied by a latent period of as long as 6 months.

Following infection, cellular proliferation produces lobulated epidermal growths that compress epidermal papillae, while fibrous septa between the lobules produce pear-shaped clumps with the apex upwards. The basal layer remains intact. Cells at the core of the lesion show the greatest distortion and are ultimately destroyed, resulting in large hyaline bodies (ie, molluscum bodies, Henderson-Paterson bodies) containing cytoplasmic masses of virus material. These bodies are present in large numbers and appear as a white depression at the center of fully developed lesions. Occasionally, the lesions can progress beyond local cellular proliferation and become inflamed with attendant edema, increased vascularity, and infiltration by neutrophils, lymphocytes, and monocytes.

As with other poxviruses, MCV does not appear to develop latency but evades the immune system through the production of virus-specific proteins. Cell-mediated immunity is most important in modulating and controlling the infection. Children and patients with HIV infection generally have more widespread lesions. Prevalence of MCV in patients with HIV may be as high as 5-18%, and the severity of infection is inversely related to the CD4 T-lymphocyte count. More extensive and resistant infections also are noted in patients receiving prednisone and methotrexate.

The virus is not strongly immunogenic, as it infrequently induces antibody formation. Specific antibodies have been found in approximately 80% of patients and in about 15% of control subjects. A role for humoral immunity in regression of lesions is not established. Reinfection is common.

Frequency

United States

MC is a common infection throughout the United States and accounts for approximately 1% of all skin disorders diagnosed. Data reported from 1969-1983 by the National Disease and Therapeutic Index Survey show an increasing number of patient visits. The prevalence rate in patients with HIV is reported to be 5-18%, and, if the CD4 cell counts are less than 100 cells/μ L, the prevalence of MC is reported to be as high as 33%.

International

The virus occurs throughout the world, and its incidence in most areas is not reliably known. It is more prevalent in tropical areas. In Mali, MC is among the most frequent dermatoses in children, with an incidence of 3.6%.2 In Australia, an overall seropositivity rate of 23% is reported.3 The lowest antibody prevalence was in children aged 6 months to 2 years (3%), and seropositivity increased with age to reach 39% in persons aged 50 years or older.

Childhood MC is common in Papua New Guinea, Fiji, and certain parts of Africa. During a regional outbreak in East Africa, it was estimated that 17% of the village population and as many as 52% of children older than 2 years developed lesions. Epidemiological studies suggest that transmission may be related to poor hygiene and climatic factors such as warmth and humidity. In England and Wales at STD clinics, incidence increased approximately 10-fold from 1971-1978.

Mortality/Morbidity

  • MC is generally a benign and self-limited infection.
  • For the most part, morbidity is caused by temporary adverse cosmetic results. Morbidity is higher in immunocompromised patients because they tend to have more lesions and more widespread infection. Most lesions resolve with no permanent residual skin defect; however, occasional lesions may produce a slightly depressed scar. This may represent deeper skin damage in lesions that were particularly inflammatory or secondarily infected. Involvement of the margin of the eyelids may produce keratoconjunctivitis.

Race

  • During a US longitudinal study performed from 1977-1981, 2-4 times as many cases were found in whites than in persons of other races.4 Whether the noted difference was secondary to differences in access to medical care, other socioeconomic factors, or genetic predisposition is unclear.

Sex

  • Several studies have shown that males are affected more commonly than females.
  • In STD clinics in England and Wales, slightly more than twice as many men are diagnosed as women.

Age

  • The disease is rare in children younger than 1 year, perhaps because of maternally transmitted immunity and a long incubation period; otherwise, incidence seems to reflect exposure to others. The greatest incidence is in children younger than 5 years and young adults. The peak among the pediatric age group correlates with casual contact, whereas the peak in young adults correlates with sexual contact.
  • Spread of the virus among households is common in warm-climate countries where children are lightly dressed and in close contact with one another and where personal hygiene may be poor. The age of peak incidence is reported to be 2-3 years in Fiji and 1-4 years in the Congo (formerly Zaire). In New Guinea, the annual infection rate for children younger than 10 years was 6%. In cooler climates, spread within households is less common, and infection is more common at a later age. Use of school swimming pools is correlated with childhood infections, with a peak incidence in children aged 10-12 years in Scotland and 8 years in Japan. Prevalence appears to be increasing in all age groups.

Clinical

History

  • Molluscum contagiosum (MC) is usually asymptomatic; however, individual lesions may be tender or pruritic.
  • In general, the patient does not experience systemic symptoms, such as fever, nausea, or malaise.
  • The patient may recall contact with an infected sexual partner, family member, or other person.
  • Patients who report having multiple sexual partners or unprotected sex have an increased risk of infection.
  • Contact may be reported in children sharing a bath or in athletes sharing gymnasium equipment and benches.
  • If the patient has skin conditions that disrupt the epidermal layer, molluscum tends to spread more rapidly.
    • The patient may notice new lesions developing along a scratch in areas of involved skin.
    • Patients with atopic dermatitis may have more extensive disease. Patients with atopic dermatitis may have a positive family history of atopy (eg, eczema, asthma, hayfever).
  • Duration of the individual lesion and of the attack is variable. Although most cases resolve without therapy within 6-9 months, some persist for 3-4 years. Individual lesions seldom persist more than 2 months.
  • Patients with HIV or those receiving prednisone, methotrexate, or other immunosuppressive medications may have more extensive and resistant infections.

Physical

  • Lesions are discrete, nontender, flesh-colored, dome-shaped papules that show a central umbilication (more apparent when lesion is frosted with liquid nitrogen).
  • Lesions are usually 2-6 mm in diameter (rarely up to 3 cm) and may be present in groups or widely disseminated. Immunocompetent children and adults usually have fewer than 20 lesions. Larger lesions may have several distinct clumps of molluscum bodies. Beneath the umbilicated center is a white curdlike core that contains molluscum bodies. Some lesions become confluent to form a plaque (agminate form).
  • Lesions may be located anywhere; however, a predilection for the face, trunk, and extremities is observed in children and a predilection for the groin and genitalia is observed in adults. Lesions are seldom found on palms and are rarely documented on the soles, oral mucosa, and conjunctiva.
  • In sexually active individuals, the lesions may be confined to the penis, pubis, and inner thighs.
  • Distribution is influenced by the mode of infection, type of clothing worn, and climate.
  • Hundreds of lesions may develop in intertriginous areas, such as the axillae and intercrural region.
  • Patients with atopic dermatitis occasionally develop large numbers of lesions, which are confined to areas of lichenified skin.
  • Widespread and persistent MC may occur in patients with AIDS and may be the presenting complaint.
  • Approximately 10% of patients develop eczema around the lesions. This is attributed to toxic substances produced by the virus or to a hypersensitivity reaction to the virus.
  • Eczema that is associated with molluscum lesions subsides spontaneously following removal.
  • Lesions may spontaneously resolve or following minor trauma. Inflammatory changes result in suppuration, crusting, and eventual resolution of the lesion. This inflammatory stage does not usually represent secondary infection and seldom requires antibiotic therapy.
  • MC may be randomly associated with other lesions, such as epidermal cysts, nevocellular nevi, sebaceous hyperplasias, and Kaposi sarcoma. Pseudocystic MC, giant MC, and MC associated with other lesions are responsible for frequent clinical misdiagnosis.
  • Disfiguring lesions may occur in patients with the following conditions:
    • AIDS: Facial and perioral MC are most commonly observed as a manifestation of HIV infection, particularly in homosexual men with HIV. At the time of MC diagnosis, the CD4 count is low.
    • Sarcoidosis
    • Lymphocytic leukemia
    • Congenital immunodeficiency
    • Selective immunoglobulin M (IgM) deficiency
    • Thymoma
    • Treatment with prednisone and methotrexate
    • Disseminated malignancy
    • Refractory atopic dermatitis
    • Immunocompromise: Lesions are especially common and extensive on the face and neck.

Causes

  • MC is a viral disease caused by a DNA poxvirus and is largely, if not exclusively, a disease of humans. It is an unclassified member of the Poxviridae family (ie, poxviruses), with features intermediately between the Orthopoxvirus and Parapoxvirus groups. The poxviruses are a large group of viruses with a high molecular weight. They are the largest animal viruses, only slightly smaller than the smallest bacteria, and are just visible using light microscopy. They are complex DNA viruses that replicate in the cytoplasm and are especially adapted to epidermal cells. They cannot be grown in tissue culture or eggs. MCV has been grown in human foreskin grafted to athymic mice but not in other laboratory animals.
  • Humans are the host for the following 3 types of MCV:
    • Orthopoxvirus: This resembles variola (smallpox) and vaccinia, which are ovoid (300 X 250 nm).
    • Parapoxvirus: These are orf and milkers nodule viruses, which are cylindrical (260 X 160 nm).
    • Unclassified (with features that are intermediately between the orthopox and parapox groups): These are intermediate in structure (275 X 200 nm). They include MCV and tanapox.
  • In 1996, the primary structure and coding capacity of MCV was determined by Senkevich et al.5 Analysis of the MCV genome has revealed that it encodes approximately 182 proteins, 105 of which have direct counterparts in orthopoxviruses.
  • Restriction endonuclease analysis of the genomes has identified 4 types.
    • MCV I and MCV II have genomes of 185 kilobases (kb) and 195 kb, respectively.
    • MCV III and IV are very rare.
    • No relationship between virus type and lesional morphology or anatomical distribution is known.
    • MCV encodes an antioxidant protein (MC066L), selenoprotein, which functions as a scavenger of reactive oxygen metabolites and protects cells from UV or peroxide damage. The particular role of this protein is not known.
  • In one study, type I caused 96.6% and type II caused 3.4% of infections in 147 patients, but no relationship was observed between virus type and lesional morphology or anatomical distribution.1

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References
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Further Reading

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Keywords

molluscum contagiosum, MC, molluscum contagiosum virus, MCV, molluscum verrucosum, molluscum contagiosum cornutum, viral infection, Poxviridae, HIV infection, Koebner phenomenon, psoriasis, lichen planus, atopic dermatitis, sexually transmitted disease, STD, acquired immunodeficiency syndrome, AIDS, Henderson-Paterson bodies, poxvirus, keratoconjunctivitis, atopy, eczema, asthma, hayfever, epidermal cysts, nevocellular nevi, sebaceous hyperplasias, Kaposi sarcoma, sarcoidosis, lymphocytic leukemia, thymoma, orthopoxvirus, parapoxvirus, pseudocystic molluscum contagiosum, giant molluscum contagiosum, syphilis, gonorrhea

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Contributor Information and Disclosures

Author

Mark A Crowe, MD, Assistant Clinical Instructor, Department of Medicine, Division of Dermatology, University of Washington School of Medicine
Mark A Crowe, MD is a member of the following medical societies: American Academy of Dermatology and North American Clinical Dermatologic Society
Disclosure: Nothing to disclose.

Medical Editor

Kevin P Connelly, DO, Clinical Assistant Professor, Department of Pediatrics, Division of General Pediatrics and Emergency Care, Virginia Commonwealth University; Medical Director, Paws for Health Pet Visitation Program
Kevin P Connelly, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation

Managing Editor

Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi
Disclosure: Nothing to disclose.

CME Editor

Merrily P M Poth, MD, Professor, Department of Pediatrics and Neuroscience, Uniformed Services University of the Health Sciences
Merrily P M Poth, MD is a member of the following medical societies: American Academy of Pediatrics, Endocrine Society, and Lawson-Wilkins Pediatric Endocrine Society
Disclosure: Nothing to disclose.

Chief Editor

William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System
William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology
Disclosure: elsevier Royalty Other

 
 
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