Continuing Education Activity

Molluscum contagiosum is a common, benign epidermal eruption caused by a double-stranded DNA virus of the Poxviridae family and affects children, adults, and individuals with compromised immune systems. Characteristic dome-shaped papules may mimic other dermatologic conditions, creating diagnostic uncertainty for clinicians. The infection is generally self-limited, yet its contagious nature, cosmetic visibility, potential for autoinoculation, and risk of more extensive disease in specific populations justify timely recognition and counseling. Clinical evaluation focuses on distinguishing typical lesions from mimickers such as verrucae, folliculitis, or acneiform eruptions while determining when active treatment is appropriate. Understanding transmission patterns, natural history, and potential complications enhances clinical decision-making and facilitates the reduction of spread through informed patient education.

This activity provides clinicians with an in-depth review of the etiology, epidemiology, pathophysiology, clinical features, differential diagnosis, and evidence-based management of molluscum contagiosum. Participants learn to select between observation, topical therapies, and procedural interventions based on lesion severity, patient age, comorbidities, and treatment goals. Enhanced collaboration among interprofessional healthcare team members, including clinicians, nurses, and dermatology specialists, promotes consistent counseling, coordinated care plans, and improved patient outcomes. The activity strengthens competence in diagnostic accuracy, communication strategies, and therapeutic decision-making to support high-quality, patient-centered care.

Objectives:

• Identify the characteristic clinical features and key differential diagnoses of molluscum contagiosum to support its timely and accurate recognition and appropriate management.
• Apply current evidence-based management strategies to guide individualized decisions on initiating therapy versus observation for molluscum contagiosum.
• Implement effective patient education and infection control strategies to decrease transmission and recurrence of molluscum contagiosum.
• Implement effective collaboration and communication among interprofessional team members to develop coordinated care and infection-control strategies for patients with molluscum contagiosum, ensuring consistent counseling, aligned treatment plans, and effective family education. 

Introduction

Molluscum contagiosum (MC) is a common, benign epidermal eruption caused by a virus that affects both children and adults, including healthy and immunocompromised individuals. Characteristic lesions are skin-colored, dome-shaped papules that may resemble other dermatologic conditions, making accurate diagnosis challenging at times. Although MC is typically harmless and self-limited, its contagious nature, cosmetic impact, and risk of complications in specific populations warrant clinical attention and patient education. 

MC is common in childhood, and the virus may also be sexually transmitted or linked to participation in contact sports in teenagers and adults.[1][2][3] Additionally, it is associated with immunodeficiency, infecting individuals with inherited disorders, HIV infection, or those on immunosuppressive therapy. Transmission occurs directly through skin-to-skin contact or indirectly via fomites from contaminated objects such as towels, clothing, gym equipment, toys, swimming pool surfaces, and sports gear. It can also spread through autoinoculation, where affected individuals transfer the virus to nearby or distant skin areas by scratching or touching existing lesions. The incubation period typically ranges from 2 to 6 weeks. The duration of lesions varies, but in most cases they are self-limited and resolve within a year.[4] See Image. Molluscum Contagiosum.

Etiology

The molluscum contagiosum virus (MCV) is a double-stranded DNA virus from the Poxviridae family. MCV belongs to a different genus than other poxviruses that infect humans, such as vaccinia, variola, and mpox. There are 4 MCV genotypes, with MCV-1 responsible for about 90% of cases in the United States, followed by MCV-2. Infections caused by MCV-3 and MCV-4 are uncommon globally but have been reported primarily in Asia and the South Pacific.[5] Most pediatric cases are caused by MCV-1, whereas MCV-2 is more often associated with sexually transmitted infections in immunocompetent adolescents and adults and with more severe or disseminated cutaneous involvement in immunocompromised individuals.[6][7]

Transmission occurs through direct skin-to-skin contact, autoinoculation, and exposure to contaminated fomites such as shared towels, clothing, razors, sports equipment, and pool or bath toys, which can retain infectious material from disrupted lesions. Fomite transmission is particularly relevant in settings with close contact, such as households and locker rooms. Children, sexually active adolescents and adults, and immunocompromised individuals remain the groups at highest risk. Vertical transmission of MCV, although rare, has been documented in case reports of neonates born to mothers with active infection. Transmission is believed to result from contact with maternal genital lesions during vaginal delivery, with lesions appearing shortly after birth.[8]

Epidemiology

MC is most frequent in children and is rare in infants under 1 year of age. There are no gender differences in prevalence or healthcare utilization.[9] Data on the global prevalence of MC are limited, with an estimated annual incidence of approximately 8000 cases per 100,000 individuals.[5] In children, the overall prevalence ranges from 5.1% to 11.5%, with a higher frequency reported in regions with warm climates.[10][11] In the United States, MC affects approximately 6 million people annually, with the highest incidence among children aged 1 to 14 years.[9] Most cases are seen in children younger than 8, with a median age at diagnosis of 5 years.[3][12]

MC also occurs in adolescents and adults, as a sexually transmitted infection or associated with close skin contact during sports such as wrestling or gymnastics.[1] MC is more common and often more severe in individuals who are immunosuppressed. During the 1980s, reported cases increased in association with the HIV epidemic, and the prevalence among patients with HIV is estimated to be as high as 20%.[13][14] MC may also occur in patients with iatrogenic immunosuppression (eg, after organ transplantation or chemotherapy) or primary immunodeficiency syndromes.[15]

Major risk factors for MC include young age, close contact with affected individuals, shared fomites, impaired skin barrier, and immunocompromised status. Children with atopic dermatitis are at particularly high risk, likely due to frequent scratching, which disrupts the skin barrier and facilitates viral entry and autoinoculation.[14] In immunocompromised individuals, lesions may be more numerous, atypical in distribution, and long-lasting.

Pathophysiology

Humans are the only known hosts for MCV.[16] Pathogenesis begins when MCV penetrates the epidermis, usually through microabrasions or a compromised skin barrier. The incubation period typically ranges from 2 to 7 weeks, but can vary from 1 week to 6 months. The virus replicates in the cytoplasm of keratinocytes, causing local proliferation and the formation of characteristic skin lesions. 

The virus only infects epidermal keratinocytes in vivo and, unlike other poxviruses such as vaccinia, cannot be cultured in standard cell lines.[17] MCV employs multiple strategies to evade host immune and inflammatory responses, including encoding proteins that inhibit chemokine signaling and suppress local inflammatory pathways, resulting in persistent infections that may last months to years.[5][18][19] Disease progression is typically self-limited in immunocompetent hosts, with eventual clearance mediated by a delayed local inflammatory response. In patients with atopic dermatitis or immunosuppression, lesions may be more numerous, persistent, and atypical in appearance. MCV infections remain localized to the skin and do not cause viremia or systemic illness.[19]

Histopathology

MC lesions display typical histopathological features, including epidermal hyperplasia and dome-shaped papules with central craters or depressions. These craters are filled with keratin and contain large intracytoplasmic inclusion bodies, known as molluscum bodies or Henderson-Paterson bodies, which are composed of viruses. Molluscum bodies are large, eosinophilic, and serve as sites of viral replication.[6][19] The basal layer of the epidermis remains intact.

Additional histologic features include keratinocytes surrounding cells with molluscum bodies, which have prominent nucleoli, amphophilic cytoplasm, and clear cytoplasmic vacuoles. The adjacent dermis may show dilated capillaries and lymphocytic infiltration. However, inflammatory infiltrates are usually sparse unless the MC lesion is regressing, in which case a dense infiltrate of cytotoxic T cells, natural killer cells, and plasmacytoid dendritic cells may be present.[20]

History and Physical

Patients with MC typically relate a history of gradual onset of asymptomatic, small skin "bumps" over weeks to months. Lesions are usually painless, but mild pruritus or local irritation sometimes occurs. While the virus can affect adults, especially immunocompromised or sexually active individuals, the majority of cases occur in children, particularly those younger than 15. They may report a history of close skin-to-skin contact with another child, participation in contact sports, or a history of atopic dermatitis, which increases the risk of infection as well as the lesion burden. 

Physical examination shows flesh-colored, dome-shaped papules with central umbilication, typically 2 to 5 mm in diameter.[21][22] Lesions may be solitary or clustered and are most commonly found on the trunk, extremities, and face in children, or on the genital, perineal, and lower abdominal areas in sexually active adolescents and adults. The oral mucosa is rarely involved, whereas conjunctival lesions can occasionally be seen.[23] Children typically present with 10 to 20 lesions, although in severe cases the number may exceed 100. In children with underlying atopic dermatitis, the rash may develop quickly and spread more extensively.[24]

Molluscum dermatitis refers to an inflammatory rash that develops around or between MC lesions. This condition is thought to represent an immune-mediated hypersensitivity reaction to MCV antigens rather than direct viral infection of the surrounding skin. The infection appears as erythematous, scaly, or excoriated patches near or between lesions and is often considered a sign of impending lesion resolution, as the host's immune system responds to the MCV; this condition should not be mistaken for a secondary bacterial infection.[25]

Lesions in individuals with impaired immunity are typically numerous, larger, and more widely disseminated than in those with intact immunity. In severely immunocompromised individuals, such as those with advanced HIV infection or primary immunodeficiencies, lesions may exceed 10 to 15 mm in diameter ("giant" molluscum), involve atypical sites (including the face, eyelids, and mucous membranes), and persist for prolonged periods. Lesions may also be confluent and disfiguring, and are more likely to resist standard therapies.[6][26]

Evaluation

MC is a clinical diagnosis, based on the appearance of characteristic flesh-colored, dome-shaped, umbilicated papules, and does not typically require laboratory confirmation. Dermatoscopy may aid diagnosis, but further evaluation is generally unnecessary.[6] Laboratory testing, including histopathology, cytology, and polymerase chain reaction, is reserved for atypical presentations, immunocompromised individuals, or when the diagnosis is uncertain due to unusual lesion morphology or distribution.

Skin biopsy and fine-needle aspiration cytology can confirm MC by identifying pathognomonic Henderson-Paterson bodies.[27][28] Polymerase chain reaction assays targeting MCV DNA (eg, the p43K gene) from lesion swabs provide rapid, sensitive, and specific confirmation, and can differentiate between MCV1 and MCV2 subtypes. Pyrosequencing, a type of DNA sequencing technique, is occasionally used for genotyping in research or epidemiological settings.[29][30] Diagnostic imaging is not indicated in the evaluation of MC, as the disease is limited to the epidermis and does not involve deeper tissues.[19] Bacterial cultures are rarely indicated and should be considered only if there is clinical suspicion of superinfection. True bacterial superinfection of MC lesions is uncommon, and routine culturing or antibiotic use is not recommended.[31]

Treatment / Management

Observation ("benign neglect") is the first-line approach for MC in immunocompetent individuals, as most cases resolve spontaneously within months to years. Treatment is considered for persistent, symptomatic, or cosmetically concerning lesions or to reduce transmission risk. National and international guidelines, including the Cochrane review and the American Academy of Dermatology, recommend observation as a reasonable strategy, given the lack of consistently superior interventions and the self-limited nature of the infection.[32][33] 

The primary treatments for molluscum contagiosum include physical removal (curettage, cryotherapy, and electrodessication) and topical therapies, with selection guided by lesion burden, symptoms, patient preference, and risk of transmission. Recent advances in topical agents have expanded therapeutic options, complementing traditional destructive methods. Clinicians should carefully weigh the potential benefits of active treatment against the risks of procedural discomfort and scarring when deciding between intervention and watchful waiting.

Physical removal methods include curettage, cryotherapy, and electrodessication. Curettage is frequently cited as the most effective intervention, with high clearance rates and favorable cosmetic outcomes compared to electrodessication. Both curettage and cryotherapy are common in-office procedures reserved for MC lesions that are persistent, symptomatic, cosmetically concerning, or causing psychosocial distress, particularly in children with multiple or facial lesions. Curettage is generally preferred over electrodessication for children, offering better cosmetic outcomes, faster recovery, and less post-procedural pain. Cryotherapy is effective but may be painful and less tolerated in young children; it may also cause blistering and pigmentary changes.[34][4] Electrodessication is less preferred due to higher rates of lesion remnants and slower recovery.[35]

Topical therapies include cantharidin (now available as VP-102), potassium hydroxide, podophyllotoxin, and the newly Food and Drug Administration (FDA)-approved berdazimer gel (Zelsuvmi). Traditional cantharidin, typically compounded in-office, varies in concentration and delivery. In contrast, VP-102, approved by the FDA in 2020, is a standardized 0.7% cantharidin formulation in a single-use applicator, offering consistent dosing and an improved safety profile for the treatment of molluscum contagiosum. Two large phase 3 trials demonstrated that VP-102 is superior to inactive vehicle for complete clearance (46%–54% vs 13%–18% at 12 weeks), with mostly mild to moderate local adverse effects.[10]

Other topical agents, such as potassium hydroxide, benzoyl peroxide, salicylic acid, and podophyllotoxin, have variable efficacy and may irritate. Imiquimod, a topical immune response modifier, is not recommended due to its lack of effectiveness and increased risk of local application-site reactions.[32][33][34][36] Berdazimer gel (10.3%) represents a significant recent advancement, approved by the FDA in 2024 for use in adults and children aged 1 year and older. The medication is a topical antiviral therapy that disrupts viral replication and stimulates local immune responses. Multiple phase 3 trials and meta-analyses demonstrate that Berdazimer gel is significantly more effective than an inactive vehicle for achieving complete lesion clearance at 12 weeks, with a favorable safety profile. Most adverse events are mild to moderate local reactions.[9][37][38] The product is designed for once-daily topical application by patients, parents, or caregivers and is the first FDA-approved, at-home topical therapy for MC.

Immunotherapy is an emerging option for recalcitrant or widespread molluscum contagiosum, leveraging the host's cell-mediated immune response to clear lesions. Intralesional agents, including Candida antigen, measles-mumps-rubella vaccine, tuberculin purified protein derivative, and varicella zoster vaccine, have demonstrated complete clearance rates of 36% to 100%, with mostly mild local reactions. This approach is beneficial for patients with multiple, persistent, or treatment-resistant lesions, or for those seeking to avoid destructive procedures, and may be considered in immunocompromised individuals.[39][40]

Patients with impaired immunity often require individualized, multimodal therapy, as lesions tend to be more extensive and treatment-resistant. Local destructive methods, such as cryotherapy and curettage, may reduce lesion burden but are often insufficient in patients with advanced immunosuppression.[6] Topical cidofovir can be effective for giant or refractory lesions and is preferred over systemic cidofovir due to the risk of nephrotoxicity.[41] Intralesional immunotherapy is a promising option with growing evidence of efficacy even in transplant recipients and those with significant immunosuppression.[42] In patients with HIV, MC is frequently extensive, persistent, and responds poorly to standard therapies. Optimizing antiretroviral treatment is the most effective approach and often leads to gradual regression of lesions as immune function improves. 

Differential Diagnosis

The differential diagnosis of MC includes verruca vulgaris (common warts), verruca plana (flat warts), and folliculitis. Verruca vulgaris, caused by human papillomavirus (HPV), presents as flesh-colored, hyperkeratotic papules, most commonly affecting the hands and feet. They can be mistaken for MC, especially in children, but typically lack central umbilication and may have a rougher surface (see Image. Pseudo-Koebnerization).[43] Verruca plana is also HPV-induced. These flat-topped papules usually appear on the face and extremities, especially in children and young adults. They are generally smaller and less dome-shaped than molluscum and lack the characteristic central umbilication.[44] 

Folliculitis is a bacterial infection of hair follicles, most often caused by Staphylococcus aureus, and can present as grouped papules or pustules. Unlike MC lesions, folliculitis lesions are often erythematous and tender, and may have a central hair.[45] Other conditions that may resemble MC include keratosis pilaris (rough, papular lesions typically found on the upper arms, thighs, or cheeks that lack umbilication), milia (white, keratin-filled cysts usually found on the face, which are nonumbilicated and unclustered), and condyloma acuminatum (anogenital warts).[46][47] HPV types 6 and 11 cause these soft, papular, or pedunculated growths in the genital region that may resemble molluscum but lack central umbilication and are often larger or more irregular in appearance.[48]

In immunocompromised individuals, MC lesions may be atypical, larger, and mimic malignancies, such as basal cell carcinoma or keratoacanthoma (for single lesions), or fungal infections, including cryptococcosis and histoplasmosis (for extensive lesions). In rare cases, basal cell carcinoma may mimic MC, especially the nodular or superficial types. Suspicious lesions that are persistent, ulcerated, or rapidly growing require biopsy for diagnosis. [49] Mpox (formerly known as monkeypox) and other orthopoxvirus infections can present with umbilicated papules or pustules, often accompanied by systemic symptoms such as fever, myalgias, and lymphadenopathy. Diagnosis is confirmed via polymerase chain reaction analysis of swabbed lesions.[50]

Prognosis

MC generally has an excellent prognosis in immunocompetent children and adults, with spontaneous resolution expected in most cases within 6 to 18 months. In healthy children, MC is self-limited, with about 50% of lesions clearing within 12 months and 70% within 18 months, without treatment.[12] The average duration is 13 to 18 months, but some cases may persist for up to 2 to 5 years.[10][51] Persistent or recurrent disease and complications are more common in individuals who are immunocompromised.

In immunocompetent adults, MC is generally benign and self-limited, with lesions typically resolving spontaneously within 12 months, although clearance can occasionally take up to 2 to 3 years. Recurrence is uncommon, but reinfection can occur with new exposure. Sexually transmitted lesions do not affect long-term health but warrant counseling on safe sexual practices to prevent further spread. Complications in healthy children and adults are rare and usually limited to secondary bacterial infection or mild post-inflammatory changes if lesions are scratched or treated aggressively. Treatment does not reliably shorten the disease course in immunocompetent individuals.[12][32]

In immunocompromised adults, lesions can be larger, more numerous, atypical, and persistent, with slower resolution. In HIV-positive individuals, effective antiretroviral therapy often facilitates clearance. Complications include higher rates of secondary bacterial infection, inflammation, and postinflammatory pigment changes or scarring. Spontaneous resolution is less predictable than in immunocompetent individuals, and lesions may persist for years.

Complications

Most cases are uncomplicated, but potential adverse outcomes include:

• Secondary bacterial infection (rare), especially in cases of scratching or in children with atopic dermatitis.[4][10] 
• Eczematous reactions (molluscum dermatitis) are more common in children with atopic dermatitis and may cause pruritus or discomfort. Susceptibility is attributed to impaired skin barrier function and heightened pruritus, which promotes scratching and autoinoculation.[12]
• Scarring (rare), usually following significant inflammation or physical treatments.[4][9]
• Psychosocial distress due to visible lesions, especially when on the face or in school-aged children.[4][9]
• Autoinoculation and spread to other body sites or household contacts.[4] In immunocompromised populations such as patients with HIV, organ transplant recipients, or other immunodeficiencies, MC can be extensive, persistent, and atypical. Lesions may be larger, more numerous, and resistant to standard therapies.[10][51] Chronic, disfiguring lesions and increased risk of secondary infection are more frequent in this population. In HIV-positive individuals, initiation of antiretroviral therapy (ART) is the most effective intervention for MC, but lesions may persist. Occasionally, MC can be a sign of declining immune function in immunosuppressed individuals.[26]  

Deterrence and Patient Education

Patient education emphasizes the prevention of methicillin-resistant Staphylococcus aureus through behavioral and environmental strategies. Since the virus spreads through direct skin contact or contaminated fomites, patients and caregivers should avoid scratching lesions to prevent autoinoculation and secondary infections. They should also practice good hand hygiene and refrain from sharing towels, razors, clothing, or sports equipment. Lesions should be covered with clothing or a waterproof bandage, especially during school, daycare, contact sports, or swimming, to lower the risk of transmission. However, children do not need to be excluded from activities. Swimmers and athletes should keep lesions covered and refrain from sharing equipment with teammates. Shaving over affected areas should be avoided to prevent autoinoculation.

For sexually active individuals, counseling should address safe sexual practices and recognize that molluscum contagiosum can be transmitted sexually when lesions are in the genital area. Clinicians should also reassure families that the condition is typically self-limited in most healthy people, usually resolving within 6 to 12 months. However, they should also emphasize that immunocompromised individuals might require earlier evaluation and treatment due to the risk of more extensive disease. Through coordinated, clear communication, interprofessional teams can help reduce transmission, prevent recurrence, and assist patients and families in effective self-care.

Pearls and Other Issues

Pearls and other issues include the following:

• Lesions may persist up to 4 years, even in healthy individuals.
• Reinfection is possible after exposure; immunity is not long-lasting.
• Scarring is uncommon, usually only after trauma (scratching or curettage).
• Secondary bacterial infection is infrequent, and perilesional inflammation usually indicates the host's immune response, which ultimately leads to MC resolution.
• Antibiotic treatment is rarely necessary in immunocompetent individuals.
• Immunocompromised individuals may experience longer disease duration and treatment resistance.
• Malignant transformation has not been reported, reassuring for clinicians and caregivers.

Enhancing Healthcare Team Outcomes

Patients with MC often present in a variety of healthcare settings—from pediatric and primary care clinics to dermatology and infectious disease practices—highlighting the need for interprofessional collaboration to ensure accurate diagnosis, effective management, and patient-centered care. Because the infection can affect both healthy and immunocompromised individuals, clinicians must be skilled in distinguishing MC from other papular eruptions, recognizing when intervention is warranted, and addressing concerns related to transmission, contagion, and cosmetic appearance.[52][53][54]

A strategic, team-based approach enhances outcomes by combining the expertise of multiple professionals. Physicians and advanced practitioners assess lesion characteristics, risk factors, and treatment options. Nurses play a pivotal role in patient education and infection-prevention counseling. Pharmacists review topical and systemic treatments for safety and efficacy, and infection control specialists provide guidance to limit the spread in community and institutional settings.

Ethical principles such as respecting patient autonomy, privacy, and informed consent are central when discussing treatment options versus observation. Effective interprofessional communication ensures consistent messaging, reduces unnecessary interventions, and supports shared decision-making with patients and families. Through collaboration, clear communication, and shared responsibility, healthcare teams can enhance patient safety, reduce stigma, and improve outcomes for individuals with molluscum contagiosum, supporting the principles of interprofessional education and patient-centered care.

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Disclosure: Gurinder Kumar declares no relevant financial relationships with ineligible companies.

Disclosure: Jonathan Stern declares no relevant financial relationships with ineligible companies.

Disclosure: Sharon Daley declares no relevant financial relationships with ineligible companies.