Molluscum contagiosum

Meet the patient

A mother brings her healthy four-year-old in with "water warts" — a scattering of 15 small, shiny, pearly bumps with tiny central dimples across his trunk and axillae, present for three months. He has eczema and scratches. She wants them frozen off today; she is also worried they will scar.[1]

The two questions that settle the consult are the two that settle every molluscum case: does this child need any treatment at all? (most do not) and is there a red flag hiding in the distribution? (facial and giant in an adult means HIV; genital in a child means safeguarding). Get those two right and the rest is a treatment ladder.[1]

What MC is — and the word that names it

Molluscum contagiosum is a common, benign, self-limiting cutaneous infection caused by the molluscum contagiosum virus (MCV) — the only human pathogen of the genus Molluscipoxvirus in the family Poxviridae. It produces firm, dome-shaped, pearly-white papules with a pathognomonic central umbilication containing a curd-like core. The natural history in immunocompetent hosts is spontaneous resolution within months to one or two years, which makes watchful waiting a legitimate first strategy.[1]

The morphology is high-yield at every exam level because it is pathognomonic, the histology (Henderson-Patterson bodies in cup-shaped epidermal down-growths) is uniquely identifiable, and the disease illustrates transferable themes: a strictly epidermal viral infection with no viraemia, a chronic immune-mediated clearance that takes months, the HIV association, and a therapeutic ladder that spans watchful waiting through physical destruction to the first FDA-approved specific drugs.[1]

The bedside skill is threefold: distinguish the typical lesion from its mimics (verrucae, closed comedones, milia, basal cell carcinoma, cryptococcosis), recognise atypical variants (giant, eczematous, periocular, oral), and act on the red flags.[1]

Classification — genotype, morphology, and the context that drives management

MC is classified by virus genotype, by lesion morphology, and by clinical context — three axes that change prevalence, prognosis and management.[1]

By genotype, four types are recognised (MCV-1 to MCV-4), but MCV-1 causes the great majority of paediatric and adult disease worldwide (about 75 to 95 percent), while MCV-2 is over-represented in HIV and immunosuppressed adults and in some sexually transmitted cohorts. The genotypes are clinically indistinguishable in the immunocompetent individual; the distinction matters for epidemiology and a small immunocompromised subgroup.[1][3]

By morphology, the variants an examiner will probe:[1]

• Typical MC — 2 to 5 mm pearly papules with central umbilication; the commonest form in children.
• Giant MC — single or few lesions over 1 cm (some 2 to 3 cm); most often facial in adults; a strong HIV/immunosuppression signal; biopsy because the differential includes keratoacanthoma and nodular BCC.
• Agmate/clustered MC — multiple lesions grouped in one region, sometimes linear from autoinoculation along a scratch.
• Eczema molluscatum — widespread lesions on the eczematous skin of atopic dermatitis; reflects Koebner phenomenon and impaired cutaneous antiviral immunity.
• Inflammatory MC — spontaneously red, crusted or pustular; a sign the host immune response is engaging — often a prelude to resolution.
• Periocular/ocular MC — uniquely important for the risk of follicular conjunctivitis and chronic keratitis.[15]

By clinical context — the dimension that drives management:[1]

[2] [14]

How common, who, and how it spreads

MC is one of the commonest cutaneous viral infections of childhood worldwide, with an estimated global point prevalence in children of about 5 to 10 percent (higher in some tropical regions) and a peak age of 1 to 10 years. Incidence is bimodal: a primary paediatric peak (1 to 10 years) driven by skin and fomite contact, and a smaller young-adult peak (20 to 29 years) driven by sexually transmitted genital disease. It accounts for roughly 1 percent of dermatology consultations in temperate climates and more in the tropics.[1][3]

Transmission is by three overlapping routes: direct skin-to-skin contact (the dominant route among children and during sexual transmission), fomites (shared towels, sponges, baths, swimming-pool edges, gym equipment — the virus is stable for weeks on wet surfaces), and autoinoculation (scratching seeds new lesions at distant sites — the reason linear and clustered patterns are so common). There is no convincing evidence for airborne transmission, and viraemia does not occur — the virus is strictly epidermal, so systemic disease is a feature only of severe immunocompromise.[1][2]

Outbreaks cluster in nurseries, schools, swimming pools, contact-sport teams and shared-bath households. Household secondary attack rates approach 10 to 30 percent when one child is affected. The high-yield list of risk factors for extensive or refractory disease: HIV with low CD4 (the single most important), iatrogenic immunosuppression (transplant, biologics, long-term steroids), atopic dermatitis (eczema molluscatum), and tropical humid climates.[1][14]

[1] [2]

Why the poxvirus hides in the epidermis — and why clearance takes months

MCV is a large, enveloped, double-stranded DNA virus (about 190 kb genome) of the family Poxviridae, the only member of its genus to infect humans. Unlike most DNA viruses it replicates entirely in the cytoplasm of infected cells using its own DNA-dependent RNA polymerase — a feature shared with variola and vaccinia — but with the unique molluscipoxvirus property that it is almost entirely restricted to the epidermis and does not produce a productive viraemia in immunocompetent hosts.[1][3]

The viral life cycle plays out inside the epidermal keratinocyte. The infected cell becomes hugely enlarged, its cytoplasm crammed with mature virions packaged into eosinophilic inclusion bodies — the molluscum (Henderson-Patterson) bodies — that compress the nucleus into a thin crescent at the cell periphery. By the time the cell reaches the granular layer, the inclusion has effectively replaced the cytoplasm. The central umbilication of the mature lesion is the surface expression of a cup-shaped epidermal down-growth shedding virus-laden cells.[1]

Why the virus stays epidermal for months is the central puzzle. MCV has evolved a large repertoire of immune-evasion proteins: an IL-18 binding protein that blunts the Th1 response; chemokine inhibitors (MC148, MC054, MC007) that sequester host chemokines and impair dendritic-cell, NK and T-cell recruitment; a glutathione peroxidase (MC066) that neutralises reactive oxygen species; apoptosis inhibitors (MC159, MC160) that prolong the infectious window; and MHC class I downregulation to evade CD8 cytotoxic T-cells.[1]

The net effect is a chronic, locally contained infection the systemic immune system sees but cannot eliminate quickly. Clearance depends ultimately on cell-mediated immunity — when CD4 and CD8 T-cells, NK cells and IFN-gamma finally arrive in force, lesions undergo inflammation, crusting and resolution. This explains the HIV association (no T-cell help, no clearance), the delayed clearance in atopic dermatitis (Th2-skewed local immunity), and the therapeutic effect of intralesional immunotherapy (Candida antigen, PPD, MMR), which calls in a non-specific cell-mediated response that clears distant, uninjected lesions too.[1][12]

[1]

The clinical story — pearly, dimpled, and quietly spreading

The classic lesion is a firm, smooth, dome-shaped, pearly-white or skin-coloured papule, 2 to 5 mm (occasionally up to 1 to 2 cm when giant), with a central umbilication from which a curd-like, caseous core can be expressed with lateral pressure. Lesions are usually multiple (10 to 20 in immunocompetent children, occasionally hundreds in HIV) and may be grouped, linear (from autoinoculation), or scattered. They are typically asymptomatic, though inflammation and crusting signal spontaneous resolution; mild pruritus is common, and a surrounding eczematous halo (id reaction) occurs in up to 10 percent of children, especially those with atopy.[1][3]

Site distribution differs sharply between children and adults. In children: face, trunk, axillae, extremities, popliteal and antecubital fossae, sparing palms and soles (the thick stratum corneum is not permissive). In adults: the lower abdomen, genitals, pubic region and inner thighs in sexually transmitted disease. In HIV: extensive, clustered on the face (beard area, forehead, eyelids) and frequently giant. In atopic dermatitis: widespread eczema molluscatum.[1]

The natural history in immunocompetent children is spontaneous resolution in 6 to 12 months typically, almost always by 2 years. Resolution is often heralded by inflammation, crusting and a pustular or furuncle-like appearance — paradoxically a sign the lesion is on its way out.[1][2]

The differential — the umbilicated papule that is not MC

The central umbilication of a pearly papule is pathognomonic, but several conditions mimic it. The complete differential with the features that distinguish each:[1]

[1] [14]

The classic trap — a solitary umbilicated papule on an adult face called molluscum when it is a BCC or keratoacanthoma. Biopsy any solitary atypical lesion in an adult, especially in sun-exposed skin. In HIV, the dangerous mimic is cutaneous cryptococcosis, which can resemble molluscum exactly — confirm with India ink or mucicarmine and a cryptococcal antigen.[14]

The id (autoeczematisation) reaction — an itchy, eczematous rash distant from the lesions — must be distinguished from secondary bacterial infection (yellow crusts, pain, spreading erythema), scabies (burrows, web-space involvement), tinea corporis (annular, scaly), and drug reaction (temporal relation to a new agent).[1]

The bedside round — five checks and a dermoscopy glance

Diagnosis is clinical at the bedside. The sequence is short and reproducible, and is exactly the sequence an OSCE station will test: history (age, duration, tempo, symptoms, atopy, HIV, immunosuppression, contacts, sexual history); general inspection (count and map lesions, distribution, sparing of palms and soles, mucosal/periorbital/genital involvement); lesion-focused examination (confirm the pearly dome, central umbilication, and expressible curd-like core — the pathognomonic bedside demonstration); dermoscopy; and a context-driven examination (HIV stigmata in an adult with facial or genital disease; safeguarding in a child with genital lesions).[1]

[1]

Dermoscopy shows the classic white-yellow amorphous or polylobular centre with a peripheral crown of radial ("dotted" or "comma-shaped") vessels — "crown vessels" — highly specific and useful when morphology is ambiguous.[1][10]

Investigations — almost none, except to exclude mimics and find immunocompromise

The diagnosis of typical molluscum is clinical — no investigation is required. Investigation is reserved for atypical, solitary, adult, giant, treatment-refractory or immunocompromised presentations:[1]

• Dermoscopy — non-invasive; white-yellow amorphous centre with peripheral crown vessels.
• Skin biopsy (rarely needed) — for a solitary atypical lesion in an adult (exclude BCC or keratoacanthoma), giant lesions, or refractory disease. Histology is pathognomonic: a cup-shaped epidermal down-growth with intracytoplasmic eosinophilic molluscum (Henderson-Patterson) bodies compressing the nucleus.
• PCR for MCV DNA — reference laboratories; useful for atypical or HIV-associated disease and to distinguish MCV from cutaneous cryptococcosis or histoplasmosis.
• HIV serology with CD4 count — in any adult with extensive (over 50 lesions), facial, giant, genital or refractory molluscum. The single highest-yield investigation in that context.
• STI screen — in any adult with genital molluscum (chlamydia and gonorrhoea NAAT, syphilis serology, hepatitis B/C, HIV).[1][14]

Management — reassure first, then climb the ladder

Molluscum is almost never a resuscitation-level disease. The acute scenarios are few: severe secondary bacterial infection (impetiginised MC, cellulitis — oral anti-staphylococcal antibiotics); periorbital MC with keratitis (urgent ophthalmology); extensive MC in newly diagnosed HIV (initiate ART — restoration of immune function is itself the definitive therapy); and anaphylaxis to cantharidin (exceptionally rare).[1]

The decision between watchful waiting and active treatment balances the natural history (self-resolution in 6 to 12 months), the bother to the patient or parent, the lesion site (face and genitals warrant active treatment), the cohort (immunocompromised — earlier active treatment), and the treatment burden. The 2023 network meta-analysis (Chao et al.) and the 2025 comprehensive review (Ulrych et al.) provide the modern evidence base.[4][6]

Watchful waiting is appropriate for the immunocompetent, asymptomatic child with non-facial, non-genital, non-bothersome lesions, and is supported by AAP, BAD and AAD guidance. Active treatment is offered for bothersome, spreading, facial or genital lesions, for parental preference after counselling, and for any lesion in an immunocompromised patient.[1][3]

[1]

Physical destruction — fast, effective, and the first active move

Curettage is highly effective, single-visit clearance for a small number of lesions, requiring local anaesthetic (topical EMLA or intralesional lidocaine), with a small risk of scarring and pigmentary change — favoured for facial or genital lesions where rapid clearance matters.[1]

Cryotherapy (liquid nitrogen) — single or repeated freeze-thaw cycles; effective but painful, with post-treatment vesiculation and pigmentary change; less ideal in children.[1]

Cantharidin 0.7 to 0.9% is a topical vesicant that inhibits serine/threonine protein phosphatases, producing acantholysis and intraepidermal blistering. Applied in clinic, washed off at home at 2 to 6 hours (recent FDA labelling: 24 hours post-application), it produces a small blister that heals in 1 to 2 weeks. The Vakharia 2018 systematic review confirmed efficacy with a favourable tolerability profile in children, and the CAMP-1 and CAMP-2 trials demonstrated superiority over vehicle — leading to FDA approval of YCANTH (cantharidin 0.7% topical solution) in 2023, the first FDA-approved specific treatment for molluscum. Apply with care to avoid normal skin; not for use near the eyes or mucosa.[7][8][11]

Topical agents — for home use, face, and generalised disease

Berdazimer sodium 10.3% gel (Zelsuvmi) is a nitric-oxide-releasing topical, FDA-approved in 2024 on the basis of the B-SIMPLE phase 3 trials (Browning et al., JAMA Dermatology 2022), which showed significantly higher clearance rates than vehicle. Applied once daily, with a gentle inflammatory reaction as the main adverse event.[9][10]

Potassium hydroxide (KOH) 5 to 10% is applied to lesions daily until inflammation or crusting develops; a widely used parent-applied topical in paediatric MC, with mild irritant dermatitis as the main adverse event. Podophyllotoxin 0.5% is self-applied for genital MC in non-pregnant adults; contraindicated in pregnancy, breastfeeding and children. Imiquimod 5% (a TLR-7 agonist) has variable efficacy in trials and is no longer first-line for routine paediatric MC. Tea tree oil 10% and benzoyl peroxide show modest symptomatic benefit; common contact irritants.[1][13]

Intralesional immunotherapy — the refractory-disease move

A specialist approach for refractory or extensive molluscum: intradermal injection of an immunogenic antigen (Candida antigen with the most evidence, trichophytin, BCG, PPD, MMR) into one or a few index lesions recruits a systemic cell-mediated immune response that clears both injected and distant, uninjected lesions. The Wells 2020 systematic review confirmed efficacy and a favourable safety profile; injection-site reaction and post-inflammatory pigment change are the main adverse events.[12]

Molluscum in immunocompromise — restore the immune system

In HIV, the cornerstone is restoration of immune function with antiretroviral therapy (ART) — facial and giant molluscum characteristically clear as CD4 counts rise. Initiate ART promptly; adjunctive destructive and topical therapies accelerate clearance but cannot substitute for immune reconstitution. Co-existing opportunistic infection must be excluded when lesions are atypical (persistent ulceration, necrotic centres) by biopsy, fungal stains and tissue culture — cryptococcosis, histoplasmosis, Penicillium marneffei, bacillary angiomatosis, Kaposi sarcoma must remain in mind.[14]

Oral cimetidine (an H2-antihistamine with weak immunomodulatory activity) has been used in paediatric MC at 40 mg/kg/day in divided doses for 2 to 3 months; evidence is mixed and inferior to physical destruction, but it remains a parent-friendly option in children who cannot tolerate destructive treatment.[1]

The subtypes and scenarios that bite

Genital molluscum in an adult is a sexually transmitted infection. Co-existing STI testing is mandatory (chlamydia and gonorrhoea NAAT, syphilis serology, HIV, hepatitis B and C); discuss partner notification and consistent condom use. Treatment: podophyllotoxin self-applied, or curettage, cryotherapy or cantharidin. Genital MC in a child, however, is more often autoinoculation from concurrent cutaneous lesions than sexual abuse — but safeguarding assessment is mandatory in any prepubertal child with genital MC. Involve paediatrics and child protection per local protocol.[1][5]

Eczema molluscatum (MC on atopic dermatitis) reflects Koebner phenomenon and impaired local antiviral immunity. Management has two parallel tracks: control the underlying eczema (emollients, topical corticosteroids, calcineurin inhibitors) and treat the MC actively (cantharidin, curettage or KOH; intralesional immunotherapy in extensive disease).[1]

Giant molluscum — solitary or few lesions over 1 cm, predominantly in HIV or immunosuppressed adults, often on the face. The principal reason for biopsy is to exclude keratoacanthoma, nodular BCC or amelanotic melanoma.[14]

Periorbital and ocular molluscum — a lid-margin umbilicated papule can produce chronic follicular conjunctivitis, punctate epitheliopathy, keratitis with corneal scarring and pannus. Treat with ophthalmology-guided curettage or surgical excision of the lid lesion; cantharidin is contraindicated near the eye. The 20-year systematic review (Naseer et al.) confirmed the spectrum of ocular involvement.[15]

How patients come to harm — the preventable list

MC is benign and self-limiting in the immunocompetent, so the preventable harms are missed red flags and iatrogenic injury:[1]

• Failing to test for HIV in an adult with extensive, facial, genital or refractory molluscum — the missed sentinel of uncontrolled disease.
• Missing safeguarding in a prepubertal child with genital molluscum — autoinoculation is commonest, but sexual abuse must be actively excluded.
• Missing concomitant STIs in an adult with genital molluscum.
• Treating an id reaction as secondary bacterial infection with inappropriate antibiotics.
• Applying cantharidin periocularly — risk of corneal involvement; treat periocular MC only with ophthalmology input.
• Using podophyllotoxin in a pregnant patient — teratogenic.
• Calling a solitary adult facial lesion molluscum when it is a BCC or keratoacanthoma — biopsy if there is any doubt.[1]

Prognosis, disposition, and special populations

In immunocompetent children the prognosis is excellent — 70 to 90 percent spontaneously resolve within 2 years, with a median time-to-clearance of 6 to 12 months. Prolonged disease correlates with atopic dermatitis, immunosuppression, HIV and treatment delay. Recurrence is common because the virus is ubiquitous; reinfection does not imply treatment failure.[1]

In HIV, the prognosis depends on immune reconstitution. With consistent ART, facial and giant MC characteristically improve as CD4 counts rise; without ART, lesions can persist for years. Disposition is almost always outpatient; refer for atypical or uncertain diagnosis, giant lesions, extensive, facial or immunocompromised disease, treatment-refractory lesions, and periorbital involvement (co-management with ophthalmology).[1][14]

In pregnancy, molluscum is uncommon and usually self-resolves; podophyllotoxin is contraindicated (teratogenic), and curettage, cryotherapy or cantharidin are reasonable. In the elderly, a new umbilicated papule is more often a BCC, sebaceous hyperplasia or keratoacanthoma and warrants biopsy.[1]

Evidence and regional deltas

Landmark evidence and approvals: the CAMP-1 and CAMP-2 trials (Eichenfield et al., 2022-23) of cantharidin 0.7% (YCANTH) versus vehicle led to FDA approval in 2023 as the first specific pharmacological therapy for molluscum; the B-SIMPLE phase 3 trials (Browning et al., JAMA Dermatology 2022) of berdazimer 10.3% gel (Zelsuvmi) led to FDA approval in 2024; and the 2023 network meta-analysis (Chao et al.) ranked cantharidin, curettage and berdazimer among the top performers.[6][8][10]

Regional deltas: the framework (watchful waiting first, active treatment for bothersome disease) is globally consistent, but cost and access shape the choice. In the US and Canada, YCANTH and Zelsuvmi are available; in the UK and Europe, curettage, cryotherapy and KOH are first-line with intralesional immunotherapy in specialist centres; in India and South Asia, KOH, curettage and compounded cantharidin are the accessible backbone, with berdazimer limited by cost.[1]

The mantra, and the mnemonic

[1] [16]

The mantra: pearly papule, central dimple, curd-like core — reassure the child, test the HIV in the adult, and safeguard the genital child.[1]

Ward-round test — three stems, thirty seconds each

Stem 1 — the child with water warts (answer)

A healthy four-year-old with 15 pearly, umbilicated papules on the trunk and axillae, present for three months. He has eczema and scratches. His mother wants them frozen off and worries about scarring. What is the plan? Model: This is classic molluscum contagiosum in an immunocompetent child. The natural history is spontaneous resolution in 6 to 12 months (almost always by 2 years), so watchful waiting with reassurance is first-line — counsel on avoiding shared towels, covering lesions, trimming nails to limit autoinoculation, and no need for school exclusion. If the family prefers active treatment, cantharidin 0.7% (YCANTH) in clinic or parent-applied KOH 5 to 10% are the most paediatric-friendly options. Reassure the mother that scarring is not a feature of resolved molluscum.[1]

Stem 2 — the adult with giant facial molluscum (answer)

A 35-year-old man presents with dozens of umbilicated papules on his face, several over 1 cm, that have been spreading for months and resist cryotherapy. What is the single most important investigation, and what is the cornerstone of treatment? Model: Extensive, facial, giant molluscum in an adult is a sentinel of uncontrolled HIV — the single most important investigation is HIV serology with a CD4 count. The cornerstone of treatment is antiretroviral therapy (ART) — facial and giant molluscum characteristically clear as CD4 counts rise. Biopsy at least one lesion to exclude keratoacanthoma, nodular BCC and — critically in HIV — cutaneous cryptococcosis, which can mimic molluscum exactly (confirm with India ink or mucicarmine and a cryptococcal antigen). Adjunctive destructive therapy accelerates clearance but cannot substitute for immune reconstitution.[14]

Stem 3 — genital molluscum in a five-year-old (answer)

A five-year-old girl has three umbilicated papules on her vulva and several typical molluscum on her trunk. What is the safeguarding issue, and what is the most likely explanation? Model: Genital molluscum in a prepubertal child mandates a safeguarding assessment — but autoinoculation from concurrent cutaneous lesions is the commonest cause, and the presence of typical lesions elsewhere on the trunk supports that. Sexual abuse must be actively excluded, however, so involve paediatrics and child protection per local protocol for a focused history, examination, and any indicated STI testing. Treat the lesions (cantharidin is avoided on genital mucosa; curettage or watchful waiting) and address the eczema if present.[1][5]

References

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2. [2]Leung AKC, Barankin B, Hon KLE. Molluscum Contagiosum: An Update Recent Pat Inflamm Allergy Drug Discov, 2017.PMID 28521677
3. [3]Meza-Romero R, Navarrete-Dechent C, Downey C. Molluscum contagiosum: an update and review of new perspectives in etiology, diagnosis, and treatment Clin Cosmet Investig Dermatol, 2019.PMID 31239742
4. [4]Ulrych JM, Krupa J, Malinowski M, et al. Molluscum contagiosum: a comprehensive review of treatment modalities Wiad Lek, 2025.PMID 40847879
5. [5]Stulberg DL, Hutchinson AG. Molluscum contagiosum and warts Am Fam Physician, 2003.PMID 12674451
6. [6]Chao YC, Ko MJ, Tsai WC, et al. Comparative efficacy of treatments for molluscum contagiosum: A systematic review and network meta-analysis J Dtsch Dermatol Ges, 2023.PMID 37199262
7. [7]Vakharia PP, Chopra R, Silverberg NB, et al. Efficacy and Safety of Topical Cantharidin Treatment for Molluscum Contagiosum and Warts: A Systematic Review Am J Clin Dermatol, 2018.PMID 30097988
8. [8]Gupta AK, Mann A, Vincent K, et al. YCANTH(TM) (Cantharidin) Topical Solution Skinmed, 2023.PMID 37945366
9. [9]Gupta AK, Mann A, Vincent K, et al. Zelsuvmi(TM) (Berdazimer) Topical Gel Skinmed, 2024.PMID 39748580
10. [10]Browning JC, Enloe C, Cartwright M, et al. Efficacy and Safety of Topical Nitric Oxide-Releasing Berdazimer Gel in Patients With Molluscum Contagiosum: A Phase 3 Randomized Clinical Trial JAMA Dermatol, 2022.PMID 35830173
11. [11]Ogilvie-Turner K, Goldman RD. Cantharidin for molluscum contagiosum Can Fam Physician, 2020.PMID 32532721
12. [12]Wells A, Saikaly SK, Schoch JJ. Intralesional immunotherapy for molluscum contagiosum: A review Dermatol Ther, 2020.PMID 33044025
13. [13]Kairey L, Agnew T, Bowles EJ, et al. Efficacy and safety of Melaleuca alternifolia (tea tree) oil for human health-A systematic review of randomized controlled trials Front Pharmacol, 2023.PMID 37033604
14. [14]Mohseni Afshar Z, Goodarzi A, Emadi SN, et al. A Comprehensive Review on HIV-Associated Dermatologic Manifestations: From Epidemiology to Clinical Management Int J Microbiol, 2023.PMID 37496761
15. [15]Naseer S, Mian SI, Hakim FE. Ocular and Periorbital Manifestations of Molluscum Contagiosum: A 20-year Systematic Review Int Ophthalmol Clin, 2025.PMID 40116404
16. [16]Clebak KT, Malone MA. Skin Infections Prim Care, 2018.PMID 30115333