Molluscum contagiosum and viral warts — short-answer questions

This stem concerns two of the commonest benign viral skin infections of childhood in an atopic child, illustrating clinical diagnosis, the expectant-versus-active treatment decision, and the role of evidence in counselling anxious parents. ^[2]

Question 1 (10 marks)

a) Give the two diagnoses, the causative viruses, and the key clinical features that identify each. (5 marks) ^[2]

The axillary lesions are molluscum contagiosum, caused by Molluscum contagiosum virus (MCV), a brick-shaped double-stranded DNA poxvirus of the genus Molluscipoxvirus. The identifying features are the small, smooth, dome-shaped, pearly, flesh-coloured papules, each with a glistening central dell (umbilication), clustered in the flexures and gradually increasing in number over months. The thumb lesion is a common viral wart (verruca vulgaris), caused by human papillomavirus (commonly HPV-2, 27 or 57); the identifying features are the rough, firm, hyperkeratotic surface with tiny black dots representing thrombosed capillary loops. ^[2]

His atopic dermatitis is relevant because the epidermal barrier defect of eczema increases susceptibility to both infections, and his weekly swimming is a recognised contributor to wart acquisition through moist, macerated skin and shared surfaces. ^[2]

b) Outline the pathophysiology of each and explain why both are self-limiting. (5 marks) ^[2]

In molluscum, the poxvirus infects lower epidermal keratinocytes; infected cells swell with large eosinophilic intracytoplasmic inclusions called molluscum (Henderson-Patterson) bodies. As these cells migrate upward, the overlying stratum corneum degenerates centrally and the viral core is extruded through the umbilicated dell. The virus evades local immunity, which explains the long indolent course until cell-mediated recognition switches on, often heralded by an inflammatory halo around the lesions. ^[2]

In warts, human papillomavirus enters basal keratinocytes through micro-trauma and drives keratinocyte proliferation and abnormal keratinisation, producing koilocytes (ballooned cells with pyknotic nuclei), hyperkeratosis, acanthosis and elongated rete ridges. Both conditions resolve through a cell-mediated (Th1-type) immune response, which is why lesions may persist for months and then vanish — the biological basis for expectant management. ^[2]