Molluscum contagiosum is an important cause of viral infection that can affect the eyelid (1,2,3,4,5,6,7,8,9,10,11,12,13). Historically seen almost exclusively in young children, it has recently been recognized with greater frequency in adults with acquired immunodeficiency syndrome (AIDS; 3). In children, transmission results from direct contact or fomites (1). In adults, it is generally a sexually transmitted disease. It is a cutaneous pox virus infection that can produce lesions on face, trunk, and proximal extremities (1).

Molluscum contagiosum infection typically occurs as one or more discrete, flesh-colored lesions that range from 1 to 5 mm in diameter. Each lesion typically has an umbilicated center, sometimes simulating basal cell carcinoma. A cheesy detritus can usually be expressed from this central pore. A chronic follicular conjunctivitis can also occur as a result of shedding of virus particles into the conjunctival fornix. If untreated, this can lead to a corneal pannus and can simulate trachoma. Eyelid molluscum contagiosum can also cause an eczematous-appearing periorbital dermatitis (1,4,5,6,7). In patients with human immunodeficiency virus infection, the lesions tend to be larger and more aggressive (4,5,6,7). Severe bilateral eyelid involvement can occur in immunosuppressed children (8). Eyelid molluscum contagiosum infection can occasionally be the first signs of AIDS (7).

Histopathologically, the typical lesion shows invasive acanthosis and degeneration of epithelial cells that fill the central cavity. Numerous intracytoplasmic inclusion bodies (Henderson-Patterson bodies) are present within the cavity (10).

The most commonly employed treatment is incision and expression or curettage of the central core (13). When the lesion is located on the eyelid margin, it can be excised by shaving. Cryotherapy and laser treatment have been employed mostly for extraocular lesions. Hyperfocal cryotherapy with local anesthesia is reported to be a safer method for multiple eyelid lesions in AIDS patients (12). Topical trichloroacetic acid tretinoin (Retin-A), salicylic acid, and cantharidin have been used (13). Once the lesion is completely eliminated, recurrence is rare.

Chalazion is a common lipogranulomatous inflammation of the sebaceous glands of the eyelids, most often the meibomian glands (1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25). It can also occur from the sebaceous glands of Zeis and appear on the eyelid margin.

Chalazion usually occurs secondary to noninfectious obstruction of the ducts of the aforementioned sebaceous glands (1,2). It usually first appears as a firm, tender, erythematous lump in the tarsal plate. As it progresses, it may break through posteriorly and appear on the palpebral conjunctiva or it may drain anteriorly through the skin. A ruptured chalazion can sometimes incite production of granulation tissue in the form of a pyogenic granuloma. In some instances, pressure on the globe by a chalazion can induce significant refractive errors (3,4,22). More aggressive chalazions have been observed in patients with hyperimmunoglobulinemia E (Job’s syndrome; 23,25), and tend to be more difficult to manage.

Chalazion generally has typical clinical features and the diagnosis can be made easily. It is reported that in 94% of cases the diagnosis is correctly made by the clinician. However, about 6% prove histopathologically to be other benign or malignant lesions (5); the most important is sebaceous carcinoma, but other malignant and benign eyelid conditions can closely mimic chalazion (5,6,7,8,9).

Histopathologically, chalazion is characterized by a lipogranulomatous reaction to liberated lipid material. A connective tissue pseudocapsule is often present around the lesion. Round clear spaces in the lesion represent fat deposition. The granulomatous reaction with giant cells may be intermixed with acute and chronic inflammatory cells. Causative organisms are not usually identified, but secondary infection can occur, particularly in patients with Job’s syndrome. The granulomas may resemble those seen with sarcoidosis, cat scratch disease, or tuberculosis (2).

Management is generally hot compresses and good eyelid hygiene. Symptomatic lesions that do not resolve can be managed by incision and curettage, with special effort to remove the pseudocapsule. A conjunctival approach using a chalazion clamp with the lid everted is generally preferred. An eyelid incision can be used for anterior lesions that are eroding through the skin (10,11). Several techniques for local anesthesia for chalazion treatment have been reported (12,13,14,15,16,17,18,19). If the lesion is typical of chalazion, intralesional injection of corticosteroids can be effective in bringing about resolution (10,15). However, such injections should be done with great care, because inadvertent corneal penetration and traumatic cataract have been rarely recognized as complications of corticosteroid injection (16).

As mentioned, some malignant neoplasms, particularly sebaceous carcinoma, can simulate a chalazion. Hence, any tissue should be sent for histopathologic studies to exclude the possibility of malignancy. The prognosis for chalazion is excellent.