[Skip to Content]
[Skip to Content Landing]
Views 683
Citations 0
JAMA Ophthalmology Clinical Challenge
October 2016

Eruption of Eyelid Target Lesions

Author Affiliations
  • 1Birmingham and Midland Eye Centre, Birmingham, England
JAMA Ophthalmol. 2016;134(10):1189-1190. doi:10.1001/jamaophthalmol.2016.0934

A teenaged boy awakened 2 days prior to presentation with a few skin lesions, which rapidly spread to the rest of his right eyelids (Figure 1). The rash caused a burning sensation; otherwise, he was feeling well. He was not taking any regular medication. His visual acuity was 20/20 OU. Examination revealed clusters of target lesions on the right upper and lower eyelids. There were papillae in the upper palpebral conjunctiva and follicles and a few pustules in the lower palpebral conjunctiva. The cornea was unremarkable with no staining, and results of a dilated ophthalmoscopy examination were normal. Ocular movements were full, and there was no proptosis. A few solitary lesions were found scattered on his nose and right cheek; however, his body was not affected. He had a tender right submandibular lymphadenopathy but was apyrexial.

Figure 1.
A healthy teenaged boy presented with multiple target lesions and erythema on his right eyelids.

A healthy teenaged boy presented with multiple target lesions and erythema on his right eyelids.

Box Section Ref ID

What Would You Do Next?

  1. Observe

  2. Prescribe oral flucloxacillin

  3. Prescribe oral aciclovir

  4. Prescribe oral cimetidine


Human herpesvirus 1, or Herpes simplex virus type 1 infection (HHV-1)

What to Do Next

C. Prescribe oral aciclovir

This teenaged boy presented with periocular target lesions. The abrupt eruption suggested a hypersensitivity reaction.1 An infection was likely the cause, given the prodromal symptoms and submandibular lymphadenopathy with conjunctivitis. Herpes simplex virus is the most commonly identified etiology, accounting for more than half of adult patients.2 In children, Mycoplasma pneumonia and fungal infection are more frequent.3 The lesions on this patient were not waxy papules or umbilicated, which would have suggested Molluscum contagiosum virus.

Early treatment with aciclovir has been demonstrated to lessen and reduce the duration of skin lesions.4 The patient took 200 mg of oral aciclovir 5 times daily and guttae chloramphenicol 4 times daily for a week. A week later, the lesions had scabbed over (Figure 2) and the conjunctivitis had resolved. The eye was quiet, and there was no corneal involvement. The scabs started to shed in the second week. He felt well, and the lymphadenopathy had resolved.

Figure 2.
Scabs formed in place of the previous target lesions, and the conjunctival papillae and follicles resolved 9 days after the lesions first erupted.

Scabs formed in place of the previous target lesions, and the conjunctival papillae and follicles resolved 9 days after the lesions first erupted.

After using polymerase chain reaction, we detected HHV-1 from swabs of the lesions. The result of the bacterial swab was normal, as were the results of the blood tests.

The eyelid lesions caused by HHV-1 are consistent with a delayed-type hypersensitivity reaction.2 The herpetic DNA fragments are transported to the skin sites by peripheral blood mononuclear cells and expressed on keratinocytes. This leads to the recruitment of HHV-1–specific CD4+ helper T cells, which respond to the viral antigens by producing interferon-γ. The latter upregulates cytokines and chemokines that amplify an acute cutaneous inflammatory cascade.2

Primary HHV-1 infection usually presents in the unilateral facial area supplied by the maxillary division of the trigeminal nerve.5 The findings for this patient of greater upper papillary and lower follicular reactions on the palpebral conjunctivae also corresponded with a published report.6 It is important to check for corneal involvement; as many as 17% of patients with HHV-1 can be affected.6

Herpes simplex virus remains latent within the trigeminal ganglion after its initial infection, and one of the main issues is that a quarter of patients can have a recurrence after the primary disease, of which up to 50% occur within 2 years.7 Topical aciclovir applied to the skin lesions does not appear to prevent herpes-associated multiforme lesions.8 However, 400 mg of acyclovir twice daily has been shown to be effective in the reduction of recurrent disease.9 Other options include 500 mg to 1 g of valaciclovir per day or 125 to 250 mg of famciclovir per day, which offer greater oral bioavailability than aciclovir and can be used in patients who do not respond to aciclovir.10 The antiviral dose may be tapered once the patient is free of recurrence for 4 months and eventually stopped.

In summary, HHV-1 eyelid infections can present with various lesion types and severity, such as in this otherwise healthy teenaged boy. Early antiviral treatment should be commenced to reduce the duration of the cutaneous disease.

Patient Outcome

After a week, the conjunctival follicles settled and the target lesions began to scab over. These lesions completely resolved at 1 month.

Back to top
Article Information

Corresponding Author: Patrick J. Chiam, FRCOphth, Birmingham and Midland Eye Centre, Sandwell and West Birmingham Hospitals NHS Trust, Dudley Road, Birmingham B18 7QH, England (pjtchiam@yahoo.com).

Published Online: July 28, 2016. doi:10.1001/jamaophthalmol.2016.0934

Conflict of Interest Disclosures: The author has completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported.

Additional Contributions: I thank the patient for granting permission to publish this information.

Lamoreux  MR, Sternbach  MR, Hsu  WT.  Erythema multiforme.  Am Fam Physician. 2006;74(11):1883-1888.PubMedGoogle Scholar
Aurelian  L, Ono  F, Burnett  J.  Herpes simplex virus (HSV)-associated erythema multiforme (HAEM): a viral disease with an autoimmune component.  Dermatol Online J. 2003;9(1):1.PubMedGoogle Scholar
Villiger  RM, von Vigier  RO, Ramelli  GP, Hassink  RI, Bianchetti  MG.  Precipitants in 42 cases of erythema multiforme.  Eur J Pediatr. 1999;158(11):929-932.PubMedGoogle ScholarCrossref
Lemak  MA, Duvic  M, Bean  SF.  Oral acyclovir for the prevention of herpes-associated erythema multiforme.  J Am Acad Dermatol. 1986;15(1):50-54.PubMedGoogle ScholarCrossref
Liesegang  TJ.  The biology of herpes simplex and varicella zoster virus infections.  Int Ophthalmol Clin. 1993;33(1):81-93.PubMedGoogle ScholarCrossref
Darougar  S, Wishart  MS, Viswalingam  ND.  Epidemiological and clinical features of primary herpes simplex virus ocular infection.  Br J Ophthalmol. 1985;69(1):2-6.PubMedGoogle ScholarCrossref
Mitchell  PC.  Herpetic keratitis.  Optom Clin. 1991;1(4):45-58.PubMedGoogle Scholar
Huff  JC.  Erythema multiforme and latent herpes simplex infection.  Semin Dermatol. 1992;11(3):207-210.PubMedGoogle Scholar
Tatnall  FM, Schofield  JK, Leigh  IM.  A double-blind, placebo-controlled trial of continuous acyclovir therapy in recurrent erythema multiforme.  Br J Dermatol. 1995;132(2):267-270.PubMedGoogle ScholarCrossref
Kerob  D, Assier-Bonnet  H, Esnault-Gelly  P, Blanc  F, Saiag  P.  Recurrent erythema multiforme unresponsive to acyclovir prophylaxis and responsive to valacyclovir continuous therapy.  Arch Dermatol. 1998;134(7):876-877.PubMedGoogle ScholarCrossref