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Varicella zoster virus immune recovery stromal keratitis in a patient with AIDS
  1. AYMAN NASERI,
  2. TODD P MARGOLIS
  1. The Francis I Proctor Foundation and the Department of Ophthalmology, UCSF, Medical Center
  2. San Francisco, USA
  1. Dr Todd P Margolis, The Francis I Proctor Foundation, UCSF, Medical Center, San Francisco, CA, 94143-0944, USA tpms{at}itsa.ucsf.edu

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Editor,—The advent of potent antiretroviral therapy has resulted in the recognition of the syndrome of immune recovery uveitis in patients with AIDS and a history of cytomegalovirus (CMV) retinitis.1 Although the pathogenesis of this disease is poorly understood, it is hypothesised to be a consequence of an improved immune response to viral antigen already present in the eye, with or without active viral replication.2 We describe a case of immune recovery varicella zoster virus (VZV) stromal keratitis in a patient with AIDS.

CASE REPORT

A 37 year old man with AIDS (CD4 = 180 cells × 106/l) developed right sided ophthalmic zoster and was treated with aciclovir (800 mg by mouth five times a day). Twelve days after onset of the rash, topical prednisolone acetate (one drop every 2 hours) was prescribed to treat multiple anterior stromal corneal infiltrates. The keratitis promptly resolved, and the corticosteroid drops were discontinued within 3 weeks. Over the next 5 months his cornea remained clear, but his HIV disease progressed with the CD4 count dropping to a nadir of 88 cells × 106/l. He was started on potent antiretroviral therapy and prophylactic aciclovir 400 mg by mouth twice daily. His cornea remained clear for the next 2 years, but as his CD4 reached 398 cells × 106/l, he presented with a complaint of redness of his right eye. On examination he had multiple anterior stromal infiltrates of his right cornea, similar in appearance to the keratitis associated with the previous episode of ophthalmic zoster (Fig 1). The recurrence of stromal keratitis occurred 2½ years after discontinuation of topical steroids and while the patient was taking aciclovir prophylaxis.

Figure 1

Slit lamp photograph of the temporal aspect of the patient's right eye shows stromal infiltrates with an intact corneal epithelium.

COMMENT

VZV associated anterior stromal keratitis is though to be due to immune recognition of residual viral antigen in the corneal stroma.3 The incidence of recurrent VZV stromal keratitis has not been well characterised, nor have factors which might precipitate recurrences. Recurrent keratitis related to immune system activation has been recognised following adenoviral infection.4 In that case, subepithelial opacities associated with a previous adenoviral follicular, keratoconjunctivitis recurred 9 months following the original infection in association with a severe upper respiratory infection. In this report, a patient with AIDS and a history of ophthalmic zoster had a recurrence of anterior corneal stromal infiltrates almost 3 years after the initial skin eruption. Recurrence of the keratitis was not associated with skin or corneal epithelial disease and occurred despite aciclovir prophylaxis. Although the recurrence of the keratitis with this patient's immune recovery may be coincidental, the significant delay between his initial zosteriform eruption and the recurrence of his stromal disease, as well as the close temporal relation between the recurrence and the patient's immune recovery, suggest that this is a case of immune recovery zoster keratitis in a patient with ophthalmic zoster.

Other examples of immune recovery disease in patients with AIDS receiving potent antiretroviral therapy are well recognised. Immune recovery uveitis has been described in patients with previous CMV retinitis.1 2 In addition, immune recovery inflammation has been seen in association with previously clinically silent systemicMycobacterium avium complex infection and in patients with cryptococcal meningitis.5 6 In at least one of the cases of meningitis, immune recovery inflammation was thought to be directed against residual cryptococcal antigen, as opposed to a delayed immune response to viable organisms. As advances in AIDS therapy continue to improve the immune status of patients, immune recovery inflammation may become increasingly recognised.

Acknowledgments

TPM is the recipient of a Research to Prevent Blindness (NY, NY) Lew Wasserman Award.

References

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