Immune recovery vitritis in an HIV patient with isolated toxoplasmic retinochoroiditis
Sendi, Parhama; Sachers, Frankb; Drechsler, Henningc; Graber, Petera
aUnit of Infectious Diseases, Basel University Medical Clinic, Liestal, Switzerland
bVista Clinic, Binningen, Switzerland
cDivision of Infectious Diseases and Hospital Epidemiology, University Hospital, Basel, Switzerland.
Received 12 June, 2006
Accepted 27 June, 2006
Isolated Toxoplasma gondii retinochoroiditis rarely occurs as a first opportunistic infection in HIV-positive patients. The benefit of specific treatment is debated and there is no consensus on the best regimen . However, HAART can lead to immune recovery inflammation syndrome, causing further therapeutic challenges. We describe a case of isolated toxoplasmic retinochoroiditis and immune recovery vitritis (IRV) after initiating HAART. Successful treatment included parabulbar steroid injection.
A 34-year-old HIV-positive man was first diagnosed with HIV in 1994, but denied further controls. In March 2005, he suffered from blurred vision of the left eye. Visual acuity was reduced to 0.4 on the left eye. Fundoscopy revealed an extensive retinochoroidal lesion in the inferonasal periphery (Fig. 1a). Polymerase chain reaction from aqueous humor was positive for T. gondii, but negative for cytomegalovirus. A magnetic resonance imaging scan of the brain showed no cerebral lesions. The CD4 cell count was 11 cells/μl and the plasma HIV viral load was 952 000 copies/ ml. Treatment with pyrimethamine and sulfadiazine was administered, but was stopped as a result of intolerance after 2 days. HAART with tenofovir, lamivudine, and lopinavir/ritonavir was started. Four weeks later, visual acuity of the left eye rapidly deteriorated further. The CD4 cell count increased to 112 cells/μl and the plasma HIV viral load decreased to 1094 copies/ml. Ophthalmological examination now revealed extensive cellular infiltrates in the anterior chamber and the vitreous (Fig. 1b). In addition, cystoid macular and papillary oedema were present. The findings were consistent with IRV. Despite treatment with oral prednisone 50 mg/day for 9 days and prednisolone eyedrops, the inflammatory reaction persisted. After a parabulbar steroid injection (triamcinolon 40 mg), inflammation regressed and visual acuity of the left eye improved to 1.0 within 4 weeks. Six months later, ophthalmological examination showed chorioretinal scarring and stable epiretinal fibroplasia without signs of inflammation (Fig. 1c). The CD4 cell count had increased to 233 cells/μl and the plasma HIV viral load was undetectable. One year after the intervention visual acuity remained normal.
The initiation of HAART can induce a vision-threatening IRV, which is mainly seen in cytomegalovirus retinitis [2,3]. In our case, isolated toxoplasmic retinochoroiditis of the left eye was the first opportunistic manifestation of HIV disease in a patient with a very low CD4 cell count (11 cells/μl). There are no evidence-based treatment recommendations in this rare setting, and the prevalence of IRV after initiating HAART is unknown. Oral steroids for IRV have been reported to be a successful option . In refractory cases, parabulbar steroid injections are an effective and safe treatment modality .
Clinical awareness of IRV in association with toxoplasmic retinochoroiditis is important, so that early diagnosis can be made and appropriate treatment administered. Good collaboration between ophthalmologists and infectious disease consultants is crucial to prevent vision loss.
This case was presented at the 14th Symposium of the International Immunocompromised Host Society in Crans-Montana, Switzerland, 2–5 July 2006.
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© 2006 Lippincott Williams & Wilkins, Inc.