Massive Mycobacterial Choroiditis dur Highly Active Antiretroviral Therapy Another Immune-recovery Uveitis? Ehud Zamir, MD, 1 Henry Hudson, MD, 2 Richard R. Ober, MD, 3 Subramanian Krishna Kumar, MD, 1 Robert C. Wang, MD, 1 Russell W. Read, MD, 1 Narsing A. Rao, MD 1 Purpose: To describe the ocularpresentation ofdisseminated mycobacterial disease occurring during immune-recovery in a patient with acquired immune deficiency syndrome (AIDS). Study design: Case report and literature review. Participants: A 41-year-old AIDS patient with a prior diagnosis of cytomegalovirus retinitis. Methods: The patient developed progressive, bilateral multifocal choroiditis with panuveitis 2 months after beginning and responding to highly active antiretroviral therapy. His left eye became blind and painful and was enucleated.Pathologic examination revealed massive choroiditis with well-formed, discrete granulomas and multiple intracellular and extracellular acid-fast organisms within the choroidal granulomas. Culture and poly- merase chain reaction of vitreous specimens revealed Mycobacterium avium complex (MAC). Results: Empiric,and later sensitivity-guided, local and systemic antibiotic therapy was used to treat the remaining right eye, but it continued to deteriorate. Despite medical therapy,three vitrectomies and repeated intravitreal injections of amikacin, a totalretinaldetachment ensued. One week after the third vitrectomy, the patient died from mesenteric artery thrombosis in the setting of disseminated mycobacterial disease. Conclusions: This is the first report of ocular inflammation as the presenting finding in the recently recognized syndrome of immune-recovery MAC disease. Pathogenesis of this entity is related to an enhanced immune response to a prior, subclinical, disseminated infection. The formation of discrete granulomas, norma absent in MAC infections in AIDS, reflects this mechanism. Ophthalmology 2002;109:2144 –2148 © 2002 by the American Academy of Ophthalmology, Inc. Mycobacterium avium complex (MAC) is a common op- portunistic infection in acquired immune deficiency syn- drome (AIDS), typically causing a multisystem disease. Ocular infections are rarely a part of its clinical spectrum. 1–5 The strongest predictor for disseminated MAC infection is a CD4 cell count of less than 0.05 ⫻ 10 9 /L. 6 Pathologically, immune-suppressed AIDS patients demonstrate a sluggish granulomatous response to MAC, with ill-defined, rather than discrete, granulomas. 7,8 With the recent introduction of highly active antiretrovi ral therapy (HAART) and the subsequent immune recovery a change in clinical pattern has occurred for several oppor tunistic infectious agents in AIDS patients. In cytomegalo- virus (CMV) retinitis, for example, the recovering immune system can elicit a delayed inflammatory response against viralantigens, causing the inflammatory syndrome known as immune recovery uveitis. 9 –12 Although the incidence of new MAC infections has declined significantly in immune- recovered patients, 13 a syndrome has recently been de- scribed in which patients with previously subclinical, dis- seminated MAC infection develop the clinically overt form of the disease shortly after initiation of HAART. As with immune recovery uveitis, this syndrome has been attribut to the large numbers of new, functionally competent im- mune cells that become available to respond to the preex- isting microbial burden. 14 –17 We report here a case of massive granulomatous cho- roiditis, which was the presenting sign of a disseminated, lethalMAC infection in an immune-recovering AIDS pa- tient. Histologic evaluation of an enucleated globe, as wel as vitreous culture and polymerase chain reaction, led to t diagnosisof systemic MAC infection. The atypical his- Originally received: April9, 2001. Manuscript no.210241. Accepted: October 22, 2001. 1 Doheny Eye Institute, Keck School of Medicine of the University of Southern California, Los Angeles, California. 2 Retina Centers, P.C.,Tucson, Arizona. 3 Retina-Vitreous Service, Department of Ophthalmology, College of Med- icine, The University of Arizona Health Science Center, Tucson, Arizona. Supported in part by National Institutes of Health Core Grant EY03040 and by an unrestricted grant from Research to Prevent Blindness, New York, New York. Dr. Zamiris the recipient of an American Physicians Fellowship for Medicine in Israel Grant, Boston, Massachusetts. Dr.Read is now affiliated with the Departments of Ophthalmology and Pathology, University of Alabama School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama. Reprint requests to Narsing A. Rao, MD, Doheny Eye Institute, University of Southern California, 1450 San Pablo Street, DVRC 211, Los Angeles, California 90033. 2144 © 2002 by the American Academy of Ophthalmology, Inc. ISSN 0161-6420/02/$–see front matter Published by Elsevier Science Inc. PII S0161-6420(01)01048-X