Diagnosis and management of minimal recurrences of macular histoplasmosis.

Disease in the macula from ocular histoplasmosis has been ascribed to (1) traction of a scar, (2) fresh areas of choroiditis, and (3) reactivation of a scar. Traction of a scar is probably a rare cause. The rationale for early use of corticosteroids in attacks of ocular histoplasmosis is based on the hypothesis that the underlying disease is an inflammation. The concept of a choroiditis could fit with what is assumed to happen in the case of second and third hypotheses, those of fresh choroiditis and reactivation of a scar. The goal of therapy is to stop the inflammation before it is clinically recognizable by the ophthalmologist, so that little or no damage to vision results. Whether corticosteroids might work by suppression of an immunological response or simply by curtailing the severity of the choroiditis, or both, is not known. We do know from clinical experience that corticosteroids do not appear to be deleterious to the ocular histoplasmosis. When they were first tried, we were wary about using them in a "fungal" disease. As experience grew, we learned that our mistakes were usually not from using too great a quantity of corticosteroids for too long a time but the opposite; from using too small amounts of corticosteroids for too short a time. Clinically, most attacks of macular histoplasmosis occur at the sites of previous scars, with little or no sign of any choroiditis. At present, there are six poorly defined hypotheses of how this may occur: (1) symbiosis, (2) secondary infection, (3) vascular decompensation [2], (4) immunological reaction [3], (5) altered structure [1], and (6) failure of precapillary arteriole [5]. Corticosteroids might be helpful in any of these instances. I believe that the attack that usually takes the form of an enlargement of the atrophic histo spot is caused by an immunological response in this area that develops into a mild spreading choroiditis. It is possible that with a reduction of the patient's resistance, live H. capsulatum or an antigenic component of it escapes from one of the viscera to lodge in the sensitized area of the atrophic choroid where a choroiditis previously existed. At this site, a fresh, mild choroiditis is activated. This choroiditis then persists for a variable period before either becoming quiescent or progressing into the neovascular stage, with the growth of a net through Bruch's membrane and the pigment epithelium and under the sensory retina. The rationale for the early and intensive use of corticosteroids is to try to abort the attack of choroiditis before it reaches the stage of becoming recognizable by the ophthalmologist.