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.