The relationship between systemic histoplasmosis and this particular clinical picutre of a central choroiditis with peripheral atrophic lesions in the fundus was postulated by Woods in 1960 [19]. Since that time there have been many studies attempting to substantiate his hyptthesis [1, 3-5, 7-18]. In a large study performed in Walkersville, Maryland, which is an area endemic for histoplasmosis [14], the prevalence of the characteristic peripheral histoplasmic lesion in the fundus was 27 per 1000 population. The prevalence was 44 per 1000 population with positive histoplasmosis skin tests. In a similar study done in sothern Ohio, the prevalence of peripheral fundus lesions was 1.6 percent of 1417 patients examined [1]. Several generalizations can be made from the information obtained in studying the students involved in the Willis flu, and these can be compared with information from the control students from Bellingham. First, the acute infection at Willis School did not cause significant ocular abnormalities. This finding is supported by the fact that no significant differences occurred in the fundus lesions seen in the control group of students who lived in the same geographic area but were not clinically ill from histoplasmosis. Our evidence shows that the eyegrounds of the individuals living in this area were different from those of the students who lived outside the central Ohio area. How do we account for the similarity of ocular lesions in the affected students and the Delaware control group? Perhaps by the age of 11 or 12, a person living in the histoplasmosis belt will have already been exposed to histoplasmosis, resulting in the characteristic scars that are seen. If, in fact, histoplasmosis is the etiological agent in the patients who are diagnosed as having presumed ocular histoplasmosis, difficulty arises in understanding why those individuals involved in the epidemic did not have more scars than the control group. Perhaps the numbers of patients examined were not large enough to reflect the difference that really may exist. An interesting observation is that 4 (67 percent) of our control students with significant lesions had negative histoplasmosis skin tests. Of course, other organisms may have caused these lesions which have not yet been implicated as causative agents in the presumed ocular histoplasmosis syndrome.