photomicrographs do not represent or­ ganisms of any type, they have been ac­ cepted by the mycologists I consulted as compatible with Histoplasma capsulatum. Moreover, Drs. Gass and Zimmer­ man ignore the fact that the organisms were also present in the lung and fre­ quently intracellularly, within macrophages in the ocular lesions and with­ in pulmonary histiocytes, findings that would be unlikely if the organisms were merely "small calcific bodies." I completely agree with the caution regarding therapeutic implications of these findings. Certainly, therapy that has such potentially serious side effects should not be based on a single histopathologic demonstration of mycotic in­ festation. Indeed, as I already pointed out, there was some evidence that the macular disciform lesions might be relat­ ed to local hypersensitivity to retained, nonviable organisms, which suggests that antifungal therapy would be of no benefit when the lesions are seen clinically. I think my report clearly demonstrates the presence of Histoplasma organisms in the ocular lesions (and in the lung) of a patient with the presumed ocular histoplasmosis syndrome and that it further advances our understanding of the pathophysiology of this entity. ALAN M. ROTH, M.D.

Sacramento, California Involutional Diabetic Retinopathy Editor: In the recent article, "Involutional dia­ betic retinopathy" (Am. J. Ophthmol., 84:851, 1977), by William J. Ramsay, Robert C. Ramsay, Richard L. Purple, and William H. Knobloch, the authors state that they did not expect to find the charac­ teristic and repeatable tritanopic vision abnormality in eight of nine diabetic pa­ tients they studied. They supposed that this acquired blue-yellow defectiveness is

MAY, 1978

associated with the optic nerve atrophy in their cases. They then refer to two papers concerning the similarities between con­ genital tritan defects and dominant optic nerve atrophy.1-2 Initially, an acquired blue-yellow de­ fectiveness was reported in elderly dia­ betics, 3-6 but it also occurs in aging nor­ mal people. 7-9 For this reason, the testing of young diabetics is particularly impor­ tant. A survey of 400 diabetics under 50 years of age with normal visual acuity revealed that up to 30% could be consid­ ered to have an acquired blue-yellow color vision defect.10 Furthermore, loss of color discrimination involving yellow and blue vision and also within the bluegreen sector both manifest themselves in diabetics by 25 years of age and gradually increase in severity.11 Optic nerve diseases generally produce an acquired type 2 red-green defect,5 ex­ cept for dominant optic nerve atrophy, which produces an acquired type 3 blueyellow defect.8,12 Several retinal diseases are characterized by an acquired blueyellow defect,8 which persists if an as­ cending optic nerve atrophy becomes evi­ dent, as in glaucoma and peripheral tapetoretinal dystrophies. The pre-existing blue-yellow defect in diabetics persists also if the diabetes causes an ascending optic nerve atrophy. It is therefore not justified to base the blue-yellow defect in diabetics on the color vision defect in dominantly inherit­ ed optic nerve atrophy. ALFRED J. PINCKERS, M.D. AUGUST F. DEUTMAN, M.D.

Nijmegen, The Netherlands REFERENCES 1. Krill, A. E., Smith, V. C , and Pokorny, J.: Similarities between congenital tritan defects and dominant optic nerve atrophy. Coincidence or iden­ tity. J. Optom. Soc. Am. 60:1132, 1970. 2. : Further studies supporting the identity of congenital tritanopia and hereditary dominant optic atrophy. Invest. Ophthalmol. 10:182, 1971.

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3. Zanen, J.: Introduction a l'etude des dyschromatopsies reetiniennes centrales acquises. Bruxelles, Imprimerie Medicale et Scientifique, 1953. 4. Zanan, J., Szucs, S., and Pirart, J.: Les seuils achromatiques et chromatiques dans le diabete. Bull. Soc. Beige Ophthalmol. 115:210, 1957. 5. Francois, J., and Verriest, G.: Les dyschromatopsies acquises. Ann. Oculistique 190:713, 812, 193,1957. 6. Cox, J.: Colour vision defects acquired in dis­ eases of the eye. Br. J. Physiol. Opt. 17:195, 1960; 18:3, 67, 1961. 7. Lakowski, R.: Is the deterioration of colour discrimination with age due to lens or retinal chang­ es? Farbe 11:69, 1962. 8. Verriest, G.: Further studies on acquired defi­ ciency of color discrimination. J. Opt. Soc. Am. 53:185, 1963. 9. Ruddock, K. H.: The effect of age upon colour vision. Vision Res. 5:37, 1965. 10. Kinnear, P. R.: The risk of colour vision deterioration in young diabetics. Luzern, Tagungsband, 1965, p. 261. 11. Lakowski, R., Aspinall, P. A., and Kinnear P. R.: Association between colour vision losses and diabetes mellitus. Ophthalmic Res. 4:145, 1972/1973. 12. Jaeger, W.: Dominant vererbte Opticusatrophie (unter besonderer Berilcksichtigung der dabei vorhandenen Frabensinnstdrungen). von Graefes Arch. Ophthalmol. 155:475, 1954.

Reply Editor: We appreciate the interest and com­ ments of Drs. Pinckers and Deutman. We have no quarrel with their discussion on developing retinal defects of blue-yellow vision in diabetics. We speculated that in addition to the retinal dyschromatopsia, the developing optic nerve atrophy may have contributed to the defect, and we appropriately hedged the supposition at the end of the same sentence quoted by Pinckers and Deutman. In our data, the high incidence of the blue-yellow dys­ chromatopsia, and the apparent "clean­ ness" of the lesion in many of our patients surprised us. In our longitudinal study (48 patients to date), all but three patients have shown blue-yellow dyschromatopsia, whereas almost one third of them show the mark­ edly delimited tritan defect (clean tritan

axes on the D-15 and F-M 100 Hue tests, little or no error on the red and green axes of the 100 Hue test, and a normal Rayleigh equation and normal acceptance limits on the Nagel anomaloscope test). Because acquired color vision defects are inherently variable and both peripher­ al and proximal retinas are involved in involutional diabetic retinopathy, we think it better to consider the possibility that the defects in color vision may be caused at multiple points rather than ex­ clusively in the distal retinal elements. WILLIAM H. KNOBLOCH, M.D. ROBERT C. RAMSAY, M.D. RICHARD L. PURPLE, P H . D.

Minneapolis, Minnesota

BOOK REVIEWS Highlights of Ophthalmology, vol. 15. Edited by Benjamin F. Boyd. Panama City, Clinica Boyd and Center for Advanced Studies in Ophthalmology, 1974. Clothbound, 900 pages, table of contents, index, 167 black and white figures, 46 color plates. $60 The 20th anniversary edition of the Highlights of Ophthalmology is a beauty. The white cover trimmed in blue and gold with a slipcover is a beautiful exam­ ple of the printer's art. Benjamin Boyd, ophthalmic interviewer extraordinaire, who has produced 15 of these volumes in the past 20 years here brings together discussions with master ophthalmologists on their preferred method of carrying out a variety of procedures. Boyd provides some 70 interviews covering such varied topics as advances in corneal surgery, traumatic hyphema, anterior vitrectomy, advances in cataract surgery, intraocular lenses, contact lenses, glaucoma, infec­ tion, ultrasonography, vitreous surgery, retinal disease, uvea, strabismus and plas-

Involutional diabetic retinopathy.

726 AMERICAN JOURNAL OF OPHTHALMOLOGY photomicrographs do not represent or­ ganisms of any type, they have been ac­ cepted by the mycologists I cons...
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