Diffuse Unilateral Subacute Neuroretinitis in South America Eduardo Cunha de
Souza, MD; Sergio Lustosa da Cunha, MD; J.
\s=b\ We describe two cases of diffuse unilateral subacute neuroretinitis in South America. These Brazilian patients presented with subretinal worms similar in size to those described in the southeastern United States. This is the first report, to our knowledge, of diffuse unilateral subacute neuroretinitis occurring outside the United States and Caribbean Islands.
(Arch Ophthalmol. 1992;110:1261-1263) unilateral subacute Diffuse tinitis (DUSN) is clinical syn¬ neurore¬
a
drome that typically affects young healthy individuals and is characterized in its early stages by unilateral visual loss, vitreitis, papillitis, retinal vasculi¬ tis, and recurrent crops of evanescent gray-white outer retinal lesions.17 Its later stages include severe visual loss, optic atrophy, retinal vessel narrowing, and widespread diffuse as well as multifocal areas of retinal pigment epithe¬ lial degeneration. It is caused by a nematode migrating in the subretinal space for up to 4 years or more. To date, DUSN has been confirmed by biomicroscopic identification of a nematode only in patients from the United States and Caribbean Islands. The purpose of this report is to describe a nematode wandering in the subretinal
Accepted
for publication March 16, 1992. From the Division of Ophthalmology, S\l=a~\oPaulo (Brazil) University Medical School (Drs Cunha de Souza and Lustosa da Cunha), and the Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami (Fla) School of Medicine (Dr
Gass).
Reprint requests to R. Bahia 563, Paulo, Brazil (Dr Cunha de Souza).
01244 S\l=a~\o
Donald M.
space of two Brazilian
DUSN.
Gass,
MD
patients with
REPORT OF CASES
Case 1.—A 15-year-old white boy had a history of poor visual acuity in the right eye that was first detected during routine school eye examination in August 1986. Other than exposure to dogs, his previous medical his¬
was unremarkable. Best corrected vi¬ sual acuity was counting fingers at 6 ft in the right eye and 20/20 in the left eye. There was an afferent pupillary defect in the right eye without evidence of strabismus. Results of slit-lamp examination showed 1+ cells and flare in the right anterior chamber and 3+ cells in the vitreous of this eye. The left eye was normal. Indirect ophthalmoscopy of the right eye disclosed a pale optic disc, moderate narrow¬ ing of the arterial retinal vessels, and diffuse degeneration of the retinal pigment epithe¬ lium that was most marked in the midperipheral fundus. There were clusters of focal yellow-white lesions that involved the deep layers of the retina and the retinal pigment epithelium in the posterior pole. Biomicroscopy, using a 90-diopter (D) Volk lens (Volk Optical, Mentor, Ohio), revealed a 400- to 500^m-long motile white subretinal nema¬ tode in the superonasal portion of the mac¬ ula. Its diameter was approximately Vaoth of its length. It propelled itself with slow coil¬ ing and uncoiling movements in the subret¬ inal space. There were no signs of larval tracks (Fig 1, left and right). The left eye was normal. We used focal argon laser to destroy the worm. Three weeks later visual acuity was 20/200 OD, the focal white outer lesions were gone, and there was less vitreous inflamma¬ tion (Fig 1, bottom). Results of the medical and laboratory investigation, including stool examination and serologie tests for toxocara, syphilis, and toxoplasma, were normal. CASE 2.—A 13-year-old white boy first noted subnormal visual acuity in his left eye
tory
Downloaded From: http://archopht.jamanetwork.com/ by a University of Auckland User on 05/16/2015
a school eye examination in June 1988. His previous medical history was neg¬ ative except for exposure to dogs. His visual acuity was 20/20 OD and 20/400 OS. There was an afferent pupillary defect in the left eye. Biomicroscopic examination showed normal anterior segment in both eyes. There were 1 + cells in the vitreous of the left eye. Indirect ophthalmoscopy revealed a slight pale optic disc and moderate narrowing of the retinal arterioles in the left eye. There were multiple diffuse chorioretinal scars and extensive areas of pigment epithelium de¬ generation with relative sparing of the mac¬ ula in this eye. In one area nasal to the optic disc were clusters of outer retinal gray-white lesions. Observation with a +90-D Volk lens re¬ vealed a white intraretinal motile worm, gen¬ tly tapered at both ends. It was 400 to 500 µ in length, and its diameter was approxi¬ mately Vfeoth of its length. It often assumed an "s"-shaped appearance. There were no signs of larval tracks in the fundus (Fig 2, top and bottom left). The right fundus was normal. We destroyed the worm with focal argon green laser. Three weeks later, visual acuity was 20/200+ eccentrically OS. The white retinal lesions were much less apparent (Fig 2, bottom right). Results of medical and lab¬ oratory investigation, including stool exam¬ ination and serologie tests for syphilis, toxocara, and toxoplasma, were normal. Aqueous humor was obtained by inserting a 27-gauge needle through the limbus. The results of an enzyme-linked immunosorbent assay for Toxocara canis were negative.
during
COMMENT
Reports to date suggest that DUSN is endemic in three areas. The greatest number of cases have occurred in the southeastern United States and the Caribbean areas. The nematodes in these areas vary in length from approx¬ imately 350 to 1000 µ . The other
Fig 1.—Case 1, right eye. Top left, Photograph of retina. Note the optic atrophy, narrowing of the retinal artendes, and the active whitish retinal lesions in the papillomacular area. The recognized worm was coiled into an open "C" shape (arrow) and there prob¬ ably was subretinal worm material near its superior portion. Top right, Note the diffuse pigment epithelial degeneration in the midperiphery of the retina. Bottom, Three weeks after laser treatment to destroy the worm (superior arrow). Note the less-apparent whitish retinal lesions (inferior arrow)
Fig 2.—Case 2, left eye. Top, Photograph of retina. Note the optic atrophy, loss of foveal reflex, and narrowing of the retinal arterioles. There was pigment reaction inferotemporal to the macula. Bottom left, Note the presence of clusters of active white lesions
nasally in the retina. In that region was found the "s"-shaped, white intraretinal worm (arrow). Bottom right, Three weeks after laser treatment (arrow). Note that the nasal retina looked better, with¬ out active lesions.
Downloaded From: http://archopht.jamanetwork.com/ by a University of Auckland User on 05/16/2015
endemie area is the north midwestern part of the United States, and the nem¬ atode there is approximately 1500 to 2000 µ in length. Except for the fact that the larger nematode causes a coarser pattern of pigment epithelial clumping and depigmentation, the acute and late stages of DUSN are sim¬ ilar to those of the smaller worm. The identification of the nematode in both cases was unknown. Suspects in¬ clude Ancylostoma caninum, the com¬ mon dog hookworm in the case of the smaller nematode, and Baylisascaris procyonis, a common intestinal parasite of raccoons, in the case of the larger nematode.4,8"10 The clinical picture of DUSN is unlike that caused by canis.n In addition, the second-stage lar¬ canis are smaller than those in vae of DUSN and patients with DUSN typi¬ cally show no serologie or skin-test ev¬ idence of exposure to canis? The clinical findings in our two pa¬ tients were typical of those described in patients with DUSN in the southeast¬ ern United States and the Caribbean area. They represent the first cases, to our knowledge, of DUSN with docu¬ mentation of the subretinal worm in South America. Although hookworm infection is common in some areas of South America, particularly that caused by Ancylostoma braziliense, our patients had no evidence of such in¬ fection. In retrospect, we believe we have seen other patients with similar findings, but prior to our finding the first nematode we failed to consider DUSN in the differential diagnosis. We believe that with a greater awareness of the various manifestations of the early and late stages of the disorder by our colleagues in South America, DUSN may prove to be endemic in some areas of this continent. Evidence to date suggests that DUSN is caused by a solitary nematode migrating in the subretinal space in pa¬ tients who usually have no other evi¬ dence of systemic disease.14 As it moves, it leaves substances in its path that cause multifocal gray-white inflam¬ matory patches at the level of the outer retina and pigment epithelium. These active lesions are nearly always con¬ fined to one small segment of the fun¬ dus, and the nematode is usually found nearby. These lesions usually fade within 7 to 10 days and most leave no visible change in the fundus. The development of successive crops
of these evanescent lesions in the wake of the worm is the most characteristic sign suggesting DUSN. In the early stages of the disease, it is accompanied by vitreous inflammation, and in some cases, optic disc edema and retinal perivasculitis. During periods of rela¬ tive inactivity of the nematode, no ac¬ tive white lesions may be present. Dur¬ ing a period of many weeks or months, progressive narrowing of the retinal vessels, optic disc pallor, and diffuse as well as multifocal areas of pigment ep¬ ithelial atrophy develop over wide areas of the fundus, often sparing the macular area.
Central visual loss in these patients is caused primarily by a toxic reaction affecting primarily the retinal ganglion cells. Visual loss may occur very rapidly during the early stages of the disease, or, in some cases, may be delayed until after development of the optic atrophy and the retinal vessel
probably
narrowing. During the early stages of DUSN, the
active outer-retinal lesions may be in¬ correctly attributed to acute posterior multifocal placoid pigment epitheliopathy, the multiple evanescent white dot syndrome, sarcoidosis, Behçet's dis¬ ease, bird-shot or vitiliginous choroidopathy, the presumed ocular histoplas¬ mosis syndrome, and those syndromes that mimic it.4 Elevation of the optic disc margins when unassociated with the white lesions may be incorrectly in¬
terpreted as nonspecific papillitis, neu¬ roretinitis, or papilledema. Visual loss in patients with relatively
normal fundi and in whom the vitreitis is overlooked may be attributed to amblyopia, retrobulbar neuritis, or other optic nerve disorders. In the later stages of the disease, extensive chorioretinal changes may be incorrectly at¬ tributed to retinitis pigmentosa, oph¬ thalmic artery occlusion, trauma, endstage chorioretinitis of unknown cause, and optic atrophy secondary to optic nerve and intracranial disorders. The unilaterality of the findings in patients with DUSN is helpful in excluding many of the simulating disorders. Diffuse unilateral subacute neurore¬ tinitis, like syphilis, is a great imitator. Patients presenting with any of the signs of DUSN35 deserve a careful ex¬ amination since observation of the worm is the only method of accurate di¬ agnosis. The worm is most likely to be found in the vicinity of the already de-
Downloaded From: http://archopht.jamanetwork.com/ by a University of Auckland User on 05/16/2015
scribed active deep retinal lesions, should they exist. Finding it may be difficult and require multiple patient visits. Destruction of the worm with photocoagulation will prevent further loss of visual function.1·35 Unfortu¬ nately, our patients were treated in a late stage, but, nevertheless, experi¬ enced some improvement in their visual acuity 2 months after treatment. Initial trials with oral antihelminthic agents were unsuccessful in destroying the worm in DUSN, presumably be¬ cause of the inability of the drugs to penetrate the blood-retinal barrier.3 Gass et al12 recently reported successful treatment, however, with orally admin¬ istered thiabendazole, in some patients with DUSN when it is associated with moderately intense vitreous inflamma¬ tion. They recommend this treatment, however, only when the worm cannot be found, and when the clinical picture is typical of the early stages of DUSN. Detection of an intense focus of retinitis presumably caused by death of the worm 1 week after administration of thiabendazole is an early sign of treat¬ ment
success.
References 1. Gass JDM, Gilbert WR Jr, Guerry RK, Scelfo R. Diffuse unilateral subacute neuroretinitis. Oph-
thalmology. 1978;85:521-545. 2. Gass JDM, Scelfo R. Diffuse unilateral subacute neuroretinitis. J R Soc Med. 1978;71:95-111.
3. Gass JDM, Braunstein RA. Further observations concerning the diffuse unilateral subacute neuroretinitis syndrome. Arch Ophthalmol. 1983; 101:1689-1697. 4. Gass JDM. Stereoscopic Atlas of Macular Diseases. Diagnosis and Treatment. 3rd ed. St Louis, Mo: Mosby-Year Book; 1987:470-475. 5. Olsen KR, Gass JDM. Diffuse unilateral subacute neuroretinitis. In: Ryan SJ, ed. Retina. St Louis, Mo: Mosby-Year Book; 1989;2:655-661. 6. Parsons HE. Nematode chorioretinitis: report of a case, with photographs, of a viable worm. Arch Ophthalmol. 1952;47:799-800. 7. Price JA Jr, Wadsworth JAC. An intraretinal worm: report of a case of macular retinopathy caused by invasion of the retina by worm. Arch
Ophthalmol. 1970;83:768-770. 8. Kazacos KR, Raymond LA,
Kazacos EA, Vestre WA. The raccoon ascarid: a probably cause of human ocular larva migrans. Ophthalmology.
1985;92:1735-1743.
9. Lewis RA. In: Kazacos KR, Raymond LA, Kazacos EA, Vestre WA. The raccoon ascarid: a probable cause of human ocular larva migrans. Ophthalmology. 1985;92:1743-1744. Discussion. 10. Kazacos KR, Vestre WA, Kazacos EA, Raymond LA. Diffuse unilateral subacute neuroretinitis syndrome: probable cause. Arch Ophthalmol.
1984;102:967-968.
11. Shields JA. Ocular toxocariasis. Surv Ophthalmol. 1984;28:361-381. 12. Gass JDM, Callanan DG, Bowman CB. Oral therapy in diffuse unilateral subacute neuroretinitis. Arch Ophthalmol. 1992;110:675-680.
Souza, MD; Sergio Lustosa da Cunha, MD; J.
\s=b\ We describe two cases of diffuse unilateral subacute neuroretinitis in South America. These Brazilian patients presented with subretinal worms similar in size to those described in the southeastern United States. This is the first report, to our knowledge, of diffuse unilateral subacute neuroretinitis occurring outside the United States and Caribbean Islands.
(Arch Ophthalmol. 1992;110:1261-1263) unilateral subacute Diffuse tinitis (DUSN) is clinical syn¬ neurore¬
a
drome that typically affects young healthy individuals and is characterized in its early stages by unilateral visual loss, vitreitis, papillitis, retinal vasculi¬ tis, and recurrent crops of evanescent gray-white outer retinal lesions.17 Its later stages include severe visual loss, optic atrophy, retinal vessel narrowing, and widespread diffuse as well as multifocal areas of retinal pigment epithe¬ lial degeneration. It is caused by a nematode migrating in the subretinal space for up to 4 years or more. To date, DUSN has been confirmed by biomicroscopic identification of a nematode only in patients from the United States and Caribbean Islands. The purpose of this report is to describe a nematode wandering in the subretinal
Accepted
for publication March 16, 1992. From the Division of Ophthalmology, S\l=a~\oPaulo (Brazil) University Medical School (Drs Cunha de Souza and Lustosa da Cunha), and the Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami (Fla) School of Medicine (Dr
Gass).
Reprint requests to R. Bahia 563, Paulo, Brazil (Dr Cunha de Souza).
01244 S\l=a~\o
Donald M.
space of two Brazilian
DUSN.
Gass,
MD
patients with
REPORT OF CASES
Case 1.—A 15-year-old white boy had a history of poor visual acuity in the right eye that was first detected during routine school eye examination in August 1986. Other than exposure to dogs, his previous medical his¬
was unremarkable. Best corrected vi¬ sual acuity was counting fingers at 6 ft in the right eye and 20/20 in the left eye. There was an afferent pupillary defect in the right eye without evidence of strabismus. Results of slit-lamp examination showed 1+ cells and flare in the right anterior chamber and 3+ cells in the vitreous of this eye. The left eye was normal. Indirect ophthalmoscopy of the right eye disclosed a pale optic disc, moderate narrow¬ ing of the arterial retinal vessels, and diffuse degeneration of the retinal pigment epithe¬ lium that was most marked in the midperipheral fundus. There were clusters of focal yellow-white lesions that involved the deep layers of the retina and the retinal pigment epithelium in the posterior pole. Biomicroscopy, using a 90-diopter (D) Volk lens (Volk Optical, Mentor, Ohio), revealed a 400- to 500^m-long motile white subretinal nema¬ tode in the superonasal portion of the mac¬ ula. Its diameter was approximately Vaoth of its length. It propelled itself with slow coil¬ ing and uncoiling movements in the subret¬ inal space. There were no signs of larval tracks (Fig 1, left and right). The left eye was normal. We used focal argon laser to destroy the worm. Three weeks later visual acuity was 20/200 OD, the focal white outer lesions were gone, and there was less vitreous inflamma¬ tion (Fig 1, bottom). Results of the medical and laboratory investigation, including stool examination and serologie tests for toxocara, syphilis, and toxoplasma, were normal. CASE 2.—A 13-year-old white boy first noted subnormal visual acuity in his left eye
tory
Downloaded From: http://archopht.jamanetwork.com/ by a University of Auckland User on 05/16/2015
a school eye examination in June 1988. His previous medical history was neg¬ ative except for exposure to dogs. His visual acuity was 20/20 OD and 20/400 OS. There was an afferent pupillary defect in the left eye. Biomicroscopic examination showed normal anterior segment in both eyes. There were 1 + cells in the vitreous of the left eye. Indirect ophthalmoscopy revealed a slight pale optic disc and moderate narrowing of the retinal arterioles in the left eye. There were multiple diffuse chorioretinal scars and extensive areas of pigment epithelium de¬ generation with relative sparing of the mac¬ ula in this eye. In one area nasal to the optic disc were clusters of outer retinal gray-white lesions. Observation with a +90-D Volk lens re¬ vealed a white intraretinal motile worm, gen¬ tly tapered at both ends. It was 400 to 500 µ in length, and its diameter was approxi¬ mately Vfeoth of its length. It often assumed an "s"-shaped appearance. There were no signs of larval tracks in the fundus (Fig 2, top and bottom left). The right fundus was normal. We destroyed the worm with focal argon green laser. Three weeks later, visual acuity was 20/200+ eccentrically OS. The white retinal lesions were much less apparent (Fig 2, bottom right). Results of medical and lab¬ oratory investigation, including stool exam¬ ination and serologie tests for syphilis, toxocara, and toxoplasma, were normal. Aqueous humor was obtained by inserting a 27-gauge needle through the limbus. The results of an enzyme-linked immunosorbent assay for Toxocara canis were negative.
during
COMMENT
Reports to date suggest that DUSN is endemic in three areas. The greatest number of cases have occurred in the southeastern United States and the Caribbean areas. The nematodes in these areas vary in length from approx¬ imately 350 to 1000 µ . The other
Fig 1.—Case 1, right eye. Top left, Photograph of retina. Note the optic atrophy, narrowing of the retinal artendes, and the active whitish retinal lesions in the papillomacular area. The recognized worm was coiled into an open "C" shape (arrow) and there prob¬ ably was subretinal worm material near its superior portion. Top right, Note the diffuse pigment epithelial degeneration in the midperiphery of the retina. Bottom, Three weeks after laser treatment to destroy the worm (superior arrow). Note the less-apparent whitish retinal lesions (inferior arrow)
Fig 2.—Case 2, left eye. Top, Photograph of retina. Note the optic atrophy, loss of foveal reflex, and narrowing of the retinal arterioles. There was pigment reaction inferotemporal to the macula. Bottom left, Note the presence of clusters of active white lesions
nasally in the retina. In that region was found the "s"-shaped, white intraretinal worm (arrow). Bottom right, Three weeks after laser treatment (arrow). Note that the nasal retina looked better, with¬ out active lesions.
Downloaded From: http://archopht.jamanetwork.com/ by a University of Auckland User on 05/16/2015
endemie area is the north midwestern part of the United States, and the nem¬ atode there is approximately 1500 to 2000 µ in length. Except for the fact that the larger nematode causes a coarser pattern of pigment epithelial clumping and depigmentation, the acute and late stages of DUSN are sim¬ ilar to those of the smaller worm. The identification of the nematode in both cases was unknown. Suspects in¬ clude Ancylostoma caninum, the com¬ mon dog hookworm in the case of the smaller nematode, and Baylisascaris procyonis, a common intestinal parasite of raccoons, in the case of the larger nematode.4,8"10 The clinical picture of DUSN is unlike that caused by canis.n In addition, the second-stage lar¬ canis are smaller than those in vae of DUSN and patients with DUSN typi¬ cally show no serologie or skin-test ev¬ idence of exposure to canis? The clinical findings in our two pa¬ tients were typical of those described in patients with DUSN in the southeast¬ ern United States and the Caribbean area. They represent the first cases, to our knowledge, of DUSN with docu¬ mentation of the subretinal worm in South America. Although hookworm infection is common in some areas of South America, particularly that caused by Ancylostoma braziliense, our patients had no evidence of such in¬ fection. In retrospect, we believe we have seen other patients with similar findings, but prior to our finding the first nematode we failed to consider DUSN in the differential diagnosis. We believe that with a greater awareness of the various manifestations of the early and late stages of the disorder by our colleagues in South America, DUSN may prove to be endemic in some areas of this continent. Evidence to date suggests that DUSN is caused by a solitary nematode migrating in the subretinal space in pa¬ tients who usually have no other evi¬ dence of systemic disease.14 As it moves, it leaves substances in its path that cause multifocal gray-white inflam¬ matory patches at the level of the outer retina and pigment epithelium. These active lesions are nearly always con¬ fined to one small segment of the fun¬ dus, and the nematode is usually found nearby. These lesions usually fade within 7 to 10 days and most leave no visible change in the fundus. The development of successive crops
of these evanescent lesions in the wake of the worm is the most characteristic sign suggesting DUSN. In the early stages of the disease, it is accompanied by vitreous inflammation, and in some cases, optic disc edema and retinal perivasculitis. During periods of rela¬ tive inactivity of the nematode, no ac¬ tive white lesions may be present. Dur¬ ing a period of many weeks or months, progressive narrowing of the retinal vessels, optic disc pallor, and diffuse as well as multifocal areas of pigment ep¬ ithelial atrophy develop over wide areas of the fundus, often sparing the macular area.
Central visual loss in these patients is caused primarily by a toxic reaction affecting primarily the retinal ganglion cells. Visual loss may occur very rapidly during the early stages of the disease, or, in some cases, may be delayed until after development of the optic atrophy and the retinal vessel
probably
narrowing. During the early stages of DUSN, the
active outer-retinal lesions may be in¬ correctly attributed to acute posterior multifocal placoid pigment epitheliopathy, the multiple evanescent white dot syndrome, sarcoidosis, Behçet's dis¬ ease, bird-shot or vitiliginous choroidopathy, the presumed ocular histoplas¬ mosis syndrome, and those syndromes that mimic it.4 Elevation of the optic disc margins when unassociated with the white lesions may be incorrectly in¬
terpreted as nonspecific papillitis, neu¬ roretinitis, or papilledema. Visual loss in patients with relatively
normal fundi and in whom the vitreitis is overlooked may be attributed to amblyopia, retrobulbar neuritis, or other optic nerve disorders. In the later stages of the disease, extensive chorioretinal changes may be incorrectly at¬ tributed to retinitis pigmentosa, oph¬ thalmic artery occlusion, trauma, endstage chorioretinitis of unknown cause, and optic atrophy secondary to optic nerve and intracranial disorders. The unilaterality of the findings in patients with DUSN is helpful in excluding many of the simulating disorders. Diffuse unilateral subacute neurore¬ tinitis, like syphilis, is a great imitator. Patients presenting with any of the signs of DUSN35 deserve a careful ex¬ amination since observation of the worm is the only method of accurate di¬ agnosis. The worm is most likely to be found in the vicinity of the already de-
Downloaded From: http://archopht.jamanetwork.com/ by a University of Auckland User on 05/16/2015
scribed active deep retinal lesions, should they exist. Finding it may be difficult and require multiple patient visits. Destruction of the worm with photocoagulation will prevent further loss of visual function.1·35 Unfortu¬ nately, our patients were treated in a late stage, but, nevertheless, experi¬ enced some improvement in their visual acuity 2 months after treatment. Initial trials with oral antihelminthic agents were unsuccessful in destroying the worm in DUSN, presumably be¬ cause of the inability of the drugs to penetrate the blood-retinal barrier.3 Gass et al12 recently reported successful treatment, however, with orally admin¬ istered thiabendazole, in some patients with DUSN when it is associated with moderately intense vitreous inflamma¬ tion. They recommend this treatment, however, only when the worm cannot be found, and when the clinical picture is typical of the early stages of DUSN. Detection of an intense focus of retinitis presumably caused by death of the worm 1 week after administration of thiabendazole is an early sign of treat¬ ment
success.
References 1. Gass JDM, Gilbert WR Jr, Guerry RK, Scelfo R. Diffuse unilateral subacute neuroretinitis. Oph-
thalmology. 1978;85:521-545. 2. Gass JDM, Scelfo R. Diffuse unilateral subacute neuroretinitis. J R Soc Med. 1978;71:95-111.
3. Gass JDM, Braunstein RA. Further observations concerning the diffuse unilateral subacute neuroretinitis syndrome. Arch Ophthalmol. 1983; 101:1689-1697. 4. Gass JDM. Stereoscopic Atlas of Macular Diseases. Diagnosis and Treatment. 3rd ed. St Louis, Mo: Mosby-Year Book; 1987:470-475. 5. Olsen KR, Gass JDM. Diffuse unilateral subacute neuroretinitis. In: Ryan SJ, ed. Retina. St Louis, Mo: Mosby-Year Book; 1989;2:655-661. 6. Parsons HE. Nematode chorioretinitis: report of a case, with photographs, of a viable worm. Arch Ophthalmol. 1952;47:799-800. 7. Price JA Jr, Wadsworth JAC. An intraretinal worm: report of a case of macular retinopathy caused by invasion of the retina by worm. Arch
Ophthalmol. 1970;83:768-770. 8. Kazacos KR, Raymond LA,
Kazacos EA, Vestre WA. The raccoon ascarid: a probably cause of human ocular larva migrans. Ophthalmology.
1985;92:1735-1743.
9. Lewis RA. In: Kazacos KR, Raymond LA, Kazacos EA, Vestre WA. The raccoon ascarid: a probable cause of human ocular larva migrans. Ophthalmology. 1985;92:1743-1744. Discussion. 10. Kazacos KR, Vestre WA, Kazacos EA, Raymond LA. Diffuse unilateral subacute neuroretinitis syndrome: probable cause. Arch Ophthalmol.
1984;102:967-968.
11. Shields JA. Ocular toxocariasis. Surv Ophthalmol. 1984;28:361-381. 12. Gass JDM, Callanan DG, Bowman CB. Oral therapy in diffuse unilateral subacute neuroretinitis. Arch Ophthalmol. 1992;110:675-680.
