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Case Report Submacular Parasite Masquerading as Posterior Pole Granuloma Jatinder Singh 1 and Rajbir Singh 2 1 Aravind Eye Hospital & Postgraduate Institute of Ophthalmology, 1 Anna Nagar, Madurai, Tamil Nadu 625020, India 2 S.B. Dr. Sohan Singh Eye Hospital, Katra Sher Singh, Chowk Farid, Amritsar, Punjab 143001, India Correspondence should be addressed to Jatinder Singh; [email protected] Received 27 February 2015; Revised 17 May 2015; Accepted 28 May 2015 Academic Editor: Alexander A. Bialasiewicz Copyright © 2015 J. Singh and R. Singh. is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Parasites enter the eye through hematogenous spread. e interaction with host immune system may result in its destruction but not without collateral damage to the vital retinal structures. Currently, the accepted treatment for ocular parasitosis is surgical removal or direct laser photocoagulation. A 24-year-old Indian woman presented with abrupt painless loss of vision to 5/300. A large yellow-white lesion centered at macula was observed with associated retinal and subretinal hemorrhage and neurosensory retinal detachment. A parasite was seen protruding at the center of the lesion. Fluorescein angiography demonstrated disc leakage and vessel wall staining. Ultrasonography demonstrated a highly reflective subretinal lesion with aſtershadowing. Serological test was positive for anti-cysticercus (IgM) antibody. Treatment with prednisolone and albendazole resulted in resolution of the lesion within 2 months with improvement of visual acuity to 20/400. A noncystic form of subretinal cysticercosis is likely with suggestive B-scan ultrasonography and serological investigations. 1. Introduction Parasites transit the vascular tunic of eye prior to entering the subretinal or intraocular space. Host immune response triggered by the parasite antigens may incite inflammation of the ocular structures. According to Lech, “to leave the parasite in the eye is to condemn the patient to blindness or total loss of the eye” [1]. e treatment advocated is urgent surgical removal or direct laser photocoagulation of the live parasite. Surgical removal of parasite from the subretinal space is com- plex and would necessitate performing a retinotomy. Laser photocoagulation needs precision and can be complicated by increased inflammation and development of scotoma when placed in the macula. Antihelminthic therapy for intraocular parasite carries risk of systemic adverse effects, limited effec- tiveness, and exacerbation of intraocular inflammation. Prior or concurrent administration of corticosteroids may help reduce the worsening of inflammation induced by the death of parasite. Monitoring of liver function and blood counts is essential if long-term antihelminthic therapy is contemplated. We report a case of submacular live parasite masquerad- ing as posterior pole granuloma treated with systemic anti- helminthics and corticosteroids. 2. Case Description A 24-year-old Indian woman presented with abrupt loss of vision in the right eye of 1-week duration. Best-corrected visual acuity was 5/300 OD and 20/20 OS. e swinging flash light test demonstrated a positive relative afferent pupillary defect in the right eye. Slit lamp biomicroscopy revealed 3+ cells in the anterior vitreous. Intraocular pressure was in the normal range. A yellow-white subretinal lesion larger than 6-disc area size with adjacent satellite lesions, retinal and subretinal hemorrhage, and a serosanguineous detach- ment of neurosensory retina was observed in the posterior pole (Figure 1(a)). ere was associated disc hyperemia and sheathing of the retinal vessels. A motile larval parasite was seen protruding from the center of the lesion. e leſt eye was normal. Fluorescein angiography demonstrated leakage from the disc and the retinal vessels (Figures 1(b) and 1(c)). Ultrasonography demonstrated a focal highly reflective sub- retinal lesion with aſtershadowing (Figure 2). e magnetic resonance imaging study of the brain was normal. Blood counts were normal. Microscopic examination of stool sam- ple did not demonstrate any evidence of parasites. Serological tests using enzyme-linked immunosorbent assay (ELISA) Hindawi Publishing Corporation Case Reports in Ophthalmological Medicine Volume 2015, Article ID 910383, 3 pages http://dx.doi.org/10.1155/2015/910383

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Page 1: Case Report Submacular Parasite Masquerading as Posterior …downloads.hindawi.com/journals/criopm/2015/910383.pdf · 2019-07-31 · Case Report Submacular Parasite Masquerading as

Case ReportSubmacular Parasite Masquerading asPosterior Pole Granuloma

Jatinder Singh1 and Rajbir Singh2

1Aravind Eye Hospital & Postgraduate Institute of Ophthalmology, 1 Anna Nagar, Madurai, Tamil Nadu 625020, India2S.B. Dr. Sohan Singh Eye Hospital, Katra Sher Singh, Chowk Farid, Amritsar, Punjab 143001, India

Correspondence should be addressed to Jatinder Singh; [email protected]

Received 27 February 2015; Revised 17 May 2015; Accepted 28 May 2015

Academic Editor: Alexander A. Bialasiewicz

Copyright © 2015 J. Singh and R. Singh.This is an open access article distributed under theCreative CommonsAttribution License,which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Parasites enter the eye through hematogenous spread. The interaction with host immune system may result in its destruction butnot without collateral damage to the vital retinal structures. Currently, the accepted treatment for ocular parasitosis is surgicalremoval or direct laser photocoagulation. A 24-year-old Indian woman presented with abrupt painless loss of vision to 5/300. Alarge yellow-white lesion centered at macula was observed with associated retinal and subretinal hemorrhage and neurosensoryretinal detachment. A parasite was seen protruding at the center of the lesion. Fluorescein angiography demonstrated disc leakageand vessel wall staining. Ultrasonography demonstrated a highly reflective subretinal lesion with aftershadowing. Serological testwas positive for anti-cysticercus (IgM) antibody. Treatment with prednisolone and albendazole resulted in resolution of the lesionwithin 2 months with improvement of visual acuity to 20/400. A noncystic form of subretinal cysticercosis is likely with suggestiveB-scan ultrasonography and serological investigations.

1. Introduction

Parasites transit the vascular tunic of eye prior to enteringthe subretinal or intraocular space. Host immune responsetriggered by the parasite antigens may incite inflammation ofthe ocular structures. According to Lech, “to leave the parasitein the eye is to condemn the patient to blindness or total lossof the eye” [1]. The treatment advocated is urgent surgicalremoval or direct laser photocoagulation of the live parasite.Surgical removal of parasite from the subretinal space is com-plex and would necessitate performing a retinotomy. Laserphotocoagulation needs precision and can be complicated byincreased inflammation and development of scotoma whenplaced in the macula. Antihelminthic therapy for intraocularparasite carries risk of systemic adverse effects, limited effec-tiveness, and exacerbation of intraocular inflammation. Prioror concurrent administration of corticosteroids may helpreduce the worsening of inflammation induced by the deathof parasite. Monitoring of liver function and blood counts isessential if long-termantihelminthic therapy is contemplated.

We report a case of submacular live parasite masquerad-ing as posterior pole granuloma treated with systemic anti-helminthics and corticosteroids.

2. Case Description

A 24-year-old Indian woman presented with abrupt loss ofvision in the right eye of 1-week duration. Best-correctedvisual acuity was 5/300 OD and 20/20 OS.The swinging flashlight test demonstrated a positive relative afferent pupillarydefect in the right eye. Slit lamp biomicroscopy revealed 3+cells in the anterior vitreous. Intraocular pressure was inthe normal range. A yellow-white subretinal lesion largerthan 6-disc area size with adjacent satellite lesions, retinaland subretinal hemorrhage, and a serosanguineous detach-ment of neurosensory retina was observed in the posteriorpole (Figure 1(a)). There was associated disc hyperemia andsheathing of the retinal vessels. A motile larval parasite wasseen protruding from the center of the lesion. The left eyewas normal. Fluorescein angiography demonstrated leakagefrom the disc and the retinal vessels (Figures 1(b) and 1(c)).Ultrasonography demonstrated a focal highly reflective sub-retinal lesion with aftershadowing (Figure 2). The magneticresonance imaging study of the brain was normal. Bloodcounts were normal. Microscopic examination of stool sam-ple did not demonstrate any evidence of parasites. Serologicaltests using enzyme-linked immunosorbent assay (ELISA)

Hindawi Publishing CorporationCase Reports in Ophthalmological MedicineVolume 2015, Article ID 910383, 3 pageshttp://dx.doi.org/10.1155/2015/910383

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2 Case Reports in Ophthalmological Medicine

(a) (b)

(c) (d)

Figure 1: (a) Color fundus photograph showing yellow-white submacular granuloma. Also observed are satellite lesions, retinal hemorrhage,perivascular sheathing, and serosanguineous detachment of neurosensory retina extending beyond temporal vascular arcades.The arrowheadindicates the site of observed motile parasite. (b) Fluorescein angiography (early phase) demonstrates patchy blocked fluorescence bysubretinal blood. (c) Late phase of fluorescein angiogram shows disc and retinal vascular leakage at and around posterior pole. (d) Colorphotograph documents resolution of the granuloma with resultant pigmented macular scar. The status remained stable till 4 years followingtreatment with albendazole and oral corticosteroids.

Figure 2: Vertical macula B-scan ultrasonogram demonstratinga calcific subretinal focus (arrow) with acoustic aftershadow ofretrobulbar fat.

was negative for Toxoplasma and Toxocara but positive foranti-cysticercus (IgM) antibody.

Treatment was initiated with prednisolone 60mg per dayto be tapered by 10mg per day every week. Albendazole400mg twice daily for 2 weeks was advised to be started fromday 3 of therapy. Ten days following the instituted therapy,the subretinal lesion appeared to be organized with reducedsubretinal fluid and associated vasculitis (supplementary

figure file in Supplementary Material available online athttp://dx.doi.org/10.1155/2015/910383). A dense white (opa-que) plaque-like lesion located at the site of motile parasitewas observed with no activity indicating the response toalbendazole therapy (Figure 1(d)). The uveitis remained qui-escent and the patient’s vision improved to 20/400 over thenext 2 months. The status remained unchanged over 4 yearsof follow-up.

3. Discussion

Our region is endemic to some parasites particularly cys-ticercosis [2]. Cysticercus larvamay rarely present without itscharacteristic cystic form. Nainiwal et al. have reported withhistopathological confirmation of a free-floating live cysticer-cus larva removed from the vitreous cavity [3]. Wender et al.reported 8 (36.4%) eyes of patients who presented with rup-tured cyst; four of them were located in the subretinal space[4]. It is possible that the disruption of cyst wall and extrusionof its contents induced severe granulomatous reaction in ourpatient. The ultrasonographic appearance of calcification inour case supports a possible diagnosis of subretinal cysticer-cus larva. The lack of fluid-filled sac however did not pro-vide the classic sonographic demonstration. Inflammationinduced by the cystic contents of cysticercosis may be severe.

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Case Reports in Ophthalmological Medicine 3

Agarwal et al. reported a case of intraocular cysticercosis sim-ulating retinoblastoma in a 5-year-old child [5]. The lack ofneuroradiological and histopathological evidence fails to cor-roborate the diagnosis of a subretinal cysticercus larva. Theimportance of serological investigation in an endemic regionfor a disease is debatable [6]. Moreover, the prohibitive costand limited utility as a guide for treatment restrict its generaluse. In our case, the result of serological tests provided somecorroborative evidence. Surgical removal of cyst in toto is theaccepted treatment for intraocular cysticercosis. However, inour case the atypical manifestation and submacular locationprecluded a safe removal of the parasite.The specific locationof the parasite at the macula amidst subretinal exudates in aninflamed eye limits the options of surgical and laser therapy.Lim and Chee successfully treated a subretinal cysticercosiswith use of albendazole coupled with immunosuppressivedose of oral steroids [7]. Our case illustrates that a high indexof suspicion in a patient from endemic region, a detailedexamination under high magnification, and investigationsmay provide a clue to the diagnosis. The management withalbendazole and oral corticosteroids helped in abolishing theparasite in our patient’s eye without any further complication.

Conflict of Interests

The authors have no financial/proprietary interest in anymaterials or equipment used in the study. They have noconflicts/potential conflicts to declare.

References

[1] Lech Jr., “Ocular cysticercosis,” American Journal of Ophthal-mology, vol. 32, no. 4, pp. 523–548, 1949.

[2] K. N. Prasad, A. Prasad, A. Verma, and A. K. Singh, “Humancysticercosis and Indian scenario: a review,” Journal of Bio-sciences, vol. 33, no. 4, pp. 571–582, 2008.

[3] S. Nainiwal, M. Chand, L. Verma, S. P. Garg, H. K. Tewari,and S. Kashyap, “Intraocular live cysticercus larva,”OphthalmicSurgery Lasers and Imaging, vol. 34, no. 6, pp. 464–466, 2003.

[4] J. D.Wender, S. R. Rathinam, R. E. Shaw, and E. T. CunninghamJr., “Intraocular cysticercosis: case series and comprehensivereview of the literature,”Ocular Immunology and Inflammation,vol. 19, no. 4, pp. 240–245, 2011.

[5] B. Agarwal, G. K. Vemuganti, and S. G. Honavar, “Intraocularcysticercosis simulating retinoblastoma in a 5-year-old child,”Eye, vol. 17, no. 3, pp. 447–449, 2003.

[6] H. H. Garcia, A. E. Gonsalez, C. A.W. Evans, and R. H. Gilman,“Taenia solium cysticercosis,”The Lancet, vol. 361, pp. 547–556,2003.

[7] W.-K. Lim and S.-P. Chee, “Nonsurgical management of sub-retinal cysticercosis,” Retina, vol. 24, no. 3, pp. 469–471, 2004.

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