Bilateral Ophthalmomyiasis Interna Posterior: Report of a Case with Severe Visual Loss
M.S. Farahvash MD, Z. Aalami Harandi MD
Department of Ophthalmology, Tehran University of Medical Sciences, Tehran, Iran
A 70-year-old woman presented with gradual painless blurring of vision in both eyes for approximately ten years. Her medical and family history were unremarkable. Her visual acuity was counting fingers at 0.5 meter in the right eye and hand motion in the left. The anterior segments were notable only for the presence of early nuclear cataracts. The fundus of both eyes revealed the pathognomonic appearance of rail-road tracks in the retinal pigment epithelium. The linear tracks were especially numerous in the mid-periphery. There was fibrous macular proliferation in the left eye and severe macular degeneration in the right. Fluorescein angiography revealed numerous hyperfluorescent tracks with no leakage. There was early hyperfluorescence in the macula of left eye with late staining. This is the first report of bilateral Ophthalmomyiasis interna posterior in Iran.
Myiasis is the invasion of human tissues and other vertebrates by fly larvae.1,2 Ophthalmomyiasis (ophthalmic myiasis) is the infestation of the human eye, by the maggot of certain flies from the order of Diptera, Host animals include cattle, sheep, horse, deer and rodents. Human infestation occurs via the penetration of intact skin, orbits or nasal cavities. Adult flies, vectors (such as ticks and mosquitos) and patient's hands may transport eggs and larvae to the surface of the eye. No history of insect bite is usually present.3
Ophthalmomyiasis externa (orbital or external ocular tissue involvement) is occasionally observed, Ophthalmomyiasis interna (anterior or posterior), however, is extremely rare. Because of lower mechanical resistance of sclera to maggot's penetration, ophthalmomyiasis interna is more frequent in children.
Suggested routes by which the maggot enters or exits the eye are through the sclera, blood stream or optic nerves.2
Tissue destruction is caused by a symbiosis between the larva and the associated proteolytic bacteria carried by the maggot. The larva destroys the tissue with toxin and thus makes proteins available for the bacterial proteolytic enzymes. Enzymatic digestion, in turn, provides suitable nutrient proteins for the maggot.
A 70-year-old woman, presented to The Farabi Eye Hospital, Tehran, with gradual painless blurring of vision in both eyes, for approximately ten year. She lived in a village in the northern part of Iran (Mazandaran province). Her medical and family history were unremarkable. She also gave no history of being struck in the eye by a fly. Itching sensation, floaters, pain, or photophobia were not present. Laboratory studies gave normal values for electrolytes, liver enzymes, blood sugar, complete blood count and urinalysis. Chest X-ray was also normal.
At the time of our examination in November 1997, her best corrected visual acuity was counting fingers at 0.5 meter in the right eye and hand motions in the left. The patient's anterior segments were notable only for the presence of early nuclear sclerosis. Intraocular pressures were normal. No relative afferent pupillary defect was detectable. There was no inflammatory reaction in the anterior or posterior segments, with no vitreous reaction or organization.
The fundus of both eyes revealed the pathognomonic, and unusually widespread pattern of rail-road tracks in the retinal pigmented epithelium (RPE) (Fig. 1). The hypopigmented curvilinear tracks were especially numerous in the mid-peripheral and posterior pole. The worm tracks were multiple and criss-crossing of a random nature. The caliber of retinal vessels and the color of the optic nerve heads were unaffected. There were fibrous macular proliferation in the left eye and severe macular degeneration in the right. Several areas of pigment clumping was observed in the mid-peripheral retina of both eyes. No organism, either alive or dead could be found at the examination of both eyes.
Fluorescein angiography revealed normal filling of the retinal vasculature in both eyes, with numerous transmission hyperfluorescent tracks, and no leakage (Fig. 2). There was early hyperfluorescence in the macula of the left eye with late staining. Visual acuity remained unchanged in periodical follow-up, and the appearance of lesions did not change.
This is the first report of bilateral Ophthalmomyiasis interna posterior in Iran.
The eye displays a wide variety of reaction to maggot. It may remain asymptomatic as in our patient (the larvae may remain in the eye for years without inducing a significant inflammatory reaction). They may also cause mild uveitis or severe inflammatory reaction.1-3 Signs of inflammation usually develop after the death of the maggot. It may be related to differences in species and heterogenic antigenicity between different varieties of botfly.4
Pathognomonic appearance of linear pigment epithelial disturbances throughout the fundus (rail-road tracks) is secondary to toxic or mechanical disturbance of the retinal pigment epithelium.5 Fluorescein angiography helps to document them. Extensive subretinal larval migration through the macular area, does not necessarily cause central visual loss or dramatic symptoms.
Visual loss may be a result of inflammation/uveitis, extension of the subretinal track through the macula (the only apparent cause of visual loss in our patient), retinal detachment, hemorrhage, subluxated lens, invasion of the optic nerve head a chronic retinal damage caused by the inflammatory process.
Suggested mechanisms of bilateral intraocular involvement are migration of a maggot from one eye to the other (through ocular coats and perforating vessels) and separate involvement in each eye.6?8
Management depends on the location of the maggot and presence of inflammation and include:1-3,6-8
1. A maggot within the vitreous cavity could be left alone, if the inflammatory response is mild.
2. Steroid therapy in the cases of mild to moderate uveitis.
3.If the maggot is subretinal, photocoagulation should be performed promptly to prevent further decrease in vision due to continued tunneling.9
4. Pars plana vitrectomy and retinectomy.
5. Removal of Iarvae from the anterior chamber, by aspiration or forceps (with or without iridectomy).
1 Ziemianski MC, Lee KY, Sabates FN. Ophthalmomyiasis interna. Arch Ophthalmol 1980; 98:1588-9.
2 Steadly LP, Peterson CA. Ophthalmomyiasis. Ann Ophthalmol 1982; 14:137-9.
3 Edward KM, Meredith TA, Hagler WS, Healy GR. Ophthalmomyiasis interna causing visual loss. Ann J Ophthalmol 1984; 97:605-10.
4 Slusher MM, Holland WD, Weaver RG, Tyler ME. Ophthalmomyiasis interna posterior: Subretinal tracks and introcular larvae. Arch Ophthalmol 1979; 97:885-7.
5 Gass JDM, Lewis RA. Subretinal tracks in Ophthalmomyiasis. Arch Ophthalmol 1976; 94:1500-5.
6 Mason GI. Bilateral Ophthalmomyiasis interna. Am J Ophthalmol 1981; 91:65-70.
7 Vine AK, Schatz H. Bilateral posterior ophthalmomyiasis. Ann Ophthalmol 1981; 13:1041-3.
8 Jakobs SM, Adelberg DA, Lewis JM, et al. Ophthalmomyiasis interna posterior, report of a case with optic atrophy. Retina 1997; 17:310-4.
9 Fitzgerald CR, Rubin ML. Intraocular parasite destroyed by photocoagulation. Arch Ophthalmol 1974; 91:162-4.
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