Year : 2007 | Volume
: 55 | Issue : 1 | Page : 67--69
Persistent corneal edema secondary to presumed dead adult filarial worm in the anterior chamber
Samar K Basak, Tushar K Hazra, Debasish Bhattacharya
Disha Eye Hospitals and Research Centre, Barrackpore, Kolkata - 700 120, West Bengal, India
Samar K Basak
Disha Eye Hospitals and Research Centre, Barrackpore, Kolkata - 700 120, West Bengal
We present three cases of persistent corneal edema secondary to presumed dead adult filarial worms lying in the anterior chamber with their attachment to the endothelium. Two of them were initially diagnosed as descemetźSQ╗s fold with corneal edema. Two patients underwent penetrating keratoplasty and in one case, surgical removal was partly possible with clearing of cornea.
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Basak SK, Hazra TK, Bhattacharya D. Persistent corneal edema secondary to presumed dead adult filarial worm in the anterior chamber.Indian J Ophthalmol 2007;55:67-69
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Basak SK, Hazra TK, Bhattacharya D. Persistent corneal edema secondary to presumed dead adult filarial worm in the anterior chamber. Indian J Ophthalmol [serial online] 2007 [cited 2022 Nov 26 ];55:67-69
Available from: https://www.ijo.in/text.asp?2007/55/1/67/29501
Live filarial worms in the anterior chamber are known.,,, They may present with decreased vision, secondary glaucoma and uveitis. There has been no report of corneal decompensation and edema with live or dead filarial worm in the anterior chamber.
We present three cases of persistent corneal edema secondary to presumed dead adult filarial worm lying in the anterior chamber attached to the endothelium. "After a careful MEDLINE/ PubMed search, we were unable to find a similar report in the literature and probably, this is the first report of this kind".
This 23-year-old male was referred to our hospital for penetrating keratoplasty (PKP) with a diagnosis of corneal edema in the right eye (RE). He had progressive dimness of vision with photophobia in the RE for four months. There was no history of acute pain, redness, ocular trauma or acute systemic illness in the recent past. On examination, his best corrected visual acuity (BCVA) in the RE was 10/200 and 20/20 in the left eye (LE). The right cornea was thick, cloudy and grossly edematous. A long thread-like structure was detected in the anterior chamber which was partly attached to the temporal half of the endothelial surface of the cornea [Figure 1]. Anterior chamber depth and digital tension was normal. The posterior segment could not be visualized due to gross corneal edema. The corneal thickness was 670 Ám in the RE and 512 Ám in the LE. The LE was essentially normal with an endothelial cell count of 2460 cells/mm 2. The USG B-scan of the RE did not show any abnormality. There was no sign of systemic filariasis. Night peripheral blood smear including the absolute eosinophil count was normal. The patient underwent PKP in the affected eye under cover of oral prednisolone, 40 mg daily in tapering doses over a period of three weeks. The BCVA improved to 20/40p after six months postoperatively. The specific diagnosis of the worm could not be possible from the morphologically altered dead worm lying firmly attached on the endothelial surface.
A 38-year-old lady referred for PKP in the RE, had a history of recurrent redness, photophobia and dimness of vision for six weeks. She was diagnosed elsewhere as descemet's folds with corneal edema. There was no history of ocular trauma or systemic illness. On examination, her BCVA was 20/120 in the RE and 20/20 in the LE. In the RE, there was mild circumcorneal congestion. The cornea was thick and edematous with few keratic precipitates. A slender thread-like dead worm was noticed in the anterior chamber with its attachment to the endothelium [Figure 2]. The part which was attached to the endothelium was partly broken in places. The dead worm was about 1-1.5 mm in thickness and 30-35 mm in length. Anterior chamber reaction was mild with 2+ flare and 2+ cells and with normal depth. Goldman applanation tension was 22 mm of Hg. The posterior segment did not reveal any abnormality. Corneal thickness was 580 Ám in the RE and 506 Ám in the LE. The LE was unremarkable with an endothelial cell count of 2145 cells/mm 2. There was no sign of systemic filariasis. Night peripheral blood smear was normal and did not reveal any microfilaria.
The loose part of the dead worm lying in the anterior chamber was removed surgically under cover of oral prednisolone 50 mg/day in tapering doses for 25 days. But the patient's visual acuity further deteriorated due to progressive corneal edema. The patient underwent PKP in the RE after six weeks and the BCVA improved to 20/60 after six months. The specific diagnosis of the worm could not be possible from the removed pieces of the dead worm under light microscopy.
This 28-year-old female had similar history and clinical signs like Case 2 [Figure 3]A and B. Corneal thickness was 574 Ám in the RE and 498 Ám in the LE. The LE was normal with endothelial cell count of 2584 cells/mm 2. The loose part of the dead worm was removed surgically. Some part of the fossil-like dead worm could not be removed because of its firm attachment with the endothelium. The central cornea became clear and patient's visual acuity improved to 20/30p after six months. Like the previous two cases, the specific diagnosis of the worm could not be possible from the removed parts of the dead worm.
Adult filarial worms are thread-like structures live in the subcutaneous tissues and the lymphatic system. They sexually reproduce microfilaria, the first larval stage. Microfilariae are ingested by hematophagus arthropods, in which they develop into infective larvae that grow in the vertebrate host and mature into adult worms. The exact route of invasion of microfilaria into the eye is still unknown. Probably, they enter the eye through the long and short posterior ciliary vessels, cerebrospinal fluid or the optic nerve sheath. One interesting observation is that in all three patients, the right eye was affected. This is probably due to the fact that the right common carotid artery is the direct branch of the arch of aorta.
Corneal edema in young subjects is mostly due to blunt injury, acute primary or secondary glaucoma, chemical injury, recurrent disciform keratitis, chronic hydrops or endothelial dystrophies. But corneal edema due to dead filarial worm in the anterior chamber with attachments to the endothelium is not known in the literature. It is probable that the dead worm liberates toxin into the anterior chamber which is lethal for the endothelium and that leads to corneal edema.
Two of our cases were initially diagnosed as descemet's folds with corneal edema. Careful slit-lamp examination with elevated thread-like structure on the endothelial surface with parts in the anterior chamber confirmed the diagnosis of a dead adult filaria, though the diagnosis was only presumptive in all three cases. The definitive diagnosis of the type of filarial worm in these cases could not be possible from light microscopy, because the morphological identity was lost in all cases as the worms were dead since long and had changed like fossils.
Beaver in his review on intraocular filariasis reported eight such cases (out of 56) where the filarial worms were removed but not satisfactorily described or identified. The appearance through edematous cornea, distorted morphology of the dead worm and the rarity of such an occurrence, can lead to misdiagnosis. So the ophthalmologists of the tropical countries should consider dead filarial worm attached to the endothelium as a part of differential diagnosis of corneal edema with descemet's folds or tear.
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