Introduction
The basic aim behind presenting this case
report was how a non responding case of corneal ulcer in non contact lens wearers is misdiagnosed as ulcer. It is a case of acanthamoeba keratitis. The reported incidence of ac. Keratitis varies from 1-3%. In any set up the commonest misdiagnosis done in cases of acanthamoeba are 1) Fungal ulcer and the 2) herpes ulcer; reasons for misdiagnosing are.
Fungal misdiagnosis
- Satellite lesions present in few cases may point towards it.
- Endothelial exudates
- Commonest aetiology corneal ulcer à 50% of ulcer in Indian set up
Herpetic misdiagnosis
- Pseudodentritis
- Early epithelopathy changes in acanthamoeba before the stromal changes.
Case Report
We had 45 yr/m average built, non diabetic non hypertensive chronic alcoholic patient operated for RE ECCE with pciol
Patient was alright for follow up in a month with the eye being quiet and post – op RE visual acuity - 6/24. with Pinhole 6/6.
After post – op 1 month; he presented with redness, pain and watering in right eye since 3 days
History of diminution of vision
There was no history of trauma, foreign body.
On post cataract follow up –
There was no history of epithelial defect, bullous keratopathy
Post op – VA good in each visit
Past history
No history of redness / pain / watering in right eye
No history of TB, DM, IHD, leprosy.
On ocular examination
RE ® Vn : was reduced to HM from 6/24
Iids – were oedematous both upper / lower
Conjunctiva – had circumciliary congestion
Cornea – large corneal ulcer
Shape – oval
Size – 6.5 mm X 5.00 mm
Floor – at base deep central infiltration with 1-2 salellite lesion
Dense fibrous thick hypopyon (>2/3 of chamber)
No radial keratoneuritis
No ring infiltrate
No immune ring of Wesley
Anterior chamber (AC) – was filled 2/3 by hypopyon.
Iris, lens, pupil, details were not seen.
Left eye – was WNL
Provisional diagnosis made was fungal ulcer
Final diagnosis – made with 1) corneal scrapping 2) conjunctival swab done – provided no confirmatory diagnosis and most importantly ulcer was progressing and non responding to medical – antifungal treatment.
Cornea became thin ectatic and about to perforate.
So paracentesis was done and sterile pus (hypopyon) send for culture and sensitivity, KOH mount, Gram staining, Giemsa staining to rule out trophozoites of acanthamoeba seen, latter.
Fig.1 |
Fig.2 |
Treatment given
After definitive diagnosis of acanthamoeba keratitis other toxic antifungals are withdrawn from treatment and started on eye drop ocupol e/d itraconazole e/d Neosporin ointment, oc atropine and e/d iotim with this regime :- keratitis responded in 4 days, the ulcer size began decreasing in size : hypopyon decreased and patient was symptomatically better.
Corneal ulcer was healed with corneal opacity; eye became quiet.
Discussion
Corneal ulceration is a major cause of monocular blindness in developing countries.
A reported incidence of acanthamobea keratitis in India varies from 1-3%. In various published series. Most important thing in this is that large number of cases from this are formed by non contact lens wearers which had different presentation than that from contact lens wearers acanthamoeba keratitis. The majority of such patients are then treated as fungal keratitis. Instead the contact lens wearer acanthaemaeba resembles H. simplex keratitis.
The satellite lesions present in some patient may point towards – misleading fungal aetiology.
Radial keratoneuritis described as atypical for acanthamoeba keratitis was also uncommon in such non contact lens wearers.
Trauma and exposure to contaminated water have been identified as major risk factor. Use of traditional eye medicine may be added as another risk factor.
Again the delayed presentation with big ulcer size because of lack of severe pain and low economic status. This is in contrast to contact lens wearer acanthamoeba keratitis wearer ulcer size is small.
Pathophysiology
Acanthamoeba keratitis occur in patients with minor corneal trauma usually due to wearing contact lenses / splashing of contaminated water the amoeba are introduced via contaminated solution such as home made sodium chloride solution. The subsequent inflammatory reaction results in some neo vascularization. .
Causative organism :- acanthamoeba castellani; an opportunistic free living soil amoeba.
- Exists in trophozoite and cystic form
- Cystic form – highly resistant and able to survive for prolonged periods under hostile environmental condition – chlorinated swimming pools, hot tubs and subfreezing temperature under appropriate condition the cyst turn into trophozoites which produce a variety of enzymes that aid tissue penetration and destruction.
In early cases
- l Corneal epithelium often localized to diffuse punctate epitheliopathy or dendrite epithelial lesion (case of epithelial dendrite often is diagnosed as H. simplex keratitis)
- Stromal infection :- Typically occur in the
- Central cornea and early cases had the grey white non suppurative infiltration
- Small patchy stromal peripheral infiltration
- Gradual enlargement and colescens of the infiltration to form central / paracentral ring abscess.
References
- Larkins DFP. Acanthamoeba keratitis. Int Ophthalmol 1991; 39 : 163.
- Cohen E.J. perlato CJ Arcntscn JJ, et al. Medical and surgical treatment acanthamoeba ketratitis. AMJ Ophthalmol 1987; 104 : 87.
- Holland GH, Doniz PB. AMJ Ophthalmol 1987; 104 : 87.
- Perry S. Binder Cornea 1991; 8 : 106.
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The Lancet, 2006; 367 : 1120. |
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