Contact lens–related keratitis can be associated with significant ocular morbidity. Predisposing risk factors for microbial keratitis can vary with geographical location. Most contact lens–associated keratitis cases are caused by Pseudomonas aeruginosa. Although uncommon, Acanthamoeba is associated with the occurrence of keratitis in contact lens users, especially with poor contact lens hygiene. Prompt diagnosis is of paramount importance to prevent severe and permanent visual loss. Most of the treatment, as in any other instance of keratitis, is guided by microbiological results, culture, and sensitivity reports. There is one case published in the literature reporting coinfection of Pseudomonas and Acanthamoeba related to contact lens use.1 We herein report a case of contact lens–associated keratitis coinfected with Pseudomonas and Acanthamoeba, in which the diagnosis of Acanthamoeba was missed initially.
A 20-year-old woman presented to the emergency department of our hospital with a 4-day history of progressively increasing pain, redness, photophobia, mucopurulent discharge, and diminution of vision in her right eye. She was being treated for contact lens–related Pseudomonas keratitis in another hospital before presentation. Her hospital records showed that she had presented 3 days previously with a ring-shaped corneal infiltrate (1.2 by 0.8 mm) in her right eye. Gram-negative bacilli were isolated from corneal scrapings during the initial microbiological evaluation. No other organisms were isolated on microbiological evaluation, as shown in the referral letter. Topical therapy was initiated in the form of hourly fortified gentamycin 1.3% and fortified cefazolin 5%. However, the infiltrates continued to progress rapidly. Consequently, the patient was referred to our hospital. At the time of initial presentation to our department, her best-corrected visual acuity was hand motions OD and 20/20 OS. Slit lamp examination of the right eye showed a central stromal infiltrate (5.8 by 4.6 mm) with radial spokes (Fig. 1). There was severe anterior chamber reaction (>50 cells/high-power field), and intraocular pressure was elevated on digital examination. Ultrasonography showed an anechoic posterior segment. Gram stain of corneal scrapings revealed gram-negative bacilli. Both Gram stain and 10% KOH wet mount showed the presence of Acanthamoeba cysts. High-contrast double-walled cystic structures suggestive of Acanthamoeba cysts were visualized on confocal microscopy. Topical amebicidal therapy was started in the form of hourly chlorhexidine 0.02%, propamidine 0.1%, polymyxin B 30,000 IU eye drops, and neosporin (neomycin, bacitracin, polymyxin) eye ointment four times a day. In addition, topical atropine 1% TDS and oral acetazolamide 250 mg BD were started. Microbiological cultures obtained from the corneal scrapings, contact lenses (two pairs), and contact lens storage case showed the presence of both P. aeruginosa and Acanthamoeba. Pseudomonas was sensitive to polymyxin B.
Within 48 hours of institution of therapy, the patient showed symptomatic improvement, along with a decrease in the density of infiltrates and a reduction in the anterior chamber reaction. Repeat corneal scrapings on day 10 showed Acanthamoeba but no bacilli. Hourly amebicidal treatment was continued for about 3 weeks. Progressive resolution of the infiltrate was noted. Epithelialization was complete by day 24, following which the amebicidal therapy was tapered during the next 4 weeks to four times a day. Seven weeks later, the patient had a vascularized central corneal opacity (Fig. 2), with a best-corrected visual acuity of counting finger at 0.5 ft. She is now on maintenance therapy with chlorhexidine 0.02% four times a day and is awaiting a corneal graft.
Although contact lens wear remains the major risk factor for microbial keratitis in the developed world, it is still considered a minor predisposing cause in developing countries.2 Pseudomonas is the most common causative organism isolated in contact lens–related keratitis. In India, the incidence of Acanthamoeba keratitis is very rare, and most of such cases are non–contact lens related.2–4 This is in marked contrast to reports from other Southeast Asian countries like Singapore, where most cases of Acanthamoeba keratitis are related to contact lens wear.5,6
It has been noted that when cells of Acanthamoeba species were incubated with P. aeruginosa and Staphylococcus epidermidis in a contact lens system, Acanthamoeba showed significantly increased binding with Pseudomonas but not with S. epidermidis.6 Both Acanthamoeba and P, aeruginosa share many characteristics as eye pathogens. Both can adhere to, colonize, and invade injured corneal tissue,7 can produce tissue-destructive enzymes,8,9 and have been recovered individually as contaminants of contact lens care systems.10 Despite these similarities, there is only one case of coinfection with these microbes reported so far.1 Acanthamoeba and P. aeruginosa have been shown to act as selectively exclusive ocular pathogens because the latter induces amebicidal activity when cocultivated with Acanthamoeba in vitro as a result of a toxin-mediated phenomenon.11
Early diagnosis and specific antiamebic therapy prevents rapid destruction of eye by microbes. The sensitivity of 10% KOH wet mount preparation (87 to 91%) has been reported to be higher than that of Gram-stained smear (58 to 66%) and Giemsa-stained smear (45 to 59%) in detecting Acanthamoeba cysts in various Indian studies.3,4,12 Our case highlights that 10% KOH wet mount is a simple and quick tool to identity Acanthamoeba cysts so that timely treatment can be initiated. Also, confocal microscopy is a rapid modality for diagnosis of Acanthamoeba keratitis. Demonstration of amebic cysts on confocal imaging is considered as level II evidence, with a sensitivity and specificity of 100% and 84%, respectively.13,14
Most successful treatment regimens for Acanthamoeba keratitis have used a combination of polyhexanide or chlorhexidine and propamidine isethionate.15 This combination therapy is believed to lower the risk of drug resistance, developing as a result of a low-dose, single-drug therapy.15
Both P. aeruginosa and Acanthamoeba are potentially devastating causes of microbial keratitis. Our case highlights the importance of considering the possibility of such a coinfection especially in cases with contact lens–related keratitis.
Dr. Rajendra Prasad Centre for Ophthalmic Sciences
All India Institute of Medical Sciences
Ansari nagar, New Delhi 110029
Received September 14, 2012; accepted October 29, 2012.
1. Dini LA, Cockinos C, Frean JA. Unusual case of Acanthamoeba polyphaga
and Pseudomonas aeruginosa
keratitis in a contact lens wearer from Gauteng, South Africa. J Clin Microbiol 2000; 38: 826–9.
2. Sharma S, Gopalakrishnan S, Aasuri MK, Garg P, Rao GN. Trends in contact lens–associated microbial keratitis in southern India. Ophthalmology 2003; 110: 138–43.
3. Bharathi JM, Srinivasan M, Ramakrishnan R, Meenakshi R, Padmavathy S, Lalitha PN. A study of the spectrum of Acanthamoeba
keratitis: a three-year study at a tertiary eye care referral center in South India. Indian J Ophthalmol 2007; 55: 37–42.
4. Manikandan P, Bhaskar M, Revathy R, John RK, Narendran V, Panneerselvam K. Acanthamoeba
keratitis—a six-year epidemiological review from a tertiary care eye hospital in South India. Indian J Med Microbiol 2004; 22: 226–30.
5. Cheng CL, Ling ML, Lim L. A case series of Acanthamoeba
keratitis in Singapore. Singapore Med J 2000; 41: 550–3.
6. Gorlin AI, Gabriel MM, Wilson LA, Ahearn DG. Effect of adhered bacteria on the binding of Acanthamoeba
to hydrogel lenses. Arch Ophthalmol 1996; 114: 576–80.
7. Ramphal R, McNiece MT, Polack FM. Adherence of Pseudomonas aeruginosa
to the injured cornea: a step in the pathogenesis of corneal infections. Ann Ophthalmol 1981; 13: 421–5.
8. He YG, Niederkorn JY, McCulley JP, Stewart GL, Meyer DR, Silvany R, Dougherty J. In vivo
and in vitro
collagenolytic activity of Acanthamoeba castellanii
. Invest Ophthalmol Vis Sci 1990; 31: 2235–40.
9. Ferrante A, Bates EJ. Elastase in the pathogenic free-living amoebae Naegleria
spp. Infect Immun 1988; 56: 3320–1.
10. Donzis PB, Mondino BJ, Weissman BA, Bruckner DA. Microbial contamination of contact lens care systems. Am J Ophthalmol 1987; 104: 325–33.
11. Qureshi MN, Perez AA 2nd, Madayag RM, Bottone EJ. Inhibition of Acanthamoeba
species by Pseudomonas aeruginosa
: rationale for their selective exclusion in corneal ulcers and contact lens care systems. J Clin Microbiol 1993; 31: 1908–10.
12. Sharma S, Garg P, Rao GN. Patient characteristics, diagnosis, and treatment of non-contact lens–related Acanthamoeba
keratitis. Br J Ophthalmol 2000; 84: 1103–8.
13. Kaufman SC, Musch DC, Belin MW, Cohen EJ, Meisler DM, Reinhart WJ, Udell IJ, Van Meter WS. Confocal microscopy: a report by the American Academy of Ophthalmology. Ophthalmology 2004; 111: 396–406.
14. Kanavi MR, Javadi M, Yazdani S, Mirdehghanm S. Sensitivity and specificity of confocal scan in the diagnosis of infectious keratitis. Cornea 2007; 26: 782–6.
15. Larkin DF, Kilvington S, Dart JK. Treatment of Acanthamoeba
keratitis with polyhexamethylene biguanide. Ophthalmology 1992; 99: 185–91.