Phaco Training : Adenoviral Conjunctivitis

By | September 1, 2013

Adenoviral conjunctivitis


Etiology: Epidemic keratoconjunctivitis (EKC) is one of the most common ocular viral infections caused by adenoviruses. Adenovirus family consists of different serotypes. Serotypes 8, 11 19 and 37 are held responsible for EKC and it is known that especially serotypes 8 and 19 cause epidemics [1,2].

Clinical Presentation: Disease presents itself after an incubation period which usually takes 2 to 14 days. Mixed papillary and follicular response of the conjunctiva, eye pain, burning eyes, itching of the eyes, diffuse hyperemia, chemosis, serous discharge and ipsilateral periauricular lymphadenopathy can be observed during the course of the disease. In approximately 80% of the cases, keratitis in the form of diffuse superficial punctate keratitis, focal epithelial punctate keratitis, and subepithelial infiltrates (SEI) follow the conjunctivitis in a manner of 1 to 3 weeks. Subepithelial infiltrates are small, round and grayish lesions. They are composed of residues of antigen and lymphocyte accumulations adhered to surface stromal cells. The lesions disappear without causing scarring or neovascularization. They are usually bilateral and frequently asymmetrical. They may stay dormant in the cornea for months or years, or they may cause acute symptoms such as decrease in visual acuity, halo, glare, and photophobia [3,4].


Treatment: Antibiotics and antiviral eye drops are NOT effective.

Topical corticosteroids may suppress the symptoms and findings of EKC, however due to extended use of these agents problems such as cataract, glaucoma, and tendency to super infections may occur [57].

Cyclosporine A (CsA)

Since 2002, a topical emulsion of ciclosporin for treating inflammation caused by keratoconjunctivitis sicca (dry eye syndrome) has been marketed under the trade name Restasis (0.05%).

SunPharma has Cyclumune e/d both as 0.1% and 0.05%

In ocular adenovirus infections, virus static agents; such as trifluridine, vidarabine and ganciclovir; were tried but none were found to be effective in treatment [1214].

  1. Ward JB, Siojo LG, Waller SG: A prospective, masked clinical trial of trifluridine, dexamethasone, and artificial tears in the treatment of epidemic keratoconjunctivitis.

Cornea 1993, 12:216-221. PubMed Abstract | Publisher Full Text

  1. Little JM, Lorenzetti DW, Brown DC, Schweem HH, Jones BR, Kaufman HE: Studies of adenovirus type 3 infection treated with methisazone and trifluorothymidine.

Proc Soc Exp Biol Med 1968, 127:1028-1032. PubMed Abstract

  1. Hutter H: Epidemic keratoconjunctivitis: treatment results during an epidemic.

Klin Monbl Augenheilkd 1990, 197:214-217. PubMed Abstract | Publisher Full Text

Rx. Not responding to steroids

Cylcomune e/d 0.1% (Sun Pharma) 2 times for 3 months

Or Cyclomune e/d 0.05 % 4 times for 3 months

Restasis 0.05 % (Allergan)

With Flarex e/d 4 times 1 wk

3 times 1 wk

2 times 1 wk

1 times  1 wk

Mechanism of Action of CsA:

In medicine, the most important effect of ciclosporin is to lower the activity of T cells and their immune response.

Ciclosporin binds to the cytosolic protein cyclophilin (immunophilin) of lymphocytes, especially T cells. This complex of ciclosporin andcyclophilin inhibits calcineurin, which, under normal circumstances, is responsible for activating the transcription of interleukin 2. In T-cells, activation of the T-cell receptor normally increases intracellular calcium, which acts via calmodulin to activate calcineurin. Calcineurin then dephosphorylates the transcription factor nuclear factor of activated T-cells (NFATc), which moves to the nucleus of the T-cell and increases the activity of genes coding for IL-2 and related cytokines. Ciclosporin prevents the dephosphorylation of NF-AT by binding to cyclophilin.[25] It also inhibits lymphokine production and interleukin release and, therefore, leads to a reduced function of effector T-cells. It does not affect cytostaticactivity.

Ciclosporin affects mitochondria by preventing the mitochondrial permeability transition pore from opening, thus inhibiting cytochrome c release, a potent apoptotic stimulation factor. This is not the primary mechanism of action for clinical use, but is an important effect for research on apoptosis.

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