Cytomegalovirus disease of external eye is rare and its anterior segment presentations are extraordinary. Cytomegalovirus can be latent without manifestation in immunocompromised patients and CMV- induced retinitis is an important cause of blindness in this group. One previously described an adult suffering from CMV keratitis with a history of cardiac transplant recipient suffering from acquired CMV infection due to transpalation.  Positive corneal culture results indicated the presence of the disease, and unilateral dendritic epithelial keratitis resolved after superficial debridement. Also, CMV epithelialithis along with endotheliitis has been reported in patients with AIDS without retinitis. 
Likewise, intravitreal inoculation of CMV in healthy mice showed that CMV caused a self-limiting and temporary affecting anterior segment of the eye. In contrast, in mice with suppressed immunity, necrotizing retinitis occurred. [ 4]
In our patient, CMV manifested only as dendritic epithelial lesions (see Fig. 1) akin to formerly described case who mimicked the epithelial keratitis due to herpes zoster. [ 5]. The linear lesion did not develop terminal bulbs or epithelial ulceration. PCR test of the sample taken with the applicator from dendritic epithelial lesions of both eyes confirmed CMV infection of the corneal epithelium.
Dendritic epithelial lesions can be caused by the HSV virus, and HSV-induced keratitis is also often unilateral, but in this patient bilateral dendritic manifestations was appeared. Varicella Zoster Virus can also cause these manifestations but epithelial keratitis of dendritic type is unusual, however is common in HZO.  In HZO, the branched and Medusa-like lesions plaques are prominent. These lesions do not have central ulcers and have minimal staining with fluorescein. Meanwhile, the bulbous end is not seen.  Nevertheless, in this patient the dendritic lesions were different from those of HZO including painful skin lesions, with no distributed dermatome.
We could not identify how the patient was infected. Still, no investigational model of CMV keratitis is developed by topical challenge 8 although occasional intravitreal inoculation caused corneal infiltrates. 9 In most cases, CMV does not manifest in the corneal of AML patients, viral reactivation at a non- ocular site may extend to the anterior segment. Moreover, Viremia with conjunctival or limbal contamination and lacrimal gland involvement are probable mechanisms that the corneal epithelium can be infected throughout a systemic CMV contamination.
In this case peripheral involvement of the cornea shows a systemic CMV infection that most probably has arisen from the limbus. In other words, diminishing immune activity presumably permits infection of the ocular surface. During primary infection, CMV infects myeloid precursors CD34 +. Such cells are capable of differentiating into macrophages and dendritic cells as a whole and the body allows the virus to spread.  Therefore, redistribution of the virus leads to a range of CMV-induced diseases, including asymptomatic diseases in patients without immunodeficiency to severe multisystem diseases and even loss of life in patients with weak immune system as well as infants.
Ocular presentations of CMV contain conjunctivitis, microphthalmos, cataract, optic nerve abnormalities, eye inflammation, retinitis and inflammation of the cornea. While CMV keratitis is rare, but its manifestation is growing.  Delayed diagnosis of CMV keratitis often causes serious problems including stromal keratitis and endothelialitis 
In summary, although, herpes simplex virus and varicella- zoster virus are usual origins of corneal infection during immunodeficiency and CMV-induced keratitis often involve endothelium, bilateral corneal epithelial keratitis manifestations will be confirmed as a newly identified consequence of AML. Therefore, investigating risk factors of the host and viral genomics can pave the way for further intuition regarding the pathogenesis of CMV keratitis in otherwise immunocompetent individuals.