In the United States,<unk>  is nearly always associated with soft contact lens use.<unk>  spp. is most commonly introduced to the eye by contact lenses that have been exposed to the organism through the use of contaminated lens solution, using homemade saline-based solution or tap water, or from wearing contact lenses while bathing or swimming. However, it may also be introduced to the eye by exposure to soil or vegetation, or by trauma. In fact, the first case of<unk>  described was due to ocular trauma. Once on the contact lens,<unk>  is able to survive in the space between the contact lens and the surface of the eye. Soft contact lenses are more adherent to the corneal surface than hard lenses, which allows the<unk>  organism to bind to mannosylated glycoproteins on the corneal surface. Expression of these proteins on the corneal surface is increased by contact lens use. This increase in glycoprotein content, along with microtrauma to the corneal epithelial surface due to contact lens use increases the risk for infection. Once the organism has gained access to the surface of the eye, it is able to invade through the epithelium and Bowman's layer. In some cases, the infection can then group around corneal nerves, producing radial deposits (radial keratoneuritis), and causing extreme pain. These are features also seen in viral and bacterial keratitis, and may be misleading. The organism is also capable of invading deeper into the cornea; using metalloproteases it is able to penetrate deep into the stroma of the cornea. As the disease progresses, it may penetrate through the cornea but very rarely causes infection inside the eye (endophthalmitis) due to a robust neutrophil response in the anterior chamber. While the vast majority of cases of<unk>  occur in contact lens wearers, there have been many cases of<unk>  described in those who do not wear contact lenses, especially outside the United States. In non-contact lens users, the greatest risks for developing<unk>  infection are trauma and exposure to contaminated water. Further predisposing factors include contaminated home water supply, and low socioeconomic status. Infection is also more commonly seen in tropical or sub-tropical climates. Beyond the route of inoculation into the eye and external risk factors, host factors are also likely to play a significant role in the development of<unk> . In fact, studies of contact lens users in the United Kingdom, Japan, and New Zealand found that 400 to 800 per 10,000 asymptomatic contact lens users had lens storage cases contaminated with<unk>  spp. However, the rate of<unk>  among these patients was only 0.01 to 1.49 per 10,000 contact lens users. Although the exact host factors have not been fully described, it is likely that corneal epithelial defects, tear film composition, eye surface pH, and the level of anti-Acanthamoeba IgA antibodies in the tear film play a role in the development of<unk> . Life cycle Species within the genus,<unk> , are generally free-living trophozoites. These trophozoites are relatively ubiquitous and can live in, but are not restricted to, tap water, freshwater lakes, rivers and soil. In addition to the trophozoite stage, the organism can also form a double-walled cyst which may also be present in the environment, and can be very difficult to eradicate through medical treatment. Both of these stages are usually non-nucleated and reproduce by the means of binary fission.<unk>  trophozoite. Scale bar: 10 μm
Acanthamoeba keratitis
Herpes simplex keratitis
Fungal keratitis
Nummular keratitis
Neurotrophic keratitis
Diffuse lamellar keratitis
Peripheral ulcerative keratitis
Interstitial keratitis