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Dahl, A.A. Stoppler M.C., 2011. Keratitis. http://www.medicinenet.com/keratitis/ar ticle.htm. Diakses tanggal 4 Desember 2011 What is keratitis? Keratitis is the medical term for inflammation of the cornea. The cornea is the dome-shaped window in the front of the eye. When looking at a person's eye, one can see the iris and pupil through the normally clear cornea. The cornea bends light rays as a result of its curved shape and accounts for approximately two-thirds of the eye's total optical power, with the lens of the eye contributing the remaining one-third.. Only the very thin tear film lies between the front of the cornea and our environment. The cornea is about 0.5 millimeter thick. The back of the cornea is bathed in the aqueous fluid that fills the anterior chamber of the eye. The cornea has a diameter of about 13 millimeters (½ inch) and, together with the sclera (the white part of the eye) forms the entire outer coat of the eye. What are the causes of keratitis? Keratitis, the eye condition in which the cornea becomes inflamed, has many potential causes. Various types of infections, dry eyes , injury, and a large variety of underlying medical diseases may all lead to keratitis. Some cases of keratitis result from unknown factors. What are the different types of keratitis?

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Dahl, A.A. Stoppler M.C., 2011. Keratitis. http://www.medicinenet.com/keratitis/article.htm. Diakses tanggal 4 Desember 2011

What is keratitis?

Keratitis is the medical term for inflammation of the cornea. The cornea is the dome-shaped window in the front of the eye. When looking at a person's eye, one can see the iris and pupil through the normally clear cornea. The cornea bends light rays as a result of its curved shape and accounts for approximately two-thirds of the eye's total optical power, with the lens of the eye contributing the remaining one-third.. Only the very thin tear film lies between the front of the cornea and our environment.

The cornea is about 0.5 millimeter thick. The back of the cornea is bathed in the aqueous fluid that fills the anterior chamber of the eye. The cornea has a diameter of about 13 millimeters (½ inch) and, together with the sclera (the white part of the eye) forms the entire outer coat of the eye.

What are the causes of keratitis?

Keratitis, the eye condition in which the cornea becomes inflamed, has many potential causes. Various types of infections, dry eyes, injury, and a large variety of underlying medical diseases may all lead to keratitis. Some cases of keratitis result from unknown factors.

What are the different types of keratitis?

Keratitis can be classified by its location, severity, and cause.

If keratitis only involves the surface (epithelial) layer of the cornea, it is called superficial keratitis. If it affects the deeper layers of the cornea (the corneal stroma), it is called stromal keratitis or interstitial keratitis . It may involve the center of the cornea or the peripheral part of the cornea (that portion closest to the sclera) or both. Keratitis may affect one eye or both eyes.

Keratitis may be mild, moderate, or severe and may be associated with inflammation of other parts of the eye. Keratoconjunctivitis is inflammation of the cornea and the conjunctiva. Kerato-uveitis is inflammation of the cornea and the uveal tract, which consists of the iris, ciliary body, and choroid.

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Keratitis may be acute or chronic. It may occur only once or twice in an eye or be recurrent. It may be limited in its effects on the eye or be progressive in its damage.

The various causes of keratitis may result in different clinical presentations, so defining the location, severity, and frequency of the condition can often assist in pinpointing the exact cause. Other helpful facts in establishing the cause of keratitis can include demographic information such as the age, sex, and geographic location of the patient. A medical history is often useful as well in finding the cause of keratitis.

Infection is the most frequent cause of keratitis. Bacteria, viruses, fungi, and parasitic organisms may all infect the cornea, causing infectious or microbial keratitis.

• Bacteria most frequently responsible for keratitis include Staphylococci, Hemophilus, Streptococci, and Pseudomonas. If the front surface of the cornea has been damaged by a small scratch and the surface is not intact, almost any bacteria, including atypical mycobacteria, can invade the cornea and result in keratitis. Ulcerations of the cornea may occur, a condition known as ulcerative keratitis. Before the advent of antibiotics, syphilis was a frequent cause of keratitis.

• Viruses that infect the cornea include respiratory viruses, including the adenoviruses and others responsible for the common cold. The herpes simplex virus is another common cause of keratitis. There are about 20,000 new cases of ocular herpes in the United States annually, along with more than 28,000 reactivations of the infection. There are about 500,000 people in the U.S. with a history of herpes simplex eye disease. The herpes zoster virus (the virus responsible for chickenpox and shingles) may also cause keratitis if shingles involve the forehead.

• Fungi such as Candida, Aspergillus, and Nocardia are unusual causes of microbial keratitis, more frequently occurring in people who are immunocompromised because of underlying illnesses or medications. Fusarium keratitis, a type of fungal infection, occurs primarily in contact-lens wearers. Bacterial co-infection can complicate fungal keratitis.

• Contact-lens wearers are also susceptible to acanthamoeba keratitis caused by an amebic parasite. "River blindness," or onchocercal keratitis, is another parasitic infection of the cornea, rarely seen in developed countries but very common in the Third World.

Physical or chemical trauma is a frequent cause of keratitis. The injury may become secondarily infected or remain noninfectious. Retained corneal foreign bodies are frequent sources of keratitis. Ultraviolet light from sunlight (snow blindness), a tanning light or a welder's arc, contact-lens overwear, and chemical agents, either in liquid form splashed into the eye or in gases in the form of fumes can all result in noninfectious keratitis. Chemical injury or contact lens-related keratitis often causes superficial punctate keratitis, in which the examiner notices myriads of injured surface

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cells on the affected cornea.

Disturbances in the tear film may lead to changes in the corneal surface through drying of the corneal epithelium. This type of keratitis is usually superficial and most commonly is related to dry eyes and is known as keratitis sicca. If the eyes are extremely dry, the surface cells may die and form attached filaments on the corneal surface, a condition known as filamentary keratitis. Inability to close the eyelids properly can also lead to cornea drying, which is a condition termed exposure keratitis.

Allergies to airborne pollens or bacterial toxins in the tears may also cause a noninfectious type of keratitis. Autoimmune diseases create a similar appearance, often affecting the periphery of the cornea, termed marginal keratitis or limbic keratitis.What are the risk factors for keratitis?

Major risk factors for the development of keratitis include any break or disruption of the surface layer (epithelium) of the cornea.

The use of contact lenses increases the risk for the development of keratitis, especially if when poor hygiene, improper solutions, or overwear are associated with contact-lens use.

A decrease in the quality or quantity of tears predisposes the eye to the development of keratitis.

Disturbances of immune function through diseases such as AIDS or the use of medications such as corticosteroids or chemotherapy also increase the risk of developing keratitis.

What are keratitis symptoms and signs?

The symptoms of keratitis usually include pain, tearing, and blurring of vision. The pain may be mild to severe, depending on the cause and extent of the inflammation. Sensitivity to light may also be present. To the observer, the eye may appear red, watery, and if the cornea has extensive keratitis, the normally clear cornea may look gray or have white to gray areas.

How is keratitis diagnosed?

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The diagnosis of keratitis is made by an ophthalmologist (a physician who specializes in diseases and surgery of the eye) through a history and a physical examination. The history consists of questions documenting a past medical and ocular history and the symptoms specific to the current visit. The eye examination will consist of checking your vision and careful inspection of the corneas using a slit lamp, which is a microscope with excellent illumination and magnification to view the ocular surface and the cornea in detail. Special dye in the form of eyedrops may be placed in the eyes to assist with the examination.

In cases in which infection is suspected, a culture may be taken from the surface of the eye for specific identification of the bacteria, virus, fungus, or parasite causing the keratitis. Blood tests may also be done in certain patients with suspected underlying disease.What is the treatment for keratitis?

Treatment depends on the cause of the keratitis. Infectious keratitis generally requires antibacterial, antifungal, or antiviral therapy to treat the infection. This treatment can involve prescription eyedrops, pills, or even intravenous therapy. Any corneal or conjunctival foreign body should be removed. Wetting drops may be used if disturbance of the tears is suspected to be the cause of the keratitis. Steroid drops may often be prescribed to reduce inflammation and limit scarring. This must be done carefully and judiciously, since some infections can be worsened with their use.

Contact-lens wearers are typically advised to discontinue contact-lens wear, whether or not the lenses are related to the cause of the keratitis.

What are the possible complications of keratitis?

Superficial keratitis involves the superficial layers of the cornea and commonly does not lead to scarring. More extensive keratitis involves deeper layers of the cornea, and a scar may develop upon healing. This will affect the vision if the central portion of the cornea is involved. With severe ulcerative keratitis, the cornea may perforate, which is an extremely serious situation.

With proper diagnosis and appropriate treatment including follow-up care, keratitis can usually be managed without causing permanent visual disturbances.

Can keratitis be prevented?

The risk of keratitis can be reduced through the use of safety precautions to avoid eye injury, careful contact-lens care including proper cleaning of contact lens cases, and

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the prompt treatment of early ocular symptoms.

Keratitis At A Glance

• Keratitis is the medical term for inflammation of the cornea.

• Keratitis has many causes, including infection, dry eyes, physical and chemical injury, and underlying medical diseases.

• The diagnosis of keratitis is made by the use of a slit lamp.

• If keratitis is treated correctly and promptly, permanent damage to the eye can usually be avoided.

REFERENCES:Acharya, N.R., M. Srinivasan, J. Mascarenhas, et al. "The Steroid Controversy in Bacterial Keratitis." Arch Ophthalmol. 127.9 Sept. 2009: 1231.American Academy of Ophthalmology Cornea/External Disease Panel, Preferred Practice Patterns Committee. "Bacterial Keratitis." San Francisco: American Academy of Ophthalmology (AAO), 2008.Morgan, P.B., N. Efron, N.A. Brennan, et al. "Risk Factors for the Development of Corneal Infiltrative Events Associated With Contact Lens Wear." Invest Ophthalmol Vis Sci. 46.9 Sept. 2005: 3136-3143.Poggio, E.C., R.J. Glynn, and O.D. Schein. "The Incidence of Ulcerative Keratitis Among Users of Daily-Wear and Extended-Wear Soft Contact Lenses." N Engl J Med. 321.12 Sept. 21, 1989: 779-783.

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Kamaruddin, F.A., 2011. Gambaran Penggunaan Lensa Kontak di Kalangan Mahasiswa FK USU Dikaitkan dengan Resiko Terjadinya Keratitis. USU

ABSTRAK

Lensa kontak digunakan untuk mengoreksi kesalahan refraksi, tujuan kosmetik dan sebagai terapi dalam penyakit mata. Meskipun penggunaan lensa kontak adalah umum di seluruh dunia, namun masih ramai pengguna tidak menyadari bagaimana cara penggunaan dan perawatan yang benar.

Untuk menilai tindakan pemakaian lensa kontak pada mahasiswa kedokteran dan mengkaji mengidentifikasi faktor-faktor yang menyebabkan komplikasi mata seperti keratitis. Penelitian ini adalah studi deskript if berbentuk cross sectional. Enam puluh pengguna lensa kontak dari mahasiswa Fakultas Kedokteran USU yang memakai lensa kontak diidentifikasi dan ditanya melalui kuesioner tentang aspek yang berbeda melalui kuesioner yang merangkumi semua aspek tujuan studi.

Di antara semua pengguna lensa kontak 90% memiliki kemungkinan risiko rendah untuk mendapatkan keratitis dan 10% memiliki risiko sedang. Sebagian besar mahasiswa menggu nakan lensa kontak harian. Sembilan puluh tujuh persen mahasiswa menggunakan lensa kontak lunak. Sebagian kecil tapi tetapi sangat dikhawatiri (20%) dari mahasiswa kadang-kadang tidak melepaskan lensa mereka saat tidur . Sejumlah besar (20%) dari mahasiswa juga kadang-kadang tidak mencuci tangan mereka sebelum memegang lensa kontak. Selain itu 5% dari mereka tidak pernahmencuci penyimpanan lensa mereka. Sebanyak (73%) dari mereka selalu menjaga kebersihan lense mereka sebagai pencegahan dari terjadinya komplikasi mata.

Sebilangan besar mahasiswa kedokteran menyadari penanganan dan perawatan lensa kontak yang tepat. Hanya beberapa dari mereka yang tidak menyadari komplikasi potensial yang terkait dengan penggunaan lensa kontak yang jelek.

Kata kunci: keratitis, lensa kontak, tindakan

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Ibrahim, W.Y., Boase, D.L., Cree, I.A.,, 2007. How could contact lense wearers be at risk of Acanthamoeba infection. J Optom; 2: 60-66

AbstractContact lens wear is highly influential on the incidence of ulcerative keratitis worldwide, particularly in developed countries. The association between Acanthamoeba keratitis and contact lens wear is firmly established; it may account for up to 95% of the reported cases. Before the popularisation of soft contact lens wear, Acanthamoeba keratitis was extremely rare. In 2000 it was estimated that the number of contact lens wearers worldwide was about 80 million, out of whom 33 million were in the United States and 90% of them wore hydrogel soft lenses. Contact lens-related problems depend on many factors, such as lens material, wearing modality, lens hygiene, type of lens-caring solution, the degree of compliance of the lens user with lens wear and care procedures, lens overwear, sleeping in lenses, rate of changing lenses, and lens case hygiene. This paper is a thorough review of the literature aiming to highlight the role of one of the main risk factors of infectious keratitis, contact lens wear, and also to show the responsibility of lens users in aggravating this risk.Keywords: Acanthamoeba. keratitis. contact lenses. contact lens wearer. lens overwear.

Full TextIntroductionAcanthamoeba is a ubiquitous pathogen that can be found worldwide with different incidence rates, showing the ability to survive in very harsh environmental circumstances.1. Acanthamoeba keratitis is a potentially blinding corneal infection2. that may aggressively affect both eyes3.,4. with the possibility to recur after penetrating keratoplasty.4. Contact lens wear remains the main risk factor in transmitting Acanthamoeba trophozoites and cysts to the cornea.5.,6. A 7-year 1997-2003 survey7. showed an increase in the number of hospitalised patients due to contact lens-related corneal ulcers, which correlated with the increase in the number of lens wearers. Acanthamoeba has a great affinity for the attachment to the corneal epithelium8. and to contact lenses.9. The tendency for Acanthamoeba to adhere to surfaces is a key first step in the pathogenesis of Acanthamoeba keratitis, particularly in contact lens wearers. Contact lenses affect corneal epithelium integrity in two different ways: directly, through the associated fitting-related abrasions10. and indirectly, by altering the normal physiological and metabolic cellular activities.11. These later changes render the

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epithelial cells in a hypoxic status that eventually alters their integrity. Corneal oxygenation is significantly reduced during contact lens overwear, particularly for those who sleep in their lenses overnight.12. However, patient's compliance and some basic hygienic standards can effectively minimise the risk of Acanthamoeba keratitis.13.

Contact Lens-Related ProblemsContact Lens-Induced TraumaDirect Traumatic Effect of Lenses. The corneal epithelium, with its tight junctions, creates an important barrier against Acanthamoeba invasion to the underlying corneal structures. Corneal epithelial cells are more resistant to the cytopathic effect of Acanthamoeba trophozoites than keratocytes.14. Contact lens wear cause minor corneal abrasions, which is the key initial step for Acanthamoeba infection. Martinez et al.10. suggested that corneal trauma was the crucial factor for Acanthamoeba infection, rather than immunosuppression. The adherence of the Acanthamoeba protozoon to an intact corneal epithelium without trauma did not lead, in animal models, to the development of keratitis. Corneal abrasion was absolutely essential for the induction of Acanthamoeba keratitis in hamsters infected with contaminated contact lenses.15.

Corneal epithelial defects make it possible for the Acanthamoeba protozoon to attach to the epithelium and to subsequently invade the rest of the underlying stromal layers. Corneal injury exposes protein sites known as mannose glycoproteins on the surface of injured corneas. The adhesion of the Acanthamoeba to the corneal epithelial cells is the result of mutual interaction between corresponding mannose-binding glycoproteins on the adjacent surface membranes.8.,16.,17. Sugar inhibition assays16.,18. revealed how Acanthamoeba can selectively bind with high affinity to mannose saccharides and not to non-mannosylated neoglycoproteins, such as galactose, fucose, galactosamine or lactose. The corneal surface mannose receptors stimulate Acanthamoeba to secrete pathogenic proteases16. which, in turn, induce epithelium apoptosis19. and facilitate amoeba invasion to the underlying stroma. Alizadeh et al.20.

showed that contact lens wear exacerbated Acanthamoeba keratitis through the secretion of mannose-induced protease 133. In addition, the attachment of Acanthamoeba to corneal epithelial cells helps the phagocytosis and digestion of bacteria21. that provide an important nutrition source for Acanthamoeba. However, Sharma et al.22. found no difference between the adherence ability of Acanthamoeba to corneal epithelial cells of normal non-lens wearers and that of asymptomatic contact lens wearers.Indirect Traumatic Effect of Lenses. Contact lens wear is usually associated with corneal epithelial hypoxia and hypercapnia, particularly when sleeping in lenses or when using lenses having low oxygen transmissibility.11. Carbon dioxide accumulation alters the normal metabolic pathways, which leads to a series of micro-

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structural changes affecting all corneal layers, such as epithelial microcysts, depletion of epithelial glycogen storage, lactic acid accumulation, corneal acidosis, epithelial oedema,11. decreased mitotic rate, increased central corneal thinning,23. corneal hypoesthesia,24. compromised junctional integrity, increased epithelial cells permeability,25. increased cellular epithelial fragility, epithelial punctation, microscopic abrasion, sloughing of the epithelium and, eventually, corneal ulceration. In addition, changes in tear film thickness and stability26. and alteration of the normal profile of conjunctival commensals27. have been recognised. All these changes collectively breach the natural extra ocular protective mechanisms, rendering the cornea an easy target to a wide array of pathogens, including the Acanthamoeba.Attachment of Acanthamoeba to Contact LensesContact lenses serve as a vehicle for the harbouring, transmission and delivery of microorganisms to the eye. Acanthamoeba has a high affinity for contact lens surfaces, a property that plays an important role in the pathogenesis of Acanthamoeba keratitis and creates an actual threat to contact lens wearers.28. The adherence of Acanthamoeba trophozoites and cysts to contact lenses can be detected and quantified using different methods and techniques.9.,29.,30.,31. The ability of Acanthamoeba to attach to contact lenses is influenced by several factors:Contact Lens Material, Ionicity, and Water Content. The manufacturing material affects contact lens ability as a mechanical host allowing attachment and transfer of Acanthamoeba trophozoites or cysts onto the corneal surface. The incidence of Acanthamoeba is much lower with rigid lenses, as compared with the soft type. The lower incidence of Acanthamoeba keratitis found in the Netherlands32. was attributed to the greater proportion of Dutch contact lens wearers that used rigid gas-permeable lenses. Rigid gas-permeable lenses were recommended to hospital staff members wearing lenses, with the aim of minimising the risk of infectious keratitis, due to the easy removal of the attached Acanthamoeba trophozoites and cysts from the surface of this type of contact lenses.33. Kilvington et al.34. showed that cyst attachment occurred only for soft lenses, but not for gas-permeable ones. However, a significant adherence of trophozoites was detected in the case of rigid gas-permeable lenses, as compared with soft contact ones35., with greater affinity for the silicone acrylate material of rigid lenses than for the fluoropolymer material of those same lenses.36.

The greater affinity of Acanthamoeba trophozoites for silicone hydrogel lenses, as compared with conventional hydrogel lenses (P<0.001) was attributed to the attachment characteristics of the polymer of silicon type.37.,38. The attachment of Acanthamoeba trophozoites to different soft contact lens materials, such as polymacon, etafilcon A, lidofilcon A, and bufilcon A varied significantly, with the greatest adherence being observed for

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lidofilcon A and the least for the etafilcon A lenses.29. Adherence of cysts and trophozoites was found to be higher for the non-ionic than for the ionic disposable lenses.28. Simmons et al.39. suggested that the attachment of Acanthamoeba was highly dependant on the ionic nature and the water content of soft contact lenses. Collectively, these reasons could explain why Acanthamoeba adherence is higher for disposable and extended-wear soft lenses than for the conventional soft daily and rigid lenses.Duration of Exposure and Protozoon Concentration. Both cysts and trophozoites showed an immediate adherence to contact lenses, which was observed to happen within 10 seconds after exposure.36. Acanthamoeba adherence to lens surface increased significantly for longer exposure durations and for higher concentrations of inoculum.29.,40. The higher water content of disposable soft contact lenses allows longer time of lens wear and, in turn, gives enough time of exposure for the lenses to be loaded with Acanthamoeba. This could add to the reasons why disposable soft contact lenses wearers are at greater risk of suffering from Acanthamoeba keratitis than those wearers of other types of contact lenses. However, Sharma et al.22. found no difference in Acanthamoeba adherence to different contact lenses with increasing exposure time.Acanthamoeba-Life Stage. Acanthamoeba trophozoite shows a greater tendency to adhere to contact lenses, as compared with the cystic form.29.,36.,40.,41.,42. In contrast to the cystic form, Sharma et al.36. noticed more adherence of trophozoites to rigid gas-permeable lenses than to soft ones. Similarly, Kelly et al.29. observed more preference of trophozoites to adhere to rigid gas-permeable lenses and polymethylmethacrylate (PMMA) contact lenses compared with the cystic form, which showed non specific similar rates of adherence to a variety of lenses, such as rigid gas-permeable, PMMA, daily and disposable soft lenses.Lens Surface Deposits. Attachment of trophozoites and cysts to contact lenses is highly influenced by the presence of protein deposits on the lens surface. Protein deposits on contact lens surface increase the adhesion of other bacterial microbes like Pseudomonas aeruginosa, on which Acanthamoeba feeds.43. Protein and lipid deposition on lens surface is mediated by the chemical structure of the lens material and its water content. The high water content and the ionic material of some disposable soft lenses allow for more deposition of proteins, a fact that could explain the greater affinity of the Acanthamoeba protozoon for worn lenses than for unworn ones.39. Jones et al.44. reported significant deposition of low levels of lysozyme and high levels of lipid on silicone hydrogel contact lens materials, as compared with ionic contact lens materials. The adhesion of Acanthamoeba in unwashed worn versus unwashed unworn contact lenses showed a significantly lower adherence of Acanthamoeba to new lenses.40.,41. The serine protease subtilisin A enzyme used for protein removal from contact lenses

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has been found to have no cysticidal action even after 24 hours of exposure.45. However, it could lower the number of protozoa attached to lens surface through protein removal.Mechanical Ways Used in Contact Lens Care. While shaking showed no significant effect on adherence, a post-incubation wash using phosphate buffered saline decreased the number of adherent cysts and trophozoites.28.

Several studies suggested that a good wash significantly decreased the adherence of trophozoites and cysts to the contact lens surface,40.,42. though one study46. suggested that washing had no effect on either Acanthamoeba stage. Rinsing contact lenses in saline using the flow method was significantly more effective than the immersion technique in removing adherent Acanthamoeba trophozoites from rigid gas-permeable lenses.41. Wiping, rinsing, and rubbing of contact lenses and lens cases with multipurpose disinfecting solutions dislodged adherent cysts and trophozoites and reduced the associated microbiological load.47. Recent studies, showed that multipurpose contact lens solutions that employed a manual rub regime were more effective in removing adherent looselybound deposits48. and different pathogenic microbes49. from soft hydrogel lenses than rinsing or soaking alone.Associated Bacterial Organisms. The contamination of lens care systems with bacteria is an essential association in the development of Acanthamoeba keratitis. The bacterial microorganisms that adhere to the surfaces of contact lenses provide a good medium that facilitates attachment, feeding, survival, and growth of Acanthamoeba. Acanthamoeba can easily attach and grow on a lens surface previously loaded with bacterial microorganisms. Gorlin et al.50. found that about 50% of the eyes infected with Acanthamoeba had positive cultures for bacteria. Other study51. showed that 85% of contact lens systems infected with Acanthamoeba were contaminated with bacterial strains, mainly with the aerobic gram-negative bacilli P. aeruginosa and Xanthomonas maltophilia.Other bacterial microorganisms, such as Flavobacterium breve, P. paucimobilis, P. fluorescens, Staphylococcus aureus, Staphylococcus epidermidis, Escherichia coli, Enterobacter agglomerans, Flavobacterium indolgenes, Salmonella enterica, Corynebacterium xerosis, Serratia marcescens and Klebsiella pneumoniae were isolated in patients with Acanthamoeba keratitis. 20.,52.,53.,54.,55.,56. Alizadeh et al.20. showed that Acanthamoeba could secrete increased amounts of pathogenic mannose-induced protease 133 upon exposure to C. xerosis.Acanthamoeba trophozoites and cysts could retain viable bacteria with human pathogenic potential.57. Intra-Acanthamoeba detection, survival, growth, and multiplication of salmonellae56. and P. aeruginosa58.,59. were reported, with the possibility of reisolating58. P. aeruginosa from Acanthamoeba cysts. P. aeruginosa could significantly enhance Acanthamoeba trophozoite attachment to hydrogel contact lenses,60. but not to silicone ones.37. The

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combination of P. aeruginosa and Acanthamoeba was assumed to be selectively exclusive, causing potentially devastating ocular infections in contact lens wearers. 33.,61. Sodium salicylate reduced trophozoite attachment to hydrogel lenses when inoculated with P. aeruginosa. This effect was attributed to the inhibition of bacterial biofilmformation, interference with the biofilm-amoebal attachment, or modification of the lens surface.60.

Contact Lens Disinfecting Solutions. The use of ineffective contact lens disinfecting solutions is strongly linked to the threat of Acanthamoeba infection in contact lens wearers. A 10-year survey (1994-2004)62. showed that Acanthamoeba was isolated in contact lenses and contact lens disinfecting solutions in all cases of Acanthamoeba keratitis. The one-step 3% hydrogen peroxide and multipurpose solutions were found to be ineffective in killing Acanthamoeba cysts and trophozoites, as well as bacteria and fungi. However, in addition to the broad antimicrobial activity of multipurpose solutions, they were found to be capable of reducing the adherence capability of Acanthamoeba to contact lenses.63. Opti-Free express multipurpose solution significantly reduced the adherence of trophozoites and cysts when used to clean, rinse, and soak soft contact lenses.64. Complete Easy Rub multipurpose solution was effective in removing bacteria, fungi and Acanthamoeba from silicone hydrogel lenses.49.

Problems Caused by Contact Lens WearersContact Lens OverwearCorneal overwear-related problems could develop in the long term for any type of contact lenses, including those designed for extended wear. The overwear problems were influenced by the rate of oxygen transmission and permeability through the lens material, lens thickness, lens type, wearing modalities, replacement schedule, repeated wear of disposable lenses, and overnight sleep in lenses. A lower incidence of microbial keratitis was reported for silicone hydrogel lenses with high oxygen permeability than for other soft lenses having low oxygen permeability used with an extended wear scheme.65.,66. However, occasional pathophysiological problems, such as diffuse corneal infiltration,67. development of mucin balls, superior epithelial arcuate lesions, contact lens papillary conjunctivitis, corneal erosions,11.,68. corneal dryness and discomfort,69. central corneal thinning,70. and thickened conjunctival epithelium due to increased metaplasia71. were reported with the overwear of silicone hydrogel lenses with high oxygen permeability. A significantly higher risk of bacterial keratitis and a greater incidence of complications, such as limbal neovascularisation and corneal oedema, were reported in wearers whose daily wear time was higher than 12 hours.72.

Overnight Sleep in Different Types of Contact LensesThe cornea gets its oxygen supply directly from the air when the eye is opened and from the surrounding blood vessels when it is closed. The new versions of rigid and soft contact lenses were

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designed to allow oxygen delivery to the cornea at an almost similar level under either opened or closed-eye conditions.73. However, corneal hypoxia, subepithelial infiltrations, immune ring formation,12.

changes in corneal curvature, central corneal thinning,70. alteration in the number of polymorphonuclear leukocytes, and variations in the level of different inflammatory mediators in the tear film74. were reported upon wearing contact lenses for multiple sleep cycles. The results of various surveys75.,76.,77.,78. suggested that the overnight wear of contact lenses was the main cause of microbial keratitis, with a greater concern for the immunocompromised patients, where the risk of unusual infections was very high.79.

The overnight wear-related corneal changes and the risk of ulcerative keratitis was found to be significantly dependant on the lens type. Overnight wear of rigid gas-permeable contact lenses was associated with higher levels of corneal hypoxia and epithelial oedema, as compared with soft lenses. 25. However, Graham et al.80. stated that the severity of corneal swelling with rigid gas-permeable lenses was not a reliable predictor of ocular complications. No significant difference was recognised in the bacterial binding ability to the corneal epithelium between the overnight wear of either conventional or hyper-oxygen transmissible rigid contact lenses.81. However, central corneal epithelial thinning with visual impairment82.

and the increased risk of bacterial83.,84. and Acanthamoeba keratitis84.,85.,86.,87.,88.,89. were reported with the overnight wear of orthokeratology contact lenses.The overnight wear of extended wear lenses increased the risk of ulcerative keratitis,90. with the possibility of conjunctival cytologic changes.71.,75.,76. Schein et al.76. mainly attributed the high risk of microbial keratitis among the users of extended wear lenses to the overnight wear, rather than to lens hygiene or lens type. However, Brennan91. contradicted the common perception of optometrists in Western societies, who state that the use of extended wear lenses could increase the risk of microbial keratitis and the loss of vision. Brennan correlated the safety of the overnight wear to the high oxygen transmissibility of silicone hydrogel contact lenses. Other surveys92.,93. denied the occurrence of clinically serious events of microbial keratitis with daily disposable contact lenses. Corneal hypoxic changes, such as epithelial oedema and microcysts were not recognised among the overnight wearers of extended wear lenses, with no significant difference in limbal redness between them and the non-lens users.94. Kenyon et al.95. suggested that neither the level of overnight corneal swelling nor the period between removals could influence the incidence or the severity of corneal problems of extended wear lenses.Non-Compliant Contact Lens UsersThe compliance of contact lens wearers with the recommended lens care hygiene procedures is crucial to reduce the risk of serious infections. D’Aversa et al.96. reviewed the medical records of 12 patients and found that substandard lens-care methods were used

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in 13 out of 14 (92.9%) eyes infected with Acanthamoeba. The use of tap water for the care of contact lenses was widely accepted as the main risk factor in Acanthamoeba infection.5.,85.,97.,98.,99.,100.,101.,102.

In the United Kingdom, 91% of the soft contact lens wearers and 94% of the rigid lens wearers avoided the disease by the complete avoidance of water and the use of powerful lens disinfecting solutions.5. In the USA, the withdrawal of salt tablets from the market was responsible for the decrease in the incidence of Acanthamoeba keratitis in the mid 80s.98. A recent study103. showed that the Chicago-area tap water contained a highly virulent Acanthamoeba strain that was contributing to the increased incidence rate of Acanthamoeba keratitis in this area. Swimming, diving, showering or washing the face while wearing contact lenses was reported to cause Acanthamoeba keratitis.97.,104.,105.,106.,107.,108. The 50-fold increase in the risk of Acanthamoeba keratitis among disposable contact lens users was largely attributable to repeated wear of lenses, lack of disinfection, and use of saline and chlorine-based solutions.75.

The compliance of contact lens users with the recommended care procedures is ineffective if these solutions do not manage to kill Acanthamoeba.6.,105.,109. To avoid the persistent use of non-sterile solutions by non-compliant lens wearers, Moore13. recommended heat disinfection of lenses—between 70 and 80°C for 10 minutes—and the use of 3% hydrogen peroxide for 2-3 hours, 0.001% thimerosal with edetate for 4 hours, 0.005% benzalkonium chloride with edetate for 4 hours, 0.001% chlorhexidine for 4 hours or 0.004% chlorhexidine for 1 hour. Better compliance of contact lens wearers was achieved with the introduction of multipurpose solutions. The multipurpose solutions replaced the need for an additional rinsing solution, offering a single solution for the cleaning, disinfection and contact lens storage.110. The multipurpose solutions provided potent antimicrobial protection with less toxic and less allergenic effects.48.,49.,75.

The non-compliance of contact lens users could occur in the case of deliberate reuse of daily disposable contact lenses, when wearing expired lenses without replacement or if using cheap contact lenses purchased from unlicensed vendors.111. Old contact lenses could colonise more microorganisms due to the increased lens surface tear and wearrelated scratches40. or to the accumulated deposits.43.,44.,45. The relationship between repeated use of daily disposable lenses and risk of Acanthamoeba112.,113. and microbial keratitis93.,114. is well established.Daily disposable lenses were designed for single use only, where a new sterile set should be opened every morning and discarded in the evening. This wear modality aimed to provide a great hygienic advantage, by avoiding the necessity and the cost of disinfecting solutions and storage cases. For hygienic purposes, daily disposable lenses were recommended for those lens wearers having jobs entailing a great potential risk of infection, such as hospital staff

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members.33. Dart et al.115. reported that vision loss was less likely to occur for daily disposable than for reusable soft lens wearers, though no significant reduction in the risk of microbial keratitis was found for users of daily disposable and silicone hydrogel lenses. However, the assumed lens wearers’ compliance could sometimes divert the attention of professionals from considering Acanthamoeba infection in daily disposable contact lens wearers. A delay of 17 days before starting the anti-Acanthamoeba treatment was reported.116.

Radford et al.75. stated that the low care philosophy of daily disposable lens use has resulted in an absolute absence of care, and emphasised the importance of warning patients against the increased risk of infection upon reuse of daily disposable contact lenses. The non-compliance of contact lens users has been attributed to the convenience of using multipurpose or one-step solutions instead of using twostep hydrogen peroxide solutions. Financial savings achieved by reusing daily disposable contact lenses is another factor.117.

ConclusionContact lens wear is the main cause of ulcerative keratitis, which could get seriously complicated with corneal scarring and lead to permanent vision loss. The association between Acanthamoeba keratitis and contact lens wear is firmly established. Contact lenses have a great impact on corneal epithelium integrity. This, added to the greater affinity of Acanthamoeba to adhere to either corneal or lens surfaces, increase the risk of keratitis in contact lens wearers. Lens hygiene, lens care solutions, wearing modalities and the compliance of lens users are important factors in the lens-keratitis relationship. Every lens wearer should be aware of what the main risk factors are and, when given the routine instructions regarding lens fitting and care, they should also be provided with a thorough explanation of how contact lens misuse can seriously affect vision.Received 4 September 2008 Received 1 March 2009 Accepted 2 March 2009Corresponding author. [email protected] YW, Boase DL, Cree I.A. Factors affecting the epidemiology of Acanthamoeba keratitis. Ophthalmic Epidemiol. 2007; 14:53-60. 2.Awwad ST, Heilman M, Hogan RN, et-al. Severe reactive ischemic posterior segment inflammation in Acanthamoeba keratitis: a new potentially blinding syndrome. Ophthalmology. 2007; 114:313-20. 3.Hassanlou M, Bhargava A, Hodge W.G. Bilateral Acanthamoeba keratitis and treatment strategy based on lesion depth. Can J Ophthalmol. 2006; 41:71-3. 4.Rama P, Matuska S, Vigano M, Spinelli A, Paganoni G, Brancato R. Bilateral Acanthamoeba keratitis with late recurrence of the infection in a corneal graft: a case report. Eur J Ophthalmol. 2003; 13:311-4.

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5.Radford CF, Lehmann OJ, Dart J.K. Acanthamoeba keratitis: multicentre survey in England 1992-6. National Acanthamoeba Keratitis Study Group. Br J Ophthalmol. 1998; 82:1387-92. 6.Butler TK, Males JJ, Robinson LP, et-al. Six-year review of Acanthamoeba keratitis in New South Wales, Australia: 1997-2002. Clin Experiment Ophthalmol. 2005; 33:41-6. 7.Verhelst D, Koppen C, Van Looveren J, Meheus A, Tassignon MJ, The Belgian Keratitis Study Group. Contact lens-related corneal ulcers requiring hospitalization: a 7-year retrospective study in Belgium. Acta Ophthalmol Scand. 2006; 84:522-6. 8.Jaison PL, Cao Z, Panjwani N. Binding of Acanthamoeba to mannose-glycoproteins of corneal epithelium: effect of injury. Curr Eye Res. 1998; 17:770-6. 9.Beattie TK, Seal DV, Tomlinson A, McFadyen AK, Grimason A.M. Determination of amoebicidal activities of multipurpose contact lens solutions by using a most probable number enumeration technique. J Clin Microbiol. 2003; 41:2992-3000. 10.Martinez AJ, Janitschke K. Acanthamoeba, an opportunistic microorganism: a review. Infection. 1985; 13:251-6. 11.Liesegang T.J. Physiologic changes of the cornea with contact lens wear. CLAO J. 2002; 28:12-27. 12.Klein P. Corneal immune ring as a complication of soft extended wear contact lens use. Optom Vis Sci. 1991; 68:853-7. 13.Moore M.B. Acanthamoeba keratitis and contact lens wear: the patient is at fault. Cornea. 1990; 9:S33-5. 14.Kinnear F.B. Acanthamoeba pathogenicity for corneal cells. J Infect. 2004; 49:310-6. 15.Van Klink F, Alizadeh H, He YG, et-al. Chinese hamster model of Acanthamoeba keratitis: role of contact lenses, trauma, and Langerhans cells. Invest Ophthalmol Vis Sci. 1993; 34:1937-44. 16.Yang Z, Cao Z, Panjwani N. Pathogenesis of Acanthamoeba keratitis: carbohydrate-mediated host-parasite interactions. Infect Immun. 1997; 65:439-45. 17.Garate M, Alizadeh H, Neelam S, Niederkorn JY, Panjwani N. Oral immunization with Acanthamoeba castellanii mannose-binding protein ameliorates amoebic keratitis. Infect Immun. 2006; 74:7032-4. 18.Cao Z, Jefferson DM, Panjwani N. Role of carbohydrate-mediated adherence in cytopathogenic mechanisms of Acanthamoeba. J Biol Chem. 1998; 273:15838-45. 19.Zheng X, Uno T, Goto T, Zhang W, Hill JM, Ohashi Y. Pathogenic Acanthamoeba induces apoptosis of human corneal epithelial cells. Jpn J Ophthalmol. 2004; 48:23-9. 20.Alizadeh H, Neelam S, Hurt M, Niederkorn J.Y. Role of contact lens wear, bacterial flora, and mannose-induced pathogenic protease in the pathogenesis of amoebic keratitis. Infect Immun. 2005; 73:1061-8. 21.Allen PG, Dawidowicz E.A. Phagocytosis in Acanthamoeba. (I). A mannose receptor is responsible for the binding and phagocytosis of

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yeast. J Cell Physiol. 1990; 145:508-13. 22.Sharma S, Sankaridurg PR, Venkata N, et-al. Adherence of Acanthamoeba to human corneal epithelial cells recovered from normal non-lens wearers and asymptomatic contact lens wearers. Cont Lens Anterior Eye. 1999; 22:110-5. 23.Myrowitz EH, Melia M, O’Brien T.P. The relationship between longterm contact lens wear and corneal thickness. CLAO J. 2002; 28:217-20. 24.Ahuja M. Contact lens wear and microbial keratitis. J Indian Med Assoc. 2002; 100:664-6. 25.Lin MC, Graham AD, Fusaro RE, Polse K.A. Impact of rigid gas-permeable contact lens extended wear on corneal epithelial barrier function. Invest Ophthalmol Vis Sci. 2002; 43:1019-24. 26.Tutt T, Bradley A, Begley C, Thibos L.N. Optical and visual impact of tear break-up in human eyes. Invest Ophthalmol Vis Sci. 2000; 41:4117-23. 27.Barequet IS, Jabbur NS, Barron Y, Osterhout GJ, O’Brien T.P. Perioperative microbiologic profile of the conjunctiva in photorefractive keratectomy. J Refract Surg. 2001; 17:55-62. 28.Ramachandran L, Janakiraman D, Sharma S, Rao G.N. Effect of time and washing on the adhesion of Acanthamoeba to extended wear disposable hydrogel contact lenses. CLAO J. 1997; 23:113-6. 29.Kelly LD, Xu L. The effect of Acanthamoeba concentration on adherence to four types of unworn soft contact lenses. CLAO J. 1995; 21:27-30. 30.John T, Desai D, Sahm D. Adherence of Acanthamoeba castellanii cysts and trophozoites to unworn soft contact lenses. Am J Ophthalmol. 1989; 108:658-64. 31.Mathers WD, Sutphin JE, Folberg R, Meier PA, Wenzel RP, Elgin R.G. Outbreak of keratitis presumed to be caused by Acanthamoeba. Am J Ophthalmol. 1996; 121:129-42. 32.Cheng KH, Leung SL, Hoekman HW, et-al. Incidence of contactlens-associated microbial keratitis and its related morbidity. Lancet. 1999; 354:181-5. 33.Hay J, Seal D.V. Contact lens wear by hospital health care staff: is there cause for concern?. J Hosp Infect. 1995; 30:275-81. 34.Kilvington S, Larkin D.F. Acanthamoeba adherence to contact lenses and removal by cleaning agents. Eye. 1990; 4:589-90. 35.Cohen EJ, Fulton JC, Hoffman CJ, Rapuano CJ, Liabson P.R. Trends in contact lens-associated corneal ulcers. Cornea. 1996; 15:566-70. 36.Sharma S, Ramachandran L, Rao G.N. Adherence of cysts and trophozoites of Acanthamoeba to unworn rigid gas permeable and soft contact lenses. CLAO J. 1995; 21:247-451. 37.Beattie TK, Tomlinson A, McFadyen AK, Seal DV, Grimason A.M. (II). Enhanced attachment of Acanthamoeba to extended-wear silicone hydrogel contact lenses: a new risk factor for infection?. Ophthalmology. 2003; 110:765-71. 38.Beattie TK, Tomlinson A, Seal D.V. Surface treatment or material characteristic: the reason for the high level of Acanthamoeba

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attachment to silicone hydrogel contact lenses. Eye Contact Lens. 2003; 29:S40-3. 39.Simmons PA, Tomlinson A, Connor R, Hay J, Seal D.V. Effect of patient wear and extent of protein deposition on adsorption of Acanthamoeba to five types of hydrogel contact lenses. Optom Vis Sci. 1996; 73:362-8. 40.Sehgal R, Saini J, Singh KD, Bhatti H.S. Acanthamoeba adherence to soft contact lens and human corneal stroma. Indian J Pathol Microbiol. 2002; 45:63-7. 41.Cancrini G, Iori A, Mancino R. Acanthamoeba adherence to contact lenses, removal by rinsing procedures, and survival to some ophthalmic products. Parassitologia. 1998; 40:275-8. 42.Seal DV, Hay J, Kirkness C.M. Chlorhexidine or polyhexamethylene biguanide for Acanthamoeba keratitis. Lancet. 1995; 345:136. 43.Butrus SL, Klotz S.A. Contact lens surface deposits increase the adhesion of Pseudomonas aeruginosa. Curr Eye Res. 1990; 9:717-24. 44.Jones L, Senchyna M, Glasier MA, et-al. Lysozyme and lipid deposition on silicone hydrogel contact lens materials. Eye Contact Lens. 2003; 29:S75-9. 45.Hughes R, Kilvington S. Comparison of hydrogen peroxide contact lens disinfection systems and solutions against Acanthamoeba polyphaga. Antimicrob Ag Chemother. 2001; 45:2038-43. 46.John T. Interactions of bacteria and amoebae with ocular biomaterials. Cells and Materials. 1991; 1:129-39. 47.Niszl IA, Markus M.B. Treatment of Acanthamoeba keratitis. S Afr Med J. 1996; 86:566. 48.Cho P, Cheng SY, Chan WY, Yip W.K. Soft contact lens cleaning: rub or no-rub?. Ophthalmic Physiol Opt. 2009; 29:49-57. 49.Kilvington S, Lonnen J. A comparison of regimen methods for the removal and inactivation of bacteria, fungi and Acanthamoeba from two types of silicone hydrogel lenses. Cont Lens Anterior Eye. 2009; 32:73-7. 50.Gorlin AI, Gabriel MM, Wilson LA, Ahearn D.G. Effect of adhered bacteria on the binding of Acanthamoeba to hydrogel lenses. Arch. Ophthalmol. 1996; 114:576-80. 51.Kelly LD, Xu L. The effect of concurrent Pseudomonas or Xanthomonas exposure on adherence of Acanthamoeba castellanii to soft contact lenses. Graefes Arch Clin Exp Ophthalmol. 1996; 234:311-4. 52.Bottone EJ, Madayag RM, Qureshi M.N. Acanthamoeba keratitis. Synergy between amoebic and bacterial co-contaminants in contact lens care systems as a prelude to infection. J Clin Microbiol. 1992; 30:2447-50. 53.Clark BJ, Harkins LS, Munro FA, Devonshire P. Microbial contamination of cases used for storing contact lenses. J Infect. 1994; 28:293-304.

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54.Wang X, Ahearn D.G. Effect of bacteria survival and growth of Acanthamoeba castellanii. Curr Microbiol. 1997; 34:212-5. 55.Willcox MD, Low R, Hon J, Harmis N. Does Acanthamoeba protect Pseudomonas aeruginosa from the bactericidal effects of contact lens disinfecting systems?. Aust N Z J Ophthalmol. 1998; 26:S32-5. 56.Tezcan-Merdol D, Ljungstrom M, Winiecka-Krusnell J, Linder E, Engstrand L, Rhen M. Uptake and replication of Salmonella enterica in Acanthamoeba rhysodes. Appl Environ Microbiol. 2004; 70:3706-14. 57.Marciano-Cabral F, Cabral G. Acanthamoeba spp. as agents of disease in humans. Clin Microbiol Rev. 2003; 16:273-307. 58.Walochnik J, Picher O, Aspöck C, Ullmann M, Sommer R, Aspöck H. Interactions of “Limax amoebae” and gram-negative bacteria: experimental studies and review of current problems. Tokai J Exp Clin Med. 1999; 23:273-8. 59.Michel R, Burghardt H, Bergmann H. Acanthamoeba, naturally intracellularly infected with Pseudomonas aeruginosa, after their isolation from a microbiologically contaminated drinking water system in a hospital. Zentralbl Hyg Umweltmed. 1995; 196:532-44. 60.Tomlinson A, Simmons PA, Seal DV, McFadyen A.K. Salicylate inhibition of Acanthamoeba attachment to contact lenses: a model to reduce risk of infection. Ophthalmology. 2000; 107:112-7. 61.Dini LA, Cockinos C, Frean JA, Niszl IA, Markus M.B. 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. 62.Tzanetou K, Miltsakakis D, Droutsas D, et-al. Acanthamoeba keratitis and contact lens disinfecting solutions. Ophthalmologica. 2006; 220:238-41. 63.Borazjani RN, Kilvington S. Effect of a multipurpose contact lens solution on the survival and binding of Acanthamoeba species on contact lenses examined with a no-rub regimen. Eye Contact Lens. 2005; 31:39-45. 64.Kilvington S, Anger C. A comparison of cyst age and assay method of the efficacy of contact lens disinfectants against Acanthamoeba. Br J Ophthalmol. 2001; 85:336-40. 65.Holden BA, Sweeney DF, Sankaridurg PR, et-al. Microbial keratitis and vision loss with contact lenses. Eye Contact Lens. 2003; 29:S131-4. 66.Bialasiewicz A.A. Infection immunology in silicone hydrogel contact lenses for continuous wear--a review. Klin Monatsbl Augenheilkd. 2003; 220:453-8. 67.Skotnitsky C, Jalbert I, O’Hare N, Sweeney DF, Holden B.A. Case reports of three atypical infiltrative keratitis events with high Dk soft contact lens wear. Cornea. 2002; 21:318-24. 68.Dumbleton K. Noninflammatory silicone hydrogel contact lens complications. Eye Contact Lens. 2003; 29:S186-9. 69.Fonn D, Dumbleton K. Dryness and discomfort with silicone hydrogel contact lenses. Eye Contact Lens. 2003; 29:S101-4.

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70.Gonzalez-Meijome JM, Gonzalez-Perez J, Cervino A, Yebra-Pimentel E, Parafita M.A. Changes in corneal structure with continuous wear of high-Dk soft contact lenses: a pilot study. Optom Vis Sci. 2003; 80:440-6. 71.Gurdal C, Aydin S, Kirimlioglu H, Toprak E, Sengor T. Effects of extended-wear soft contact lenses on the ocular surface and central corneal thickness. Ophthalmologica. 2003; 217:329-36. 72.Rapkin J.S. The effect of daily wear time on contact lens complications. CLAO J. 1988; 14:139-42. 73.Weissman B, Mondino B.J. Why daily wear is still better than extended wear. Eye Contact Lens. 2003; 29:S145-6. 74.Thakur A, Willcox M.D. Contact lens wear alters the production of certain inflammatory mediators in tears. Exp Eye Res. 2000; 70:255-9. 75.Radford CF, Bacon AS, Dart JK, Minassian D.C. Risk factors for Acanthamoeba keratitis in contact lens users: a case-control study. BMJ. 1995; 310:1567-70. 76.Schein OD, Buehler PO, Stamler JF, Verdier DD, Katz J. The impact of overnight wear on the risk of contact lens-associated ulcerative keratitis. Arch Ophthalmol. 1994; 112:186-90. 77.Lam DS, Houang E, Fan DS, Lyon D, Seal D, Wong E. Incidence and risk factors for microbial keratitis in Hong Kong: comparison with Europe and North America. Eye. 2002; 16:608-18. 78.Landers JA, Crompton J.L. Microbial keratitis associated with overnight wear of silicone hydrogel contact lenses. Med J Aust. 2006; 185:177-8. 79.Sridhar MS, Laibson PR, Rapuano CJ, Cohen E.J. Infectious crystalline keratopathy in an immunosuppressed patient. CLAO J. 2001; 27:108-10. 80.Graham AD, Fusaro RE, Polse KA, Lin MC, Giasson C.J. Predicting extended wear complications from overnight corneal swelling. Invest Ophthalmol Vis Sci. 2001; 42:3150-7. 81.Cavanagh HD, Ladage P, Yamamoto K, Li SL, Petroll WM, Jester J.V. Effects of daily and overnight wear of hyper-oxygen transmissible rigid and silicone hydrogel lenses on bacterial binding to the corneal epithelium: 13-month clinical trials. Eye Contact Lens. 2003; 29:S14-6. 82.Alharbi A, Swarbrick H.A. The effects of overnight orthokeratology lens wear on corneal thickness. Invest Ophthalmol Vis Sci. 2003; 44:2518-23. 83.Lau LI, Wu CC, Lee SM, Hsu W.M. Pseudomonas corneal ulcer related to overnight orthokeratology. Cornea. 2003; 22:262-4. 84.Sun X, Zhao H, Deng S, et-al. Infectious keratitis related to orthokeratology. Ophthalmic Physiol Opt. 2006; 26:133-6. 85.Watt K, Swarbrick H.A. Microbial keratitis in overnight orthokeratology: review of the first 50 cases. Eye Contact Lens. 2005; 31:201-8. 86.Hutchinson K, Apel A. Infectious keratitis in orthokeratology. Clin Experiment Ophthalmol. 2002; 30:49-51.

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87.Lu L, Zou L, Wang R. Orthokeratology induced infective corneal ulcer. Zhonghua Yan Ke Za Zhi. 2001; 37:443-6. 88.Xuguang S, Lin C, Yan Z, et-al. Acanthamoeba keratitis as a complication of orthokeratology. Am J Ophthalmol. 2003; 136:1159-61. 89.Wilhelmus K.R. Acanthamoeba keratitis during orthokeratology. Cornea. 2005; 24:864-6. 90.Schein OD, Poggio E.C. Ulcerative keratitis in contact lens wearers. Incidence and risk factors. Cornea. 1990; 9:S55-8. 91.Brennan N.A. Is there a question of safety with continuous wear?. Clin Exp Optom. 2002; 85:127-40. 92.Levy B, McNamara N, Corzine J, Abbott R.L. Prospective trial of daily and extended wear disposable contact lenses. Cornea. 1997; 16:274-6. 93.Sankaridurg PR, Sweeney DF, Holden BA, et-al. Comparison of adverse events with daily disposable hydrogels and spectacle wear: results from a 12-month prospective clinical trial. Ophthalmology. 2003; 110:2327-34. 94.Sweeney D.F. Clinical signs of hypoxia with high-Dk soft lens extended wear: is the cornea convinced?. Eye Contact Lens. 2003; 29:S22-5. 95.Kenyon E, Polse KA, Seger R.G. Influence of wearing schedule on extended-wear complications. Ophthalmology. 1986; 93:231-6. 96.D’Aversa G, Stern GA, Driebe W.T. Diagnosis and successful medical treatment of Acanthamoeba keratitis. Arch Ophthalmol. 1995; 113:1120-3. 97.Seal DV, Dalton A, Doris D. Disinfection of contact lenses without tap water rinsing-is it effective?. Eye. 1999; 13:226-30. 98.Mathers WD, Sutphin JE, Lane JA, Folberg R. Correlation between surface water contamination with amoeba and the onset of symptoms and diagnosis of amoeba-like keratitis. Br J Ophthalmol. 1998; 82:1143-6. 99.Jeong HJ, Yu H.S. The role of domestic tap water in Acanthamoeba contamination in contact lens storage cases in Korea. Korean J Parasitol. 2005; 43:47-50. 100.Visvesvara G.S. Epidemiology of infections with free-living amebas and laboratory diagnosis of microsporidiosis. Mt. Sinai J. Med. 1993; 60:283-8. 101.Cohen EJ, Buchanan HW, Laughrea PA, et-al. Diagnosis and management of Acanthamoeba keratitis. Am. J. Ophthalmol. 1985; 100:389-95. 102.Moore MB, McCulley JP, Newton C, Cobo LM, Foulks GN, O’Day D.M. Acanthamoeba keratitis. A growing problem in soft and hard contact lens wearers. Ophthalmology. 1987; 94:1654-61. 103.Shoff ME, Joslin CE, Tu EY, Kubatko L, Fuerst P.A. Efficacy of contact lens systems against recent clinical and tap water Acanthamoeba isolates. Cornea. 2008; 27:713-9. 104.Radford CF, Minassian DC, Dart J.K. Acanthamoeba keratitis in England and Wales: incidence, outcome, and risk factors. Br J

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Ophthalmol. 2002; 86:536-42. 105.Stehr-Green JK, Bailey TM, Brandt FH, Carr CH, Bond WW, Visvesvara G.S. Acanthamoeba keratitis in soft contact lens wearers: a case-control study. JAMA. 1987; 258:57-60. 106.Ondriska F, Mrva M, Lichvar M, Ziak P, Murgasova Z, Nohynkova E. First cases of Acanthamoeba keratitis in Slovakia. Ann Agric Environ Med. 2004; 11:335-41. 107.De Jonckheere J.F. Epidemiological typing of Acanthamoeba strains isolated from keratitis cases in Belgium. Bull Soc Belge Ophtalmol. 2003; 287:27-33. 108.Kaji Y, Hu B, Kawana K, Oshika T. Swimming with soft contact lenses: danger of Acanthamoeba keratitis. Lancet Infect Dis. 2005; 5:392. 109.Niszl IA, Markus M.B. Anti-Acanthamoeba activity of contact lens solutions. Br J Ophthalmol. 1998; 82:1033-8. 110.Stevenson RW, Seal D.V. Has the introduction of multi-purpose solutions contributed to a reduction in Acanthamoeba keratitis in contact lens wearers?. Contact Lens Anterior Eye. 1998; 21:89-92. 111.Gagnon MR, Walter K.A. A case of Acanthamoeba keratitis as a result of a cosmetic contact lens. Eye Contact Lens. 2006; 32:37-8. 112.Blades K, Tomlinson A, Seal D.V. Acanthamoeba keratitis occurring with daily disposable contact lens wear. Br J Ophthalmol. 2000; 84:805. 113.Woodruff SA, Dart J.K. Acanthamoeba keratitis occurring with daily disposable contact lens wear. Br J Ophthalmol. 1999; 83:1088-9. 114.Stapleton F. Contact lens-related microbial keratitis: what can epidemiologic studies tell us?. Eye Contact Lens. 2003; 29:S85-9. 115.Dart JK, Radford CF, Minassian D, Verma S, Stapleton F. Risk factors for microbial keratitis with contemporary contact lenses: a case-control study. Ophthalmology. 2008; 115:1647-54. 116.Niyadurupola N, Illingworth C.D. Acanthamoeba keratitis associated with misuse of daily disposable contact lenses. Cont Lens Anterior Eye. 2006; 29:269-71. 117.Hiti K, Walochnik J, Haller-Schober EM, Faschinger C, Aspock H. Viability of Acanthamoeba after exposure to a multipurpose disinfecting contact lens solution and two hydrogen peroxide systems. Br J Ophthalmol. 2002; 86:144-6.

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Qu W., Busscher H.J., Hooymans J.M., van der Mei H.C.. 2011. Surface thermodynamics and adhesion forces governing bacterial transmission in contact lens related microbial keratitis. J Colloid Interface Sci Jun 15; Vol. 358 (2), page 430-6

J Colloid Interface Sci. 2011 Jun 15;358(2):430-6. doi: 10.1016/j.jcis.2011.03.062. Epub 2011 Mar 23.Surface thermodynamics and adhesion forces governing bacterial transmission in contact lens related microbial keratitis.Qu W, Busscher HJ, Hooymans JM, van der Mei HC.SourceDepartment of Biomedical Engineering, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands.

AbstractContact lens induced microbial keratitis results from bacterial transmission from one surface to another. We investigated the adhesion forces of Pseudomonas aeruginosa, Staphylococci and Serratia to different contact lenses, lens cases and corneal surfaces using AFM, and applied a Weibull analysis on these adhesion forces to calculate bacterial transmission probabilities from lens case to corneas with a contact lens as an intermediate. Also a new surface thermodynamic parameter was introduced, the interfacial free energy of transmission,

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which in essence compares the interfacial free energies of bacterial adhesion, calculated from measured contact angles with liquids on the donating and receiving surfaces in the transmission process. Bacterial adhesion forces were generally strongest among all eight strains for the lens case (-6.5 to -12.0 nN) and corneas (-3.5 to -11.5 nN), while contact lenses (-0.6 to -13.1 nN) exerted slightly smaller adhesion forces. Consequently, bacterial transmission from lens case to contact lens yielded a smaller contribution in the final transmission than from contact lens to cornea. Bacterial transmission probabilities as derived from force analyses were higher when the interfacial free energies of transmission were more negative, which is in line with surface thermodynamic principles. Therewith this parameter could provide useful in analyzing other bacterial transmission phenomena between donating and receiving surfaces as well.

Martinez, A.J., Janitschke, 1985. Acanthamoeba, an opportunistic microorganism:a review. Infection; 13: 251-256.

SummaryGranulomatous amebic encephalitis due toAcanthamoeba spp. usually occurs in chronically ill and debilitated individuals. Some of these patients may have received immunosuppressive therapy. Another infection due toAcanthamoeba spp. has been corneal ulcerations which usually occur after minimal trauma to the corneal epithelium (1). In contrast, primary amebic meningoencephalitis due toNaegleria fowleri usually occurs in healthy, young individuals with a history of swimming in heated swimming pools, in manmade lakes or with recent contact with contaminated water and practising water-related sports. Subclinical infections due to free-living amebas are probably common in healthy individuals with the protozoa living as “normal flora” in the nose and throat. It is possible that in humans, antibodies and cell-mediated immunity protect the host in such ordinary circumstances against invasive infection. In debilitated and chronically ill individuals,

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depressed cellmediated immunity may allow these protozoa to proliferate, allowing a fulminant “opportunistic” infection to develop. In the case of acanthamoebic keratitis, it is important to keep in mind that the temperature and moist environment of the eye serve as a good medium for the growth and proliferation of the amebas and is not necessarily associated with immunosuppression but rather with trauma. This review confirms that opportunistic free-living amebic infections occur with increased frequency in patients treated with steroids, radiotherapy, chemotherapeutic drugs or with broad-spectrum antibiotics and suggest that the mechanism of such infection may be depressed cell-mediated immunity or some other alteration of the immune system, like acquired immunodeficiency syndrome (AIDS).

Sharma, S., Ramachandran L, 1995. Adherence of cysts and trophozoites of Acanthamoeba to unworn rigid gas permeable and soft contact lenses.CLAO J; 21: 247-451.

CLAO J. 1995 Oct;21(4):247-51.Adherence of cysts and trophozoites of Acanthamoeba to unworn rigid gas permeable and soft contact lenses.Sharma S, Ramachandran L, Rao GN.SourceLate Sri Devchand Nagardas Jhaveri Microbiology Centre, Hyderabad, India.

AbstractContact lens related Acanthamoeba keratitis has been more often associated with the use of soft contact lenses than with the use of rigid gas permeable (RGP) contact lenses. We studied the adherence of Acanthamoeba cysts and trophozoites to unworn RGP (silicone acrylate and fluoropolymer) and low and high water content soft contact lenses marketed in India. A human corneal isolate of Acanthamoeba polyphaga suspended in saline (1 x 10(5) amoebae/mL) was used. Lens segments were exposed to A. polyphaga cysts or trophozoites with or without shaking. After exposure for zero to 7 hours, lenses were

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either washed or not washed and the adherence was determined using light microscopy and a hemocytometer (per square millimeter of the lens). Both cysts and trophozoites immediately adhered to all four types of lenses. Adhesion increased with an increase in exposure time. The number of adherent cysts and trophozoites was higher (P = 0.043-0.0003) in the unwashed group of lenses at all exposure times for all lenses. Among washed groups, adherence was greatest with RGP silicone acrylate and high water content soft lenses. Trophozoites of Acanthamoeba showed greater adherence to RGP lenses, whereas cysts showed greater adherence to high water content soft lenses. Shaking did not have a significant effect on adherence. Adhesion of Acanthamoeba to contact lenses may play an important role in the pathogenesis of Acanthamoeba keratitis.

Rahayu, T., 2011. Tak Semua Orang Cocok Pakai Lensa Kontak. http://www.go4healthylife.com/articles/4567/1/Tak-Semua-Orang-Cocok-Pakai-Lensa-Kontak/Page1.html. Diakses tanggal 15 Januari 2012

Tak Semua Orang Cocok Pakai Lensa Kontak•  Redaksi Go4HealthyLife.com 11 Juli 2011 Useful Articles Belum ada Rating

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Go4HealthyLife.com, Jakarta – Lensa kontak untuk sebagian orang lebih nyaman dan praktis dikenakan dibandingkan mengenakan kacamata untuk mengoreksi penglihatan. Namun tak semua orang bisa menggunakan lensa kontak.

“Orang dengan mata yang sedang mengalami infeksi dan atau peradangan aktif sebaiknya tidak menggunakan lensa kontak,” Dr Tri Rahayu, SpM, FIACLE dalam acara bincang media tentang keamanan penggunaan lensa kontak yang diselenggarakan Ciba Vision di Bunga Rampai Jakarta, Senin (11/7). "Mereka yang mengalami kontra indikasi relatif juga perlu pengawasan secara hati-hati jika ingin mengenakan lensa kontak.”

Kepala Divisi Refraksi dan Lensa Kontak Departemen Mata FKUI-RSCM lebih lanjut menjelaskan mereka yang dikategorikan dengan kontra indikasi relatif antara lain yang mengalami gangguan mata kering dan atau orang dengan gangguan perabaan, seperti kepekaan kornea yang berkurang.

“Untuk mereka yang mengalami mata kering ringan masih diperbolehkan menggunakan kontak lensa tapi dengan pengawasan ketat. Namun jika gangguan mata kering berat maka tidak disarankan memakai lensa kontak. Pakai saja kacamata,” saran Dr Tri.

Sementara mereka yang kepekaan korneanya berkurang sebaiknya menghindari lensa kontak karena jika terjadi sesuatu yang tidak nyaman dengan korneanya bisa berbahaya. "Terlambat menyadari adanya rasa tidak nyaman pada kornea bisa berakibat buruk," ujarnya.

Berkurangnya kepekaan kornea umumnya disebabkan oleh sejumlah penyakit saraf di wajah, dtroke ringan, namun jarang terjadi akibat bawaan lahir.

Dr Tri mengingatkan untuk tidak sembarangan menggunakan lensa kontak, apalagi asal beli untuk sekadar bergaya tanpa terlebih dahulu memeriksakan kondisi mata.

Disarankan  selama pemakaian lensa kontak sebaiknya lakukan pemeriksaan rutin setiap 6 bulan sekali. “Namun jika ada keluhan, jangan tunggu sampai 6

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bulan, segera hubungi dokter mata terdekat,” tandas Dr Tri.