Keratitis, Herpes Simplex Introduction Background Herpes simplex virus (HSV) keratitis encompasses a variety of disease processes that HSV can cause in the human cornea. A variety of clinical manifestations of infectious and immunologic etiologies, such as infectious epithelial keratitis, neurotrophic keratopathy, necrotizing stromal keratitis, immune stromal keratitis (ISK), and endotheliitis, can affect all levels of the cornea. Although more common as a manifestation of recurrent HSV infection, HSV keratitis may also be seen during a primary infection. Pathophysiology
Keratitis, Fungal Introduction Background Fungal keratitis was first described by Leber in 1879. This entity is not a common cause of corneal infection, but it represents one of the major causes of infectious keratitis in tropical areas of the world. Considering fungus as a possible cause of infectious keratitis is important because devastating ocular damage can result if it is not diagnosed and treated promptly and effectively.
Keratitis, Bacterial Introduction Background Bacterial keratitis is a sight-threatening process. A particular feature of bacterial keratitis is its rapid progression; corneal destruction may be complete in 24-48 hours with some of the more virulent bacteria. Corneal ulceration, stromal abscess formation, surrounding corneal edema, and anterior segment inflammation are characteristic of this disease. Pathophysiology
Dystrophy, Map-dot-fingerprint Introduction Background Corneal map-dot-fingerprint dystrophy is by far the most common corneal dystrophy and is named from the appearance of its characteristic slit lamp findings. Map-dot-fingerprint dystrophy is also known as Cogan’s dystrophy, Cogan microcystic epithelial dystrophy, epithelial basement membrane dystrophy, and anterior basement membrane dystrophy.
Dystrophy, Macular Introduction Background Macular dystrophy is an autosomal recessive condition, which is the least common but the most severe of the 3 major stromal corneal dystrophies. It is characterized by multiple, gray-white opacities that are present in the corneal stroma and that extend out into the peripheral cornea.
Dystrophy, Lattice Introduction Background Lattice dystrophy usually is an autosomal dominant condition, and it is the most common of stromal dystrophies. Like granular and Avellino dystrophy, the genetic defect of lattice dystrophy has been mapped to the BIG H3 gene on chromosome 5q. Onset of the corneal changes usually occurs in the first decade of life, although patients may remain asymptomatic for years. Examination of the cornea in the second to third decade of life will reveal branching, refractile lattice…
Dystrophy, Granular Introduction Background Granular dystrophy is an autosomal dominant, bilateral, noninflammatory condition that results in deposition of opacities in the cornea by adulthood. It specifically affects the middle portion of the cornea (stroma) and eventually can cause decreased vision and eye discomfort. Severe cases of granular dystrophy can be treated with either excimer laser ablation or by replacing cornea (corneal transplant). Pathophysiology
Dystrophy, Fuchs Endothelial Introduction Background Fuchs endothelial dystrophy is characterized by an asymmetrical, bilateral, slowly progressive edema of the cornea in elderly patients. When inherited, the transmission is autosomal dominant. The root cause of the condition is a slowly progressive formation of guttate lesions between the corneal endothelium and the Descemet membrane. These wartlike, anvil- or mushroom-shaped excrescences are said to be abnormal elaborations of basement membrane and fibrillar collagen by distressed or dystrophic endothelial cells. As the lesions enlarge,…
Dystrophy, Crystalline Introduction Background Schnyder crystalline corneal dystrophy (SCCD) is a rare autosomal dominant stromal dystrophy that is characterized by bilateral corneal opacification, resulting from an abnormal accumulation of cholesterol and lipid. The causative gene for this disease is UBIAD1, which is present on 1p36. The gene is involved in cholesterol metabolism. Van Went and Wibaut first described crystalline dystrophy in the Dutch literature in 1924, and it was delineated further by Schnyder in the Swiss literature in 1929.1,2
Dermoid, Limbal Introduction Background Limbal dermoids are benign congenital tumors that contain choristomatous tissue (tissue not found normally at that site). They appear most frequently at the inferior temporal quadrant of the corneal limbus. However, they may occasionally present entirely within the cornea or may be confined to the conjunctiva. They may contain a variety of histologically aberrant tissues, including epidermal appendages, connective tissue, skin, fat, sweat gland, lacrimal gland, muscle, teeth, cartilage, bone, vascular structures, and neurologic tissue, including…