This presentation is on infective keratitis. Infective keratitis is a common sight threatening condition encountered by ophthalmologists in the acute setting. A wide variety of pathogens and host responses may be involved. Prompt diagnosis and management is required to prevent significant ocular morbidity and visual loss. The spectrum of infective keratitis includes bacteria, fungal, parasital, and viral keratitis. For assessment, we begin with history taking. The symptoms of infective keratitis include an acute red eye, pain, tearing, photophobia, discharge, and blurring of vision. You should note the onset and duration of symptoms. And some cases of the infective keratitis may present insidiously. The risk factors for infective keratitis may be divided into ocular or systemic risk factors. Ocular risk factors include trauma, contact lens use, Iatrogenic causes, poor cooler surface, or lid disease. Systemic risk factors include immunosuppression or nutritional cause. In examination, we should always include the visual acuity and characteristics of the infective lesion. You should note whether the lesion is single or multiple, the signs of the infiltrate and associated epithelial defect, the location, the depth, the amount of stromal inflammation, and any other characteristic features which may suggest the underlying etiology. You should look out for complications such as significant corneal thinning, perforation, limbal and scleral involvement, severe intraocular inflammation, and endophthalmitis. You should also look out for predisposing ocular factors, such as poor ocular surface, lid disease and exposure, reduced cornea sensation, and any signs of corneal trauma and surgery. For investigation there should always be photography documentation. Early and adequate corneal scrapes should be performed. These include gram stain, blood and chocolate agar, Sabouraud’s medium, thioglycolate, and brain-heart infusion broth. The contact lens and cases should also be sent for culture. Specialized stains, culture mediums, and imaging modalities specific to the organisms may also be performed. In the management of a patient with infective keratitis, we must first obtain samples for identification of the infective organism. Empirical broad spectrum topical antimicrobials should be started. Systemic treatment is indicated if there is impending or actual perforation, limbal or scleral involvement, risk of intraocular extension in deep infections, and history of prior intraocular penetration. We should always monitor progress and watch for complications. The culture results should be considered and treatment modified as necessary. Surgical intervention is reserved as a last resort for severe infections refractory to maximal medical therapy for extended periods of time. Bacterial keratitis is the most common cause of infective keratitis. There is often rapid onset and disease progression. The pathophysiology involves, firstly, a disruption of corneal epithelial barrier, entrance and proliferation of bacteria and stroma with release of proteases, migration of neutrophils into the cornea from limbal vasculature and tear film, and lastly, the release of metalloproteinases break down extracellular matrix, causing inflammatory necrosis. The spectrum of organisms may be gram positive, gram negative, or atypical mycobacteria. Common gram positive organisms include staphylococcus aureus, staphylococcus, epidermis, streptococcus pneumoniae, and bacillus. In staphylococcal infections, there is usually a round, well-circumscribed white or yellow-white stromal infiltrate with distinct borders. The surrounding cornea is usually clear. In streptococcal infections, there’s usually a serpinginous ulcerative keratitis with hypopyon. And in bacillus cereus infections, there is an association with soil-contaminated injury, and there’s often rapid progression to ring ulcer with deep abscess formation. Gram negative organisms include pseudonomas aeruginosa, neisseria gonorrhoeae. And other less common organisms include Moraxella, Proteus, Klebisella, and Escherichia coli. In pseudonomal infection, there’s often a central suppurative keratitis with surrounding ground glass appearance, and is associated with a history of contact lens wear or trauma. In neisseria gonorrhoeae infection, there is rapidly progressive conjunctivitis and fulminant keratitis. The organism is capable of penetrating intact and causing stromalysis with acute perforations. It is sexually transmitted in adults, and an important cause of ophthalmia neonatorum. Atypical mycobacterium includes mycobacterium fortitum and mycobacterium chelonei. They cause an intractable recalcitrant post-traumatic keratitis and requires staining for acid fast baccili Lowenstein-Jensen medium for culture, The management of bacterial keratitis involves the use of broad spectrum topical antibiotics. There should be an intensive loading dose for 48 to 72 hours and gradual taper according to response and culture. The common agents in use include fortified cefazolin and gentamicin. Monotherapy with fluoroquinolones, such as ciprofloxacin and levofloxacin may also be considered in small peripheral ulcers. Oral antibiotics should be considered in selective cases, and cycloplegis may be considered for pain relief. Anti-inflammatory medications may also be used. However, the role of steroids is controversial. Fungal keratitis is a major ophthalmic problem in warm, tropical climates. Fungus can be classified into filamentous, yeast, or dimorphic fungus. The risk factors include ocular trauma, especially vegetative or soil-contaminated injuries; inappropriate use of topical steroids; local, ocular, or systemic immunosuppression. The inflammatory manifestations of fungal keratitis are usually milder than those in bacterial keratitis in initial phase. There can be progression to intense inflammation subsequently. Yeast infections commonly occur in immunosuppressed eyes with structural abnormalities. There’s usually a whitish infiltrate, which may be more superficial than that seen in filamentous fungal infections. There may also be crystalline keratopathy. Tremendous fungal keratitis is often trauma related. There’s usually a deep grey-white infiltrate with irregular feathery borders, satellite lesions, and endothelial plaques. Investigations include special stains, such as Periodic Achid-Schiff, Giemsa, Acridine orange, cultures such as Sabouraud’s, molecular diagnostic techniques, such as PCR, and corneal biopsy. In the management of fungal keratitis, topical antifungal therapy is started hourly initially, then tapered over six to eight weeks. Adjunctive systemic therapy may be considered in severe disease. Superficial corneal debridement may be useful in improving drug penetration and removal of inciting organisms. Anti-fungal agents may be divided into polyenes, which include Amphotericin B, and Natamycin; azoles, which include Voriconazole, Ketoconazole, and fluconazole; and fluorinated pyrimidines, such as Flucytosine. In Acanthamoeba keratitis, the free-living amoeba found in tap water, swimming pools, fresh water and soil is involved. The two forms include active trophozoites, which produce enzymes which aid tissue penetration and destruction, and dormant cysts, which are resilient and able to survive in unfavorable conditions. A major risk factor is contact lens wear, especially with exposure to contaminated water. Clinical features of Acanthamoeba keratitis include heat, epithelial irregularity, punctate epithelial erosions, radial keratoneuritis– in advanced cases, a grey-white diffuse stromol infiltrate with overlying epithelial defect, which may progress to ring infiltrate and stromal melt. Other findings may include scleritis, uveitis, and hypopyon. The investigations for Acanthamoeba keratitis include microscopy, with special stains, such as Calcofluor white and Giemas, culture with non-nutrient agar with E coli overlay. In vivo confocal microscopy may be used to detect cysts and trophozoites. And corneal biopsy may be considered in culture negative and medically unresponsive cases. In the management of Acanthamoeba keratitis, early diagnosis and treatment is key. Treatment is often prolonged and clinical relapse common. This involves the use of intensive topical antiamoebic agents, such as Biguanide, aromatic diamidines, aminoglycosides, and imidazoles. Viral keratitis may include herpes simplex keratitis or herpes zoster ophthalmicus, which is caused by the herpes simplex virus and Varicella zoster virus , respectively. Herpes simplex keratitis is usually caused by HSV-1 virus and, less commonly, HSV-2. Primary infection usually occurs in childhood through skin and nucleus membrane contact with oral lesions and secretions. Clinical features may include fever, malaise, flu-like symptoms, oro-facial, ocular, or systemic manifestations. The virus then ascends via the sensory nerve axons to establish a dormant infection in the corresponding ganglia. In recurrent disease, viral reactivation occurs when the virus travels along the nerve axon to the sensory nerve endings, and then to the epithelium, where it replicates. Potential triggers include sunlight, trauma, surgery, heat, infectious disease, or emotional stress. Herpes simplex keratitis may be classified according to the layer of cornea, which is predominantly affected. Epithelial disease is due to active viral infection. Non-necrotizing stromal disease, endothelial disease, and uveitis are immune mediated. Necrotizing stromal keratisis involves both a severe inflammatory response and active viral replication. In epithelial keratitis, there are punctate epithelial erosions, with terminal end bulbs, branching dendrites with borders lined by swollen epithelial cells– which stains with the rose Bengal– and an ulcerated base, which stains with fluorescein. The affected areas may coalesce and enlarge to form a more expansive geographic ulcer. In necrotizing stromal keratitis, there is a dense white necrotic stromal infiltrate, with overlying epithelial defect, progressive thinning and perforation, and stromal vascularization. In non-necrotizing, or interstitial keratitis, there is often unifocal or multi-focal stromal haze, stromal edema, anterior chamber reaction, with no overlying epithelial defect. In disciform endothelial keratitis, there’s a disc-shaped stromal and epithelial edema, usually involving the central cornea. there may be keratic precipitates, a mild anterior chamber inflammation, and Wessley’s ring. Your patients may also have a high intraocular pressure in the presence of trabeculitis. The management of herpes simplex keratitis is as follows. Epithelial disease is treated with topical antiviral agent, such as Acylovir ointment five times a day. Necrotizing stromal keratitis is treated with systemic antiviral therapy, with judicious use of low-dose topical steroids to control inflammation. In non-necrotizing stromal keratitis, topical steroids with systemic antiviral treatment is recommended. Similarly, in endothelial disease, topical steroids with systemic antiviral treatments is used. We should always monitor for response and complications, and also consider prophylaxis in selected patients. Complications may include recurrence of epithelial disease with topical steroid use, progressive corneal thinning and perforation, secondary bacterial infection, uveitiis and glaucoma. Lastly, prophylaxis should be considered in patients with frequent recurrences, ocular surface disease, patients who are only-eyed, and patients who have bilateral involvement. Herpes Zoster Ophthalmicus is due to the reactivation of Varicella zoster virus that resides in a latent form in the sensory trigerminal ganglion after primary chicken pox. The ophthalmic branch is most commonly affected. HZO usually occurs in healthy, elderly individuals. Always suspect immunodeficiency in a young patient with HZO. In Hutchinson’s sign, the nasociliary branch of V1 innervates the skin on the tip of the nose, as well as intraocular structures. Skin vesicles on the tip of the nose are associated with a high risk of ocular involvement. Ocular manifestations usually follow the acute skin rash by weeks. The ocular manifestations may be corneal or extra-corneal. The extra-conical features include conjunctivitis, episcleritis, scleritis, or sclerokeratitis, uveitis, retinitis, choroiditis, optic neuritis, or cranial palsies, encephalitis, and post-herpetic neuralgia. Corneal involvement in HZO includes epithelial keratitis. This occurs within the first few days of rash and resolve spontaneously a few days later. The clinical features include punctate epithelial erosions and pseudodendrites. Nominal keratitis may occur about 10 days after the onset of rash. They may multiple round granular sub-epithelial deposits surrounded by stromal haze. Disciform keratitis occurs three weeks after the onset of rash and is usually preceded by nummular keratitis. The clinical features are similar to HSV disciform keratitis. Lastly mucus plaque keratitis may occur three to six months after the onset of rash. There may be elevated mucus plaques that stained brightly with rose Bengal. They usually have a linear grey branching appearance. Other complications include neurotrophic keratitis, exposure keratopathy, secondary to cicatricial lid changes, and lipid keratopathy. The management of HZO involves the use of systemic antiviral therapy, such as oral acyclovir 800 milligrams five times a day. Intravenous acyclovir may be required if the patient is immunosuppressed. Epithelial disease is treated with topical acyclovir ointment and lubricants. Stromal, nummular, or disciform keratitis are treated with topical steroids. And lastly, mucus plaques may be treated with Antimucolytics. Thank you.