Early Deep Anterior Lamellar Keratoplasty (DALK) for Acanthamoeba Keratitis Poorly Responsive to Medical Treatment.

PURPOSE: To evaluate the success (eradication of infection) or failure (recurrence of infection in the cornea or sclera, or endophthalmitis) of early therapeutic deep anterior lamellar keratoplasty (DALK) for active Acanthamoeba keratitis (AK) poorly responsive to medical treatment. METHODS: Retrospective, noncomparative case series of 11 patients (11 eyes) affected by active AK poorly responsive to medical treatment who underwent early therapeutic DALK. Surgery was performed in all cases within 30 to 60 days from the onset of symptoms. Corneal ulcer depth was less than 300 µm in all cases. A 3-drug combination (chlorhexidine gluconate, propamidine isethionate, and neomycin sulfate) was the antiamoebic protocol used preoperatively and postoperatively. Cannula big bubble and "layer-by-layer" manual dissection techniques were performed. Eradication of infection, episodes of rejection, postoperative endothelial cell density, and the best spectacle-corrected visual acuity were evaluated. Histologic examination of surgical margins was performed, and margin clearance was assessed. Mean follow-up was approximately 2 years. RESULTS: Four descemetic DALK and 7 predescemetic DALK were performed. One small Descemet membrane rupture occurred. Peripheral surgical margins were free of infection in all cases. Deep surgical margins not free from infection were found in 2 cases. However, no episode of infection recurrence was observed. The postoperative average best spectacle-corrected visual acuity was 0.8 (range, 0.6-1.0). No case of rejection was recorded. CONCLUSIONS: Early therapeutic DALK could be considered a new approach to eradicate active infection in AK cases poorly responsive to medical treatment, with significant ulcer in the optical zone. Further studies are needed to validate this new indication for DALK.

Persistent corneal edema secondary to presumed dead adult filarial worm in the anterior chamber.

We present three cases of persistent corneal edema secondary to presumed dead adult filarial worms lying in the anterior chamber with their attachment to the endothelium. Two of them were initially diagnosed as descemet's fold with corneal edema. Two patients underwent penetrating keratoplasty and in one case, surgical removal was partly possible with clearing of cornea.

Failure of Acanthamoeba castellanii to produce intraocular infections.

PURPOSE: This study examined possible mechanisms to explain why Acanthamoeba castellanii remains restricted to the cornea and rarely produces intraocular infections. The first hypothesis proposed that trophozoites cannot penetrate Descemet's membrane and the corneal endothelium to enter the anterior chamber (AC). The second hypothesis proposed that the trophozoites can enter the AC; however, the aqueous humor (AH) contains factors that either induce encystment or kill the amoebae. METHODS: Descemet's membrane was isolated from pig corneas and was used to determine whether Acanthamoeba trophozoites could penetrate this membrane in vitro. In addition, the capacity of trophozoites to survive in AH was determined in vitro. Trophozoites (10(6)) were injected into the AC of hamster eyes, and the number of amoebae in the AC was determined by histopathology 1 to 15 days later. RESULTS: The amoebae penetrated Descemet's membrane within 24 hours of in vitro culture. Penetration was prevented by addition of serine protease inhibitors or a chicken monoclonal antibody against the Acanthamoeba serine protease MIP-133. Although AH induced encystment of the amoebae, cysts remained viable. Injection of amoebae into the AC induced a robust neutrophil infiltrate, which was associated with complete clearance by day 15 after AC injection. CONCLUSIONS: The findings suggest that A. castellanii is capable of penetrating Descemet's membrane and entering the AC. However, a robust neutrophil response is associated with the disappearance of intraocular trophozoites and suggests that cells of the innate immune apparatus are important in preventing Acanthamoeba keratitis from progressing to become an intraocular infection.

[Post-varicella keratoendothelitis]. / Cheratoendotelita postvaricela.

The female patient, convalescent after varicella, presented in the tenth day after disappearance of the cutaneous eruption the first ocular symptoms with perikeratic congestion, endothelial precipitations, folds of the Descemet membrane, thick stroma, endothelial edema with appearance like keratoendothelitis. Ocular manifestations in varicella are produced through sanguine circulation of the virus like a varicella uveitis. The paper insists on various ocular manifestations in varicella.