Chronic microsporidial stromal keratitis in an immunocompetent, non-contact lens wearer.

An 82-year-old healthy man with unilateral chronic stromal keratitis, initially diagnosed to have viral keratitis and refractory to medical therapy, showed numerous oval, microsporidial organisms, measuring 4-5 m in length in the corneal biopsy. Penetrating keratoplasty, followed by treatment with systemic albendazole and topical propamidine isethionate resulted in resolution of the infection. Electron microscopy of the keratoplasty specimen demonstrated sporoblasts with diplokaryotic nuclei and multiple coils of the filament. The light and electron microscopic features were consistent with microsporidial keratitis.

Acanthamoeba adherence to soft contact lens and human corneal stroma.

In the present study, the adhesibility of Acanthamoeba castellani trophozoites and cysts to hydrogel contact lenses and to human cornea was investigated. Segments of unworn contact lenses were prepared (120 segments in total). In addition, 8 corneal buttons were obtained from 8 enucleated eyes. And each cornea cut into 8 radial segments. To these lens and corneal segments, 1.2 x 106/ml and 1.3 x 106/ml of cysts and trophozoites respectively were added under varying conditions. The adhesion was checked at 0, 3 and 24 hours after the exposure. Adhesion analysis showed that the trophozoites adhered equally well to lens or cornea. There is an increase in the number of trophozoites adhering to contact lenses as well as cornea. This difference is more significant for contact lenses. Washing of contact lenses significantly decreased the adherence of the trophozoites after 3 hours of incubation. When the comparison of adhesion was done between the unwashed worn and unwashed unworn contact lenses, it was observed that there was a significant difference in adherence to new lenses where the adherence was much lower. The study shows that washing of contact lenses does decrease the chances of colonization by Acantamoeba catellani and also that older lenses have higher chances of getting colonized probably due to the occurrence of scratches et. on the surface which may help in colonization.

Keratocyte loss in Acanthamoeba keratitis: phagocytosis, necrosis or apoptosis?

PURPOSE: Pathogenesis of Acanthamoeba keratitis involves breakdown of epithelial barrier, stromal invasion by Acanthamoeba, loss of keratocytes, inflammatory response and finally stromal necrosis. The loss of keratocytes, believed to be due to the phagocytic activity of the parasite, occurs disproportionate to and independent of the parasite load, thereby suggesting additional modes of cell loss. To test our hypothesis that the loss of keratocytes in Acanthamoeba keratitis is due to apoptosis, we did both histology and histochemistry on the corneal tissues. METHODS: Routine Haematoxylin and Eosin, Gomori's Methenamine Silver and Periodic acid Schiff stained sections of five corneal tissues from penetrating keratoplasty and eviscerated eyes were reviewed. TUNEL staining was done for morphological detection of apoptosis in three cases, using formalin-fixed, paraffin-processed tissues. RESULTS: Histological changes were epithelial ulceration, loss of keratocytes in all layers, inflammation in anterior two-thirds of the stroma with necrosis, and deeper quiet stroma. Acanthamoeba trophozoites were found in the anterior stroma while the cysts were more in the deeper stroma, with minimal or no inflammatory response. TUNEL staining was positive in keratocytic nuclei in all layers. CONCLUSIONS: This study demonstrates that one of the modes of keratocyte loss in Acanthamoeba keratitis is by apoptosis, possibly in addition to the necrotic process and phagocytic activity of the parasite. The death of inflammatory cells also appears to be mediated by apoptosis.