Clostridium perfringens endophthalmitis after penetrating keratoplasty with contaminated corneal allografts: a case series.

PURPOSE: To report the postoperative clinical course of 3 patients who underwent corneal transplantation with corneal allografts contaminated with Clostridium perfringens and to evaluate the risk factors for anaerobic contamination in 2 donors. METHODS: Patient records and adverse reaction reports from a single eye bank related to cases of posttransplant C. perfringens endophthalmitis were reviewed. Records regarding the mated corneas, donor autopsy reports, and other pertinent data were also reviewed. RESULTS: Three adverse reactions associated with transplantation of corneal allografts contaminated with C. perfringens were reported. Two cases were from mated corneas. Both patients developed fulminant endophthalmitis after undergoing uncomplicated penetrating keratoplasty and required subsequent enucleation. Another isolated case (with no adverse reaction in the mate cornea) developed hypopyon postoperatively that resolved with intravitreal and topical antibiotics. Possible risk factors for anaerobic tissue contamination in the donors included illicit drug use in the first donor and exposure to sewage at the time of death in the second donor. CONCLUSIONS: Clostridial endophthalmitis is an aggressive rapidly progressive infection with potentially poor visual outcomes that can be transmitted from infected corneal allografts. Further investigation is needed to clarify the role of anaerobic donor rim cultures and the donor risk factors associated with recovering corneal allograft tissue contaminated with C. perfringens.

Conjunctival papilloma.

Conjunctival papillomas are some of the most common tumors of the conjunctiva and are well-described in ophthalmology textbooks. However, they have not be well-recognized by the dermatologic community. These lesions may be encountered by the dermatologist during a full skin examination or they may be the presenting concern of a patient.

Retinal toxicity of chloroquine hydrochloride administered by intraperitoneal injection.

Chloroquine is quinolone derivative known to exert dose-related retinal toxicity, albeit in a variable manner. It is thought that variability in the presentation of chloroquine retinopathy may be the result of perturbations in drug bioavailability subsequent to oral ingestion. In order to better understand the ramifications of bioavailability on the development of retinal injury subsequent to chloroquine use, this study investigated the relationship between retinal injury and chloroquine administration via intraperitoneal rather than oral administration. Four-week-old C57/6J mice underwent daily intraperitoneal injection of 10 mg kg(-1) chloroquine hydrochloride for a total of 62 days. Following treatment, tissue was fixed in preparation for analysis by light and transmission electron microscopy. Treated animals demonstrated marked abnormality of the outer retinal layers described as complete loss of the outer plexiform layer as well as photoreceptors and photoreceptor nuclei. The retinal pigmented epithelium demonstrated focal atrophy, loss of nuclei and pigment irregularity. Findings in the inner retina were notable for the loss of Müller cells and the presence of membranous cytoplasmic bodies. Retinae of control animals were entirely normal. In contrast to previous studies in the murine model examining chloroquine retinopathy subsequent to oral administration, this study suggests that intraperitoneal chloroquine administration facilitates retinal toxicity, presumably due to heightened drug absorption and bioavailability. It is posited that an increased rate of drug accumulation within the retina leads to an enhanced lysosomotrophic drug effect due to inability of the lysosome to compensate for chloroquine-induced elevation in pH through re-acidification of the intra-lysosomal content.

Noninvasive diagnosis of epithelial downgrowth after penetrating keratoplasty using immunohistochemical analysis of resected corneal buttons.

PURPOSE: To describe a noninvasive technique that can be used to support a clinically suspected diagnosis of epithelial downgrowth in patients who have previously undergone penetrating keratoplasty (PK). METHODS: Previously resected corneal buttons of 14 patients who developed signs suggestive of epithelial downgrowth after PK were examined retrospectively using immunohistochemical analysis to determine if occult epithelial cells were in fact present on the posterior surface of the cornea. Many of these patients were diagnosed with pseudophakic corneal edema or graft failure and had undergone multiple intraocular surgical procedures. In all cases, the initial histopathologic evaluation did not disclose the presence of epithelial cells using light microscopy after standard handling and staining techniques. Fourteen age- and diagnosis-matched control specimens were also examined. RESULTS: Thirteen of 14 specimens (92.9%) exhibited positive staining with anti-keratin AE1/AE3 markers, indicating that epithelial cells were already present on the endothelial surface at the time of the original PK. None of the control specimens displayed positive staining of the retrocorneal surface. CONCLUSION: Retrospective immunohistochemical analysis of corneal specimens can establish the diagnosis of epithelial downgrowth in a noninvasive manner. Early diagnosis may allow for this condition to be treated more successfully if aggressive intervention is undertaken. Alternatively, it may spare the patient from additional (and potentially futile) intraocular surgery. In the clinical setting of suspected epithelial downgrowth, ophthalmic pathologists should re-evaluate PK specimens from patients initially diagnosed with pseudophakic corneal edema or graft failure.

Toxicity and dose-response studies of 1alpha-hydroxyvitamin D2 in a retinoblastoma xenograft model.

BACKGROUND: Although calcitriol (1,25-dihydroxycholecalciferol) and vitamin D(2) inhibit retinoblastoma growth in the athymic (nude) mouse xenograft (Y-79 cell line) model of retinoblastoma, they can cause severe toxicity. OBJECTIVE: To examine the toxicity of and dose-dependent response for the inhibition of tumor growth for 1alpha-hydroxyvitamin D(2) (1alpha-OH-D(2)), an analogue with reduced systemic toxicity, in the athymic Y-79 mouse model. METHODS: Mice were randomized into treatment and control groups for 5-week toxicity and dose-response studies. Treatment was via oral gavage 5 times per week. Dose-response studies measured tumor inhibition and drug serum levels. Tumor size and body weight were measured weekly together with various criteria for toxicity. Animals were euthanized at the end of the treatment period. Tumors and kidneys were harvested, and serum was analyzed for calcium and drug levels. RESULTS: Doses of 0.1 to 1.2 microg/d were selected on the basis of toxicity studies for the dose-response trial. Tumor weight and volume in the 0.2-microg and 0.3-microg doses were significantly lower than in controls. Mortality rates and kidney calcification in mice treated with doses of 0.1 to 0.3 microg were lower than those observed in studies of calcitriol and vitamin D(2). CONCLUSION: A vitamin D analogue, 1alpha-OH-D(2), inhibits tumor growth in this xenograft model of retinoblastoma with less toxicity than calcitriol and vitamin D(2).