Protracted Aspergillus versicolor endophthalmitis caused by corneal microperforation.

BACKGROUND: Here we describe the characterization of a protracted Aspergillus versicolor endophthalmitis caused by a corneal microperforation. HISTORY AND SIGNS: A 58-year-old patient noticed blurred vision two weeks after he was hit in the eye by an old cable in a dilapidated house. A traumatic cataract and an intraocular inflammation were diagnosed and treated elsewhere with phacoemulsification and anti-inflammatory drugs. Vitreous samples were sterile. Despite topical steroids visual acuity continued to decrease and the patient presented in Lausanne 6 months later with a visual acuity of counting fingers, major inflammation of the anterior segment and a small corneal scar. Fundus examination revealed massive vitreous inflammation with a voluminous whitish chorioretinal infiltrate temporally. THERAPY AND OUTCOME: Vitrectomy with dissection of a protuberant epiretinal filamentous tissue in the temporal fundus was performed, and Amikacine, Vancomycine and Amphothericine were injected intravitreally. Bacteriological work-up revealed Aspergillus versicolor. Visual acuity improved to 0.2 with topical steroids and oral antifungal drugs. CONCLUSIONS: Corneal microperforations may cause a protracted endophthalmitis due to Aspergillus versicolor, a rare fungus, which is commonly found in insulation materials and cables in dilapidated houses.

Pneumococcal meningitis induces apoptosis in recently postmitotic immature neurons in the dentate gyrus of neonatal rats.

Bacterial meningitis is associated with high rates of morbidity and mortality, despite advances in antibiotic therapy. Meningitis caused by Streptococcus pneumoniae is associated with a particularly high incidence of neurological sequelae including deficits resulting from damage to the hippocampus. Previous studies have documented that in neonatal rats with experimental pneumococcal meningitis, cells in the subgranular layer of the dentate gyrus undergo apoptosis. The aim of the present study was to define in more detail the nature of the dying cells in the dentate gyrus. Using bromodeoxyuridine labeling at different times before infection combined with immunocytochemistry, we identified the vulnerable cells as those which underwent mitosis 6-10 days before infection. A majority of these cells are of neuronal lineage. Thus, immature neuronal cells several days after the last cell division are preferentially triggered into apoptosis during pneumococcal meningitis. The loss of these cells may contribute to the long-lasting impairment of hippocampal function identified in animal models and in humans after bacterial meningitis.

Re-emergence of hidden residual intraocular silicone oil bubble after previous silicone oil removal.

BACKGROUND: We describe the re-emergence of a hidden residual intraocular silicone oil bubble after previous silicone oil removal. HISTORY AND SIGNS: A 57-year-old patient underwent vitrectomy with silicone oil for a complicated retinal detachment. Six weeks later silicone oil was removed via the pars plana and phakoemulsification with lens implantation was performed. Subsequent clinical follow-up showed an attached retina without residual silicone oil bubbles. However, more than 2 years later the patient suffered sudden visual loss. Clinical examination showed a bubble of silicone oil wedged between a remaining layer of anterior vitreous and the capsular bag, reducing central visual acuity. THERAPY AND OUTCOME: Complete extraction of the silicone oil bubble was performed via the pars plana. CONCLUSIONS: Residual silicone oil bubbles may wedge themselves into vitreous pockets in the ophthalmoscopically invisible regions of the pars plana. Over time these bubbles may migrate into the retrolental space with obstruction of the visual axis.

Oxidative stress in brain during experimental bacterial meningitis: differential effects of alpha-phenyl-tert-butyl nitrone and N-acetylcysteine treatment.

Antioxidant treatment has previously been shown to be neuroprotective in experimental bacterial meningitis. To obtain quantitative evidence for oxidative stress in this disease, we measured the major brain antioxidants ascorbate and reduced glutathione, and the lipid peroxidation endproduct malondialdehyde in the cortex of infant rats infected with Streptococcus pneumoniae. Cortical levels of the two antioxidants were markedly decreased 22 h after infection, when animals were severely ill. Total pyridine nucleotide levels in the cortex were unaltered, suggesting that the loss of the two antioxidants was not due to cell necrosis. Bacterial meningitis was accompanied by a moderate, significant increase in cortical malondialdehyde. While treatment with either of the antioxidants alpha-phenyl-tert-butyl nitrone or N-acetylcysteine significantly inhibited this increase, only the former attenuated the loss of endogenous antioxidants. Cerebrospinal fluid bacterial titer, nitrite and nitrate levels, and myeloperoxidase activity at 18 h after infection were unaffected by antioxidant treatment, suggesting that they acted by mechanisms other than modulation of inflammation. The results demonstrate that bacterial meningitis is accompanied by oxidative stress in the brain parenchyma. Furthermore, increased cortical lipid peroxidation does not appear to be the result of parenchymal oxidative stress, because it was prevented by NAC, which had no effect on the loss of brain antioxidants.

Marked elevation in cortical urate and xanthine oxidoreductase activity in experimental bacterial meningitis.

Experimental bacterial meningitis due to Streptococcus pneumoniae in infant rats was associated with a time-dependent increase in CSF and cortical urate that was approximately 30-fold elevated at 22 h after infection compared to baseline. This increase was mirrored by a 20-fold rise in cortical xanthine oxidoreductase activity. The relative proportion of the oxidant-producing xanthine oxidase to total activity did not increase, however. Blood plasma levels of urate also increased during infection, but part of this was as a consequence of dehydration, as reflected by elevated ascorbate concentrations in the plasma. Administration of the radical scavenger alpha-phenyl-tert-butyl nitrone, previously shown to be neuroprotective in the present model, did not significantly affect either xanthine dehydrogenase or xanthine oxidase activity, and increased even further cortical accumulation of urate. Treatment with the xanthine oxidoreductase inhibitor allopurinol inhibited CSF urate levels earlier than those in blood plasma, supporting the notion that urate was produced within the brain. However, this treatment did not prevent the loss of ascorbate and reduced glutathione in the cortex and CSF. Together with data from the literature, the results strongly suggest that xanthine oxidase is not a major cause of oxidative stress in bacterial meningitis and that urate formation due to induction of xanthine oxidoreductase in the brain may in fact represent a protective response.