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Background Corneal ulcer or keratitis is defined as a loss of corneal epithelium with underlying stromal infiltration and suppuration associated with signs of inflammation. Corneal blindness is a significant public health problem worldwide; infectious keratitis is one of the predominant preventable causes of blindness. Several studies have evaluated microbial infectious keratitis's etiology, management, and outcome. However, there are regional variations in corneal ulcers' prevalence, risk factors, and outcome. The objective of this study was to isolate and identify the bacterial, fungal, viral, and protozoal etiological organisms causing infectious corneal ulcers along with their prevalence and antimicrobial sensitivity pattern. Methods A prospective observational study was done in the Department of Microbiology and RIO, Medical College & Hospital, Kolkata, for a period of 1 year (February 2019 to January 2020) after obtaining clearance from the Institutional Ethics Committee. Informed consent, demographic data, history of disease onset, duration of symptoms, associated co-morbidities, etc., were taken from the patients fulfilling the inclusion criteria. Corneal scraping samples were collected sterilely to detect bacterial, fungal, parasitic, and viral isolates and identified by standard laboratory procedures. Results A total of 80 patients were included in the study. The risk factors included foreign body in 24 (30%), blunt trauma in 10 (12.5%), steroid use in 8 (10%), contact lens user 4 (5%), and spontaneous in 34 (42.5%). Among these 80 patients, 18 showed growth of bacteria, including Staphylococcus aureus, Streptococcus pneumoniae, Streptococcus pyogenes, and Pseudomonas aeruginosa; four had growth of fungi, including Aspergillus spp. and Fusarium spp, and two were positive for Herpes simplex virus by IFA. Conclusion Early diagnosis and prompt keratitis treatment are critical for preventing visual loss. The identification of the various causative agents of keratitis is essential for the proper management of the cases.
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PURPOSE: Retinal nerve fibre layer (RNFL) is a sensitive structure, which is affected by anaemia due to hypoxia. A timely detection of RNFL thinning may aid preventing devastating complications. Optical coherence tomography (OCT) measures RNFL thinning with accuracy and helps in detecting thinning of the retinal layer in anaemic patients. This study was destined to evaluate thinning of RNFL in anaemic patients and their correlation with the haemoglobin level. METHODS: It was a prospective comparative study. Total of 151 patients were included in this study. Patients with retinal diseases were excluded from this study. After initial evaluation, haematological and ophthalmological parameters were measured. RNFL was measured with OCT and corroborated with the Hb level and analysed accordingly. EPI and SPSS softwares were used for detail analysis and the correlation between RNFL thinning and the Hb level. Initially, each eye was separately assigned a value (0, 1, and 2) (normal, borderline, and abnormal, respectively) as per the severity of thinning, and then, the sum of the scores of both eyes were considered as a separate variable, and a multiple linear regression analysis was performed with the independent variables. RESULTS: RNFL thinning was found to be significant in each group of patients. There was a strong correlation of RNFL thinning with degree of anaemia. CONCLUSIONS: Thalassaemia, iron deficiency anaemia, and anaemia of chronic diseases are associated with the significant damage to RNFL. Degree of anaemia is the most important parameter for such thinning of the RNFL layer.
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Although the mechanism of action of topiramate is not fully understood, its anticonvulsant properties may result, at least in part, from an interaction with AMPA/kainate receptors. We have recently shown that topiramate selectively inhibits postsynaptic responses mediated by GluR5 kainate receptors. To determine if this action of topiramate is relevant to the anticonvulsant effects of the drug in vivo, we determined the protective activity of topiramate against seizures induced by intravenous infusion of various ionotropic glutamate receptor agonists in mice. Topiramate (25-100 mg/kg, i.p.) produced a dose-dependent elevation in the threshold for clonic seizures induced by infusion of ATPA, a selective agonist of GluR5 kainate receptors. Topiramate was less effective in protecting against clonic seizures induced by kainate, a mixed agonist of AMPA and kainate receptors. Topiramate did not affect clonic seizures induced by AMPA or NMDA. In contrast, the thresholds for tonic seizures induced by higher doses of these various glutamate receptor agonists were all elevated by topiramate. Unlike topiramate, carbamazepine elevated the threshold for AMPA- but not ATPA-induced clonic seizures. Our results are consistent with the possibility that the effects of topiramate on clonic seizure activity are due to functional blockade of GluR5 kainate receptors. Protection from tonic seizures may be mediated by other actions of the drug. Together with our in vitro cellular electrophysiological results, the present observations strongly support a unique mechanism of action of topiramate, which involves GluR5 kainate receptors.