ABSTRACT
Purpose. To present a case of acute idiopathic maculopathy (AIM) and illustrate primary choroidal perfusion defect using multimodal imaging. Case Description. We report a case of a 24-year-old man with a paracentral scotoma of the right eye and recent flu-like illness. The patient was found to have a unilateral ovoid-shaped, placoid lesion just inferior to the fovea. Multimodal imaging confirmed findings most consistent with a diagnosis of acute idiopathic maculopathy (AIM). Serologic studies confirmed a strongly positive immunoglobulin G (IgG) titer for coxsackievirus A. Spectral-domain optical coherence tomography angiography (SD-OCTA) showed bilateral areas of vascular reduction at the level of the choriocapillaris and choroid, sparing the retinal circulation. Conclusions and Importance. The changes in outer retina and retinal pigment epithelium, classically described in AIM, are likely secondary to choroidal hypoperfusion.
ABSTRACT
This paper presents a case demonstrating repair of traumatic macular hole and submacular hemorrhage with intravitreal gas tamponade and t-PA in an office setting.
Subject(s)
Hemangioblastoma/diagnosis , Macula Lutea/pathology , Retinal Neoplasms/diagnosis , von Hippel-Lindau Disease/complications , Adolescent , Cervical Cord/pathology , Diagnosis, Differential , Hemangioblastoma/complications , Humans , Magnetic Resonance Imaging , Male , Predictive Value of Tests , Retinal Neoplasms/complications , Tomography, Optical Coherence , von Hippel-Lindau Disease/diagnosisABSTRACT
PURPOSE: To report a novel clinical finding associated with familial exudative vitreoretinopathy in three patients using fundus photography, fluorescein angiography, and histopathology. METHODS: Observational case series of three patients with familial exudative vitreoretinopathy, an ophthalmic examination with fundus photography, and fluorescein angiography were used to document clinical findings between January 2007 and January 2015. Surgical specimens from one case were examined using standard histopathologic techniques, as well as transmission electron microscopy and energy dispersive x-ray analysis. RESULTS: Distinctive white preretinal granules were noted in all cases and were found to be extramacular in location. Histopathology in one case revealed the granules to be crystalline structures with a regular pattern evident on higher magnification. The chemical constitution was found to be carbon, oxygen, and fluorine. CONCLUSION: Our case series represents the first description of white preretinal granules in association with familial exudative vitreoretinopathy. The authors have not seen these granules in other forms of retinopathy and their presence may aid in differentiating this disease from other entities.
Subject(s)
Retinal Diseases/pathology , Child , Eye Diseases, Hereditary , Familial Exudative Vitreoretinopathies , Female , Fluorescein Angiography , Fundus Oculi , Humans , Infant , Male , Retinal Diseases/diagnostic imagingABSTRACT
Enteroaggregative Escherichia coli (EAEC) is an important cause of acute and persistent diarrhea. The defining stacked brick adherence pattern of Peruvian EAEC isolate 042 has previously been attributed to aggregative adherence fimbriae II (AAF/II), which confer aggregative adherence on laboratory E. coli strains. EAEC strains also show exceptional autoaggregation and biofilm formation, other phenotypes that have hitherto been ascribed to AAF/II. We report that EAEC 042 carries the heat-resistant agglutinin (hra1) gene, also known as hek, which encodes an outer membrane protein. Like AAF/II, the cloned EAEC 042 hra1 gene product is sufficient to confer autoaggregation, biofilm formation, and aggregative adherence on nonadherent and nonpathogenic laboratory E. coli strains. However, an 042 hra1 deletion mutant is not deficient in these phenotypes compared to the wild type. EAEC strain 042 produces a classic honeycomb or stacked brick pattern of adherence to epithelial cells. Unlike wild-type 042, the hra1 mutant typically does not form a tidy stacked brick pattern on HEp-2 cells in culture, which is definitive for EAEC. Moreover, the hra1 mutant is significantly impaired in the Caenorhabditis elegans slow kill colonization model. Our data suggest that the exceptional colonization of strain 042 is due to multiple factors and that Hra1 is an accessory EAEC colonization factor.
