De novo lesions in presumed ocular histoplasmosis-like syndrome. (1/118)

Two patients with multifocal choroiditis similar or identical to POHS are presented. Colour photographs and fluorescein angiography document the occurrence of de novo lesions in the originally involved eye. The cases also demonstrate the development of new choroidal lesions within the originally involved eye, the early evolution of the "basic choroidal lesion", and the need for fluorescein angiography for visualizing the underlying choroidal lesion.  (+info)

New animal model for human ocular toxocariasis: ophthalmoscopic observation. (2/118)

BACKGROUND/AIMS: Although human ocular toxocariasis causes severe vision defect, little is known about its aetiology, diagnosis, and treatment. To develop a new animal model for human ocular toxocariasis, ophthalmological findings of fundi in Mongolian gerbils, Meriones unguiculatus, and BALB/c mice were investigated following infection with Toxocara canis. METHODS: Using an ophthalmoscope, which was specifically developed to observe the fundi of small animals, ocular changes of fundi of 20 gerbils and 11 mice were monitored after oral infection with embryonated eggs of T canis. RESULTS: Vitreous, choroidal, and retinal haemorrhages were consistently observed in Mongolian gerbils, but rarely in mice. Severe exudative lesions and vasculitis were often present in gerbils but not in mice. Migrating larvae were also frequently observed in gerbils. CONCLUSION: Mongolian gerbils are more appropriate animal model for human ocular toxocariasis than previously used experimental animal such as mice, guinea pigs, rabbits, and monkeys because of its high susceptibility of ocular infection.  (+info)

Detection of specific immunoglobulin E during maternal, fetal, and congenital toxoplasmosis. (3/118)

Toxoplasma immunoglobulin E (IgE) antibodies in 664 serum samples were evaluated by using an immunocapture method with a suspension of tachyzoites prepared in the laboratory in order to evaluate its usefulness in the diagnosis of acute Toxoplasma gondii infection during pregnancy, congenital infection, and progressive toxoplasmosis. IgE antibodies were never detected in sera from seronegative women, from patients with chronic toxoplasma infection, or from infants without congenital toxoplasmosis. In contrast, they were detected in 86.6% of patients with toxoplasmic seroconversion, and compared with IgA and IgM, the short kinetics of IgE was useful to date the infection precisely. For the diagnosis of congenital toxoplasmosis, specific IgE detected was less frequently than IgM or IgA (25 versus 67.3%), but its detection during follow-up of children may be interesting, reflecting an immunological rebound. Finally, IgE was detected early and persisted longer in progressive toxoplasmosis with cervical adenopathies, so it was also a good marker of the evolution of toxoplasma infection.  (+info)

Toxoplasma gondii infection induces gene expression and secretion of interleukin 1 (IL-1), IL-6, granulocyte-macrophage colony-stimulating factor, and intercellular adhesion molecule 1 by human retinal pigment epithelial cells. (4/118)

We have used human retinal pigment epithelial (HRPE) cultures to investigate the primary cellular responses of retinal resident cells to intracellular Toxoplasma gondii replication. At 4 days postinoculation, when all of the cells were infected, the secretion of interleukin 1beta (IL-1beta), IL-6, granulocyte-macrophage colony-stimulating factor (GM-CSF), and intercellular adhesion molecule 1 (ICAM-1) was augmented by 23-, 10-, 8-, and 5-fold, respectively, over the control. Northern and reverse transcriptase PCR analyses showed significant upregulation of steady-state levels of mRNA for IL-1beta, IL-6, GM-CSF, and ICAM-1. The secretion of these molecules by HRPE cells may play a critical immunoregulatory role in the pathophysiological processes associated with T. gondii-induced retinochoroiditis.  (+info)

Childhood blindness and visual loss: an assessment at two institutions including a "new" cause. (5/118)

PURPOSE: This study was initiated to investigate the causes of childhood blindness and visual impairment in the United States. We also sought a particular etiology--congenital lymphocytic choriomeningitis virus (LCMV)--which has been considered exceedingly rare, in a fixed target population of children, the severely mentally retarded. METHODS: We undertook a library-based study of the world literature to shed light on the causes of childhood blindness internationally and to put our data in context. We prospectively examined all consented children (159) at 2 institutions in the United States to determine their ocular status and the etiology of any visual loss present. One of the institutions is a school for the visually impaired (hereafter referred to as Location V), in which most of the students have normal mentation. The other is a home for severely mentally retarded, nonambulatory children (hereafter referred to as Location M). This institution was selected specifically to provide a sample of visual loss associated with severe retardation because the handful of cases of LCMV in the literature have been associated with severe central nervous system insults. Histories were obtained from records on site, and all children received a complete cyclopleged ophthalmic examination at their institution performed by the author. Patients at Location M with chorioretinal scars consistent with intrauterine infection (a possible sign of LCMV) had separate consents for blood drawing. Sera was obtained and sent for standard TORCHS titers, toxoplasmosis titers (Jack S. Remington, MD, Palo Alto, Calif), and ELISA testing for LCMV (Centers for Disease Control and Prevention, Atlanta, Ga). RESULTS: The diagnoses at Location V were varied and included retinopathy of prematurity (19.4%), optic atrophy (19.4%), retinitis pigmentosa (14.5%), optic nerve hypoplasia (12.9%), cataracts (8.1%), foveal hypoplasia (8.1%), persistent hyperplastic primary vitreous (4.8%), and microphthalmos (3.2%). The most common diagnosis at Location M was bilateral optic atrophy, which was found in 65% of the patients examined who had visual loss. Of these, the insults were most often congenital (42.6%), with birth trauma, prematurity, and genetics each responsible for about 15% of the optic atrophy. The second most common diagnosis was cortical visual impairment (24%), followed by chorioretinal scars (5%), which are strongly suggestive of intrauterine infection. Of 95 patients examined at Location M, 4 had chorioretinal scars. Two of these had dramatically elevated titers for LCMV, as did one of their mothers. One of the other 2 children died before serum could be drawn, and the fourth had negative titers for both TORCHS and LCMV. CONCLUSIONS: At both locations studied, visual loss was most often due to congenital insults, whether genetic or simply prenatal. The visual loss at Location V was twice as likely as that at Location M to be caused by a genetic disorder. The genetic disorders at Location V were more often isolated eye diseases, while those among the severely retarded at Location M were more generalized genetic disorders. Our study identified optic atrophy as a common diagnosis among the severely mentally retarded with vision loss, a finding that is supported by previous studies in other countries. In our population of severely retarded children, the target etiology of lymphocytic choriomeningitis virus was responsible for half the visual loss secondary to chorioretinitis from intrauterine infection. This is more common than would be predicted by the few cases previously described in the literature, and strongly suggests that LCMV may be a more common cause of visual loss than previously appreciated. We believe that serology for LCMV should be part of the workup for congenital chorioretinitis, especially if the TORCHS titers are negative, and that perhaps the mnemonic should be revised to "TORCHS + L." Childhood blindness and visual impairment are tragic and co  (+info)

Population based assessment of uveitis in an urban population in southern India. (6/118)

AIM: To assess the prevalence of active and inactive uveitis unrelated to previous surgery or trauma in an urban population in southern India. METHODS: As part of the Andhra Pradesh Eye Disease Study, 2522 subjects (85.4% of those eligible), a sample representative of the population of Hyderabad city in southern India, underwent interview and detailed dilated eye examination. Presence of sequelae of uveitis without current active inflammation was defined as inactive uveitis. RESULTS: Unequivocal evidence of active or inactive uveitis unrelated to previous surgery or trauma was present in 21 subjects, an age-sex adjusted prevalence of 0.73% (95% confidence interval (CI) 0.44-1.14%). Active uveitis was present in eight subjects, an age-sex adjusted prevalence of 0.37% (95% CI 0. 19-0.70), of which 0.06% was anterior, 0.25% intermediate, and 0.06% posterior. The 0.36% (95% CI 0.17-0.68%) prevalence of inactive uveitis included macular chorioretinitis scars (0.26%), anterior (0. 07%) and previous vasculitis involving the whole eye (0.03%). The prevalence of visual impairment due to uveitis of less than 6/18 in at least one eye was 0.27%, less than 6/60 in at least one eye was 0. 16%, and less than 6/60 in both eyes was 0.03%. CONCLUSION: These population based cross sectional data give an estimate of the prevalence of various types of uveitis in this urban population in India. Active or past uveitis that might need treatment at some stage was present in one of every 140 people in this population.  (+info)

Rapid progressive subacute sclerosing panencephalitis in a 2-year-old child with congenital athyreosis. (7/118)

We present the unique case of a 2-year-old girl with congenital athyreosis who acquired primary measles virus infection at the age of 18 months, coincidentally with an Epstein-Barr virus infection. First neurologic symptoms of subacute sclerosing panencephalitis appeared 5 months later, and the girl died within 6 months after a rapid progressive illness. Factors possibly predisposing to this extraordinary disease course-primary measles virus infection at an early age and lack of evidence for immunodeficiency-are discussed.  (+info)

Effect of Fas and Fas ligand deficiency in resistance of C57BL/6 mice to HSV-1 keratitis and chorioretinitis. (8/118)

PURPOSE: To investigate the effect of Fas and Fas ligand (FasL) deficiency on the development of herpes stromal keratitis and on the von Szily model of herpes retinitis in C57BL/6 mice, which are ordinarily resistant to development of both of these herpetic diseases. METHODS: Anterior chamber inoculation of the right eye of each mouse with various titers of HSV-1 (KOS strain) was performed. Both eyes of each mouse were enucleated on postinoculation day 15 and processed for histopathologic examination. HSV-1 was inoculated into one cornea of other mice, and the severity of stromal keratitis was scored. RESULTS: Contralateral destructive chorioretinitis developed in susceptible Balb/cByj mice (19/23); ipsilateral chorioretinitis did not occur (0/23). Stromal keratitis developed in susceptible C.AL-20 mice (15/16). None of the C57BL/6 (0/10 for keratitis or 0/20 for retinitis) developed inflammation. Neither did B6.SMN.C3H.gld (FasL deficient; 0/12 or 0/28) or B6.MRL.lpr (Fas deficient; 0/11 or 0/34) mice (keratitis or contralateral chorioretinitis). Minimal scattering of inflammatory cells in the contralateral retina but not destructive chorioretinitis was observed in two C57BL/6, three B6.SMN.C3H.gld, and five B6.MRL.lpr mice. Few inflammatory cells were also found in the ipsilateral vitreous and vitreoretinal interface (but not destructive chorioretinitis) of all C57BL/6, two gld, and three lpr mice. CONCLUSIONS: Immune dysregulation secondary to deficiency in Fas or FasL system does not influence the resistance of the C57BL/6 mice to develop herpes simplex keratitis or destructive herpes simplex chorioretinitis.  (+info)

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