Molero, C. (AZOOR) is an ocular disease characterized by a rapid loss of visual function (13). Common characteristics of this disease include (i) acute loss of retinal peripheral vision in one or both eyes, (ii) normal funduscopic examination results in the early stages of the disease, and (iii) considerable abnormalities in retinograms whereas evoked potentials are normal (14, 17, 23, 36). A mixed dysfunction of rods and cones is usually observed, although cones are usually more affected. In the early stages of the disease, visual acuity and angiographic test Reactive Blue 4 results are normal despite marked deterioration of the visual field. Some patients exhibit abnormal pupillary reflex, suggesting some type of neuropathy. In fact, inflammation of the central nervous system has been found in a patient with AZOOR (16). In some cases, photophobia occurs, and the appearance of photopsias, referred to as wavy lights, is common. A typical AZOOR patient is usually a young myopic woman who is otherwise healthy; indeed, according to a recent study, about 80% of patients with this disease are women (13). Ever since this disease was first explained, it has been associated with multiple evanescent white dot syndrome (12, 19, 34, 38). Moreover, similarities between AZOOR, multiple evanescent white dot syndrome, multifocal choroiditis, punctate inner choroidopathy, acute macular retinopathy, and acute idiopathic blind spot enlargement have been explained previously (4, 5, 20, 37, 40). Some of these conditions have been Reactive Blue 4 associated with histoplasmosis (8, 14). In line with these observations, we reported that AZOOR may be caused by a fungal contamination (6). AZOOR was previously considered an immune disorder or a disease caused by an unidentified infectious agent (2, 12, 18). Serpiginous choroiditis (SC) is usually a progressive and usually recurrent inflammatory disorder of the choroid, retinal blood vessels, and pigment epithelium. This disease is usually chronic and usually affects both eyes, leading to vision loss (24, 38). The cause of SC remains unknown, although the possibility that it is an autoimmune disorder has been proposed. In fact, patients suffering from SC are treated with immunosuppressive brokers (28, 35). In the present statement we provide further evidence that AZOOR and SC may have a fungal origin. MATERIALS AND METHODS Yeast growth. Yeasts were produced in YEPD medium (1% yeast extract, 2% peptone, and 2% glucose) with incubation at 30C. The same medium, made up of agar, was used to isolate individual colonies. Antibodies. Rabbit antisera against were obtained by inoculation of 0.5 ml of phosphate-buffered saline (PBS) made up of 1 or 2 2 mg of yeast after autoclaving and lyophilization. Each inoculum had been previously mixed with the same volume of Freund’s adjuvant. Rabbits were inoculated up to four occasions, and the antibody titer and specificity of the serum samples were tested by immunofluorescence and Western blotting. Immunofluorescence. For species, a Euroimmun commercial kit (Medizinische Labordiagnostika Rabbit Polyclonal to NOX1 AG) was used in accordance with the manufacturer’s instructions and using the same serum dilutions as for for 20 min. Pellets were resuspended in 1 ml of triple-distilled filtered water and were incubated at room heat for 20 min. Samples were centrifuged for 3 min at 20,000 Reactive Blue 4 and washed twice more with triple-distilled filtered water. Pellets recovered from your last centrifugation were resuspended in 300 l of PBS. Samples were boiled for 10 min and then incubated for 2.