Abstract. Equine recurrent uveitis (ERU) is the most frequent cause of blindness in horses worldwide. Leptospira has been implicated as an etiologic agent in some cases of ERU and has been detected in fresh ocular tissues of affected horses. The objective of this study was to determine the presence of Leptospira antigen and DNA in fixed equine ocular tissues affected with end-stage ERU. Sections of eyes from 30 horses were obtained. Controls included 1) 10 normal equine eyes and 2) 10 equine eyes with a nonrecurrent form of uveitis. The experimental group consisted of 10 eyes diagnosed with ERU based on clinical signs and histologic lesions. Sections were subjected to immunohistochemical staining with an array of rabbit antiLeptospira polyclonal antibodies. DNA extractions were performed by using a commercial kit designed for fixed tissue. Real-time PCR analysis was completed on extracted DNA. The target sequence for PCR was designed from alignments of available Leptospira 16S rDNA partial sequences obtained from GenBank. Two of 10 test samples were positive for Leptospira antigen by immunohistochemical assay. Zero of 20 controls were positive for Leptospira antigen. All test samples and controls were negative for Leptospira DNA by realtime PCR analysis. Leptospira was detected at a lower frequency than that previously reported for fresh ERUaffected aqueous humor and vitreous samples. Leptospira is not frequently detectable in fixed ocular tissues of horses affected with ERU when using traditional immunohistochemical and real-time PCR techniques.
The objective of this study was to describe method of placement, and frequency and severity of complications associated with a subpalpebral lavage system placed in the medial aspect of the equine inferior eyelid. The inferomedial subpalpebral lavage (ISPL) tube is positioned deep in the medial aspect of the inferior conjunctival fornix so that the footplate lies flat between the lower eyelid and the anterior surface of the nictitans. Retrospective data from the placement of 92 ISPL systems placed in 86 horses during a 31-month period were examined. Tube placement was performed using sedation and regional anesthesia only in 59% of horses. The median duration of tube placement was 19 days (range: 1-61 days). Seventy-one horses were treated for up to 55 days following discharge from hospital with an ISPL tube in place. No complications were reported with 59% of ISPL systems. Non-ocular complications were found in 38% of ISPL systems and included tube displacement from the conjunctival fornix (18%), suture loss requiring resuturing of the system to the horse's head (14%), and damage necessitating replacement of the injection port (6%). Ocular complications were recorded in 3% of horses and were limited to inferior eyelid swelling. Vision was retained in 88% of horses. The ISPL system is easily and safely placed, and well tolerated for extended periods. It appears to be associated with infrequent and minor complications when compared with placement of subpalpebral lavage tubes in the superior eyelid.
Herpetic stromal keratitis (HSK) is an inflammatory disease of the cornea that often results in blindness.It is mediated by a host immune response which is triggered by herpes simplex virus (HSV) infection. Immune effector mechanisms are hypothesized to be important in disease development. We investigated, in a mouse model, whether perforin-dependent cytotoxicity is an important effector mechanism in the production of HSK. Wild-type (C57BL/6) and perforin-deficient (PKO) mice were infected intracorneally with HSV-1 strain F. Clinical disease and histologic lesions of the cornea at 23 days postinfection (p.i.) were significantly less severe in HSV-1-infected PKO mice than in infected wild-type mice. mRNA for the chemokine macrophage inflammatory protein 1␣ (MIP-1␣) was detected by reverse transcription-PCR in the corneas of infected wild-type mice but not in the corneas of infected PKO mice at 23 days p.i. Adoptive transfer of wild-type HSV-1 immune T-cell-enriched splenocytes into HSV-1-infected PKO mice restored the disease phenotype which was seen in infected wild-type mice. In contrast, mice carrying a null-function mutation in the Fas ligand, which is involved in an alternative cytotoxic mechanism, developed clinical disease and histologic lesions which were comparable to those in wild-type mice. Viral clearance from the eyes of PKO mice was not impaired. There was no significant difference between the infectious viral titers isolated from the eyes of PKO and wild-type mice. Our findings show that perforin is important in the pathogenesis of HSK.Herpetic stromal keratitis (HSK) is a chronic inflammation of the cornea which is a consequence of infection by herpes simplex virus (HSV). It is the main nontraumatic cause of corneal blindness in people in developed countries (54). HSV-1-induced corneal inflammation in the mouse model is an immunopathological condition mediated by T lymphocytes (11, 20-22, 38, 48, 49, 54). T-cell-deficient mice, such as athymic nude mice, scid mice, or thymectomized mice, do not develop keratitis following intracorneal infection with HSV-1. However, these mice develop HSK upon intracorneal HSV-1 infection if they have previously received an adoptive transfer of HSV-1 immune T lymphocytes (3,11,12,21,37,43,58).The main effector mechanisms mediated by T lymphocytes are the secretion of soluble factors such as cytokines and chemokines and the lysis of target cells. Cytokines, such as gamma interferon, have been proposed as mediators of HSK (2,20,24). However, studies of gamma interferon knockout mice failed to demonstrate a role for gamma interferon in the pathogenesis of HSV-induced stromal keratitis (5). Chemokines have also been postulated to be involved in the development of HSK (55, 57, 59). There is evidence that macrophage inflammatory protein 1␣ (MIP-1␣), a beta chemokine involved in lymphocyte recruitment, plays a role in the development of HSK (60).Immune cytotoxic effector mechanisms play a role in the development of many immune-mediated disorders. The two main cytotoxic ef...
A 23-year-old captive female California sea lion (Zalophus californianus) developed an inferiotemporal subconjunctival swelling of the right eye. Surgical excision of the mass was performed and a diagnosis of orbital fat prolapse was confirmed histopathologically. There was no recurrence of orbital fat prolapse at 15 months post operatively. This is the first known case of orbital fat prolapse in the California sea lion.
The formalin-fixed, amber-colored right globe from a 12-week-old female silver Labrador Retriever dog was submitted to the Comparative Ocular Pathology Laboratory of Wisconsin for light microscopic evaluation. The clinical history described a collapsed anterior chamber and multifocal nodular lesions in the peripheral iris. Histologically, immunohistochemically, and ultrastructurally, the uveal mass was consistent with a malignant schwannoma; there was extension along peripheral nerves within the sclera. The signalment and behavior of the neoplasm distinguish it from the uveal schwannoma of blue-eyed dogs and bear some resemblance to the ocular lesions in human neurofibromatosis. The dilute color mutation may contribute to the cause. Six weeks later, the dog did not develop any additional masses.
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