• DOI:10.1177/030098589002700215
• Corpus ID: 34177731

Pars Plicata in Equine Recurrent Uveitis

@article{Cooley1990ParsPI,
  title={Pars Plicata in Equine Recurrent Uveitis},
  author={P L Cooley and Milton Wyman and O R Kindig},
  journal={Veterinary Pathology},
  year={1990},
  volume={27},
  pages={138 - 140}
}

• P. L. Cooley, M. Wyman, O. Kindig
• Published 1 March 1990
• Medicine
• Veterinary Pathology

Equine recurrent uveitis (ERU) is one of the most devastating and frequent ocular diseases in the horse. Current hypothesis is that ERU is involved in a delayed hypersensitivity reaction with persistence of immunologically sensitized cells that respond to systemic re-exposure to an antigen. 1.2.6 Light micrographs have revealed a nongranulomatous response. l .2 Essentially no research has been performed with regard to ultrastructural or immunologic events in ERU. A major component of the blood-aqueous barrier in many species is the tight junctions of the lateral intercellular spaces of the non-pigmented ciliary epithelium.* This barrier is broken in uveitis. This study compares the ultrastructural morphology of the non-pigmented ciliary epithelium and pigmented epithelium of the pars plicata in normal horses and in horses affected with ERU. Ocular examinations were done with a hand-held biomicroscope and an indirect ophthalmoscope. Horses of various ages and both sexes were used. Diagnosis of ERU was based on history of previous uveitis and detection of residual lesions (synechiae, lack of corpora nigra, cataract, keratic precipitates, chorioretinal scars, vitreal traction bands, or retinal detachment) and detection of miosis or flare with or without signs of an exacerbated uveitis (photophobia, hypopyon, hyphema, or fibrin in the anterior chamber). There was no evidence of corneal penetration in the ERU eyes. Seven affected ERU eyes and six normal eyes were included in the study. General anesthesia was induced, sector iridocyclectomy was done at the 12:OO to the 3:OO position under a limbal based scleral pedicle, and the horse was euthanatized. Sections of the pars plicata were immersed into a fixative solution conta’ining 2% paraformaldehyde and 2.5% glutaraldehyde in 0.1 M sodium cacodylate buffer (pH 7.4), with 0.2% calcium chloride added, and remained in the fixative for 3 hours. Specimens were rinsed with a 0.1 M phosphate buffer for 2 five minute washes and were placed into a second fixative that contained 0.5% paraformeldehyde, 3% glutaraldehyde, and 1.2% tannic acid in Sorenson phosphate buffer (pH 7.4) for 2 hours. After two rinses with Sorenson phosphate buffer (pH 7.45) containing 0.1 M sucrose, the sections were post-fixed in 1% osmium tetroxide solution that contained 0.1 M phosphate (pH 7.4). This was followed by routine processing for transmission electron microscopy. Electron micrographs of all ERU eyes revealed disruption of non-pigmented ciliary epithelium cell borders, infiltration of mononuclear cells, and rod-shaped intracytoplasmic inclusions in the non-pigmented ciliary epithelium cells (Fig. 1). Less frequently, the rod inclusions were found in the pigmented epithelium cytoplasm. With increased magnification (62,000 x ), the rods appeared in crystalloid arrangement and were associated with rough endoplasmic reticulum. Within one eye with a very active uveitis in situ, double membrane-bound rods were observed in the non-pigmented ciliary epithelium (Fig. 2). The rods were not found in surrounding connective tissue or within mononuclear cells. Mononuclear cells were found throughout the pars plicata. None of the above lesions were found in normal eyes. In contrast to the normal eyes, the nonepigmented ciliary epithelium of cases of ERU had fewer tight junctions and mitochrondria. Tight junctions observed between non-pigmented ciliary epithelium and non-pigmented ciliary epithelium/pigmented epithelium were similar to those reported in other species. The reduction of tight junctions of non-pigmented epithelium of cases of ERU may represent a tissue effect of inflammatory cell infiltration and chemical mediator release, with a result of blood-aqueous barrier breakdown. The crystalloid rod inclusions appear to be produced within the epithelial cell cytoplasm. The double membrane-bound borders observed in one eye resemble those of mitochrondrial borders. Mitochondria in ERU eyes were fewer in number, and most were elongated. Mitochondria1 loss may be attributed to dissolution into vesicles of smooth or rough endoplasmic r e t i c ~ l u m . ~ It is plausible that giant mitochondria were present with crystalloid inclusions, which became single membrane bound once further disruption of internal mitochondrial architecture occurred. Giant mitochondria may form through a fusion of several mitochondria, growth of a single mitochondria, or both.4 Giant mitochondria with crystalline inclusions have been reported in many s~ecies,~.~O including a horse with histiocytic lymphosarcoma with similar inclusions noted in histiocytic neoplastic cells.1o Whether these inclusions represent degenerative change of the mitochondrial cristae, protein storage, or crystallized mitochondria1 enzymes is ~nknown.~JO Cytoplasmic crystalline inclusions have been observed in both neoplastic and inflammatory conditions of several species 3,4,7,9 and are thought to be composed predominately of prot e i ~ ~ . ~ Translocation of the crystalloid from its site of formation can occur, making it difficult to label it as belonging to a specific cell ~ompar tmen t .~ Interestingly, intracytoplasmic crystalline inclusions observed in a horse with a granular cell variant of proliferative optic neuropathy also were double membrane bound.9 Similarities were evident between intracytoplasmic crystalloids noted in mononuclear cells found in plasmacytic conjunctivitis in a young human female,’ in human immunocytoma patients’ circulating lym-