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Bilateral multifocal corneal opacity was detected in a 4.5-year-old male captive gray mouse lemur (Microcebus murinus) without other clinical ocular changes. Histopathological examination revealed a severe diffuse granulomatous scleritis and focal keratitis with intralesional cholesterol, consistent with xanthomatous inflammation. This is the first report of xanthomatous inflammation in a gray mouse lemur. This condition may be the result of systemic factors (lipid metabolism disorders) and/or local predisposing factors such as hemorrhage or inflammation. The pathogenesis in this case could not be fully determined. Further studies on lemurs are required for a better understanding of their lipid metabolism, as well as for diagnosing and evaluating the incidence of xanthomatous inflammation in these species., (© 2016 American College of Veterinary Ophthalmologists.)

We report on a case of necrotizing keratoscleritis in primary Sjogren's syndrome. A 66-year-old female patient who was complaining of ocular pain, tearing and decreased vision in her right eye for the previous two days was admitted to our hospital. Visual acuity in the right eye was hand movement, and initial examination showed a 3.0 × 1.8 mm uveal mass bulging through a corneoscleral melting site in the nasal region of the right eye. Positive anti-nuclear antibody was identified at a titer of 1:320 with a speckled pattern, and both Sjogren's syndrome A and Sjogren's syndrome B antibody tests were positive, with titers >200 U/mL. A technetium 99m pertechnetate salivary scan revealed chronic sialoadenitis in the submandibular glands. We diagnosed the lesion as necrotizing keratoscleritis due to primary Sjogren's syndrome. A corneoscleral patch graft was performed, followed by immunosuppression including oral cyclosporin and topical prednisolone. During a follow-up period of 12 months, the corneoscleral graft was well maintained with no recurrence.

This article provides a brief review of human episcleritis and scleritis, because the pathogenesis, diagnosis, and treatment of these disorders are perhaps the best understood of all species of animals. The clinical and light microscopic manifestations, therapeutic options, and prognosis for primary and secondary episcleritis and scleritis in dog are also reviewed. The focus of this article is on primary and secondary inflammatory conditions that originate in the episclera and sclera caused by idiopathic or known etiologies.

Purpose: A case of keratectasia is reported as a severe presentation of surgically induced necrotizing sclerokeratitis (SINS)., Methods: A 72-year-old white woman had a painful, raised lesion on the superior cornea of her right eye 3 years after uncomplicated extracapsular cataract extraction with intraocular lens implantation. Examination showed a large ectatic area of the superior cornea with inflamed sclera adjacent to the surgical wound, which was diagnosed as SINS., Results: No underlying systemic autoimmune condition or vasculitis was identified on investigation. Progressive painful keratectasia necessitated enucleation, which confirmed on histopathologic examination features of chronic nodular episcleritis and nongranulomatous scleritis with evidence of keratitis and fibrovascular scarring., Conclusion: The predominant inflammatory response in the cornea represents surgically induced necrotizing keratoscleritis (SINK) as a new variant presentation of SINS. Oral corticosteroids and immunosuppressive agents should not be delayed to prevent progressive tissue destruction and poor outcome.

Purpose: This documents the evaluation and management of a patient with an unusual destructive external ocular disorder in the context of progressively disfiguring dermatitis., Methods: Observational case report including ophthalmologic examination with conjunctival and corneal scraping, radiologic studies of the sinuses and chest, skin, conjunctival, and scleral biopsies, and serologic studies., Results: Biopsies, cultures, and serologic testing led to the conclusion that the patient had pyoderma gangrenosum. Therapy with dapsone resulted in preservation of vision and resolution of the oculocutaneous inflammation., Conclusions: Pyoderma gangrenosum is a rare autoimmune disorder that can affect the eye. Biopsy of affected tissue is the key to diagnosis. Immunomodulating therapy can be a useful adjunct to the traditional steroid therapy.

In patients with rheumatoid arthritis (RA), necrotizing scleritis, an ocular manifestation of a systemic vasculitic process, is associated with significant ocular morbidity and high mortality. We present a 60-year-old man with RA who developed necrotizing scleritis and peripheral ulcerative keratitis. The scleritis was refractory to local measures, systemic corticosteroids, and cyclophosphamide but responded rapidly to infliximab. Our case illustrates that biologic agents may be considered in refractory cases of sight- and life-threatening scleritis.

Ocular inflammation in children is of substantial epidemiologic importance, particularly since uveitis in children produces more vision loss than it does in adults. This is partially because there is a higher rate of posterior uveitis in childhood uveitis than in the adult population. Treatment of ocular inflammation in children, ranging from conjunctivitis to keratitis to scleritis to uveitis, depends, of course, on whether or not the problem is microbial, traumatic, malignant, or autoimmune. Most of the cases that are vision threatening are autoimmune, and corticosteroids represent the mainstay of short-term therapy. However, abundant evidence exists which shows that all too often imprudent, prolonged use of corticosteroids is employed with resultant iatrogenic damage, including cataract, glaucoma, and secondary infection.A new paradigm for treating ocular inflammation (uveitis in particular) is espoused in this article. It is based on a limited tolerance to corticosteroid use and a more proactive approach to corticosteroid-sparing immunomodulatory therapy in an effort to induce a durable remission off all corticosteroids.

Purpose: To report a case of surgically induced necrotising sclerokeratitis (SINS) with imminent uveal prolapse following uncomplicated cataract surgery., Methods: Case report., Results: The causative agent was found to be a subtarsal abscess and the condition responded to drainage of the localised infection and a course of topical antibiotics., Conclusion: This report represents the first account of postoperative scleral necrosis arising from a subconjunctival abscess, and illustrates the importance of identifying all aetiopathogenic factors in cases of postsurgical necrotizing scleritis.

Background: A case of Scedosporium prolificans corneoscleritis is reported in a patient who had developed scleral necrosis following pterygium surgery, with adjunctive beta-irradiation. This fungus has been reported to be the causative organism in only two previous cases of corneoscleritis., Methods: The patient presented with signs and symptoms typical of corneoscleritis. When the fungus was isolated from a biopsy specimen, aggressive scleral debridement was carried out and intensive antifungal therapy was instigated., Results: After a prolonged course, the eye was rendered sterile., Conclusion: Early conjunctival recession and aggressive scleral debridement combined with intensive instillation of antifungals are crucial to the successful management of fungal corneoscleritis.

A 71-year old woman complains of painless inflammation, discharge and decreased vision at the right eye since two weeks. Eight years before she was operated at this eye for a nasally located pterygium and received adjuvant radiotherapy. On examination a necrotizing scleritis was seen which rapidly involved the cornea and was infected by Pseudomonas. Despite intensive antibiotherapy the sclerokeratitis extended further and eventually lead to enucleation. Surgically induced scleritis-especially after pterygium surgery with adjuvant radiotherapy-and complicating Pseudomonas infection are discussed.

Background: The fungus Scedosporium prolificans was first described as a human pathogen in 1984, and has been associated with metastatic endophthalmitis and one previously reported case of sclerokeratitis., Methods: We report a case of S. prolificans sclerokeratitis in the setting of late scleral necrosis complicating pterygium surgery with adjunctive beta-irradiation., Results: A poor clinical response to topical natamycin and amphotericin B, and systemic itraconazole and ketoconazole was encountered. Enucleation was required, with subsequent microbiological cure. Pathological correlation is described., Conclusions: S. prolificans infections often respond poorly to medical therapy. Early surgical intervention is indicated in culture-proven scleritis due to Scedosporium prolificans.

Sixteen years old patient presents bilateral tuberculous sclerokeratitis and papulonecrotic cutaneous tuberculids-type acnitis. The patient is a bearer of a latent tuberculous focere following a prolonged contact with a cavitar bacillary. The positive diagnosis was much facilitated by the association with acneiform dermic tuberculids at face, intense and positive local reaction to PPD and a favourable therapeutic response to tuberculostatics. The particularity of the case consists in a concomitant, cutaneous and ocular affection since the first episode, the affection evolving as a typical bilateral tuberculous sclerokeratitis.

A 23-year-old male presented with bilateral sclerokeratitis. He reported recent bronchitis, sinusitis, dyspnea on exertion, hemoptysis, arthralgias and myalgias. Wegener's granulomatosis was diagnosed by a positive antineutrophil cytoplasmic autoantibody (ANCA) test and a nasal and subglotic biopsy showing granulomatous inflammation. Treatment with cyclophosphamide, systemic corticosteroids and trimethoprim/sulfamethoxazole resulted in resolution of the sclerokeratitis and remission of the disease.

The ocular and systemic features of 10 patients whose Wegener's granulomatosis presented with corneoscleral inflammatory disease are described. Marginal corneal infiltrates were seen in all patients with anterior scleritis and were a valuable sign of disease activity. Nine out of 10 patients had symptoms of systemic vasculitis on presentation; seven had renal impairment; three had chest x-ray abnormalities. Autoantibodies against neutrophil cytoplasmic determinants (ANCA) were present in all cases. In seven patients the scleritis responded well to pulsed immunosuppressive therapy followed by long term oral steroids and cyclophosphamide. Oral steroid therapy alone failed to control severe disease. Corneoscleral disease was not a cause of visual loss. It is important to realise that inflammatory corneoscleral disease may be the presenting feature of a severe systemic vasculitis.

Two cases of necrotizing sclerokeratitis following uncomplicated extracapsular cataract extraction are reported. Enucleation became necessary in the first case despite initially successful immunosuppressive treatment. In the second case, a stable condition was achieved by covering the affected area with a patch of lyophilized dura. Two years later, however, phthisis bulbi developed.

Pterygium excision was complicated by bacterial corneoscleritis and endophthalmitis in two patients, one who had received postoperative beta irradiation and the other topical thiotepa. These complications followed surgery by two and six weeks. Causative organisms were Streptococcus pneumoniae and Pseudomonas aeruginosa, respectively. Despite aggressive therapy, visual outcome was poor in both cases. These cases demonstrate that, although infrequent, complications of pterygium excision can be destructive and visually disabling.

A number of cases of necrotic sclerokeratitis following eye surgery have been reported in recently published literature. The condition was presumably triggered by surgical inflammation and caused by localized occlusive vasculitis: in one case deposits of immune complexes in vessel walls were demonstrated. The authors report on three cases of necrotic sclerokeratitis which developed five to 16 months after uncomplicated cataract extraction. Clinical examination showed disappearance of vessels in affected sclera, together with tissue necrosis. None of the patients had any systemic immune disease and no immune complexes were found in biopsy material obtained from two eyes (of which one was enucleated and the other two healed under steroid treatment). In all three affected eyes cataract extraction was performed via a corneoscleral incision. In two of the three cases communicated here cataract extraction was performed in the fellow eye without any postoperative complications. Since postsurgical sclerokeratitis is presumably triggered by vascula inflammation, clear corneal incisions may be preferable to corneoscleral incisions in cases where immune reactions are anticipated.