Nonulcerative bullous keratitis associated with Pseudomonas alcaligenes infection in a Thoroughbred mare

A 5‐year‐old Thoroughbred mare presented with an intermittently mildly painful right eye with a nonulcerative corneal opacity of several weeks' duration that had improved with topical steroids but recurred when steroids were withdrawn. Ophthalmic examination demonstrated a focal region of moderate corneal oedema and midstromal corneal infiltrate centrally but no other significant ocular abnormalities, and suggested a diagnosis of immune‐mediated keratitis. Empirical courses of both topical and systemic anti‐inflammatory drugs, both nonsteroidal and steroidal, led to initial improvement but bullous keratopathy developed when corneal oedema became profound. Due to the rapidly progressive nature of the bullous keratopathy combined with poor response to medical therapy, a keratectomy and conjunctival graft were performed under general anaesthesia. Intraoperative corneal culture of the keratectomy site grew Pseudomonas alcaligenes, a common soil and water contaminant. Histopathology of the keratectomy specimen revealed neutrophilic inflammation. Keratectomy and conjunctival graft led to resolution of ocular pain and inflammation, with an acceptable cosmetic and visual outcome. This report describes an unusual case of a nonulcerative Pseudomonas keratitis that responded well to surgical therapy, and underscores the complicated nature of nonulcerative keratitis in horses.     

Primary closure of the corneas of two Great Horned owls after resection of nonhealing ulcers

Two Great Horned owls were presented to the Colorado State University Veterinary Teaching Hospital for evaluation of corneal lesions. Each bird had a corneal ulcer and bullous keratopathy. Following unsuccessful attempts at medical and surgical management, the corneal defects in each bird were treated with penetrating keratoplasties and conjunctival pedicle grafts. In each bird the cornea healed well and regained approximately its normal shape. Both birds fully recovered and have been released into the wild.     

Efficacy of two chondroitin sulfate ophthalmic solutions in the therapy of spontaneous chronic corneal epithelial defects and ulcerative keratitis associated with bullous keratopathy in dogs

OBJECTIVE: To determine the efficacy of two antimicrobial-chondroitin sulfate ophthalmic solutions in the therapy of spontaneous chronic corneal epithelial defects (SCCED) and ulcerative keratitis associated with bullous keratopathy in dogs. ANIMALS STUDIED: Eighty dogs with SCCED and 14 dogs with ulcerative keratitis associated with bullous keratopathy. PROCEDURE: Following manual debridement of nonadherent epithelium, dogs were treated topically with a chondroitin sulfate ophthalmic solution containing either tobramycin or ciprofloxacin. Patients were re-evaluated at 2-week intervals for 4 weeks. RESULTS: After 2 weeks of treatment, 53.6% of eyes with SCCED and 17.6% of eyes with ulcerative keratitis associated with bullous keratopathy had healed. After 4 weeks of treatment, 81.0% of eyes with SCCED and 23.5% of eyes with ulcerative keratitis associated with bullous keratopathy had healed. There were no statistically significant differences in healing percentages between the tobramycin-chondroitin sulfate solution treatment groups and the ciprofloxacin-chondroitin sulfate solution treatment groups. Two dogs with SCCED, one treated with the tobramycin-chondroitin sulfate solution and the other treated with the ciprofloxacin-chondroitin sulfate solution, developed sterile corneal stromal abscesses during the study. CONCLUSIONS: Topical therapy with an antimicrobial-chondroitin sulfate ophthalmic solution combined with manual debridement of nonadherent epithelium compares favorably with other published medical and surgical therapies for SCCED; however, these compounds are only equivocally more effective than therapy with manual debridement alone. These solutions appear to be ineffective in the treatment of ulcerative keratitis associated with bullous keratopathy. The significance of the two cases of corneal stromal abscessation is unknown at this time and warrants further investigation.     

Treatment of corneal ulceration and bullous keratopathy using a nictitating membrane flap in two horses

Objective

The aim of this study was to describe placement of a nictitating membrane flap as a treatment for corneal ulceration and bullous keratopathy in two horses.

Animals Studied

A 13-year-old American Saddlebred mare presented for severe corneal edema, superficial stromal ulceration, and a central bulla of the left eye. A 4-year-old Trakhener stallion also presented with a large axial bulla of the left eye with concurrent severe corneal edema and a deep stromal ulcer.

Procedure

A complete ophthalmic examination was performed. Samples were obtained for corneal cytology, and both horses were started on aggressive medical therapy. Both underwent general anesthesia for placement of a nictitating membrane flap and a subpalpebral lavage system (SPLS).

Results

Corneal cytology for each horse revealed a mixed bacterial population. Moderate Pseudomonas aeruginosa was cultured from the mare, while Aspergillus species and a few Enterococcus gallinarum were cultured from the stallion. The bullae in both horses resolved at 3 and 4 weeks and vision returned in the affected eye 4.5 and 3 months postoperatively at the last follow-up, respectively.

Conclusion

Aggressive medical management with concurrent placement of a nictitating membrane flap is effective to treat bullous keratopathy in two horses. The described treatments could be used to treat horses that develop severe or progressive bullous corneal lesions.     

An unusual case of feline acute corneal hydrops: atypical disease presentation and possible in vivo detection of Descemet's membrane detachment in the cat's unaffected eye

A 1‐year‐old, female spayed, domestic shorthair cat presented for blepharospasm of the right eye. Slit‐lamp biomicroscopic examination showed focal corneal ulceration and presumptive keratomalacia of the right eye. Examination of the left eye was normal apart from a focal endothelial opacity. Within the first 24 h of medical management, the right eye developed marked corneal edema and globular anterior protrusion of the corneal surface consistent with feline acute corneal hydrops (FACH). Surgical management consisted of a bridge conjunctival graft, nictitating membrane flap, and temporary tarsorrhaphy. Resolution of corneal edema and pain occurred in the right eye within 24 days. Spectral domain optical coherence tomography (SD‐OCT) of the anterior segment was performed in both eyes. Conjunctival tissue from the bridge graft precluded examination of deeper corneal structures in the right eye. The left eye displayed a focal separation of the corneal endothelium and Descemet's membrane from the overlying stroma. These SD‐OCT findings are similar to the analogous syndrome found in humans and represent a potential etiology for FACH of the right eye in the case presented here. Unfortunately, the cat was lost to follow‐up and the progression of this lesion to FACH in the left eye could not be determined.     

Acute corneal hydrops of presumed traumatic origin: An uncontrolled case series (three horses)

This case series describes acute corneal hydrops in three young horses. Due to similarities in the clinical appearance and progression of the disease with that which is reported in humans and cats with acute corneal hydrops, traumatic Descemet’s membrane rupture was suspected to be the underlying aetiology in these equine cases. The horses presented with acute severe corneal oedema with intrastromal bullae formation and anterior bulging of the corneal contour. Focal posterior corneal changes were also seen in two of three cases. Mild anterior uveitis was also present. Other causes of corneal oedema (e.g. glaucoma) were ruled out based on presentation and clinical examination. Treatment approaches were medical and included various combinations of prophylactic topical antimicrobial therapy in case of secondary corneal ulceration, anti-inflammatory therapy for uveitis, targeted oedema therapy with topical hypertonic saline and corneal cross-linking, and placement of a temporary partial tarsorrhaphy for corneal tamponade. The outcome was excellent in all cases, with rapid resolution of the ocular changes. Acute corneal hydrops of presumed traumatic Descemet’s membrane rupture origin should be considered in cases of young horses presenting with acute corneal oedema. However, further studies are warranted to better characterise the disease and to try to confirm the suspected aetiology.     

Calcific band keratopathy in an alpaca

A 4‐year‐old female Suri alpaca was presented for evaluation of acute onset weakness, lethargy, and recent development of opacities in both eyes. On ophthalmic examination, bilaterally symmetrical corneal opacities were noted along the interpalpebral fissures with a few corneal blood vessels intermingled. A presumed diagnosis of calcific band keratopathy was made based on location and appearance. The patient was euthanized a short while after diagnosis due to reasons unrelated to the eyes and histologic examination of the corneas revealed subepithelial calcium and vascularization, consistent with calcific band keratopathy. This case report is the first to document this ocular condition in an alpaca.     

Subepidermal bullous dermatosis due to topical corticosteroid therapy in dogs

Six adult dogs were presented with an unusual bullous dermatosis affecting the glabrous skin of the ventral abdomen and medial thighs. Clinically, flaccid bullae were accompanied by erythema, ulceration, haemorrhage and hyperpigmentation in four of six dogs; the remaining two dogs had thin skin without grossly apparent bullae. Histologically, subepidermal bullae and clefting, vascular proliferation and dilatation (phlebectasia), and alteration in the density and staining of superficial dermal collagen were seen in all dogs. In all cases, corticosteroid-containing topical products had been applied to the affected areas prior to the development of the dermatosis; skin lesions resolved when topical corticosteroids were withdrawn. Follow-up biopsy of three dogs showed resolution of the previously abnormal collagen and subepidermal clefting. Residual lesions included phlebectasia, comedones and hyperpigmentation. The authors postulate that subepidermal clefting was due to local, corticosteroid-induced skin fragility. This is the first report, to our knowledge, of bullous skin disease in dogs resulting from topical corticosteroid therapy.     

Amiodarone-induced keratopathy in healthy dogs

Amiodarone has a broad spectrum as an antiarrhythmic agent and is indicated for patients with atrial and ventricular arrhythmias. Amiodarone-induced corneal deposits are the most common reversible side effect (70-100%) in humans. Additional ocular effects in humans include deposits in the lens, retina and optic nerve. This study was conducted to determine ocular effects of chronic oral amiodarone in healthy dogs. Six chronically amiodarone-treated dogs and four controls were used for this study. Ophthalmic examination was performed using biomicroscopy and indirect ophthalmoscopy at the end of 4th, 7th and 11th weeks when dogs received amiodarone. Corneal microdeposits were observed at the end of the 7th week in one eye and at end of the 11th week in the other eye of one dog. Immediately following euthanasia, corneas and optic nerves were harvested for light and electron microscopic analysis. Light microscopic analysis showed corneal deposits in the basal epithelial cells of the cornea of the clinically affected dog. In addition, a significant increase in basal cell turnover as indicated by mitotic index was observed in the affected dog compared to both nondeposit amiodarone and control groups. All remaining animals were normal. One out of six dogs treated with amiodarone demonstrated corneal deposits (16%). This prevalence is low compared to humans. Explanations for this may include species variations particularly in volume of lacrimal secretion, or the need for longer administration. In addition, sunlight is believed to exacerbate the corneal deposits in humans and all dogs in this study were housed indoors.     

Survey of ocular abnormalities in draft horses

Objective

To determine the prevalence of ocular disease in draft horses in the United States.

Animals

Draft horses of various breeds and ages.

Procedure

Nondilated ophthalmic examination was performed using slit lamp biomicroscopy and indirect ophthalmoscopy. Intraocular pressures were measured when possible.

Results

One hundred sixty-five draft horses were examined. Age range: 10 days to 33 years (mean 10.8 years, median 10 years); 87 geldings (52.7%), 71 mares (43.0%), 7 stallions (4.2%); 64 Percherons (38.8%), 51 Belgians (30.9%), 29 Clydesdales (17.6%), 15 Shires (9%), and 6 other draft breed (3.6%). Intraocular pressure: mean 24.7 mmHg OD, range 13-37 mmHg; mean 25.0 mmHg OS, range 11-37 mmHg. Vision-threatening disease was present in 9 horses (5.5%): complete cataracts 1, post-traumatic optic nerve atrophy 1, uveitis and secondary glaucoma 1, retinal detachment 1, large chorioretinal scar 3, phthisis bulbi 2. Non-vision-threatening ocular disease was present in 56 horses (33.9%) involving one or more ocular structures: eyelid trauma/notch defect 14 (8.5%), SCC-type adnexal lesions 12 (7.3%), corneal scars 16 (9.7%), keratitis 6 (3.6%), corpora nigra cyst 15 (9.1%), incipient/punctate cataract 50 (30.3%), vitreous degeneration 10 (6.1%), asteroid hyalosis 1, “bullethole” chorioretinal scars 3, RPE coloboma 1. Linear keratopathy was present in 28 horses (17%) with 2/28 having concurrent vision threatening ocular disease.

Conclusions

Ocular abnormalities, in particular minor cataracts, were relatively common in this population, but not typically vision-threatening. Additionally, this survey demonstrated a greater prevalence of linear keratopathy in draft horses compared with reports in other breeds; however, it does not appear to be associated with concurrent ocular disease.     

Nerve growth factor in dogs: Assessment of two immunoassays and selected ocular parameters following a nicergoline challenge per os

Impairment of corneal nerves can result in the development of ocular surface diseases such as aqueous tear deficiency and neurotrophic keratopathy. This study investigates oral nicergoline, an α‐adrenoceptor antagonist shown to enhance endogenous secretion of nerve growth factor (NGF) by the lacrimal gland, as a potential therapy for these conditions. Five female spayed Beagle dogs received a 2‐week course of oral nicergoline (10 mg twice daily). Drug safety was evaluated with ophthalmic and physical examinations, blood pressure monitoring, bloodwork, and urinalysis. The effect of nicergoline on the ocular surface was assessed with corneal esthesiometry, Schirmer tear test‐1, and tear film breakup time. Drug effect on NGF levels was assessed by collecting tears and blood at baseline and completion of therapy using a bead‐based immunoassay and an enzyme‐linked immunosorbent assay. Although nicergoline was well tolerated in all dogs, it did not have a significant impact on corneal sensitivity, tear production, or tear stability. Of note, NGF was below the limit of quantification in all tear samples and was only detected in 8/20 serum samples with no significant difference between levels at baseline (189.4 ± 145.1 pg/mL) and completion of therapy (149.4 ± 79.4 pg/mL). Further validation of NGF analytical assays is warranted before nicergoline is investigated in clinical patients.     

Ocular lesions in Watanabe heritable hyperlipidemic rabbits

Hyperlipidemic ocular lesions are described for Watanabe heritable hyperlipidemic (WHHL) rabbits. Male WHHL rabbits 8 months old exhibited serum hyperlipidemia and ophthalmoscopically yellowish-white lesions along the corneoscleral junction and in the iris. Histopathologically, foamy macrophages aggregated in the stroma of the cornea, iris, and ciliary body were observed. These findings have been interpreted as lipid keratopathy. In addition, multiple clusters of a large number of foamy macrophages occurred throughout the choroid and sclera in association with the blood vessels. The lesions in the choroid and sclera could not be detected ophthalmoscopy, yet were much more prominent than those in the cornea, iris, and ciliary body, suggesting greater involvement and earlier onset of lipidosis at these sites associated with hyperlipidemia in WHHL rabbits.