Treatment of bullous keratopathy with corneal collagen cross-linking in two dogs.

OBJECTIVE: Corneal collagen cross-linking with riboflavin and UV-A (CXL) decreases corneal oedema and increases visual acuity in human patients with bullous keratopathy. Presumed mechanisms are an increase in collagen packing density and a reduction in stromal swelling pressure. We present two cases in which CXL was used to treat bullous keratopathy in dogs. PROCEDURES: Four eyes of two dogs with painful bullous keratopathy-induced corneal erosions that were resistant to prior therapy were treated with CXL. Both corneas of the second patient were dehydrated to ± 400 µm corneal thickness using topical 70% glycerol solution immediately prior to CXL. Follow-up included slit-lamp examination, fluorescein staining and photographic documentation in both cases and high-resolution ultrasound examination in the second patient. RESULTS: All four eyes were comfortable and fluorescein negative at 1-week post-CXL and remained so for the rest of the follow-up period (17.5 months for case 1 and 6 months for case 2). The owner of the first patient reported a less oedematous cornea and improvement in vision that lasted for 6 months. Despite a reported lack of improvement in vision in the second patient, corneal thickness initially decreased, but was back at baseline thickness at the 4-month recheck. CONCLUSIONS: Similar to humans, CXL might become a useful treatment option for bullous keratopathy-induced therapy-resistant corneal erosions in dogs. Patient comfort was greatly improved, but corneal thickness decrease was not as long-lasting as reported for humans. The presently used protocols might need modification to fit the dog cornea.

Canine neurogenic Keratoconjunctivitis sicca: 11 cases (2006-2010).

OBJECTIVE: To describe the clinical data of dogs with neurogenic Keratoconjunctivitis sicca (KCS) and an ipsilateral dry nose without other neurologic deficits. PROCEDURE: The retrospective case study included 11 dogs diagnosed with neurogenic KCS and an ipsilateral dry nose between 2006 and 2010. Medical records were reviewed for breed, age, sex, history, suspected cause of neurogenic KCS, clinical signs, and treatment modalities. Follow-up information was obtained by re-examination of patients or completion of a telephone survey with the referring veterinarian or the owners. RESULTS: Mean age of the dogs was 6.6 ± 4.5 years. Neurogenic KCS was diagnosed in three females, five spayed females, one male, and two castrated males representing 10 different breeds. Ophthalmic signs of KCS (mean Schirmer tear test [STT] value of 1.9 ± 2.9 mm/min) combined with an ipsilateral dry nose were diagnosed in seven left and four right eyes. The suspected cause of neurogenic KCS was idiopathic in nine and trauma in two cases. Systemic therapy consisted of oral pilocarpine 1-2% eye drops combined with case-specific topical treatment with cyclosporine 0.2% and tear substitutes. Duration of systemic treatment with pilocarpine until healing was 125 days (range 84-204, median 98 days) for five dogs. One dog was lost to follow-up, and the remaining five dogs are still under systemic treatment with pilocarpine. CONCLUSIONS: Neurogenic KCS with an ipsilateral dry nose seems to be a predominantly idiopathic disease of middle-aged female dogs without breed predisposition, which may be self-limiting in some cases.

Unusual Presentation of Feline Leprosy Caused by Mycobacterium lepraemurium in the Alpine Region.

A 9-year-old cat was referred with multiple, raised, ulcerative and non-ulcerative nodules in the periocular area, sclera and ear-base region, and on the ventral aspect of the tongue. In addition, a progressive ulcerative skin nodule on the tail was observed. Fine-needle aspirations of multiple nodules from the eyelid and sclera revealed the presence of histiocytes with numerous acid-fast intracellular bacilli. The replication of slowly growing mycobacteria in liquid media was detected from biopsied nodules after three months of incubation. The molecular characterization of the isolate identified Mycobacterium (M.) lepraemurium as the cause of the infection. The cat was treated with a combination of surgical excision and a four-week course of antimicrobial therapy including rifampicin combined with clarithromycin. This is an unusual manifestation of feline leprosy and the first molecularly confirmed M. lepraemurium infection in a cat with ocular involvement in Europe. The successful combination of a surgical and antimycobacterial treatment regimen is reported.

Bilateral vision loss in a captive cheetah (Acinonyx jubatus).

The following case report describes a 1-year-old female cheetah (Acinonyx jubatus) with bilateral blindness and unresponsive pupils. For comparison, a second healthy 2.5-year-old male cheetah without visual deficits was also examined. Clinical examination of both animals included biomicroscopy, indirect ophthalmoscopy, tonometry, and electroretinography. The young female cheetah showed no menace response, no direct or indirect pupillary light reflex, and no dazzle reflex in either eye. Fundus lesions, as detected by indirect ophthalmoscopy, are described for the female animal. In both eyes, the fundus color was green/turquoise/yellow with multiple hyperpigmented linear lesions in the tapetal area around the optic nerve. The optic nerve head was dark gray and about half the normal size suggesting bilateral optic nerve hypoplasia and retinal dysplasia or differentially optic nerve atrophy and chorioretinal scarring. The ERG had low amplitudes in the right eye but appeared normal in the left eye compared with the male cheetah. Blood levels did not suggest current taurine deficiency. This is addressed to some degree in the discussion. Bilateral optic nerve hypoplasia or optic nerve atrophy is a rare anomaly in cats and has not yet been described in a cheetah.