Visual outcome in cats with hypertensive chorioretinopathy.

Purpose: To investigate factors associated with long-term visual outcome in cats with hypertensive chorioretinopathy.

Animals Studied: Eighty-eight client-owned cats diagnosed with hypertensive chorioretinopathy.

Procedure: Medical records from cats with systemic hypertension and associated retinal lesions were reviewed.

Clinical therapeutic efficacy of mycophenolate mofetil in the treatment of SARDS in dogs-a prospective open-label pilot study.

Objective: Sudden acquired retinal degeneration syndrome (SARDS) is a leading cause of irreversible blindness in dogs, yet no treatment has been objectively evaluated, or proven to be effective. Consensus of opinion is that SARDS is immune-mediated, although corticosteroid medications may exacerbate associated systemic signs. We examined the effect of sole-agent treatment with mycophenolate mofetil (MMF), a potent immunosuppressive medication unlikely to exacerbate associated systemic signs.

Enucleation or exenteration in two dogs with previous parotid duct transposition: parotid duct ligation versus reverse parotid duct transposition.

Two dogs with previous parotid duct transpositions presented with unrelated ocular disease. In both cases, ophthalmic examination revealed the need for enucleation or exenteration. In case 1, systemic coccidioidomycosis was diagnosed with panuveitis and secondary glaucoma of the left eye.

AAV gene transfer delays disease onset in a TPP1-deficient canine model of the late infantile form of Batten disease.

The most common form of the childhood neurodegenerative disease late infantile neuronal ceroid lipofuscinosis (also called Batten disease) is caused by deficiency of the soluble lysosomal enzyme tripeptidyl peptidase 1 (TPP1) resulting from mutations in the TPP1 gene. We tested whether TPP1 gene transfer to the ependyma, the epithelial lining of the brain ventricular system, in TPP1-deficient dogs would be therapeutically beneficial. A one-time administration of recombinant adeno-associated virus (rAAV) expressing canine TPP1 (rAAV.

Enzyme replacement therapy attenuates disease progression in a canine model of late-infantile neuronal ceroid lipofuscinosis (CLN2 disease).

Using a canine model of classical late-infantile neuronal ceroid lipofuscinosis (CLN2 disease), a study was conducted to evaluate the potential pharmacological activity of recombinant human tripeptidyl peptidase-1 (rhTPP1) enzyme replacement therapy administered directly to the cerebrospinal fluid (CSF). CLN2 disease is a hereditary neurodegenerative disorder resulting from mutations in CLN2, which encodes the soluble lysosomal enzyme tripeptidyl peptidase-1 (TPP1). Infants with mutations in both CLN2 alleles develop normally but in the late-infantile/early-childhood period undergo progressive neurological decline accompanied by pronounced brain atrophy.