Objectives This study aimed to describe the epidemiology and clinical presentation of presumed hereditary or presumed breed-related ocular diseases in a population of cats in France. Methods Medical records from between September 2013 and August 2017 were reviewed to identify cats with at least one presumed hereditary or breed-related ocular disease. Cats with concurrent, or a history of, ocular or systemic infectious diseases were excluded. Signalment, history and clinical findings were recorded. Results Of the 1161 cats that presented to our institution during the study period, 129 were diagnosed with at least one presumed hereditary or presumed breed-related ocular disease (11.1%, 95% confidence interval [CI] 9.3–12.9). Five ocular abnormalities had a prevalence of >1%: entropion, corneal sequestration, persistent pupillary membrane, cataract and retinal dysplasia. The prevalence of entropion was 2.2% (95% CI 1.3–3.0), with Persians ( P = 0.03), Maine Coons ( P <0.01) and male cats ( P <0.01) being over-represented. The prevalence of corneal sequestration was 2.4% (95% CI 1.5–3.3), with Persians ( P <0.01) and Exotic Shorthairs ( P = 0.02) being over-represented. Persistent pupillary membranes and cataracts had the same prevalence of 2.3% (95% CI 1.5–3.2), with no particular sex or breed significantly over-represented. Retinal dysplasia had a prevalence of 1.6% (95% CI 0.8–2.3) and Persian cats were over-represented ( P = 0.04). Anterior segment dysgenesis had a low prevalence (0.9%, 95% CI 0.4–1.5), with all affected cats being domestic shorthairs and this breed therefore being over-represented ( P = 0.04). Conclusions and relevance In a French population of cats, presumed hereditary or breed-related ocular diseases accounted for 11.1% of all ocular diseases. Cataracts, corneal sequestration, persistent pupillary membrane, entropion and retinal dysplasia were the most common conditions. Statistical breed over-representation was observed for entropion, corneal sequestration and retinal dysplasia. We recommend that more systematic screening of feline species is conducted.

Background In a previous study, telmisartan suppressed aldosterone secretion in healthy cats but not in cats with primary hyperaldosteronism (PHA). Hypotheses Telmisartan suppresses aldosterone secretion in middle‐aged healthy cat and cats with diseases that may result in secondary hyperaldosteronism, but not in those with PHA. Animals Thirty‐eight cats: 5 with PHA; 16 with chronic kidney disease (CKD), subclassified as hypertensive (CKD‐H) or non‐hypertensive (CKD‐NH); 9 with hyperthyroidism (HTH); 2 with idiopathic systemic arterial hypertension (ISH); and 6 healthy middle‐aged cats. Methods Prospective, cross‐sectional study. Serum aldosterone concentration, potassium concentration, and systolic blood pressure were measured before and 1 and 1.5 hours after PO administration of 2 mg/kg of telmisartan. The aldosterone variation rate (AVR) was calculated for each cat. Results No significant difference in the minimum AVR was observed among groups (median [quartile 1 (Q1); quartile 3 (Q3)]: 25 [0; 30]; 5 [−27; −75]; 10 [−6; −95]; 53 [19; 86]; 29 [5; 78]) for PHA, CKD, HTH, ISH, and healthy cats, respectively (P = .05). Basal serum aldosterone concentration (pmol/L) was significantly higher in PHA cats (median [Q1; Q3]: 2914 [2789; 4600]) than in CKD‐H cats (median [Q1; Q3]: 239 [189; 577], corrected P value = .003) and CKD‐NH cats (median [Q1; Q3]: 353 [136; 1371], corrected P value = .004). Conclusions and Clinical Importance The oral telmisartan suppression test using a single dose of 2 mg/kg telmisartan did not discriminate cats with PHA from healthy middle‐aged cats or cats with diseases that may result in secondary hyperaldosteronism.

A four-year-old, male, captive-born African helmeted turtle (Pelomedusa subrufa) was presented for an ocular disorder of three days duration. Physical examination showed edema of all limbs and blepharedema of the left eye. Ophthalmic examination revealed severe blepharoconjunctivitis, a large melting corneal ulcer and stromal densification that prevented evaluation of the anterior chamber. Examination of the right eye was unremarkable. Ultrasonography of the left eye revealed corneal perforation associated with severe anterior uveitis. Enucleation was performed based on the poor prognosis for the eye and the risk of septicemia. Providencia rettgeri was identified from bacterial culture. Fungal culture was negative. Histopathology of the eyeball revealed a corneal perforation associated with edema and heterophilic infiltration of the corneal stroma. Three weeks after surgery, the enucleation wound had healed. P. rettgeri has been reported as a rare cause of keratitis in humans. A systematic literature review showed one case of a melting corneal ulcer in an Asian rhinoceros (Rhinoceros unicornis) associated with this infectious agent. This is the first report of corneal perforation associated with P. rettgeri in a reptile.

Description du cas. Une jument de race Frison, âgée de 11 ans, est référée pour la prise en charge d’un ulcère cornéen chronique à l’œil gauche ne rétrocédant pas au traitement médical prescrit. Un ulcère cornéen d’aspect similaire avait été pris en charge à droite environ deux ans auparavant. En dépit des traitements médicaux, cet ulcère s’était dégradé et une énucléation avait été réalisée. A son admission, la jument présente une perte de substance cornéenne para-axiale temporo-ventrale, d’environ 2/3 de l’épaisseur cornéenne et de 4 mm de diamètre. Aucun signe de douleur ou d’uvéite antérieure n’est présent. Le test à la fluorescéine est négatif. Une dystrophie cornéenne du Frison est suspectée sur les critères cliniques et épidémiologiques. Prise en charge. Une chirurgie de greffe conjonctivale est réalisée sous anesthésie générale, permettant une stabilisation de la cornée durant tout le suivi post-opératoire. L’analyse histopathologique révèle une désorganisation des fibres de collagène, en faveur de notre suspicion clinique. Discussion. La pathogénie de cette maladie cornéenne du Frison n’est pas connue, mais une altération de la production des fibres de collagènes, éventuellement reflet d’un défaut multisystémique, est suspectée. Plusieurs modalités de prise en charge sont rapportées. La technique chirurgicale de greffe conjonctivale est majoritairement décrite.