Results suggested that dogs treated long term with phenobarbital or with phenobarbital and bromide may develop hypertriglyceridemia. Fasting serum triglyceride concentration should be periodically monitored in dogs treated with phenobarbital because hypertriglyceridemia is a risk factor for pancreatitis.

Primary lipid disorders causing fasting triglyceridaemia have been documented infrequently in Burmese cats. Due to the known increased risk of diabetes mellitus and sporadic reports of lipid aqueous in this breed, the aim of this study was to determine whether healthy Burmese cats displayed a more pronounced pre- or post-prandial triglyceridaemia compared to other cats. Serum triglyceride (TG) concentrations were determined at baseline and variably at 2, 4 and 6h after ingestion of a high-fat meal (ie, an oral fat tolerance test) in a representative sample of Burmese and non-Burmese cats. The median 4 and 6h serum TG concentrations were significantly higher in Burmese cats (4h - 2.8mmol/l; 6h - 8.2mmol/l) than in other pedigree and domestic crossbred cats (4h - 1.5mmol/l; 6h - 1.0mmol/l). The non-Burmese group had post-prandial TG concentrations ranging from 0.6 to 3.9mmol/l. Seven Burmese cats had post-prandial TG concentrations between 6.6 and 19.0mmol/l, five had concentrations between 4.2 and 4.7mmol/l, while the remaining 15 had post-prandial concentrations between 0.5 and 2.8mmol/l. None of these Burmese cats had fasting triglyceridaemia. Most Burmese cats with a 4 h TG > 6.0 mmol/l had elevated fasting very low density lipoprotein (VLDL) concentrations. This study demonstrates that a proportion of Burmese cats in Australia have delayed TG clearance compared to other cats. The potential repercussions of this observation with reference to lipid aqueous, pancreatitis and diabetes mellitus in Burmese cats are discussed.

A 7-year-old cat was presented initially with multiple draining sinuses on the metatarsal region of its right hindlimb. Another lesion had appeared at the same time on the fifth proximal interphalangeal joint of the left forelimb. Histopathological examination of a biopsy from the right hindlimb lesion revealed chronic pyogranulomatous inflammation associated with yeast-like bodies and septate mycelia; a fungus was cultured on conventional media but not identified further. Culture of a swab collected from the left forelimb lesion demonstrated a pigmented fungus, also not characterised further. Although there was initially a favourable response to ketoconazole (Nizoral, Janssen-Cilag Pty. Ltd) and beta-lactam therapy, the infection in the hind limb relapsed subsequently, and Fusarium chlamydosporum was cultured from deep biopsy specimens. Clinical improvement followed debridement and itraconazole (Sporanox, Janssen-Cilag Pty. Ltd; 100 mg orally once daily), however amputation of the limb represented the best chance for a cure. The cat made an uncomplicated recovery following surgery and remained well for five months until the lesion on the left forelimb recurred. Amputation of the distal fourth digit was then performed, and the resected tissue submitted for culture. The dematiaceous fungus Microsphaeropsis arundinis was subsequently cultured. The cat remained well for several months, until a further F. chlamydosporum infection developed on the body wall. This was excised 7 months ago, and no lesions have recurred in this area. Importantly, this is the first reported case of M. arundinis infection in a mammalian host.

1 meter had greater accuracy in the range of 140 to 400 mg/dL and was therefore well suited to detect hypertriglyceridemia. The other meter was accurate with triglyceride values < 140 mg/dL and yielded results similar to those of the veterinary laboratory in the range of 140 to 400 mg/dL, therefore being suitable for determination of triglyceride concentrations in nonfed dogs and dogs with mildly high concentrations.

A proportion of Burmese cats in Australia have an exaggerated post-prandial triglyceride (TG) response after an oral fat tolerance test (OFTT). The aim of this study was to determine (a) whether Burmese cats with presumed lipid aqueous (PLA) had exaggerated post-prandial triglyceridaemia, (b) if Burmese cats with exaggerated post-prandial triglyceridaemia ('affected' cats) had decreased lipoprotein lipase (LPL) activity and (c) whether affected cats were more insulin resistant than normal Burmese cats. Of cats with a history of PLA, 4/5 were shown to be lipid intolerant (4h TG>4.5mmol/l). Four affected Burmese cats were age, gender and body condition matched to four normal Burmese cats. Serum TG, insulin, non-esterified fatty acids (NEFA), lipoprotein and apolipoprotein concentrations were determined 2 weeks after commencing a standardised high-protein diet, with an OFTT performed 4 weeks later. Affected Burmese cats did not have significantly different fasting insulin, fructosamine, NEFA, apolipoprotein or lipoprotein concentrations compared to control cats. During the OFTT, affected cats had significantly higher 4h and 6h serum TG and NEFA concentrations than normal cats. There was a trend for lower LPL activity, higher insulin concentrations (at 4 and 6h) and higher insulin area under the curve (AUC) during the OFTT in affected Burmese cats compared to controls, although these results failed to reach significance, probably due to the small number of cats studied. Further investigations using larger numbers of cats should focus on reduced LPL activity and insulin resistance as potential causes of delayed TG clearance.