H. Beaufrère, Dr Med Vet, PhD, Dipl ABVP (Avian), Dipl ECZM (Avian),
J. Nevarez, DVM, PhD, Dipl ACZM, Dipl ECZM (Herpetology),
N. Wakamatsu, DVM, PhD, Dipl ACVP, S. Clubb, DVM, Dipl ABVP (Avian),
C. Cray, DVM, PhD, and T. Tully, DVM, MS, Dipl ABVP (Avian), Dipl ECZM (Avian)
Summary Style Manuscript
Affiliation: From the Health Sciences Centre (Beaufrère), Ontario Veterinary College, University of Guelph, 50 Stone Rd, Gueph, N1G 2W1, ON, Canada; the Department of Veterinary Clinical Sciences (Nevarez, Tully) and Pathobiological Sciences (Wakamatsu), School of Veterinary Medicine, Louisiana State University, Skip Bertman Dr, Baton Rouge, LA 70803, USA; the Rainforest Clinic for Birds and Exotics (Clubb), 3319 E Rd, Loxahatchee, FL 33470, USA; and the Avian and Wildlife Laboratory (Cray), Department of Pathology, Miller School of Medicine, University of Miami, FL 33136, USA.
Avian models for the experimental investigation of atherosclerotic lesions have extensively been used, in particular pigeons, quails, and chickens. Captive psittacine birds are susceptible to atherosclerosis and a large retrospective study suggests that the raw prevalence of advanced lesions is about 7% on postmortem. However, an experimental psittacine model has not been established.
Sixteen young Quaker parrots were randomized into 4 treatment groups and 2 control groups. Treatment groups were fed a pelletized psittacine atherogenic diet composed of 1% cholesterol while the control groups were fed a maintenance pelletized diet. Treatment groups were euthanized every 2 months and all remaining parrots were euthanized at 8 months. Plasma biochemistry, complete blood count, and lipoprotein panels were performed monthly. At the end of each treatment period, major arteries were harvested and processed for histopathology and transmission electron microscopy and atherosclerotic lesions were characterized. Arterial cholesterol con- centration, plasma hydrogen peroxide, and cholesteryl ester transfer protein concentrations were also measured. Statistical analysis was performed using Kruskall-Wallis ANOVA and linear mixed modeling.
Results demonstrated a progressive increase in arterial cholesterol content, plasma LDL, and cholesterol over time in treatment groups. Histopathologic lesions were advanced starting at 2–4 months with significant arterial luminal stenosis.
In this study, we were able to induce advanced atherosclerotic lesions by feeding a 1% cholesterol atherogenic diet and Quaker parrots readily experienced significant dyslipidemia characterized by hypercholesterolemia with increased LDL fraction. This experimental model may be useful to further study the pathogenesis, diagnosis, treatment, and prevention of psittacine atherosclerosis.