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Cardiovascular Disease in Rabbits: More questions than answers|
Barbara Deeb, DVM
Wooly was a 3 year old Jersey Wooly. His human companion reported that he had been sitting in a hunched posture and trying to walk on his toes. Physical examination, X-rays and blood tests were not diagnostic. Tests for Encephalitozoon cuniculi and Pasteurella multocida were negative. Other blood tests were within normal limits. Later his right rear leg lost muscle tone and was out of alignment. Weakness progressed to paralysis, and he was unable to use even his front legs. He developed swelling around his genitals and toes; and about 6 weeks after he first showed signs, Wooly became very lethargic, stopped eating, drinking and passing feces. Despite treatment for GI stasis, he died.
Post mortem examination and histopathology showed degenerative cardiomyopathy, liver degeneration and GI stasis. The liver changes and GI stasis were likely secondary to inability of the heart to pump normally. How did this young rabbit develop cardiomyopathy? Could his lameness have been due to thromboembolism? If detected earlier, what might have helped him medically?
Sylvie, a 6 year old Netherland Dwarf, developed severe acute loud breathing noises in her nose and lungs. Radiographs revealed an enlarged heart and increased lung density and GI stasis. Ultrasound of the organs in the chest showed right-sided heart enlargement, enlargement of the large veins and indicated high blood pressure in the lungs. She was treated with an antibiotic and drugs to make breathing easier. About 2 weeks after signs first appeared, Sylvie developed gastric bloat and died.
The post mortem exam and histopathology revealed an enlarged, flabby heart. The lungs had chronic pneumonia and fluid accumulation. The nose and sinuses were filled with exudate. Sylvie died from shock, bloat and heart failure. Was the degenerative heart disease brought on so quickly by the acute respiratory problem or did a weak heart exacerbate the respiratory disease?
Emily, a checkered giant, was 2 years old when she began to have choking episodes. On oral examination nothing abnormal was seen, but endoscopy revealed an elongated soft palate, which may have interfered with her ability to regulate swallowing and breathing. Blood tests showed Emily to be slightly anemic, have a high white cell count and be high positive for encephalitozoonosis, so she was treated with an antibiotic and antiparasite drug. One evening she appeared to have vomited, then choked, became uncoordinated, gasped for breath and died.
The most notable post mortem findings were hemorrhage in the trachea, acute and chronic bronchopneumonia due to aspiration of foreign material into the lungs. The heart appeared grossly to be flabby and whitish, microscopically to be infiltrated by scar tissue and fatty deposits. Additionally the heart, liver and kidneys showed microscopic evidence of infection with E. cuniculi. Emily probably died because of the aspiration of food. Changes in the heart were chronic and acute. Did heart disease influence Emily's respiratory problem or was it simply coincidental?
Fiver was rescued as a young feral bunny. He was about a year and a half old when he had his first veterinary exam because of lameness of has left front foot. The leg was painful, but no other abnormality could be found, and the lameness resolved in a few days. A few months later Fiver returned because he was losing weight, and his balance was poor. Blood tests for P. multocida and E. cuniculi were negative. Other blood tests pointed to an early kidney problem. Over the next few months, he lost mobility, had excessive thirst, urination and weight loss despite eager consumption of a high quality diet. He was given regular fluid therapy, but Fiver was found dead one morning.
Fiver had amazingly advanced arterial calcification throughout his body. All visible arteries were white and stiff. The histopathologic diagnosis was calcium deposition and scarring of the kidneys, severe mineralization of the arteries and scarring of both heart ventricles. What may have been the cause of this dramatic cardiovascular mineralization and disposition of scar tissue in a young rabbit?
Harry was a 6 or 7 year old Angora who had a home change when he was 1 or 2. His medical history included conjunctivitis (probably due to allergies), middle ear infection and head tilt. He was also positive for both P. multocida and E. cuniculi infections, was treated for both and apparently recovered. Thereafter, he had repeated episodes of enteritis. Changes in feces seemed related to changes in diet, but he was offered the best greens and hay a rabbit could want. One evening he developed a high fever, head tilt, difficult breathing, and died on his way to the clinic.
Post mortem analysis showed overdistension of lung tissue with air and fluid, acute pneumonia, cardiomyopathy and thromboembolism. Additionally, there was severe mineralization of the large vessels and lungs, plus mild liver and kidney disease. Several disease processes were at work; bacterial infection in the bloodstream (what was the source?), inability of the heart to pump properly and supply oxygen to the tissues, and mineralization of the vessels and lungs. Were the bouts of enteritis secondary to poor oxygenation?
Comments: Vet to Vet
Cardiomyopathy and cardiac insufficiency may develop as a result of damage to the heart muscle, possibly as a result of infections, such as corona virus, Clostridum piliformis (Tyzzers disease) other toxin-producing bacteria or even E. cuniculi. Nutritional deficiencies or imbalances may predispose to cardiovascular disease. A well-known cause of abnormal mineralization of soft tissues, such as arteries, is hypervitaminosis D and/or dietary calcium and phosphorus imbalances resulting in hypercalcemia and hypophosphatemia. Such blood imbalances can also be secondary to some cancers and to kidney disease with increased levels of parathormone production. But might rabbits tend to hyperparathyroidism more often than other mamals? They routinely maintain higher blood calcium and lower phosphorus levels. We can only speculate about the mechanisms which resulted in the cardiovascular diseases which shortened the lives of Wooly, Sylvie, Emily, Fiver and Harry. None had obvious cancer. All appeared to have good diets. Infectious diseases were a factor in 3 of the cases.
Detecting heart murmurs and irregularities by is more difficult in rabbits than some other animals. Signs of cardiovascular disease may mimic other ailments in rabbits, the result of oxygen deprivation or poor circulation: incoordination, weakness, weight loss, depression, enteritis, difficult breathing. If suspected, diagnostic measures are as for other animals: radiographs, ultrasound, ECGs, blood chemistries. If detected, medical management could include medications to improve cardiac contractility, reduce edema, and reduce cardiac workload. If vascular mineralization and hypercalcemia is detected, treatment would include diuresis with injections of isotonic saline and dietary changes. We can't solve cardiovascular problems in rabbits, but we can't even help if we don't recognize that they occur.
Case studies: Barbara Deeb, DVM, MS; notes and health records from All Pet Veterinary Clinic, Shoreline WA.
Figures: Ettinger, S.J., and R. L. Pyle, Textbook of Veterinary Internal Medicine,1982. W.B. Saunders Company.
McLaughlin, C.A. and R. B. Chaisson, 1990. Laboratory Anatomy of the Rabbit. William C. Brown/McGraw-Hill.
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