Susan Tornquist, DVM, M.S., PhD, Dip. A.C.V.P.
College of Veterinary Medicine, Oregon State University
Accumulation of fat in hepatocytes occurs in many species and is associated with well-known clinical syndromes in cats, cows, ponies, and humans. Hepatic lipidosis can result from a variety of pathophysiologic events. Clinical implications of this condition vary from high mortality in cats, to a mild decrease in productivity in lactating dairy cattle.
Hepatic lipidosis in camelids has been infrequently reported in the literature, but is increasingly recognized in cases of camelid illness or death. Although hepatic lipidosis is not likely to be the primary cause of death, it appears to represent metabolic disturbances that have serious implications.
At the College of Veterinary Medicine at Oregon State University, we have conducted two studies of hepatic lipidosis in camelids. One study is a review of 31 histologically-confirmed cases of naturally-occurring hepatic lipidosis in camelids. The second study, funded by the Morris Animal Foundation, created an experimental model of hepatic lipidosis in llamas using feed restrction and evaluated clinical, histologic, and biochemical changes that occur during development of this condition. The overall goal of these studies wass to understand the pathogenesis of camelid hepatic lipidosis in order to more effectively predict, prevent, and treat the condition.
Thirty-one camelids with histologically-confirmed hepatic lipidosis were identified from Veterinary Diagnostic Laboratory (VDL) records. Medical and historical information about these cases was obtained from medical records, owners, and referring veterinarians.
The 31 cases comprised 3.9% of 783 total camelid necropsy and biopsy submissions to the VDL between 1991 and 1997. Twenty-nine of 31 camelids did not survive their illness. The group included 30 llamas and 1 alpaca. Of the camelids with hepatic lipidosis 24 (77.4%) were female and 7 (22.6%) were male. Although this showed a gender distribution with more than 3 times as many females as males, it did not differ significantly from the gender distribution of camelid necropsy and biopsy submissions during the same period.
The animals ranged from 5 months to 18 years in age with a mean of 6.68 +/- 4.4 years. The predominance of animals in the age range of 6-10 years differed significantly from the reference population of camelids submitted to the VDL during the same time period.
Thirteen llamas with hepatic lipidosis were pregnant (54.1% of females) and 11 were lactating (45.8%). The most common factor documented in histories from these camelids was recent severe anorexia or weight loss (51.6%). Five llamas were reported to be clinically normal less than 24 hours prior to being found acutely ill or dead. Neurologic signs were reported in 8 animals (25.8%). Diarrhea was reported in the recent histories of 6 animals (19.4%). Changes in social or environmental conditions were documented for 10 of the animals (32.2%).
The most common serum biochemical abnormalities noted in the affected camelids were consistent with decreased hepatic function (increased bile acids), cholestasis (increased GGT and alkaline phosphatase) and leakage of enzymes from muscle and liver (increased AST). Hypoproteinemia and hypertriglyceridemia were also relatively common. About half of the animals were hyperglycemic at the time blood was taken. Non-esterified fatty acids (NEFA) and the ketone b-hydroxybutyrate (b-OH) were elevated in all 7 of the animals in which they were measured. These changes reflect negative energy balance and fat mobilization.
All animals tested for viruses and trace mineral abnormalities were negative. Bacteria were cultured from only one animal. Eperythrozoon were identified in 5 llamas. Gastrointestinal parasites were found in 6 of the cases. Analysis of feed for mycotoxins and forage analysis for nutritional deficiencies were negative when performed.
This study showed that all sick camelids should be considered at risk for developing hepatic lipidosis, especially those with anorexia or increased energy demands. Other stresses appear to contribute to the condition. Diagnosis cannot be made by serum biochemical testing alone, but the presence of high bile acids, GGT, AST, NEFA, and b-OH may indicate the development of the syndrome.
Since a history of recent anorexia or weight loss was the most common factor in the naturally-occurring cases of camelid hepatic lipidosis, we attempted to create a model of this condition by limited feed restriction. The study included 10 female llamas including 5 lactating and 5 non-lactating animals. The llamas were acclimated for several days during which time they were weighed, baseline blood work done, and ultrasound-guided liver biopsies taken. The llamas were restricted to 0.25% body weight dry matter hay fed daily, except for the initial 2 animals who received 1.0 % BW and 0.5 % BW feed daily. Free choice water was given and crias were allowed to nurse.
All llamas in the study lost significant amounts of body weight and all except 2 thin llamas mobilized fat as evidenced by elevations in NEFA. Histologically-confirmed hepatic lipidosis developed in 5 of the llamas, although anticipated clinical signs of depression and recumbency occurred in none of the llamas.
Serum biochemical changes that occurred in all the feed-restricted llamas were increases in ketones, decreases in BUN, and moderate elevations in cholesterol. The most significant differences between the feed-restricted llamas that developed hepatic lipidosis and those that didn’t was elevations of bile acids, GGT, and SDH in the former, but not the latter. In addition, hypoglycemia was not a consistent finding, but did occur only in the feed-restricted llamas that developed hepatic lipidosis.
Our conclusions from this study are that it is possible to induce hepatic lipidosis in llamas with severe feed restriction, especially in the face of increased energy demand, such as occurs in early lactation. The clinical and biochemical changes in induced camelid hepatic lipidosis are similar to those seen in dairy cow hepatic lipidosis. There are several clinical and biochemical differences between this induced camelid hepatic lipidosis and the naturally-occurring form. It is possible that in the natural-occurring hepatic lipidosis there may be a stress-induced defect in glucose utilization.
An additional conclusion from this study is that bile acids, GGT, and SDH appear to be good biochemical markers of hepatopathy and reduced hepatic function in camelids, although they are not specific for hepatic lipidosis.
Finally, we showed that hepatic lipidosis is reversible when animals are fed normal diets. It's important to realize that early detection and/or aggressive therapy can be successful in treating camelids with hepatic lipidosis.
Reproduced from www.orst.edu with permission of Susan Tornquist. Copyright © Oregon State University
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