Hepatic Lipidosis in Camelids

A brief look into the pathogenicity and prevalence of hepatic lipidosis among camelids.
Hepatic Lipidosis in Camelids - Articles
Hepatic Lipidosis in Camelids

Hepatic lipidosis is a well-known syndrome in periparturient dairy cattle and sheep, anorexic cats, and a sporadic problem with fat horses and ponies. This pathologic process has also been recognized in most other species, including humans. There are limited reports of hepatic lipidosis in llamas and alpacas in the literature; however, producer groups and practicing veterinarians have an increased interest in the pathogenesis of this disease process. We have dealt with three different herd-based problems with hepatic lipidosis in which multiple animals have been lost in the past year. These cases have prompted projects attempting to further characterize and define the pathogenesis of this disease process.

Natural Occurring Cases

A retrospective study of 31 histologically confirmed cases of hepatic lipidosis in llamas and alpacas submitted to Oregon State University Veterinary Diagnostic Laboratory revealed a predominately middle aged, pregnant or lactating female population to be affected. However 22.6% of the cases were male and age ranged from 5 months to 18 years. This is a very different demographics of affected animals compared to the disease in other ruminants. In these cases there was no significant association with any infectious, parasitic, or toxic causative agent. The most common factor documented in histories from these camelids was recent severe loss of appetite or weight loss. This period of not eating or weight loss varied from a couple of days to several weeks. Overweight, normal body condition, and thin animals were all represented in the affected group. Biochemical measures associated with negative energy balance (NEFA), liver dysfunction (bile acids), and muscle damage were consistently elevated. Lipemia and ketonemia were not consistently associated with hepatic lipidosis in this retrospective study population compared to the two literature reports. These data suggest similarities in the pathogenesis of hepatic lipidosis in camelids to other species and not just ruminants. A common theme in most cases of hepatic lipidosis in camelids is a period of anorexia prior to clinical signs.

Based on this study and on additional cases identified since it was completed, our conclusions are that camelids of a variety of ages, gender, body condition, and reproductive status are susceptible to development of hepatic lipidosis. Conditions that place increased energy demands, such as pregnancy and lactation contribute to hepatic lipidosis, but other stresses including social and environmental stresses or other illness appear to also predispose camelids to loss of appetite, weight, and accumulation of fat in the liver.

Experimentally Induced Hepatic Lipidosis

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 has included lactating and non-lactating animals. After obtaining baseline information, the llamas were weighed daily, fed a measured amount of hay, and given unrestricted access to water. Crias were allowed to nurse. Blood samples and liver biopsies were obtained throughout the study. The trial ended when there was any indication in blood work, biopsy, or clinical signs of the onset of hepatic lipidosis.

All llamas in the study lost large amounts of body weight. About half developed hepatic lipidosis. No animals became depressed or recumbent. Blood tests showed the expected increases in liver enzymes in those that developed hepatic lipidosis, but not in those that simply lost weight. This is important in telling us that our blood indicators of liver disease (bile acids) are relatively specific in llamas. When the affected llamas were returned to normal feed, we saw increases in weight, gradual changes in the blood values towards normal, and the disappearance of fat from the livers based on biopsies. This was also a significant finding in that it showed that the condition is reversible when normal levels of nutrients and calories are consumed.

This study has shown that it is difficult, but possible to induce hepatic lipidosis in llamas by feed restriction, which suggests that loss of appetite alone may not be enough to cause this problem. It has also shown that there are clinical and biochemical differences in this experimental model of hepatic lipidosis and the naturally-occurring form. We are speculating that the additional stresses involved in most of the naturally-occurring cases lead to changes in how the animals can utilize carbohydrates, proteins, and lipids. We plan to study factors that might be involved.

Conclusions

The key to preventing and treating this disease is increased understanding of the unique metabolic processes of camelids. The bottom line for prevention is to ensure adequate energy and protein intake, especially in pregnant and lactating females through good quality forage and appropriate supplementation. Adequate energy/protein intake can be easily assessed by use of hands-on body condition scoring. Close monitoring of intake in sick animals is absolutely critical to prevent deaths.

References

  • Tornquist, SJ, Cebra, CK, Van Saun, RJ, Smith, BB. Metabolic changes and induction of hepatic lipidosis during feed restriction in llamas. American Journal Veterinary Research 2001;62(7):1081-1087.
  • Van Saun, RJ. Callihan, B, Tornquist, SJ. Nutritional support for treatment of hepatic lipidosis in a llama. Journal Am Veterinary Med Assoc 2000;217(10):1531-1535.
  • Tornquist, S.J., R.J. Van Saun, B.B. Smith, C.K. Cebra and S.P. Snyder. Histologically- confirmed hepatic lipidosis in llamas and alpacas: 31 Cases (1991-1997). Journal Am Veterinary Med Assoc 1999;214(9):1368-1372.

Authors

Ruminant nutrition Dairy herd health Metabolic disease Reproduction Nutrition reproduction interactions Small ruminants Llamas and Alpacas

More by Robert J. Van Saun, DVM, MS, PhD