Hepatic Lipidosis in Camelids - Veterinary and Biomedical Sciences

Alpaca nutritional requirements: Pregnancy and hepatic lipidosis
Robert J. Van Saun, DVM, PhD
Department of Veterinary and Biomedical Sciences, Penn State University, rjv10@psu.edu
Abstract
Key Words
Nutrient requirements, pregnancy, hepatic lipidosis, alpaca, management
Introduction
The most desirable outcome from a pregnancy is to have a healthy, vigorous cria, no health complications
with the dam, and successful rebreeding within 30 days. Nothing can be more frustrating for an owner
after the long wait than to have something go wrong with their newborn cria, especially if the pregnancy
was difficult to conceive. Even more disheartening is learning that something could have been done to
prevent the problem during pregnancy.
Research with cattle and sheep has shown that nutrition in pregnancy influences colostrum quality and
quantity, milk yield and composition, neonate viability, and future fertility of the dam. These data reveal
the critical nutritional issues that need to be addressed during pregnancy. The critical issues are: energy
and protein balance relative to requirements and appropriate supplementation of minerals and fat-soluble
vitamins. From a management standpoint, issues such as level of intake, forage quality, body condition
monitoring, and environmental stressors must be considered.
For an industry that is dependent upon sound reproduction, we have little data to guide us in the proper
nutrition of our pregnant animals. Data specifically addressing pregnancy nutrition of alpacas and llamas
are scarce at best. Because there is sufficient functional similarity of anatomy and physiology between
camelids and other ruminants, extrapolation of basic concepts of pregnancy nutrition from other species
can be applied to the alpaca and llama and will be the focus of this discussion.
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.