Liver Disease


Hepatic Lipidosis - Fatty Liver Disease

Hepatic - The medical terminology for anything related to the liver.

Hepatocellular - Pertaining to or affecting liver cells.

Hepatocytes - A cell of the main tissue of the liver; liver cell.

Hepatocellular Disease - May be either an infection of the liver or cancer of the liver.

Hepatic Fibrosis - Excessive connective tissue accumulates in the liver, this tissue represents scarring in response to chronic, repeated liver cell injury.  Commonly, fibrosis progresses, disrupting hepatic architecture and eventually function, as regenerating hepatocytes attempt to replace and repair damaged tissue.  When such disruption is widespread, cirrhosis is diagnosed.
(2) Fibrosis is the formation of an abnormally large amount of scar tissue in the liver.  It occurs when the liver attempts to repair and replace damaged cells.  Fibrosis itself causes no symptoms, but severe scarring can results in cirrhosis, which can cause symptoms.

Portal - Relating to a point of entrance to an organ, especially the transverse fissure of the liver, through which the blood vessels enter.  (Transverse - lying across the long axis of the body or of a part.  Fissure - a narrow split or groove that divides an organ such as the brain lung, or liver into lobes)



What Is It?
The liver is one of the biggest and most important organs in the body and keeps the body's metabolism and function in balance.  On a biochemical level, it is responsible for many essential processes.  The failure of any of these biochemical functions could lead to the death of the animal.  The liver can be affected by diet, infection, drugs, and other toxic chemicals. 

Some of the main functions of the liver include proper handling of carbohydrates (sugars, starches), lipids (fats, cholesterol, bile acids), and proteins. Some of the important proteins produced by the liver include blood clotting factors, urea (used by the kidney to help with the body’s water preservation), and albumin (the main protein in the blood which helps maintain the proper fluid volume in the heart and blood vessels). Essential vitamins and minerals are produced, stored, or altered by the liver for proper use in the body. The liver aids in the functions of the immune system, the endocrine system, and in maintaining healthy blood cells. Bile acids are produced and stored in the liver and gallbladder, and are used in the digestive tract in the breakdown of food.

One very important function of the liver is its role as the body’s filter from the digestive tract. The entire digestive tract contains bacteria and food in various stages of breakdown. Nutrients are absorbed into the blood through tiny capillaries from the stomach and intestines. Blood from the digestive tract may be thought of as "dirty," since it is so close to a source of contamination— millions of bacteria and possibly harmful substances taken into the body through the mouth. From here, the blood enters the liver’s portal blood system, where the liver can "detoxify" any harmful substances and acts as the first line of defense against invading bacteria.

The liver has a tremendous ability for regeneration and functional reserve. It is able to tolerate injury and insult better than most organs without failing (although sickness may be very apparent in the body) and can repair itself remarkably well following damage. These are wonderful features of this vital organ, but they can also make it difficult to recognize when a serious disease of the liver is present."

Liver Disease in Camelids  (4-14-02)

David E Anderson, D.V.M., MS, Diplomate ACVS
College of Veterinary Medicine
The Ohio State University, Columbus, Ohio

Liver disease has not been widely recognized in camelids (alpacas and llamas). Although fatty liver disease is often discussed or observed during necropsy examination, primary liver diseases have been infrequently diagnosed. Recent clinical data suggest that the cause of fatty liver disease may have been overlooked in many camelids. Because camelids are not used for intensive meat or milk production in North America and they usually are not overworked by riding or carting, theories postulated for onset of liver disease in other livestock species may not apply to camelids. Investigations of camelid disease is in its infancy in the USA, and I expect that significant breakthroughs are on the horizon. We have begun investigations at Ohio State University to attempt to better determine the response of camelids to disease and stress.

I often find evidence of liver disease in camelids while working-up a case of what might be termed "Sick Camelid Syndrome" or SCS. SCS refers to a camelid that demonstrates depression, lethargy, increased periods of recumbency, and decreased appetite. Occasionally diarrhea or abdominal discomfort are observed. The results of physical examination fail to reveal any abnormalities except that the animal may be more tender to palpation of the abdomen than normal. In my opinion, laboratory testing of these animals is obligatory because of the stoic nature of these patients. A camelid may not show clinical signs of severe disease in a desperate attempt not to be singled out from the herd as a "weakened" animal by potential predators. The most important information to be gained by veterinarians from the owner is a detailed account of the animals recent lifestyle. Any changes should be discussed (nutrition, herd mates, feed bags, traveling to shows / sales / new farm, breeding activity, importation and quarantine, de-worming and vaccines or lack thereof, obesity, heat stress, emaciation, etc). Most cases of liver disease are found to be caused by or exacerbated by stress.

A thorough physical examination is required to rule-out common causes of illness in camelids: parasites, GI disturbance, C3 ulcer, starvation or malnutrition, social hierarchy, dental problems (tooth root abscess, malocclusion, etc), neurologic disease (meningeal worm, trauma, infection), pneumonia, etc. Rectal temperature, heart rate and rhythm, respiratory rate and pattern, C1 motility frequency and pattern, fecal consistency / color, urine color / clarity, peripheral lymph node palpation, and oral examination are the minimum veterinary data base. Clinical signs will dictate additional diagnostic tests, but most suffer from Sick Camelid Syndrome and, therefore, I routinely perform a complete blood cell count and serum biochemistry profile. I have seen many camelids suffering from severe liver disease demonstrate clinical signs of acute abdominal pain. These patients must be accurately differentiated from surgical colic because the stress of surgery and general anesthesia is extremely detrimental to patients with liver disease.
I have a liver and kidney profile run which includes SDH, GGT, AST, CPK, triglycerides, cholesterol, Cr, and BUN. SDH and GGT are cellular enzymes that provide a reflection of the severity of liver damage. AST and CPK are cellular enzymes that reflect muscle injury and allow some assessment for how long and how often the camelid has been lying down. Triglyceride and cholesterol are components of fat and provide an assessment of how much lipid mobilization is occurring. Creatinine and BUN are products of protein metabolism that are excreted by the kidneys and allow evaluation of general kidney function. I have found that rising BUN and Cr despite supportive therapy is a poor prognostic indicator. Electrolytes and bicarbonate status are evaluated because worsening acidosis, increasing GGT, and increasing Cr despite supportive care are indicators of a grave prognosis for survival.
Although viral and bacterial hepatitis are occasionally diagnosed in camelids, secondary bacterial infection is most common. Of particular concern is invasion of clostridia. Therefore, the complete blood cell count is evaluated for evidence of bacterial infection and the PCV and total protein examined. I have found that a rising PCV in the presence of a falling T.P. is a grave prognostic indicator. Also, I use blood immunoglobulin concentration as a screening tool to evaluate immune system status.

Diagnosis of the cause of liver disease in camelids can be an exercise in frustration. Histopathology (microscopic examination of liver tissue by means of liver biopsy) usually is not specific: hepatic lipidosis, biliary hyperplasia, lymphocytic plasmacytic hepatitis are common findings. Occasionally cholangiohepatitis (infection of the bile ducts) or cholestasis (obstruction to bile flow) are diagnosed from biopsy. Although histopathology often does not provide a definitive diagnosis, the information gained is well worth the effort. Because few specific liver diseases have been described for camelids, differential diagnoses should be broad in range: metabolic (e.g., fatty liver, cirrhosis), parasitic (e.g., liver flukes), toxic (e.g., mycotoxin, endotoxin, clostridium spp), bacterial (e.g., Salmonella spp, Clostridial spp, E coli), viral (e.g., adenovirus), fungal (e.g., Coccidioides imitis), and tumors or cancer (e.g., adenocarcinoma). I routinely perform ultrasound guided percutaneous liver biopsy and obtain samples for histopathology, virology, and bacteriology. Recently, a picornavirus has been identified at Cornell University (Dr. Susan Stehman and colleagues) which appears to cause pancreatitis and destruction of insulin producing islet cells. The result of this is insulin dependent diabetes mellitus which can lead to ketoacidosis and death.

Treatment is directed at supportive care unless a more specific diagnosis can be determined. Antibiotics, anti-inflammatory drugs, fluid therapy (I prefer oral fluids when possible), glucose supplementation, and pain therapy are useful for treatment of severe liver disease. Insulin therapy must be used judiciously so that a harmful decrease in blood glucose does not occur. When used, intravenous fluids must be administered cautiously because camelids readily develop low blood protein with liver disease. Anti-ulcer prophylaxis is critical to prevent clostridial overgrowth. I prefer to use omiprazole because this drug is more potent than Tagamet. Clostridial antitoxins or vaccination may be useful to bolster immunity.
The most critical factor for treatment of camelids with liver disease is to keep them eating. If appetite is suppressed, transfaunation (administration of the rumen fluid from a cow into the stomach) is a potent appetite stimulant. Other options include bacterial supplements products (such as probios), yogurt, B-complex vitamins, use of a companion animal, and offering a variety of feeds including frequent grazing. Camelids may lay down and refuse to get up if isolated in a stall. These animals should be walked, grazed, and a companion animal kept with them to prevent this cycle from starting. I have had the most success reversing liver disease in camelids by increasing the energy density of the diet (originally suggested by Dr. Norman Evans). I recommend that a glucose enriched electrolyte water be available at all times. Calf electrolyte solutions are excellent, but many of my clients have used Gator aid and similar products. Energy density may be increased in the diet by supplementing sweetfeed, dried molasses, syrup, etc. These supplements should be made available until liver enzymes have returned to normal.

I have performed extensive investigations into copper toxicity, mycotoxin contamination, parasite infestation, water source contamination, and have found that most cases of liver disease can not be readily explained. Therefore, recommendations for prevention are difficult. Probably, the most significant factor in the prevention of liver disease is to prevent sustained stress. I have found that the most severe cases of liver disease have been in camelids suffering severe, long-term stress. An example would be a llama or alpaca that is acquired in Peru, moved to a quarantine station in Peru, examined and treated several times by veterinarians and animal handlers, moved to a quarantine station in the United States, moved to a farm for sale, sold at auction, moved to the farm of final destination, entered into a new herd to establish a new social hierarchy, and, finally entered into the breeding pool. These events occur over approximately 8 to 12 months. Hepatic lipidosis is the most common consequence even in relatively thin animals. A common misconception is that fatty liver disease is a disease of overweight camelids. I have found that these are the exception, not the rule. To prevent the development of these adverse effects, the environment in which the animals are moved should be as free from stress as possible, animals should be vaccinated with 7-way or 8-way clostridial vaccines, high quality grass hay or grass should be available at all times, and a trace mineral mix should be available.
When I see fatty liver disease occurring in domestic camelids, I believe that the nutritional program should be intensively investigated. If the feed source has changed recently, a feed analysis is indicated to determine if the feed is low in digestible energy. The best indicator of the adequacy of the diet is to analyze mineral content in liver biopsies. Research done at Ohio State University investigated the effects of repeated liver biopsies. Despite performing biopsies at weekly intervals, no adverse effects were observed (in fact the animals gained an average of 5 pounds!). However, I recommend whole blood analysis of minerals if the animal in question is pregnant. Research done at Ohio State University has documented that Alpacas are quite resistant to fumonisin (a type of mycotoxin) intoxication. We fed up to 75 parts per million of fumonisin for up to 30 days with no adverse effects on the serum biochemistry, complete blood cell counts, and liver tissues. We are continuing to investigate liver disease and nutrition in camelids at Ohio State University. Research is critical to determine the cause of liver disease in these animals because the initial cause is usually past by the time your veterinarian gets involved in the case. Some very exciting research is being done in similar areas at Cornell University, Oregon State University, Auburn University, and Colorado State University. Hopefully, we will have better answers for you in coming years!


Action Plan for Camelids (Alpacas, Llamas) Affected with
Acute Death Associated with Liver Disease

David E Anderson, D.V.M., MS, Diplomate ACVS
College of Veterinary Medicine
The Ohio State University, Columbus, Ohio


  1. Do not change social structure of groups. Leave animals that have established a social order together. Stop all new activity on farm (e.g. show fitting and testing, re-grouping for sale, introduction of new animals, removal of animals).
  2. Evaluate all feed and water sources. Remove any suspect hay or grain sources (e.g. molded, spoiled, etc). Clean and sterilize any water containers that appear to contain algae or are not clean. Inspect all water sources for evidence of dead animals, run off, etc.
  3. Obtain samples from all feed and water sources. Have hay and feed analyzed for nutritional values and trace mineral content. Have hay and feed analyzed for aflatoxin and fumonisin mycotoxin. Have water analyzed for mineral content, pH, and bacterial inoculum.
  4. Perform liver mineral analysis and intestinal cultures on all animals that die. Perform trace mineral panel and viral profiles on all animals that have blood drawn for any other purpose.
  5. Check CBC and serum biochemistry profile on all symptomatic animals to guide additional treatment decisions. May elect to check serum biochemistry profile (the most diagnostic and prognostic testing tool) on all asymptomatic animals (optional - concern is additional stress).
  6. Perform complete post-mortem examination of all animals that die. Save necropsy specimens from heart, liver, lung, kidney, C1 content, urine, and aqueous humor for future toxicology as indicated by histopathology.


  1. Provide low stress environment - see comments above.
  2. Provide source of readily available carbohydrates. These include but are not limited to glucose and electrolyte enriched water, dried molasses, sweet feed, and high quality hay. Continue to provide plain clean water.
  3. Provide top dress in feed to include vitamin, mineral, bacterial / yeast, and methionine supplement.
  4. Treat animals symptomatically based on appearance, physical examination, and laboratory test results. Antibiotic, anti-inflammatory, and ulcer therapy are administered on a case-by-case basis. I have had the best success with sodium ceftiofur (Naxcel, 2.2 mg/kg, s.c., q24hr), banamine ( 1 mg/kg, s.c., q12hrs), and omiprazole (prilosec, 1 mg/kg, p.o., q24 hrs). Avoid any use of steroids.


  1. Maintain low stress environment (sun, shade, ventilation).
  2. Ensure proper Clostridial vaccination protocol.
  3. Ensure appropriate parasite control strategies.
  4. Minimize movement and re-grouping of animals. 5. Make long range plans for animal grouping organization so that repeated changes in group social structure can be avoided (e.g. breeding and sale activities).



Views on Fatty Liver Disease

David E. Anderson, DVM, MS, Diplomate ACVS,
Bradford B. Smith, DVM, PhD
Susan Tornquist, DVM, PhD
Robert Van Saun, DVM, PhD

Few diseases that can strike alpacas (and llamas) are as insidious as fatty liver disease. An alpaca farm that has all the good management signs of a tidy, well-run operation can lose animals to this disease as readily as a casually run operation scorned by neighboring breeders.

Animals in good body condition can be struck by it, though often animals with low body scores are susceptible. The mechanisms setting the disease into motion aren’t entirely understood, other than that diets low in protein and other essential elements create risk. The disease doesn’t normally occur until after a significant amount of time on a deficient diet. Often once one animal is stricken others follow. Any breeder experiencing a death to fatty liver disease should assume that other animals experiencing the same diet and exposure to stressors are at risk and consult a veterinarian.

The disease often appears in those alpacas in a population experiencing the most stress. A recent outbreak occurred in a group of lactating females a week after the onset of cold and wet weather. Animals not lactating in the same herd suffered no ill effects. Apparently the lactating females’ bodies were working overtime to supply milk to their crias. Later testing indicated that the rye hay they were fed contained only about 8 percent protein. Also, the animals were receiving a daily grain/pellet supplement.

Shortly after the onset of cold weather one lactating female slowly quit eating and became sluggish. Her symptoms grew more severe. A slight yellow cast in skin near her eyes and in her mouth appeared, indicating poor liver function, which blood test also verified. Unfortunately, the focus on strategies to cope with her problems began too late. The animal died in three days, at which time a second animal showed the same symptoms and died two days later.

A rapid analysis of feed was conducted. Herd owners were shocked to learn that the hay in use contained only 8 percent protein. Earlier shipments from the same supplier had always contained 12 to 15 percent protein. The lesson learned is that even with the same supplier and the same hay type, there are no guarantees feed will have the same nutritional quality from year to year. The hay in question looked very edible and was readily consumed by animals exposed to it. The grower had assured the alpaca breeder that the hay was "good quality  and like past years." It turned out that because of floods that tore away topsoil, the hay was not properly fertilized and subpar.

Other alpaca ranches also using the hay were contacted. None had lactating females, but one ranch attributed an animal’s death to fatty liver disease.

All involved farms abandoned their hay and absorbed the loss. All alpacas on several different ranches were given a richer hay (50-50 orchard-alfalfa mix) that tested at about 15 percent protein. Before the arrival of the new hay, monitoring of enzyme activities indicated that other animals had impaired liver functions and were on the verge of succumbing to the disease. After three weeks on the new diet all of the affected animals’ liver functions returned to normal.

In part the problem in the herd described above was exasperated by research and rhetoric in llama nutrition that emphasized the problem of obesity in llama herds. In the llama business the emphasis on a nutritionally balanced but not-rich diet to avoid obesity may not be as applicable to alpacas. In fact, several leading camelid veterinarians feel that alpacas may indeed thrive on a richer diet than llamas do. The two species have different dietary preferences in South America. One California breeder who has llamas and alpacas found that when he maintained both on the same diet (14 to 20 percent protein), for the most part alpacas maintained optimum body condition and llamas became obese. Could it be the two species have somewhat different dietary needs? At this time these observations are anecdotal, but research occurring at Oregon State University and Ohio State University will likely lend more understanding to the dietary needs of alpacas and how they may differ from those of llamas. —Editor



Hepatic Lipidosis in the Camelid: A Different Perspective

Bradford B. Smith, DVM, PhD
Susan Tornquist, DVM, PhD
Robert Van Saun, DVM, PhD

What is hepatic lipidosis?

As they say in the advertising field, the name says it all. Hepatic means liver; lipidosis means an accumulation of lipids or fats. Functionally it is a condition in which the liver has accumulated a large quantity of fat within the cells.

If you microscopically examine a normal liver, you will see all the usual components of a cell, including such structures (organelles) as the nucleus, mitochondria, lysosomes, and an occasional lipid (fat) droplet. The liver is one of the most metabolically active tissues in the body and plays a central role in fat metabolism, converting the lipids from one form to another as needed.

Hepatic lipidosis occurs when the amount of fat accumulating in the liver becomes excessive, compromising liver function. In this case, most of the cell becomes filled with fat droplets and the normal functions of the cell are impaired. As a consequence, the normal role of the liver in clearing toxins and other waste products is impaired, the byproducts accumulate in the blood, and the animal dies as a result of liver failure.

Understanding why apparently normal animals can have no evidence of problems and then die within a period of 3 to 4 days from acute liver failure is perplexing; even more perplexing is the apparent absence of other identifiable problems in most cases.

The first step in sorting out this mystery has been to take a retrospective look at what we know about the problem. To this end Dr. Sue Tornquist, head of Clinical Pathology at Oregon State University (OSU), called up the medical records of twenty-six llamas and alpacas with a histopathologic diagnosis (that is, the diagnosis was based upon a microscopic examination of the tissues and not just a gross anatomical evaluation) of hepatic lipidosis during the period from 1991 to 1997. Of the 771 llama and alpaca submissions to the OSU Veterinary Diagnostic Laboratory during this period, hepatic lipidosis was identified in twenty-six, or 3.4 percent, of the cases. When the twenty-six cases were more closely examined, the following observations emerged:

Sex: Twenty-two (or 88 percent of the group) were females, a significantly higher percentage of females than in the original 771 submissions.

Physiologic state: Twelve of the affected animals were known to be pregnant (52 percent of the females), and ten were known to be lactating (43 percent of the females).

Age: Ages of animals with hepatic lipidosis ranged from 5 months to 18 years of age, with a mean age and standard deviation of 7.1 ±4.6 years (66 percent of the population). In contrast, only 14 percent of the reference population in which ages were known were between 6 and 10 years of age.

Presenting signs: Although thorough history, physical exam findings, and laboratory data were not available for all cases, the most common factors were

• A history of recent severe anorexia or weight loss in 58 percent of the cases

• Neurologic signs including incoordination, blindness, and head pressing in 27 percent of the animals

Other changes were either agonal or present in only a few animals.


This retrospective work suggested that hepatic lipidosis was primarily a disease of middle-aged llamas and alpacas, with a substantially higher incidence in females, particularly females with a high metabolic demand such as late-term pregnancy and/or heavy lactation. These observations, coupled with the lack of other consistent histopathologic changes or evidence of bacterial or viral infections, has suggested that the problem may be primarily nutritional and/or metabolic in nature.

Clinical Cases

Retrospective studies tell only a portion of the story and don’t provide good information about the development of the problem. Herd outbreaks in the past several years have given us a better understanding of the dynamics of the problem within a herd, such as timeframes for the development of the problems, clinical changes, and alterations in blood parameters. To address this point, the following is a brief description of four herd outbreaks we have seen in the past couple of years.

Case 1: Four llamas developed the problem within a 4-week period. Although the quality of the forage was good, the volume of feed being provided was very low. No toxins
were identified. Other than insufficient
feed, no additional stress factors were

Case 2: Three female llamas developed hepatic lipidosis within a few weeks. All of the animals were lactating, and the forage quality was high. The onset of the problem coincided with a shift to very high temperatures. Changes in the weather and social hierarchy were identified as possible factors leading to decreased forage consumption.

Case 3: Three lactating female alpacas died within a short period of time. The onset appears to have been correlated with a shift to cold weather. The forage quality appears to have been marginal though supplement had been offered to compensate. Two animals were in good condition at onset of disease.

Case 4: A group of seven llamas died within a 3-week period. This was the only outbreak in which most of the animals were males. Unlike the females in the other cases, which for the most part were over conditioned, in this situation the pastures and hay were of poor to very poor quality and most of the animals were moderately to severely under conditioned.


All these cases support our view that we are primarily dealing with a metabolic disease with underlying nutritional problems, specifically that the animals are in a condition of very high energy demand and are not able to meet this need in an appropriate manner. As a result of the  increased energy needs, more and more fat is mobilized. For reasons that are not clearly understood, the liver is unable to handle the increased demand for energy and responds by inappropriately increasing the amount of fat stored in the liver—ultimately resulting in liver failure.

A couple of important caveats about this interpretation:

• Inappropriate energy and/or protein metabolism as the cause of the problem is a theory—not a fact—and needs to be carefully examined.

• In all cases, the problem appears to have a stress component, such as changes in social conditions, dramatic changes in the weather, or restricted food availability. While stress appears to be a triggering device, its role in the development of the problem is unclear.

It was against this background that Susan Tornquist, Bob Van Saun, and I developed a research protocol to examine the metabolic basis for hepatic lipidosis in the llama. We submitted the proposal to the Morris Animal Foundation, where it was reviewed, evaluated, ranked, and funded. (We wish to thank Andy and Cheryl Tillman for funding this project through the Morris Animal Foundation.) We are currently running a series of studies to establish how the disease develops and to characterize the clinical and biochemical changes so that the condition can be identified at a stage early enough for treatment. The project at Oregon State University has so far produced some fascinating results and generated a much better understanding of the condition.


Hepatic lipidosis is becoming a serious problem. While we still don’t have the answers, work at Oregon State University is an important first step in finding a solution. If you have had confirmed camelid deaths caused by hepatic lipidosis, we would be very interested in hearing from your veterinarians about these cases. These talks have been very useful in helping us get a more detailed and complete picture of the problem under field conditions and a better understanding of the underlying factors involved in the development of the condition. Confidentiality is maintained at all times. Contact us at College of Veterinary Medicine, Oregon State University, 105 Magruder Hall, Corvallis, OR 97331-4802, fax: 541-737-0502.

Copyright © 1998 by Brad Smith, Susan Tornquist, and Robert Van Saun.

About the Authors

David E. Anderson, DVM, MS Diplomate ACVS, is an assistant professor of farm animal medicine, College of Veterinary Medicine, Ohio State University, Columbus. He has been practicing medicine and surgery and performing research with llamas and alpacas for 8 years, focusing on reproduction, nutrition, and metabolic disease, all of which are closely interrelated. His current six research projects on alpacas and llamas are directed to developing immediate applications "on the farm."

Brad Smith, DVM, PhD: Oregon State University

Susan Tornquist, DVM, PhD, ACVCP, is the head of clinical pathology at Oregon State University. She is currently working on two Morris Animal Foundation grants dealing with camelid health issues.

Bob Van Saun, DVM, PhD, ACT, ACVN, is a double-board-certified faculty member at Oregon State University with an interest in nutrition and reproduction. He has been working with llamas and alpacas for the last 5 years and is involved in several studies.



Overview of Hepatic Disease In Large Animals  |   Acute Hepatitus In Large Animals

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