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Liver Disease in Camelids

by David E Anderson, DVM, MS, Diplomate ACVS
International Camelid Institute
College of Veterinary Medicine
The Ohio State University

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.

HISTORICAL INFORMATION

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.

PHYSICAL EXAMINATION AND CLINICAL SIGNS

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.

ETIOLOGIC INVESTIGATIONS: DIAGNOSIS?

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 STRATEGY

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.

PREVENTION OF LIVER DISEASE

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!

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