Overview of Malassimilation Syndromes in Large Animals
Malassimilation is a decreased ability of the GI tract to incorporate nutrients into the body, either due to maldigestion or malabsorption. Maldigestion is the failure of adequate degradation of dietary constituents within the GI tract, which is required to facilitate absorption due to defects in pancreatic exocrine function, bile acid content, or brush border enzymes. Malabsorption is the failure of passage of nutrients from the intestinal lumen into the bloodstream. Some disease processes involve both maldigestion and malabsorption, such as is seen in young animals with lactase deficiency. Maldigestion alone is an infrequent cause of malassimilation in large animals. In horses, diseases causing malabsorption are much more common than diseases causing maldigestion. In cattle, small ruminants, and camelids, the forestomach bacteria and protozoa contribute to nutrient degradation, which makes maldigestion a very rare condition.
Maldigestion syndromes are uncommon and poorly understood in large animals. They may be due to alterations in gastric function or activity of rumen microflora, abnormal bacterial proliferation in the small intestine, or a decrease or lack of small-intestinal brush border enzyme activity (eg, lactase deficiency). Less likely causes include drug-induced alteration in secretion or excretion of bile salts, or deficiency or inactivation of pancreatic lipase. Changes in bile salt concentration may not impair digestion in adult herbivores but may exacerbate diarrhea in milk-fed neonates. Surgical resection or bypass of the distal small intestine may facilitate bacterial overgrowth with associated bile salt abnormalities.
Lactose is a disaccharide composed of glucose and galactose. The enzyme lactase, which catalyzes the degradation of lactose into its components, is localized in the small-intestinal brush border of foals and calves. The degradation is necessary to facilitate absorption. Primary lactase deficiency is inherited as an autosomal recessive trait in people, but its occurrence and mode of inheritance in large animals is poorly documented. Acquired or secondary lactase deficiency seems to be more common in large animals. It is seen in foals, calves, and crias as a result of intestinal mucosal changes induced by viral, protozoal, and bacterial enteritis. Sloughing of the small-intestinal epithelial cells, loss of villous tips, and loss of some or all of the crypt cells result in some degree of lactase deficiency because of loss of lactase-secreting epithelial cells. Morphologic changes may include partial villous atrophy, crypt hyperplasia, and infiltration of the lamina propria. Osmotic diarrhea in lactase-deficient foals and calves occurs due to increased undigested/unabsorbed nutrients entering the caudal intestinal parts, subsequently increasing bacterial fermentation, concentration of osmotically active particles, and retention of water and electrolytes in the intestine.
A number of diseases may induce a malabsorption syndrome by altering the normal absorptive mechanisms of the small intestine. Malabsorption is commonly seen in animals with GI disease. It may arise from structural or functional disorders of the small intestine or have a multifactorial etiopathogenesis. Malabsorption is often seen concurrently with enteric protein loss. Either may cause loss of nutrients in the feces and subsequent weight loss. Malabsorption is not synonymous with diarrhea in any species, although diarrhea may be a common clinical feature. Function of the large intestine may be secondarily altered because of changes in the small intestine. Transient diarrhea may occur as abnormal quantities of carbohydrates, protein, fatty acids, and bile acids enter the large intestine in the ileal effluent. These substances can directly or indirectly enhance intestinal secretion or decrease absorption rates. Malabsorption of nutrients may result from insufficient absorptive surface area, an intrinsic defect in the mucosal or submucosal morphology of the intestinal wall, or obstruction of blood and lymphatic vessels. Rotavirus infection in younger animals may cause destruction of intestinal villous epithelial cells, which results in maldigestion due to decreased activity of brush border disaccharidase enzymes and in malabsorption due to decreased absorptive surface area. Coronavirus and cryptosporidia may have similar effects. A decreased absorptive surface area can also result from small-intestinal resection (short-bowel syndrome) or from villous atrophy due to granulomatous enteritis. Local infiltrative or inflammatory disease, edema, or lymphatic obstruction (granulomatous enteritis, lymphosarcoma) secondary to local or systemic causes may interfere with the ability of the intestinal wall to absorb nutrients. Inefficient absorption also may develop due to increased mucosal permeability caused by cellular damage. Metabolic abnormalities may alter the epithelial cells and decrease the available energy for active transport and maintenance of the carrier proteins or brush border enzymes. Congenital deficiencies of enzymes normally present on the microvilli are not well recognized in large, domestic animals. However, neonates and ruminants have low levels of maltase, and ruminants especially lack sucrase. In most mammalian species, lactase activity declines with age.
In horses, malabsorption is commonly caused by the following: 1) inflammatory or infiltrative disorders—diffuse lymphosarcoma of the small intestine (alimentary lymphoma); enteritis due to eosinophilic, lymphocytic-plasmacytic, or basophilic infiltrate; multisystemic eosinophilic epitheliotropic enterocolitis; granulomatous enteritis (inflammatory bowel disease); Lawsonia intracellularis (weanling foals, yearlings); intestinal ischemia and damage due to migration of Strongylus vulgaris larvae, small strongyles, or Strongyloides westeri (foals) infection; cryptosporidia; postinfarction inflammation; amyloid-associated gastroenteropathy; multiple abscessation in the bowel; tuberculosis; histoplasmosis; intestinal Rhodococcus equi infection; invasive enterocolitis (Salmonella spp); 2) biochemical or genetic abnormalities—congenital or acquired lactase deficiency (lactose intolerance), dietary-induced enteropathy, monosaccharide transport defect, pancreatic exocrine insufficiencies; 3) diseases causing inadequate absorptive area—villous damage or atrophy due to viral infection (rotavirus, coronavirus) or bacterial enteritides in foals, cryptosporidiosis, intestinal resection; 4) cardiovascular disorders—congestive heart failure, intestinal ischemia; 5) lymphatic obstruction—lymphosarcoma, mesenteric lymphadenopathy, intestinal lymphangiectasia, abscessation, thoracic duct obstruction; and 6) miscellaneous—drug-induced, heavy metal toxicosis, zinc deficiency.
In cattle, malabsorption syndromes are less frequently documented but likely are seen most often in calves with diarrhea. Diseases that cause malabsorption syndromes in ruminants include diarrhea caused by viruses, bacteria, or protozoa in calves and young stock. These inflammatory changes often result in maldigestion and malabsorption. Another major group of cattle suffering from malabsorption syndrome is older cattle with Mycobacterium avium subsp paratuberculosis infection (Johne’s disease). Rare underlying reasons for malabsorption in ruminants are local or generalized ischemia, protein malnutrition, congestive heart failure, lymphatic obstruction, parasitism (eg, trichostrongylosis of sheep and cattle), or tuberculosis. Oral antibiotics may cause an imbalance in GI tract flora and interfere with digestion and intestinal absorption of nutrients. Treatment with high doses of ampicillin, neomycin, or tetracycline significantly decreases and delays glucose absorption during oral glucose tolerance tests in calves.
New World camelids can be affected by most conditions that cause malabsorption syndrome in ruminants. Virus-caused diarrhea (coronavirus) is particularly a problem in young crias. Intestinal protozoa infection (eg, Eimeria macusaniensis) may result in weight loss and hypoproteinemia due to malabsorption during either the prepatent or patent phase of infection. Severe debilitation caused by coccidiosis is typically seen in young animals; however, chronic malabsorption caused by chronic enteritis can also be found in adult llamas and alpacas, which typically shed high numbers of the pathogen.
In swine, malabsorption is poorly documented; however, proliferative enteropathy (L intracellularis) can result in malabsorption. In piglets, an amylase deficiency may result in starch malabsorption during the immediate postweaning period. Diarrhea of other origin (eg, Escherichia coli) may cause malabsorption syndrome in piglets.
Clinical signs of malassimilation syndrome are variable, depending on the underlying disease condition and the presence or absence of concurrent protein-losing enteropathy. Malassimilation syndromes frequently result in a negative energy balance, and subsequently in weight loss, muscle wasting, and possibly low serum protein concentrations. Therefore, chronic weight loss or reduced growth rate is a typical clinical sign.
Appetite of affected animals may be normal, increased, or decreased and is, therefore, not very helpful as a diagnostic parameter. Polyphagia may be seen due to insufficient nutrient absorption to stimulate the satiety centers. In small-intestinal malabsorption, decreased feed intake or anorexia is present more commonly, because the primary disease process causes loss of appetite.
Feces are frequently normal in consistency and volume. Diarrhea may be present but is not a consistent feature. In adult animals, small-intestinal disease must be rather extensive before diarrhea develops, because the colon can compensate and absorb the increased fluid load. This is especially the case in llamas and alpacas. In adult horses and ruminants, diarrhea indicates involvement of the large intestine. In young animals in which colonic function is not yet fully developed, diarrhea is seen with small-intestinal and large-intestinal disease.
Clinical signs of malassimilation may also include exercise intolerance, lethargic attitude, and variable thirst. Vital signs are usually normal until late in the disease. Pyrexia may be seen with inflammatory and neoplastic conditions. Abdominal pain may result from bowel inflammation, mesenteric or mural abscesses or adhesions, or partial obstruction. Ascites, dependent edema, and weakness may develop later in the disease process, especially if enteric protein loss is present. Skin and ocular lesions, vasculitis, arthritis, hepatitis, and renal disease may indicate immunologic reactions, particularly with inflammatory bowel disease. Skin lesions seen with malabsorption-related dermatosis include a thin hair coat, patchy alopecia, and focal areas of scaling and crusting that are often symmetrically distributed.
Foals and calves with lactose intolerance commonly show diarrhea, poor growth rate, and an unthrifty appearance. Some may experience flatulence, mild abdominal discomfort, or bloating after intake of milk. In young animals with acquired lactase deficiency, clinical signs (eg, diarrhea, dehydration, weight loss) and clinicopathologic alterations (eg, acidosis, hypoglycemia. and electrolyte abnormalities) are indistinguishable from those of the primary enteropathy. The condition of the animal may improve quickly, and diarrhea may resolve when milk is withdrawn.
The carcass is thin to emaciated, depending on the duration and severity of the malassimilation disease. Specific lesions depend on the primary underlying disease process. Overt signs of malabsorption do not always correlate with gross and histopathologic changes, emphasizing the importance of functional disorders.
Small-intestinal malabsorption cannot be determined by clinical examination or by routine laboratory data. However, clinical examination may lead to a presumptive diagnosis after more common causes of weight loss have been excluded. Determination of the primary underlying pathologic process is necessary to establish an appropriate treatment regimen and prognosis.
A complete history should focus on duration of condition, precipitating factors, nutritional history, deworming and routine health care program, previous or concurrent diseases, as well as the number, age, and proximity of other affected animals. A thorough physical examination is performed to correlate physical findings with clinical signs and history. In adult horses and cattle, rectal palpation is performed to determine the presence of intra-abdominal masses, enlarged lymph nodes, adhesions, abnormal positioning or thickening of bowel segments, or abnormalities in the cranial mesenteric artery. The kidneys, bladder, and related structures should also be evaluated.
A CBC and serum biochemical parameters (eg, total protein, albumin, fibrinogen, glucose, cholesterol, bilirubin, ketones, fatty acids, CK, AST, glutamate lactate dehydrogenase) help determine general health status of the animal; presence of inflammation or an infectious process; involvement of body systems; and metabolic, electrolyte, and serum protein status. Urinalysis, abdominocentesis, and fecal examination for parasite ova, larvae, protozoa, and occult blood should also be performed to exclude more common causes of weight loss. Additionally, urinalysis should be performed to assess whether glucose or protein is being excreted via urine, which could be a further cause for chronic weight loss.
Evaluation of plasma protein electrophoresis, fecal pH, bacteriologic culture, and immunologic studies may be indicated. Intracolonic fermentation of malabsorbed carbohydrates will often reduce the fecal pH in foals and calves. Protein-losing enteropathy can be diagnosed presumptively by excluding other causes of protein loss, such as renal disease or loss into a third space (peritoneum, pleural space), and by excluding the possibility of decreased albumin production due to another condition such as liver disease. Standard and contrast radiography of the bowel may be feasible in foals and small ponies, calves, and New World camelids. Abdominal ultrasonography is a useful diagnostic tool to determine bowel-wall thickness and intestinal motility, as well as the presence of excess fluid in the abdominal cavity, masses, adhesions, abnormal positioning of bowel in the abdominal cavity, and vascular lesions in the cranial mesenteric artery.
When malassimilation is suspected, a carbohydrate absorption test may be performed to assess small-intestinal function. In horses, a gastroscopy to diagnose lesions in the stomach (eg, granulomas, tumor, ulcers) and duodenum or retention of ingesta should be accomplished before absorption tests are performed. For absorption tests, the intestinal disorder must be diffuse and/or must affect the delivery to and transit through the small intestine to be diagnostic. An abnormal or flattened absorption curve is suggestive of small-intestinal dysfunction. However, a flattened absorption curve can also be caused by other conditions. Although absorption tests may indicate the presence of malassimilation, an etiologic diagnosis requires a biopsy of intestinal mucosa and possibly lymph node. In some cases, rectal biopsy may reveal focal or diffuse inflammatory infiltration. Bacteriologic culture of the feces, biopsy samples, and fecal examination for leukocytes and epithelial cells may confirm the presence of salmonellae or other invasive organisms. In some cases, laparoscopy or exploratory celiotomy is required to obtain the intestinal or lymph node biopsies. Surgery may not be advisable in a debilitated animal, because wound healing is poor and dehiscence is a potential problem. If undertaken, intestinal and lymph node biopsies should be obtained for culture, histopathology, enzymology, and immunology. Because of the risk and cost of obtaining appropriate tissue samples, malassimilation syndrome is often presumptively diagnosed with the aid of absorption tests.
Clinically applicable absorption tests include d-glucose and d-xylose. These tests may help assess small-intestinal function in preruminant calves, foals, crias, and mature horses. Indications for an oral d-xylose absorption test in foals, calves, and possibly crias include persistent diarrhea not attributable to infectious agents, poor growth despite normal intake, and other signs of maldigestion (repeated episodes of gas colic, bloating, ileus). In monogastric animals, the test solution is administered into the stomach. In ruminants and New World camelids, the forestomachs must be bypassed (esophageal groove, abomasocentesis), because otherwise the sugars are metabolized by the forestomach flora; however, oral carbohydrate tolerance studies are not frequently used in ruminants. The d-glucose absorption test has the advantages of being easy and inexpensive, and methods to determine blood glucose concentrations are available in most clinical laboratories. The main disadvantage is that results are not only a function of intestinal absorption, but also are strongly influenced by the intensive cellular uptake and metabolism of glucose after it has been absorbed. The d-xylose absorption test more directly measures intestinal absorptive capacity and is not influenced by endogenous factors and intestinal enzymatic activity, respectively. Disadvantages are that d-xylose is more expensive, and availability of commercial laboratories that perform plasma xylose determinations is limited. However, d-xylose concentrations can be measured using classic photometric techniques, which do not require special equipment and can be performed in a clinical laboratory.
Glucose or galactose may inhibit the absorption of d-xylose; therefore, fasting is necessary before the test is performed in horses and preruminant calves. The protocols of both tests require prolonged fasting, which may be deleterious to sick young foals and calves. The results of both tests are also affected by gastric emptying rate (d-xylose has also been used to estimate abomasal emptying rate in cattle), small-intestinal transit time, diet, and length of fasting period before testing. The shape of the absorption curve is influenced by renal clearance, hypoxia, anemia, systemic and intestinal bacterial infections, and IgG concentrations in foals. The age of the animals also affects absorption and digestion of glucose, lactose, and d-xylose. Therefore, the control animals must be within a few days of age of the affected animal if reference ranges are not available for its age group.
A delayed peak in the absorption curve of both the d-glucose and d-xylose test may result from delayed gastric emptying resulting from hypertonicity of the glucose or xylose solution, excitement, pain, retained gastric contents, changes in GI transit time and motility, or partial obstruction. Further sedation of the animal decreases GI motility and secondarily the absorption. A flat absorption curve may be also seen in animals with normal absorptive capacity due to a transient decrease in intestinal blood flow or to bacteria in the lumen of the small intestine metabolizing the test sugar. The test substance rapidly equilibrates with many body fluids (eg, ascites), which lowers the blood concentration of xylose and may result in a flat curve.
d-Xylose is a pentose also known as wood sugar; only trace amounts are found in feed stuffs of plant origin. The d-xylose absorption test measures absorptive capacity of the small-intestinal mucosa because functional enterocytes actively transport d-xylose across the mucosa and into the bloodstream. Subnormal absorption supports a diagnosis of malabsorption. Age and diet also affect d-xylose absorption in healthy horses. Foals <3 mo old have a higher peak concentration of d-xylose after administration than adults. Adult horses maintained on a high-roughage, low-energy diet have a higher peak concentration of d-xylose after administration than those fed a high-energy diet. Food deprivation can alter d-xylose absorption in horses without overt GI tract disease, which must be considered when interpreting results in horses that are anorectic regardless of cause.
d-Xylose (0.5–1 g/kg in a 10% solution) is administered via nasogastric tube to a horse that has been fasted overnight (18–24 hr). Heparinized venous blood samples are collected before d-xylose administration (time 0) and at 30-min intervals afterward for 4 hr (±6 hr sample). Expected peak values (20–25 mg/dL) should occur between 60 and 120 min after dosing. The normal curve should have a bell shape or inverted V shape with a definable peak plasma xylose concentration 1–2 hr after administration. Peak absolute plasma values should be ≥15 mg/dL above baseline values in healthy horses. In adult cattle the d-xylose (0.5 g/kg in a 50% solution) must be administered by abomasocentesis to bypass the rumen. Similar to that in horses, the curve is almost bell shaped in high-yielding dairy cattle; peak values of 1.1–1.3 mmol/L (16–20 mg/dL) occur ~90 min after the solution is administered.
Glucose absorption curves are steeper in pasture-fed horses than in those fed a higher energy ration. Lower peak values are seen in horses on a high-concentrate ration. The length of the pretest fast influences the absorption curve. Prolonged fasting may delay or decrease peak glucose concentration, thus giving a false-positive result. In two studies, >90% of adult horses with evidence of “total” glucose malabsorption had severe infiltrative lesions of the small intestine. The majority of horses (18/25) classified with “partial” glucose malabsorption also had obvious pathologic abnormalities of the small intestine.
Performance of the d-glucose absorption test is similar to that of the d-xylose absorption test except samples are collected into sodium fluoride tubes. In healthy horses, blood glucose concentrations should peak 90–120 min after administration. This peak should be >85% above the resting glucose level. Reportedly complete malabsorption is defined as a peak <15% above resting concentrations; partial malabsorption is defined as a peak 15%–85% above resting levels. One of the major disadvantages to the oral glucose absorption test is that when using the conventional protocol sampling is over a 6-hr period. One reported modified protocol requires only two test samples at 0 and 120 min after administration. This modification reportedly did not affect the reliability of the test result.
Diagnosis of acquired lactase deficiency is usually presumptive based on history, clinical signs, and confirmation of presence of associated pathogens. Definitive diagnosis can be achieved with an oral lactose tolerance test. Lactose is hydrolyzed within the brush border of the small-intestinal enterocytes by lactase to constituent d-glucose and galactose before these monosaccharides can be absorbed. Oral lactose tolerance testing is directed specifically at assessing whether lactase activity is present. Adult horses (>3 yr old) are lactose intolerant, and the test is unsuitable for adult ruminants and adult New World camelids. The oral lactose tolerance test is of value in evaluating young foals and preruminant calves with diarrhea or poor growth. Lactose intolerance has been documented in foals, calves, and kids.
An oral lactose tolerance test does not distinguish maldigestion from malabsorption and requires fasting for several hours. Feeding enzymatically treated milk (lactose-free milk) to animals suspected of being lactose intolerant may be tried before subjecting animals to the lengthy fast (12–18 hr) required before this test is performed. Before performing an oral lactose intolerance test, grain and hay should be withheld for 18 hr. The calf or foal should be prevented from nursing (muzzled) for ≥4 hr before administering d-lactose at 1 g/kg as a 20% solution via nasogastric tube; the muzzle should be kept in place for the duration of the test. Blood samples are collected into tubes containing fluoride oxalate for determination of blood glucose concentrations at 30 min, and immediately before and at 30-min intervals for 3–4 hr after dosing. Blood glucose concentration should be double that of the resting values within 60–90 min of lactose administration. Peak glucose concentrations should be ≥35 mg/dL higher than the baseline in healthy foals. Abnormal results suggestive of lactose intolerance include a delayed, prolonged, or lack of increase in blood glucose concentration from baseline.
Lack of an appropriate increase in blood glucose concentration after lactose administration may be due to maldigestion or malabsorption. Therefore, if the lactose tolerance test is abnormal, a d-glucose or d-xylose absorption test should be performed to determine whether malabsorption or maldigestion alone is the problem. Casein hypersensitivity is distinguished from lactose intolerance by assessing the animal’s response to enzymatically treated and untreated milk. Definitive confirmation of lactase deficiency is through direct measurement of mucosal lactase activity in the intestinal tissue. However, this is rarely undertaken in the clinical setting, because a surgical biopsy of the mucosa is required.
A hydrogen breath test has also been described for detection of carbohydrate malabsorption in horses. In a clinical study, diseased horses showed higher fasting breath hydrogen levels than did healthy horses. However, because of the expensive laboratory procedures, the test is not widely used.
The etiology of the primary underlying disease process must be determined before specific therapy for malassimilation syndrome can be initiated. Specific therapy for most causes of malassimilation is not available, except for lesions due to parasite damage. Anticoccidial and larvacidal dewormings may improve the condition; however, a complete healing and return to full absorption capacity is not always achievable depending on the damage. Anti-inflammatory agents (eg, NSAIDs, corticosteroids) may also help decrease the inflammatory response within the affected bowel. Supportive care and facilitation of nutrient absorption from more caudal parts of the intestine must be encouraged until the intestinal epithelium recovers and new villous cells are produced. Maturation and healing of the intestinal absorptive surfaces may take weeks to months in severe cases.
Calves and foals with acquired lactase deficiency after diarrheal disease (viral, bacterial, protozoal) often respond well to supportive care (correction of acid-base, electrolyte, and glucose abnormalities) and feeding of enzymatically treated milk until the small-intestinal mucosa has regenerated. Foals and calves should be fed small amounts of high-quality roughage or grain (if they are able to tolerate it) to help meet their energy needs, although enteral feeding should be continued whenever possible. Young foals and calves that do not tolerate feedings of milk or enzymatically treated milk may benefit from short-term (<24 hr) withdrawal of milk. These animals need alternative sources of energy and nutrients such as short-term feeding (≤24 hr) of glucose-containing electrolyte solutions or, in more severe cases, partial or total parenteral nutrition. Dietary change to a soy-based, non-lactose-containing milk replacer and early weaning are advised for animals with nonresponsive lactose intolerance.
Treatment of inflammatory bowel disease in horses has been attempted but is often unsuccessful even with aggressive corticosteroid administration. Sulfasalazine and isoniazid have been recommended, but their usefulness is unproved. Similarly, the usefulness of dimethyl sulfoxide in the treatment of intestinal amyloidosis is unknown. Animals with anaerobic or aerobic bacterial overgrowth may respond to antimicrobial administration. Adequate penetration of antimicrobials into inflammatory bowel lesions (Rhodococcus equi in foals) is doubtful. Successful treatment of Lawsonia intracellularis in foals has been achieved with longterm administration of antimicrobials (erythromycin, azithromycin, clarithromycin, chloramphenicol, oxytetracycline, doxycycline) and aggressive supportive care (fluids, plasma) as dictated by the animal’s clinical condition. Any treatment attempt of cattle with clinical signs of Johne’s disease have proved to be unsuccessful; slaughter or euthanasia is recommended. Eimeria macusaniensis infections in affected camelids may successfully be treated if diagnosed early. Treatment currently involves administration of amprolium, sulfonamides, ponazuril, or toltrazuril with appropriate supportive care.
Horses with malabsorption due to a disease process or after small-bowel resection must be fed a diet that optimizes digestion of feeds in the large intestine. The diet should provide easily absorbed protein, carbohydrates, fat, and water-soluble vitamins and maintain mineral balance. Increased concentrate-to-forage ratios decrease digestion of feeds in the large intestine and should be avoided. Horses benefit from a fiber-based diet. To enhance digestion in the large intestine, easily fermentable roughages (eg, alfalfa) should be fed. High-quality fiber, metabolized in the cecum and colon to volatile fatty acids, may partially compensate for small-intestinal losses. In young animals, the diet may be supplemented with milk protein if lactase deficiency is not present. Fat may be added to the diet to enhance caloric intake. Calcium, magnesium, phosphate, zinc, copper, and iron may need to be supplemented, because they are absorbed in horses in the small intestine only. Water-soluble (especially vitamin B12) and fat-soluble vitamins should be supplemented parenterally as needed. Excessive supplementation, which could lead to toxicosis, should be avoided.
Horses that will not eat may have to be force-fed via nasogastric tube. The horse should be fed small, frequent meals to take advantage of the limited remaining absorptive ability of the small intestine without overloading it. Preruminant calves that are repeatedly tube-fed may develop ruminal acidosis due to deposition of fermentable feed material into the rumen (rumen drinker) rather than the abomasum. Partial or total parenteral nutrition may be necessary for animals that refuse to eat or that cannot tolerate force-feeding. However, total parenteral nutrition is expensive and difficult to continue on a long-term basis in horses or even impossible in ruminants.
Efforts should be made to determine an etiologic diagnosis once malassimilation has been confirmed so that an accurate prognosis can be given and appropriate therapy prescribed. Most conditions causing malassimilation in adult large animals warrant a poor prognosis, and treatment is commonly unsuccessful. However, parasitic infection of the bowel or its blood supply can respond to anthelmintic therapy. Occasionally, a non-neoplastic infiltration of the bowel may respond to corticosteroids, but the response may be transient in some cases. Calves, foals, and kids with lactase deficiency may respond well to supportive care and dietary management. Prognosis for horses with malabsorption due to inflammatory bowel disease is poor; most reported cases have been fatal.