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Are Horses Lactose Intolerant

author
Ellen Grant
• Tuesday, 13 October, 2020
• 9 min read

Submitted by Anonymous (not verified) on Sat, 08/10/2019 – 02:20 255 Conclusion Lactose intolerance with its 4 underlying causes appears to be very rare in foals.

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Contents

In contrast to the human situation it is not an issue in adolescent or adult horses as these do not drink milk or eat products containing lactose. If the condition of a foal permits, an LTT may provide more information and a better understanding of this disease in foals.

References Earlier, L., Poll, D., Del co, F., State, B., Fried, M. and Titian R.(2008) Correlation between symptoms developed after the oral ingestion of 50 g glucose and results of hydrogen breath testing for lactose intolerance. (2006) Lactose intolerance in infants, children and adolescents.

Berber, M., Oberkanins, C., Kriegshäuser, C., Hollerith, B., Offenbach- Glacier, A., Fuchs, D. and Ledochowski, M. (2007) Hydrogen breath testing versus LCT genotypic for the diagnosis of lactose intolerance: a matter of age? (2004) Equine Neonatology, Medicine and Surgery, W.B.

Kobayashi, A., Kauai, S., OBE, Y. and Kagoshima, Y. (1975) Effects of dietary lactose and a lactate preparation on the intestinal absorption of calcium and magnesium in normal infants.

(1997) Manual of Equine Neonatal Medicine, 3rd end., Live Oak Publishing, Woodland, California. (1985) Oral lactose tolerance test in foals: technique and normal values.

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(2006) Lactose intolerance in infants, children and adolescents. (1975) The development and distribution of mucosal enzymes in the small intestine of the fetus and the young foal.

Assimilation is a decreased ability of the GI tract to incorporate nutrients into the body, either due to digestion or malabsorption. Digestion 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.

In cattle, small ruminants, and came lids, the fore stomach bacteria and protozoa contribute to nutrient degradation, which makes digestion a very rare condition. 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.

The enzyme lactate, which catalyzes the degradation of lactose into its components, is localized in the small-intestinal brush border of foals and calves. It is seen in foals, calves, and cries as a result of intestinal mucosal changes induced by viral, protozoal, and bacterial enteritis.

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Morphological changes may include partial villus atrophy, crypt hyperplasia, and infiltration of the lamina Peoria. Osmotic diarrhea in lactase-deficient foals and calves occurs due to increased undigested/absorbed 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 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 villus epithelial cells, which results in digestion due to decreased activity of brush border disaccharide enzymes and in malabsorption due to decreased absorptive surface area. A decreased absorptive surface area can also result from small-intestinal resection (short-bowel syndrome) or from villus atrophy due to granulators enteritis.

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.

Oral antibiotics may cause an imbalance in GI tract flora and interfere with digestion and intestinal absorption of nutrients. Clinical signs of assimilation syndrome are variable, depending on the underlying disease condition and the presence or absence of concurrent protein-losing osteopathy.

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Assimilation syndromes frequently result in a negative energy balance, and subsequently in weight loss, muscle wasting, and possibly low serum protein concentrations. In small-intestinal malabsorption, decreased feed intake or anorexia is present more commonly, because the primary disease process causes loss of appetite.

In adult animals, small-intestinal disease must be rather extensive before diarrhea develops, because the colon can compensate and absorb the increased fluid load. 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 lesions seen with malabsorption-related dermatitis 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 thrifty appearance. In young animals with acquired lactate deficiency, clinical signs (e.g., diarrhea, dehydration, weight loss) and clinicopathologic alterations (e.g., acidosis, hypoglycemia.

Overt signs of malabsorption do not always correlate with gross and histopathologic changes, emphasizing the importance of functional disorders. A CBC and serum biochemical parameters (e.g., 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.

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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. Standard and contrast radiography of the bowel may be feasible in foals and small ponies, calves, and New World came lids.

In horses, a gastrostomy to diagnose lesions in the stomach (e.g., granular, tumor, ulcers) and duodenum or retention of ingest should be accomplished before absorption tests are performed. Although absorption tests may indicate the presence of assimilation, an etiologic diagnosis requires a biopsy of intestinal mucosa and possibly lymph node.

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 colostomy is required to obtain the intestinal or lymph node biopsies.

If undertaken, intestinal and lymph node biopsies should be obtained for culture, histopathology, etymology, and immunology. Because of the risk and cost of obtaining appropriate tissue samples, assimilation syndrome is often presumptively diagnosed with the aid of absorption tests.

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Indications for an oral d-xylose absorption test in foals, calves, and possibly cries include persistent diarrhea not attributable to infectious agents, poor growth despite normal intake, and other signs of digestion (repeated episodes of gas colic, bloating, illus). 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. 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. The shape of the absorption curve is influenced by renal clearance, hypoxia, anemia, systemic and intestinal bacterial infections, and Egg concentrations in foals.

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. The test substance rapidly equilibrates with many body fluids (e.g., ascites), which lowers the blood concentration of xylose and may result in a flat curve.

Similar to that in horses, the curve is almost bell shaped in high-yielding dairy cattle; peak values of 1.1–1.3 MML/L (16–20 mg/DL) occur ~90 min after the solution is administered. In two studies, >90% of adult horses with evidence of “total” glucose malabsorption had severe infiltrate lesions of the small intestine.

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The majority of horses (18/25) classified with “partial” glucose malabsorption also had obvious pathologic abnormalities of the small intestine. 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.

Diagnosis of acquired lactate deficiency is usually presumptive based on history, clinical signs, and confirmation of presence of associated pathogens. The oral lactose tolerance test is of value in evaluating young foals and predominant calves with diarrhea or poor growth.

An oral lactose tolerance test does not distinguish digestion from malabsorption and requires fasting for several hours. 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 digestion or malabsorption. Casein hypersensitivity is distinguished from lactose intolerance by assessing the animal’s response to enzymatically treated and untreated milk.

The etiology of the primary underlying disease process must be determined before specific therapy for assimilation syndrome can be initiated. Anticoccidial and parricidal deforming may improve the condition; however, a complete healing and return to full absorption capacity is not always achievable depending on the damage.

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Calves and foals with acquired lactate 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.

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. Treatment of inflammatory bowel disease in horses has been attempted but is often unsuccessful even with aggressive corticosteroid administration.

Successful treatment of Lawson intracellular in foals has been achieved with long term administration of antimicrobial (erythromycin, azithromycin, azithromycin, chloramphenicol, tetracycline, doxycycline) and aggressive supportive care (fluids, plasma) as dictated by the animal’s clinical condition. Any treatment attempt of cattle with clinical signs of John’s disease have proved to be unsuccessful; slaughter or euthanasia is recommended.

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.

High-quality fiber, metabolized in the cecum and colon to volatile fatty acids, may partially compensate for small-intestinal losses. Calcium, magnesium, phosphate, zinc, copper, and iron may need to be supplemented, because they are absorbed in horses in the small intestine only.

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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 assimilation has been confirmed so that an accurate prognosis can be given and appropriate therapy prescribed.

Most conditions causing assimilation in adult large animals warrant a poor prognosis, and treatment is commonly unsuccessful. Calves, foals, and kids with lactate 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.

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