Watch for these conditions that impact nutrient absorption and lead to weight loss
In some situations no matter how much a horse consumes, he still loses weight and appears unthrifty. Because most nutrient absorption occurs in the small intestine, any disease syndrome that impacts that area is likely to affect nutrient delivery within the body.
In this article we’ll describe six conditions veterinarians would suspect if your horse isn’t absorbing nutrients properly.
What’s Going on Inside?
When a horse eats, food moves from the stomach to the small intestines into the cecum, before passing into the large colon. Anything that doesn’t get absorbed passes as feces. Here, however, we’ll focus on the part of the gastrointestinal tract chiefly responsible for nutrient absorption: the small intestine.
The three segments of the small intestinal tract (the duodenum, jejunum, and ileum) are lined with mucous membrane covered in villi, which are fingerlike projections that increase surface area to maximize nutrient uptake, and crypts, which are branched, tubular pouches at the base of the villi that produce stem cells and secrete mucus. Microvilli cover the villi, increasing its surface area even more.
The villi connect to the blood and lymphatic vessels to transfer nutrients throughout the body; loss of the villi and the digestive enzymes on their surface subsequently result in reduced nutrient absorption. Any changes to the villi’s structure or form not only impair digestion due to lost digestive enzymes but also reduce the absorptive surface area for nutrients. Bacterial or viral diseases (e.g., rotavirus, coronavirus) can cause such changes by blunting or eroding the villi, as can surgical resection of diseased small intestine (short-bowel syndrome).
Indeed, a number of conditions can cause inflammation, infiltration, or lymphatic obstruction of the small intestine, troublemakers that damage cells and increase cell permeability (the ability of molecules to move across the cell membrane). Examples include lymphosarcoma (cancer of the lymph tissue), granulomatous enteritis (similar to Crohn’s disease in humans), Lawsonia intracellularis bacterial infection in foals, Cryptosporidia protozoal infection in any age horse, intestinal damage from internal parasites (small and large strongyles), and Rhodococcus bacterial infection, to name a few.
The small intestine is responsible for absorbing carbohydrates, proteins, and fatty and bile acids. When it doesn’t do this properly, the nutrients spill over into the large intestine, increasing the horse’s likelihood of developing diarrhea and experiencing protein loss. An adult horse’s colon usually is able to compensate for diarrhea—generally considered a condition of the large intestine—by absorbing large amounts of fluid. However, young animals with developing large colon capacity might experience diarrhea with both large and small intestine disease.
Now let’s delve a bit deeper into some of the specific causes of disease in the small intestine.
Foals younger than 1, particularly weanlings, are susceptible to L. intracellularis infections that can cause inflammatory bowel disease (IBD, specifically, equine proliferative enteropathy, or EPE) in the small intestine. Affected horses show signs of fever, loss of appetite, lethargy, malaise, and in about 40% of cases, diarrhea.
“(Foals in the) early stages—fever, lack of appetite—have a 94% recovery rate,” says Nicola Pusterla, DVM, PhD, Dipl. ACVIM, professor and chief of large animal medicine at the University of California’s School of Veterinary Medicine, in Davis. “Cases with advanced disease or complications that are referred to a hospital have a 13-30% mortality rate.”
The rare adult horse infected with Lawsonia, asymptomatic foals (affected but not showing signs of sickness), symptomatic foals, and other wild and domestic nonequid mammals can shed L. intracellularis in their feces, which can then get picked up by grazing foals.
Pusterla says infectious L. intracellularis doesn’t usually persist in the environment for longer than one to two weeks—even less time if heat, humidity, or other environmental factors are at play. He notes, however, that asymptomatic foals are important amplifiers of L. intracellularis. Caretakers won’t have isolated these individuals from the general population, so they become reservoirs for passing bacteria into the environment.
“In general, sick foals with clinical disease that are being treated will shed for only a few days,” says Pusterla. “However, foals can shed up to 10 days prior to developing clinical disease.” It’s critical, therefore, to practice good biosecurity in the face of an outbreak to minimize spread of infection.
Most of the damage Lawsonia causes occurs in the lower portions of the small intestine, and resulting malabsorption/maldigestion of nutrients there can cause diarrhea. “Low protein levels in the blood are specifically due to albumin (a type of protein) loss through the gastrointestinal tract,” Pusterla says. He recommends feeding affected foals a protein-rich palatable diet until they’ve fully recovered.
Veterinarians can diagnose Lawsonia several ways. A thorough diagnostic workup includes complete blood count and blood chemistry, serologic testing (titers run on blood samples), and fecal analysis.
To make a definitive laboratory diagnosis, veterinarians must screen the feces for L. intracellularis using PCR (polymerase chain reaction testing, which amplifies and detects pathogen DNA) and check the serum for antibodies against L. intracellularis using an established assay, says Pusterla.
Veterinarians also use ultrasound to see signs of disease such as intestinal wall thickening and corrugations.
It is not uncommon for foals with EPE to have concurrent disease (e.g., endoparasitism [internal parasites], pneumonia, gastric ulcers). Pusterla says endoparasitism is a predisposing factor in pigs, a species also affected by proliferative enteropathy, and this might also be the case for foals. He reports that farms with endemic EPE have been able to prevent cases by improving their parasite management programs.
Researchers have shown off-label use of a pig vaccine against Lawsonia to be very effective for preventing L. intracellularis in foals on endemic farms. They recommend vaccinating foals with 30 mL of the pig vaccine intrarectally twice, 30 days apart, one month prior to the historical annual occurrence of EPE cases on a farm.
As we’ve mentioned, intestinal damage from small and large strongyles can also impede digestion.
“Nutritional deficiencies as a result of intestinal parasite infections are likely caused by a combination of factors,” says Gabriele Landolt, DVM, PhD, assistant professor at Colorado State University’s Veterinary Teaching Hospital, in Fort Collins. “Intestinal parasites may increase nutrient loss, especially of protein, and cause decreased food intake and decreased nutrient absorption.”
She explains that protein loss most likely occurs when plasma protein leaks through parasite-damaged intestinal walls.
Fortunately, owners can work with their veterinarians to easily manage intestinal parasitism with a strategic control program that includes annual or biannual fecal egg count testing and targeted deworming based on the results.
Inflammatory Bowel Disease
This condition occurs when abnormal cells infiltrate the lining of the small intestine. Horses with IBD might have a history of mild recurrent colic, in addition to poor body condition from weight loss or failure to gain weight despite ample nutrition. Affected horses could demonstrate various degrees of colic pain due to excess gas production from the fermentation of spilled-over carbohydrates in the large colon.
“The pathogenesis of inflammatory bowel diseases (how they develop) is largely unknown, but an immune-mediated inflammatory cause has been hypothesized,” says Landolt, listing hypersensitivity reactions to inhaled, dietary, or parasitic antigens (foreign substances that induce an antibody response) as inciting factors. Conditions classified as IBD, all of which involve various types of white blood cells infiltrating the intestinal wall and other organs, include:
- Granulomatous enteritis (GE);
- Lymphocytic-plasmacytic enterocolitis (LPE);
- Multisystemic eosinophilic epitheliotropic disease (MEED); and
- Idiopathic focal eosinophilic enterocolitis (IFEE).
In some cases of GE and MEED, skin lesions seen as thin hair, patchy hair loss, crusting, and scaliness appear. “Multisystemic eosinophilic epitheliotropic disease is usually associated with severe exudative dermatitis (an oozing inflammation of the skin) and ulcers of the coronary band,” says Landolt. “The cause of MEED is unknown but is hypothesized to represent a chronic hypersensitivity reaction against undefined antigens, such as parasites, bacteria, or food allergies.”
Multisystemic eosinophilic epitheliotropic disease can affect any age or breed of horse but tends to occur in 2- to 4-year-old Standardbreds and Thoroughbreds. Eighty percent of GE cases occur in Standardbreds, with the highest incidence among those ages 1 to 5 years.
Lymphocytic-plasmacytic enterocolitis might be an early stage of lymphosarcoma. Weight loss in these horses with intestinal cancer is most likely due to a combination of gastrointestinal events. The tumor cells infiltrate the intestinal lining, reducing its absorptive surface area and replacing absorptive epithelial cells at the tip of the intestinal lining’s villi, Landolt says.
“This results in villous atrophy (wasting) and malabsorption of nutrients,” she says. “Thickening of the intestinal wall may also result in enlargement of the junctional pores between mucosal cells, which contributes to the loss of protein into the lumen (cavity of the intestines).”
In other words, rather than being absorbed into the bloodstream where it can be used as a nutrient, unabsorbed protein passes through the intestinal tract into the feces.
Veterinarians often base their presumptive diagnosis of IBD on a history of weight loss, limb and abdominal edema (fluid swelling), low blood protein, lethargy, and recurrent colic. Other diagnostic testing, such as abdominal ultrasound and rectal exam, can help veterinarians identify thickening of the small intestine. Carbohydrate absorption tests provide useful information about small intestinal efficiency.
Veterinarians use histopathology (in which they look for tissue changes caused by disease) of biopsy samples collected during small intestinal surgery to definitively diagnose and distinguish between the different forms of inflammatory/infiltrative bowel diseases.
Sand Accumulation in the Bowel
An abnormal accumulation of sand in the intestines, due to horses eating off sandy ground, can cause chronic diarrhea. This is likely due to irritation and inflammation of the colon as well as abnormal intestinal motility.
“While nutrient absorption in the small intestine should not be affected, fiber digestion and absorption of volatile fatty acids (energy derived from forage metabolism) can be affected by these changes,” says Landolt.
Management practices such as offering hay in a bedded stall (rather than on the ground outside), feeding in tire feeders or on rubber mats or concrete, and offering a psyllium product for seven consecutive days each month can help prevent sand colic.
Respiratory disease doesn’t tend to interfere with intestinal absorption, but in severe respiratory cases (e.g., recurrent airway obstruction, aka equine asthma) horses might lose weight due to increased metabolic workload and decreased food intake.
“In contrast,” says Landolt, “Severe cardiac disease, such as congestive heart failure (CHF), can interfere with nutrient absorption.” She explains that in horses with CHF, changes in intestinal wall perfusion and bowel edema can affect bowel wall permeability and nutrient absorption.
“In humans, even small changes in blood flow can lead to ischemia (inadequate blood supply) of the tips of the villi, which results in shortening of villi length and subsequent reduction in the absorptive surface,” she says. In addition, bowel wall edema can lead to malabsorption and protein loss, which she says are both thought to be major contributors to the development of cardiac cachexia, which is body wasting due to illness.
Scientists have described age-related digestive changes in rats, dogs, and humans, but Landolt says there’s little evidence of aging’s impact on equine digestion. In a 2014 study (TheHorse.com/35273) Elzinga et al. concluded that “under most practical feeding situations, differences in digestive capacity (of energy, neutral detergent fiber [a feed’s fiber content], crude protein, fat, calcium, or phosphorus) are unlikely to be present in healthy aged horses (19 to 28 years old) compared to adult horses (5 to 12 years old).”
What does influence nutrient digestibility in aged horses is dentition and the horse’s ability to chew food properly, Landolt says.
More recently, researchers have studied digestion in aged horses with pars pituitary intermedia dysfunction (PPID, also referred to as equine Cushing’s disease). At Michigan State University’s College of Veterinary Medicine, Jennifer DeVries, MS, working with Natalie Trottier, PhD, and Hal Schott, DVM, PhD, Dipl. ACVIM, authored a study in which they identified truncation of small intestinal mucosal villi and changes in the crypts in PPID horses. This was accompanied by a 50% decrease in glucose uptake and absorption.
“PPID-affected horses have altered villus morphology (form and structure) and may have decreased absorptive capacity for glucose, as compared to normal aged horses,” they wrote. This has the potential to alter energy uptake for the transport and maintenance of proteins and enzymes necessary for nutrient absorption.
“This should be considered ‘preliminary’ information because these villi changes and glucose uptake were identified in only one section of small intestine,” says Schott. “At this time, there is not enough information to extend this information globally to small intestine function and nutrient delivery.”
While further work needs to be done to better understand this finding, Schott says he suspects overall metabolic and hormonal changes contribute to the muscle wasting that occurs in advanced stages of PPID.
If your horse suffers from a small intestine issue, the first step is working with your veterinarian to address the underlying cause. Then formulate a feeding plan to help him get the most out of his meals.
“Typical feeding recommendations for horses with small intestinal malabsorptive disease include high-fiber-content diets (hay, pasture, beet pulp), since these components are fermented in the large intestine,” says Landolt. “Fat supplementation is also recommended to provide more calories.”
She also advises providing the horse access to a ration balancer and/or mineral block to balance his mineral intake. Otherwise, excesses in one can create deficiencies in another. Excess zinc, for instance, interferes with copper utilization.
For horses with a lack of appetite or difficulty keeping weight on despite a proper diet, have your veterinarian complete a thorough examination to look for underlying causes. Many disease syndromes can cause detrimental changes to the small intestine’s cellular lining that then interfere with nutrient absorption. Identifying a problem early is the best way to keep your horse healthy and in good weight.