Colitis in horses is a general term referring to an inflammatory response and disruption of the mucosal integrity in the large intestine. It can affect the large colon (colitis), cecum (typhlitis) or both (typhlocolitis). Colitis affects both mature horses and foals, but most often it affects equids between 2-10 years of age. Colitis can be chronic or acute, infectious or non-infectious and is usually associated with a range of local and/or systemic pathophysiologic events. Importantly, colitis is symptomatic of an underlying disease, so while management of the condition may be similar with all etiologies, the actual cause is critical to diagnose early in order to commence appropriate treatment and maximize the chance of a full recovery.
|Bacteria: Salmonella, Clostridium difficile, Clostridium perfringens, Lawsonia intracellularis, E.Coli, Neorickettsia risticii (Potomac Horse Fever)||Antibiotic associated diarrhea|
|Viruses: rotavirus in foals, coronavirus||Sand irritation of the large bowel|
|Parasites: small strongyles||Dietary imbalances|
|Inflammatory bowel disease|
|Plant and drug toxicities|
Often, the reason a horse develops colitis is multifactorial, and predisposing factors can include episodes of stress, perhaps from competition, travel, or antibiotic or anthelmintic treatment. In other circumstances colitis can prove idiopathic; indeed one study noted that a definitive diagnosis was made in only 35% of cases (N=66) presented (Mair, 1990), although with modern technology the ability to diagnose and classify these diseases has improved significantly.
Pathophysiological changes with colitis include widespread mucosal inflammation, with sloughing and necrosis of the mucosa and submucosa of the large intestine in the more severe forms of disease. Inflammation causes capillary dilation and increased permeability of the vascular endothelium, which in turn leads to the passive secretion of protein and fluid from the intravascular compartment into the intestinal lumen. The damage to the mucosal integrity not only reduces absorption of water, electrolytes, and nutrients but also leaves the mucosa vulnerable to further infiltration by pathogens and toxins. On postmortem examination, common findings include discoloration of the serosa (microthrombosis), mucosal edema, focal hemorrhage and necrosis (Jubb et al. 1993).
Whether acute or chronic, the disruption in colon health critically affects its structural integrity, the bacterial environment, and the ability of the equine hindgut to function optimally to maintain nutritional and overall wellness.
Clinical Signs of Colitis in Horses
Identifying colitis early is critical in securing a positive outcome for the horse, as the condition can lead to a rapid debilitation and even death. Symptoms and severity are largely dependent on the etiology as well as the susceptibility of the host – age, nutritional status, and immune status play an important role. When diagnosed quickly and treated appropriately fatality rates can be low as 10% (Larsen, 1997). The average recovery period in these cases is typically around 7-14 days.
The most overt presentation for colitis is diarrhea. Stools may range from loose and cowpie in texture, to watery and pipe stream, often accompanied by a foul smell. In severe cases there may also be blood in the diarrhea. With low-grade colitis, blood and albumin may be detectable in fecal matter, and can indicate injury to the hindgut. Colic, inappetence, ventral edema and lethargy are also typical. In some cases, horses do not develop diarrhea but instead may present with colic, fever, weight loss and/or ill thrift.
Severe diarrhea can rapidly lead to dehydration, hypoproteinemia and hypovolemic shock. This may manifest as weakness, cold extremities, a weak pulse quality and tachycardia. Persistent hypoproteinemia will lead to edema of the ventral abdomen, legs and the large intestine itself. Albumin is the most important protein within equine plasma for maintaining the intravascular oncotic pressure. Albumin has a lower molecular weight than other proteins so it is more easily lost across the damaged mucosa.
Secondary complications that can arise from colitis include:
- Septicemia and hematogenous organ colonization by bacteria
- Renal disease
- Immunosuppression and susceptibility to bacterial or fungal superinfection
- Cecum or colon infarction
- Jugular vein thrombosis
- Necrotizing enterocolitis
- and Laminitis
Diagnosis of Equine Colitis
The diagnostic work-up should include:
- A thorough history and complete physical exam
- Blood work, including a complete cell count, biochemistry, electrolytes, lactate, fibrinogen and serum amyloid A
- Abdominal ultrasound
- Fecal sample testing for:
- Occult blood and protein
- Bacterial culture
- ELISA/PCR immunoassay (such as a Equine Diarrhea PCR Panel)
- Microscopic examination for parasite larvae in fecal matter and biopsy
- +/- Rectal biopsy culture and histopathology
- +/- Xylose Absorption Test
- +/- Intestinal biopsy via exploratory laparotomy
Urgency, financial cost, invasiveness of a procedure, and prognosis must all be taken into account when formulating a plan for diagnosis. Testing for occult blood and protein is an ideal first step, using only a fresh fecal sample and yielding results stall-side in less than 15 minutes. Because of differences in the nature of albumin and hemoglobin, the presence or lack of these proteins serves to indicate where in the equine gastrointestinal tract they originate. Albumin, but not hemoglobin, is naturally degraded by acids and Proteinases (Pellegrini & Carter, unpublished), which are introduced into the duodenum via the common bile duct at a point just caudal to the pylorus. As a result, detection of albumin in a fecal sample serves as a proxy for inflammation in the hindgut. Learn more about using the SUCCEED Equine Fecal Blood Test to detect occult equine albumin and hemoglobin in a fecal sample.
Treating Colitis in Horses
The etiology of the disease will influence the required treatment. Acute severe bacteria-induced colitis requires intensive therapy in a critical care setting, while treatment for Right Dorsal Colitis is focused more on long-term nutritional therapy.
General treatment aims are:
- Correction of fluid and electrolyte balance
- Replacement of plasma protein to correct oncotic pressure and improve perfusion
- Repair of mucosal tissue
- Control of inflammation
- Ongoing nutritional management
Specific treatments may include:
- Fluid therapy with an isotonic crystalloid solution to combat hypovolemia and associated acid-base derangements
- Depending on plasma electrolyte concentrations, intravenous potassium chloride, calcium gluconate, magnesium sulfate (Epsom salts) and/or sodium administration
- Oncotic support via administration of plasma colloids, albumin and globulins and to combat hypoproteinemia
- Analgesia for abdominal discomfort
- Anti-diarrheal therapy
- Mycotoxin adsorbents, toxin neutralizing agents, and agents which prevent the synthesis, release or action of inflammatory mediators that follow endotoxin exposure
- Low dose anti-inflammatory drugs
- Possibly antimicrobial treatment
- Gastrointestinal support to promote restoration of the microbial ecology of the colon
Note that some infectious causes of colitis are transmissible, not only between horses but also across species to humans, thus isolation procedures and barrier nursing should be employed.
With appropriate treatment, signs of recovery should become apparent within 3 to 6 days (Murray, 1990) and if associated complications, such as laminitis or thrombophlebitis have been avoided then the prognosis is good and ongoing issues unlikely.
Colitis Discussion and Prevention
Specific nutrition, feeding and management regimens are required to meet the high demands placed on today’s performance horse. A diet high in energy-dense non-structural carbohydrate, but often lacking in sufficient fiber and fed intermittently, combined with prolonged stabling and the stresses that exist alongside training, competing and travel, all pose risks to digestive health.
A delicate balance of bacterial groups reside within the large colon and can be easily tipped into a state of unbalance. Diets high in non-structural carbohydrate can quickly overwhelm the small intestine, causing a failure of pre-cecal digestion and result in a significant delivery of starch to the cecum Further, transit rate may be hastened due to an increased volume of chime associated with this type of feed (Metayer et al. 2004). Under these circumstances, acidophilic anaerobes proliferate yielding lactate and propionate, which instigates a fall in pH to as low as 6.0. This acidification further reduces the population of fibrolytic populations, perpetuating disruption to the usually highly selective mucosal barrier and leaving it vulnerable to pathogenic and endotoxin infiltration.
Once this process has begun, colitis quickly follows and may very likely precede a range of disorders from colic and diarrhea to colonic ulcers and laminitis. Unfortunately, it is often the secondary complications, which govern whether an outcome is successful, or not.
Thus, treatment and prevention of colitis can both be aided by the application of careful management and feeding practices.
Some points to consider include:
- Increasing forage intake by providing free access. Minimum 1-1.5% BW of forage (DM) per day (≥40% Neutral Detergent Fiber and ≥20% Acid Detergent Fiber)
- Limiting starch intake per meal to a maximum of 2g/kg BW
- Ensuring barley, maize or wheat products are suitably processed (cooking, extruded, micronized, steam flaked or popped)
- Feeding oats preferentially over other grains
- Moderating rate of ingestion, “little and often” feeding regimes
- Avoiding dehydration
- Increasing turnout
- Avoiding turnout when fructan levels may be higher in the grass, and managing grassland effectively to reduce this risk (preferential grass species and cutting regimes)
- Avoiding sudden feed changes
- Feeding complex carbohydrates grass, hay, beet pulp for high calorie needs
- Supplementing the diet with yeasts of the Saccharomyces genus, or fructo-oligosaccharide
- Vaccinating for Potomac Horse Fever
- Providing additional hindgut health support
References & Further Reading:
- Jubb, K.V.F., Kennedy, P.C., Palmer, N.C. (1993) Pathology of domestic animals, 4th ed., Vol. 2. Academic Press. San Diego: 130-1: 213-7
- Larsen, J. (1997) Acute colitis in adult horses. A review with emphasis on aetiology and pathogenesis. Vet Q. 19 (2): 72-80
- Mair, T.S., de Westerlaken, L.V., Cripps, P.J., Love, S. (1990) Diarrhoea in adult horses: a survey of clinical cases and an assessment of some prognostic indices. Vet Rec.126(19): 479-81
- Mair, T.S., Divers, T., Ducharme, N. (2002) Manual of Equine Gastroenterology. WB Saunders. Edinburgh, UK
- Metayer, N., Lhote, M., Bahr, A., Cohen, N.D., Kim, I., Roussel, A.J., Julliand, V. (2004) Meal size and starch content affect gastric emptying in horses. EVJ. 36 (5): 436–440
- Murray, M.J. (1990) Therapeutic procedures for horses with colitis. Vet Med. 510-518
- Pellegrini, F., Carter, S. The Use of Novel Antibody Tools to Detect the Presence of Blood in Equine Feces. Unpublished
- Smith, B. P. (2015) Large Animal Internal Medicine. 5th ed. Elsevier Inc. St. Louis, MO.
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