Addressing acute diarrhea in the adult horse

dvm360dvm360 July 2020
Volume 51
Issue 7

Big colons can lead to big problems. Thats why veterinarians who treat horses should understand current diagnostic and treatment best practices for this potentially lethal condition.


Acute diarrhea is not an emergency in many animal species, but this is not always the case in horses. Because of the huge volume of fluid that can be lost from the horse's gastrointestinal (GI) tract as diarrhea, horses quickly can become profoundly hypovolemic. Horses are also exquisitely sensitive to lipopolysaccharide (endotoxin), and thus inflammation within the GI tract and translocation of bacteria through tight junctions can lead to endotoxemia, systemic inflammatory response syndrome and death.

Diarrhea can be caused by malabsorption, increased osmotically active particles in the lumen, increased secretion of water and electrolytes into the lumen, inflammation in or around the GI tract, or altered intestinal motility. It can be a primary issue or may occur secondary to disease outside the GI tract, such as endotoxemia, hypoproteinemia, or heart disease.

Most cases of acute-onset equine diarrhea are caused by an infectious agent. Infectious diseases leading to colitis and diarrhea include salmonellosis, clostridiosis, coronavirus, Potomac horse fever and larval cyathostomiasis.1 Non-infectious issues include right dorsal colitis secondary to nonsteroidal anti-inflammatory drug (NSAID) administration, inflammatory bowel disease (can also present as chronic diarrhea) and toxins such as cantharidin, hoary alyssum and arsenic.2

It is important to remember that horses with colitis do not always develop diarrhea. Therefore, many of the conditions commonly associated with diarrhea should not be ruled out simply because diarrhea is absent. For example, in a study examining the characteristics of Potomac horse fever in hospitalized horses, 34% did not have diarrhea.3 Horses can pool large volumes of fluid in their colon, which may lead to signs of colic due to distention and dysmotility, and can create significant hypovolemia without the presence of diarrhea. In some instances, patients with colitis may not develop diarrhea until fluid therapy is initiated and their fluid balance is restored.


Regardless of cause, the initial approach to examining and managing a horse with diarrhea is the same. Frustratingly, a definitive diagnosis for the inciting cause is rarely made, and most of the conditions that cause acute diarrhea present very similarly to one another. Taking a thorough history is critical when beginning the task of differentiating infectious from non-infectious causes. Medication history (specifically NSAIDs and antimicrobials), recent travel, exposure to animals with similar clinical signs, changes in feed or management, recent deworming, previous illness and duration of clinical signs are crucial pieces of information.

Clinical signs, aside from the presence of diarrhea, often include signs consistent with dehydration, fever, colic and/or endotoxemia. A complete physical examination should be performed, with extra attention paid to cardiovascular status and evidence of endotoxemia and laminitis. Initial diagnostics generally include a complete blood count and serum biochemistry panel. Useful adjuncts include measurement of blood lactate, blood gas analysis, and serum amyloid A.

Findings on complete blood counts in horses with colitis can vary drastically over as few as six to 12 hours. Initially, patients may have a normal total leukocyte count and a normal neutrophil count that can progress rapidly to marked neutropenia with a left shift and, often, toxic changes in the neutrophils. As patients improve, there is often a “rebound neutrophilia” and, finally, the counts normalize again as the patient recovers. The rapid pace at which these shifts occur supports the need for frequent monitoring of hematologic parameters to adjust therapy. Evaluation of blood smears in cases of diarrhea and colitis allows for identification of band neutrophils and toxic changes that may not be identified by an automated analyzer.

Findings on serum biochemistry panels and blood gases generally support hypovolemia, metabolic acidosis and loss of electrolytes and albumin through diarrhea. Assessment of biochemistry panels both before and after fluid therapy will allow the clinician to alter fluid therapy and rule out concurrent conditions (e.g. renal disease if blood urea nitrogen/creatinine normalize following fluid therapy). Hypovolemia can mask hypoalbuminemia, so a one-time measurement may give an incomplete clinical picture. In addition to azotemia (typically pre-renal), patients with diarrhea may have variable changes in their electrolytes. Sodium, chloride and bicarbonate are often lost through the GI tract, whereas hyperkalemia is common secondary to metabolic acidosis. Patients with normal potassium or mild hypokalemia in the face of metabolic acidosis may, in fact, be profoundly hypokalemic.

Identifying the cause of diarrhea can be challenging as not all infectious agents are shed consistently in the feces, nor can they be identified readily in the blood. Non-infectious causes of acute diarrhea can present in the same way as infectious causes. In up to 60% of cases of acute diarrhea in adult horses, the causative agent is never identified.4 Results by one method of diagnostic testing (e.g. culture for Salmonella spp.) may be negative, while another test (e.g. polymerase chain reaction) for the same agent may be positive. Formed fecal matter is more likely to yield culture-positive results as compared with feces with high water content; thus, false-negative culture results can occur.5 Currently recommended diagnostic tests for specific etiologies for diarrhea are detailed in Table 1. Commercial diagnostic laboratories often offer panels that include a combination of the tests listed below.

Table 1: Testing recommendations for specific causes of diarrhea1,2,4,5


Recommended test (sample)


Salmonella spp.

Culture (feces)

Labs will often perform PCR first and then culture positive samples. Five serial samples are recommended for culture.

PCR (feces)

Neorickettsia risticii (Potomac horse fever)

PCR (feces)

N. risticii is present in blood monocytes early in the disease course and eventually infects enterocytes and is shed in feces. Testing of both blood and feces is ideal.

PCR (whole blood)

Clostridium difficile

Toxin A/B ELISA (feces)

Toxin A/B ELISA is considered the standard diagnostic

Antigen ELISA (feces)


Culture (feces)


PCR for toxins A and B (feces)


Clostridium perfringens

Toxin ELISA (feces)



Culture (feces)

Low yield


PCR (feces)

Looks for toxin


PCR (feces)


Right dorsal colitis


Right dorsal colon wall thickness >9 mm is consistent with right dorsal colitis


Clinical, histopathology of cecal or colonic mucosa (cecal or colonic mucosa)

Histopathology will show eosinophilic inflammation, edema, +/- larvae. Fecal egg counts are rarely of use in diagnosis as the condition is caused by larval stages of parasites.2

Inflammatory bowel disease

Histopathology (biopsy of affected segment of GI tract)


ELISA = enzyme-linked immunosorbent assay; PCR = polymerase chain reaction.



Initial therapy for a horse with acute diarrhea involves restoring fluid balance, treating the underlying cause (if known, or if there is high index of suspicion for a particular etiology) and preventing or addressing endotoxemia.

Restoring fluid balance.

Fluid deficits should be addressed once a patient's approximate percentage of dehydration is determined based on clinical indices reported elsewhere (heart rate, capillary refill time, packed cell volume, urine specific gravity). An average-sized horse (450 kg [992 lb]) with watery diarrhea can produce 90 L (nearly 24 gallons) of diarrhea in a 24-hour period and thus will need significant volumes of both replacement and maintenance fluids to achieve normal hydration status.6

Initial resuscitative fluid therapy can be administered as a bolus of isotonic crystalloids (Normosol-R, Plasmalyte, lactated Ringer solution). Hypertonic saline can also be administered for rapid intravascular expansion followed by isotonic crystalloids. There is significant debate in human and small animal medicine, and to a lesser degree in equine medicine, regarding the use of colloids as a resuscitative therapy, but some clinicians advocate the use of colloids in the initial fluid plan. 7

Hydroxyethyl starch solutions and plasma both provide volume expansion of approximately three times the volume administered.7 Plasma has the added benefit of also providing immunoglobulins and coagulation factors that can attenuate the effects of endotoxemia. It can, however, be cost-prohibitive for some clients, and there is the risk of anaphylaxis and disease transmission during administration.7 While hydroxyethyl starch solutions are significantly cheaper and less likely to cause immune reactions, they have been shown to negatively affect equine platelet function and increase mortality when administered to humans with sepsis; therefore, the potential benefits must be weighed against the risks when deciding whether to use these fluids.7,8

It is imperative that patients with ongoing diarrhea be monitored closely, with fluid rates assessed frequently, to ensure that fluid losses are being replaced and daily maintenance requirements are being met. As the frequency and volume of bowel movements decrease, the volume of intravenously administered fluids can be decreased.

Treating the underlying cause.

As noted earlier, the cause of acute diarrhea is often not identified. Even in cases where testing ultimately yields a definitive diagnosis, this information usually is not available quickly enough to be useful when making an initial treatment plan. In certain cases (e.g. endemic geographical regions of Neorickettsia risticii during the appropriate season for Potomac horse fever), empirical therapy may be instituted with oxytetracycline-the antimicrobial of choice. The majority of cases, however, are not so straightforward.

Antimicrobial therapy is sometimes used in severely neutropenic animals to protect against bacteremia from translocation of primarily gram-negative bacteria via leaky tight junctions secondary to colitis.1 Intravenous gentamicin (6.6 mg/kg once daily) is an appropriate selection because it has minimal effect on anaerobic bacteria in the GI tract, and thus has a low likelihood of inducing antimicrobial-associated diarrhea. It has, however, been shown to upregulate production of β2 toxin by Clostridium perfringens and thus should be used only when clostridiosis is not present.9 Clostridial diarrhea is often responsive to metronidazole (15 mg/kg by mouth or 25 mg/kg per rectum two or three times daily). Antimicrobial therapy for salmonellosis is not used consistently because it may prolong bacterial shedding.5

Adjunctive therapies

A number of adjunct therapies have been administered in cases of diarrhea, including intestinal adsorbents, anti-endotoxin therapy, probiotics, and fecal transfaunation. Di-tri-octahedral smectite (Bio-Sponge-Platinum Performance) is an intestinal adsorbent that can bind Clostridium difficile toxins A and B, C. perfringens toxin A and endotoxin.10 Polymyxin B is a polypeptide antimicrobial agent that binds and neutralizes circulating endotoxin.11 Flunixin meglumine can also be given to attenuate endotoxemia. Laminitis prevention with cryotherapy is also recommended in many cases of acute diarrhea.1

Owing to their safety, ease of administration and affordability, probiotics are often administered as adjunct therapy in horses with acute diarrhea. However, many probiotic products may not reach the target site (large colon) effectively, and it is still largely unknown which strains of bacteria may be beneficial when administered to horses.12 Recently there has been renewed interest in the use of fecal microbial transfaunation (FMT) to reestablish normal flora following dysbiosis and colitis. FMT involves taking a fecal sample from a healthy donor and administering the feces directly into the bowel of the recipient, most commonly via nasogastric tube. Ideally, donors would be tested first for salmonellosis, C. perfringens and equine infectious anemia virus, and should have no recent history of antimicrobial administration.12


Acute diarrhea in the adult horse is a serious medical problem that requires prompt attention and therapy. It can be frustrating for veterinary clinicians and clients alike because a definitive diagnosis is often impossible to find. Luckily, however, treatment is generally the same for any case and should focus on maintaining cardiovascular status, resolving the diarrhea, and preventing endotoxemia and laminitis.


  1. Shaw SD, Stämpfli H. Diagnosis and treatment of undifferentiated and infectious acute diarrhea in the adult horse. Vet Clin Equine 2018;34:39-53.
  2. Feary DJ, Hassel DM. Enteritis and colitis in horses. Vet Clin Equine 2006;22:437-439.
  3. Bertin FR, Reising A, SLovis NM, et al. Clinical and clinicopathological factors associated with survival in 44 horses with equine neorickettsiosis (Potomac horse fever). J Vet Intern Med 2013;27:1528-1534.
  4. Oliver OE & Stämpfli H. Acute Diarrhea in the Adult Horse: Case Examples and Review. Vet Clin Equine 2006;22:73-84.
  5. Burgess BA, Morley PS. Managing Salmonella in equine populations. Vet Clin Equine 2014;30:623-640.
  6. Magdesian KG, Smith BP. Diarrhea. In: Smith BP, ed. Large Animal Internal Medicine, 4th ed. St. Louis: Mosby Elsevier; 2009:96-102.
  7. Magdesian KG. Replacement fluid therapy in horses. In: Fielding CL & Magdesian KG, ed. Equine Fluid Therapy. Ames, IA : Wiley Blackwell; 2015:161-174
  8. Blong A, Epstein K, Brainard B. In vitro effect of three formulations of hydroxyethyl starch solutions on coagulation and platelet function in horses. Am J Vet Res 2013;74:712-720.
  9. McGorum BC, Pirie RS. Antimicrobial associated diarrhoea in the horse. Part 2: Which antimicrobials are associated with AAD in the horse? Equine Vet Educ 2010;22:43-50.
  10. Weese JS, Cote NM, deGannes RVG. Evaluation of in vitro properties of di-tri-octahedral smectite on clostridial toxins and growth. Equine Vet J 2003;35:638-641.
  11. Mackay RJ. Endotoxemia. In: Smith BP, ed. Large Animal Internal Medicine, 4th ed. St. Louis: Mosby Elsevier, 2009:711-723.
  12. Schoster A, Weese JS, Guardabassi L. Probiotic use in horses-what is the evidence for their clinical efficacy? J Vet Intern Med 2014;28:1640-1652.

Kate Hepworth-Warren is an equine internal medicine specialist who currently works as a clinical assistant professor of equine medicine at North Carolina State University College of Veterinary Medicine in Raleigh, NC. Outside of work, she enjoys travelling, reading, running, and the beach.

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