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Escherichia coli (E.coli)

The bacteria Escherichia coli (E.coli) is a common inhabitant of the intestines of most mammals. It is considered to be near ubiquitous in the environment because it is shed in feces and disseminated through water and soil, where it can attach itself to, and colonize on, plants.

There is a huge variety of E.coli types. Mostly they are harmless, but there exist some notoriously virulent pathotypes of E.coliEscherichia coli O157, for example, is the pathotype that produces the Shiga Toxin. This E.coli has been associated with outbreaks of intestinal and hemolytic disease in humans and animals (

In the animal world, pigs and calves are known to be particularly susceptible to E.coli pathotypes.

E.coli and Diarrhea in Adult Horses

E.coli is a very common commensal organism in the intestinal tract of horses. The bacterium is frequently cultured from the feces of both healthy horses and horses with diarrhea.

Van Duijkeren et al. (2000) cultured E.coli from the feces of 10 horses with diarrhea and 14 horses without diarrhea. They selected 9 colonies, at random, from each fecal sample and then examined different attributes of the colonies, including the genotype and the ‘virulence factors’ that were present. They found that the genotypes of E.coli in the two groups were not significantly different. They also found that E.coli virulence factors were present in both normal horse feces and in horses with diarrhea, with the exception of the virulence factor F17 fimbriae, which was only found in horses with diarrhea. Hemolytic strains of E.coli were found in 2 horses with diarrhea.

Despite these findings, E.coli is still not considered a serious primary pathogen in horses with diarrhea, although clinicians should keep in mind that it may act as a secondary pathogen, exacerbating the primary disease pathology.

Today, the main concern with the presence of E.coli in horse feces is from a human health standpoint, as antimicrobial-resistant and multi-drug-resistant (MDR) strains of E.coli have been isolated from the feces of hospitalized horses, especially those that have been treated with oral antibiotics (Maddox et al. 2015).

E.coli, Foals and Diarrhea

Foals are highly susceptible to infection and disease from E.coli, especially as neonates.

Neonates are often exposed early to E.coli, within the first few minutes to hours of life. When a neonate is learning to nurse, early failed attempts can include sucking on the flank of the mare, or the ground, or on nearby objects. As E.coli is near ubiquitous in the environment, the foal ingests it easily.

The neonatal foal has a unique, short-lived population of cells in the intestine that persist only for the first 12-24 hours of life. These cells specialize in engulfing the large colostral proteins and transporting them to the systemic circulation. These cells can also engulf bacteria. If the foal fails to nurse adequately and does not receive the mare’s colostrum, it will likely still receive the bacteria, and subsequently develop bacteremia and then septicemia.

In foals with septicemia, E.coli is one of the most common isolates from blood culture.

E.coli can also invade the foal’s intestinal mucosa, resulting in enteritis, colitis or both. This is called Colibacillosis. In foals, colibacillosis is more commonly a secondary disease process, usually seen when the foal is being treated for another disease, often with antibiotics (Knottenbelt et al. 2004).

Knottenbelt et al. (2004) describes three forms of E.coli diarrhea in foals:

  1. Type 1 is a hypersecretory diarrhea caused by an E.coli enterotoxin. The enterotoxin does not damage the intestinal mucosa, but induces the intestinal mucosa to secrete water, electrolytes and bicarbonate into the lumen. The diarrhea is watery and profuse, however there is no protein leakage. This syndrome is not well recognized in foals.
  2. Type 2 is the more common ‘Colibacillosis’ form, where the bacteria invade the intestinal mucosa causing mucosal inflammation, often resulting in secondary septicemia. If the mucosal damage is severe, blood and protein will leak into the intestinal lumen and can be detected in feces. The clinical symptoms of septicemia often precede any diarrhea that may or may not develop.
  3. Type 3 is rare in foals. In this case, the E.coli causes destruction of the intestinal brush border resulting in malabsorption of fluid and nutrients. Protein levels in feces are likely to be high in this scenario.

Foals generally do not suffer specifically from colitis, more so enteritis or enterocolitis, which can then result in diarrhea. These syndromes are often a multifactorial affair, and can include contributions from viruses (Coronavirus and Rotavirus), other bacteria (Clostridia, Salmonella, Rhodococcus and Lawsonia), intestinal parasites (Strongyloides westerii) and the protozoa Cryptosporidium. In addition, there are the changes associated with the natural digestive maturation of the foal from a primary milk digester to a fermenter of fiber – the so-called ‘foal heat diarrhea’.

Diagnosing E. Coli in Horses

As E.coli is commonly isolated in the feces of healthy and diseased horses, it is not commonly tested for, nor considered a pathogen, until Salmonella, Clostridia, Rotavirus, Coronavirus, Lawsonia, Potomac Horse Fever and Cryptosporidium have first been ruled out. The modern diagnostic Equine Gastrointestinal PCR panels that are now available at most diagnostic laboratories can help streamline this process.

In foals, the SUCCEED Equine Fecal Blood Test can help to determine the severity of the pathology of the diarrhea. If blood and protein are present in the diarrhea as indicated by positives for hemoglobin and albumin on the FBT, then the foal may have significant damage to the intestinal wall and should be monitored closely, as prolonged antimicrobial coverage, and supplemental nutrition may be required.

Treatment and Prevention of E. Coli Infection

E.coli is generally susceptible to a wide range of antibiotics that have a Gram-negative spectrum. In most cases of equine diarrhea, the focus of the treatment will be on the primary disease, not E.coli.

New and Alternative Treatment Options to Consider

Ongoing research in other species as well as some new research in equines shows the potential utility of some other substances for managing GI health in horses.


Glutamine helps to heal the mucosa and strengthen tight junctions between enterocytes. In several animal models, functional activity of immune components including lymphocytes, macrophages and neutrophils are increased with glutamine supplementation (Newsholme, P. 2001). Treatment with glutamine in farmed animals has shown that there is improvement of gut integrity and weight gain as well as mucosal healing (Kaya, E. et al. 2007).

Glutamine is a conditionally essential amino acid. During catabolic stress of the bowel, as found in infection and sepsis, glutamine is consumed at a rate exceeding its production, warranting supplementation (Rao, R. et al. 2011).

These studies come with a caveat: although they have been conducted on GI tracts in animals as varied as chickens, cows and pigs, there are as yet no similar studies in horses. However, these studies are consistent with reports of the utility of glutamine in right dorsal colitis (Rötting, A. et al. 2004) demonstrating a clear connection between glutamine and equine GI dysbiosis.

Mannan oligosaccharide

Mannan oligosaccharide (MOS) may be useful as a bacterial “sponge”, before, during and after an E. coli infection (Flickinger, E. et al. 2003). This complex sugar resembles the mannose sugars that coat enterocytes, which are the main targets of E. coli, which binds to them with fimbrial lectins, bacterial projections which act as mannose receptors (Sharon, N. et al. 2015). E. coli fimbria preferentially latch onto MOS instead of the mannose-coated enterocytes, and the unattached pathogen can then be shed in the feces. MOS can protect equines from most pathogens as effectively as antibiotics (Spring, P. et al. 2015).

MOS may also be useful as an emergency treatment for diarrhea in horses at a rate of 100-200 mg/kg, q8-24h (Orsini, J. et al. 2013).

Antibiotics save lives, but overuse or misuse can lead to resistant bacteria. MOS has not been shown to lead to bacterial resistance, which provides a good rationale for using MOS as a substitute for antibiotics wherever possible.

MOS has no known precautions or side effects (Orsini, J. et al. 2013).


  • Feary, D. et al. (2003) “Enteritis and Colitis in Horses.” Veterinary Clinics of North America: Equine Practice 22, no. 2 (August 2006): 437–79. doi:10.1016/j.cveq.2006.03.008.
  • Flickinger, E. et al. (2003) “Nutritional Responses to the Presence of Inulin and Oligofructose in the Diets of Domesticated Animals: A Review.” Critical Reviews in Food Science and Nutrition 43, no. 1 (January 1, 2003): 19–60. doi:10.1080/10408690390826446.
  • Kaya, E. et al. (2007) “The Effect of L-Glutamine on Mucosal Healing in Experimental Colitis Is Superior to Short-Chain Fatty Acids.” The Turkish Journal of Gastroenterology: The Official Journal of Turkish Society of Gastroenterology 18, no. 2 (June 2007): 89–94.
  • Knottenbelt, D. et al. (2004) Equine Neonatology, Medicine and Surgery. Elsevier Health Sciences pp. 232.
  • Maddox, T.W. et al. (2015) Antimicrobial resistance in bacteria from horses: Epidemiology of antimicrobial resistance. Equine Veterinary Journal 47:756-765.
  • Newsholme, P. (2001) “Why Is L-Glutamine Metabolism Important to Cells of the Immune System in Health, Postinjury, Surgery or Infection?” The Journal of Nutrition 131, no. 9 (September 1, 2001): 2515S–2522S.
  • Orsini, J. et al. (2013) Equine Emergencies: Treatment and Procedures. Elsevier Health Sciences, 2013.
  • Rao, R. et al. (2011) “Role of Glutamine in Protection of Intestinal Epithelial Tight Junctions.” Journal of Epithelial Biology & Pharmacology 5, no. Suppl 1-M7 (January 2012): 47–54. doi:10.2174/1875044301205010047.
  • Rötting, A. et al. (2004) “Effects of Phenylbutazone, Indomethacin, Prostaglandin E2, Butyrate, and Glutamine on Restitution of Oxidant-Injured Right Dorsal Colon of Horses in Vitro.” American Journal of Veterinary Research 65, no. 11 (November 1, 2004): 1589–95. doi:10.2460/ajvr.2004.65.1589.
  • Sharon, N. et al. (2015) “Bacterial Adherence to Cell Surface Sugars.” Ciba Foundation Symposium 80 (1981): 119–41.
  • Spearman, K. (2016) MOS supplements in for pregnant mares have been shown to significantly increase IgG, IgM and IgA levels in colostrum. Foals from mares fed MOS have a reduced incidence of diarrhea.
  • Spring, P. et al. (2015) “A Review of 733 Published Trials on Bio-Mos®, a Mannan Oligosaccharide, and Actigen®, a Second Generation Mannose Rich Fraction, on Farm and Companion Animals.” Journal of Applied Animal Nutrition 3 (2015): e8 (11 pages). doi:10.1017/jan.2015.6.
  • Van Duijkeren, E. et al. (2000) Characterization of Escherichia coli isolated from adult horses with and without enteritis. Veterinary Quarterly 22:162-166.

Equine GI Disease Topics

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