Causes of Diarrhea in Adult Horses
Clostridium difficile is the most common cause of antibiotic-associated diarrhea and pseudomembranous colitis in humans and
horses. Risk factors in man include systemic antimicrobial use, gastrointestinal surgery, proton pump inhibitors (like omeprazole),
chemotherapy, increasing age, and lack of immune competence. The primary risk factor in horses is the use of antimicrobials
which results in disruption of the normal gastrointestinal microflora, allowing proliferation of the pathogenic C. difficile
organisms. With reduced colonization resistance, the overgrowth may be associated with toxin elaboration, and subsequent disease,
ranging from mild diarrhea to severe, life-threatening colitis. Toxins include enterotoxin (Toxin A) and cytotoxin (Toxin
B), which act synergistically to induce mucosal permeability, inflammatory cell chemotaxis, and epithelial cytotoxicity. The
d PCR can be applied to isolates once cultured to evaluate for the presence of Toxin A and B genes. Diagnosis of the disease
relies on positive fecal cultures and identification of toxins in fecal samples. Immunoassays (ELISA) are rapid, technically
easy to perform, and readily available at most commercial laboratories; they are a means of directly identifying the presence
of toxins in stool samples, however they may lack sensitivity. PCR can also be applied to isolates once cultured to evaluate
for the presence of Toxin A and B genes. Specific treatment is with metronidazole, smectite adsorbents, and supportive care
(described below). Because of its ability to form resistant spores, the microbe may survive in the environment for prolonged
periods. Most disinfectants are ineffective against spores, however peroxygen compounds and bleach can be used to decrease
Infections with Salmonella sp are clinically indistinguishable from clostridial colitis. Many serotypes of salmonellae affect
horses, including S. anatum and S. krefeld (belonging to the antigen group E), and the more invasive S. typhimurium and S.
agona (group B). In addition to diarrhea, salmonellae may produce septicemia, particularly in foals. As for clostridia, colic,
gastrointestinal surgery, anorexia and antimicrobial agents predispose horses to the development of clinical disease. Following
adherence to the gastrointestinal epithelium, salmonellae produce exotoxins, leading to ion and fluid flow from the cell,
with subsequent invasion of the cell. Salmonellae are intracellular pathogens. Once there, the bacteria result in death of
the cell through cytotoxin-induced inhibition of protein synthesis. Treatment is primarily supportive. Systemic antimicrobials
do not change the course of the GI infection. However, neonatal foals should always be covered with antimicrobials to prevent
secondary bacteremia. If kidney function is normal, amikacin should be used. If foals are azotemic, ceftiofur or other 3rd-4th
generation cephalosporin should be administered. Adult horses should be protected from bacteremia with antimicrobials (aminoglycoside
or enrofloxacin) if they are markedly neutropenic (< 1000/Ál) or febrile.
Equine monocytic ehrlichiosis (Potomac horse fever) is caused by Neorickettsia risticii, an important cause of diarrhea in
the east, as well as along the Oregon border (Shasta river) and Grass Valley in California. In addition to its geographic
restrictions, the disease occurs with summer and fall seasonality. The resulting colitis and endotoxemia are clinically similar
to that of other etiologies; however, laminitis appears to have a higher prevalence with this disease. In addition, abortion
may occur in pregnant mares. Treatment is with oxytetracycline (can be followed with doxycycline) and supportive care, although
horses must be kept well hydrated while on oxytetracycline.
Larval cyathostomiasis occurs when large numbers of small strongyle L4 larva undergo arrested development within the wall
of the gastrointestinal tract. This usually leads to chronic weight loss and diarrhea, but occasionally horses present with
acute diarrhea. Young horses housed on pasture with poor deworming histories are at highest risk. The diarrhea is often associated
with marked protein loss, leading to hypoalbuminemia. Treatment is with larvicidal doses (10 mg/kg, PO) of fenbendazole daily
for 5 days.
Newer agents currently under investigation as to their role in equine colitis include Aeromonas sp. One study found a prevalence
of 55 % of this microbe in the feces of horses with diarrhea (n=40), as compared to 0 % in those without diarrhea. However,
many of the horses in that study were concurrently infected with Salmonellae, intestinal parasites, or viruses (Hathcock,
1999). Lawsonia intracellularis has been receiving attention recently as a cause of diarrhea and protein losing enteropathies
in foals 2-18 months of age. This disease should be suspected in foals with weight loss, hypoalbuminemia, colic, and diarrhea,
or with ultrasonographic evidence of small intestinal thickening. Antemortem diagnosis can be difficult, but may be attempted
with serology (titers) and fecal PCR (several pooled samples).
Right dorsal colitis secondary to phenylbutazone and other NSAID intoxication may result in diarrhea, as well as hypoproteinemia,
colic, and signs of endotoxemia. Young performance horses, ponies, and dehydrated horses appear to be at highest risk. Inhibition
of PGE, with a subsequent reduction in perfusion of the gastrointestinal mucosa, a decrease in mucus and bicarbonate secretion,
and a delay in migration of basal epithelial cells towards the lumen, result in gastrointestinal injury. Treatment is with
Misoprostol, sucralfate, and pelleted feed. Colloids are optimal fluids, when fluid therapy is necessary.
Horses can develop diarrhea from dietary causes, such as moldy feed, or toxins such as blister beetle or oleander.