Introduction

• Cause: possible causes include:
  • Enteric salmonellosis Intestine: salmonellosis.
  • Clostridial diarrhea (Clostridium difficile Clostridium difficile, Clostridium perfringens Clostridium perfringens).
  • Potomac Horse Fever (Equine monocytic ehrlichiosis) Potomac Horse Fever.
  • Antibiotic-associated diarrhea Diarrhea: antimicrobial associated.
  • Cyathostomiasis Diarrhea: parasitic Cyathostomins: small strongyles.
  • Sand enteropathy Gastrointestinal: sand colic.
  • Carbohydrate overload.
  • Right dorsal colitis Colon: inflammation - right dorsal.
  • Intoxication, eg Blister beetle (cantharidin Toxicity: cantharidin), castor oil, hoary alyssum Poisonous plants: overview, arsenic Toxicity: arsenic.
  • Infiltrative/inflammatory bowel disease Chronic inflammatory bowel disease.
• Signs: pyrexia, diarrhea, depression and anorexia are common signs. Abdominal discomfort may be present, especially prior to onset of diarrhea.
• Diagnosis: hematology and biochemical analysis, ultrasonography, fecal testing (PCR and ELISA), serology, abdominocentesis.
• Treatment: dependent upon primary etiology.
• Prognosis: dependent upon primary etiology and patient status.

Pathogenesis

Etiology

• Salmonella spp Salmonella spp.
• Clostridium difficile Clostridium difficile.
• Clostridium perfringens Clostridium perfringens. 
• Coronavirus Coronavirus.
• Neorickettsia risticii (Potomac Horse Fever Potomac Horse Fever, equine monocytic ehrlichiosis).
• Antimicrobial-associated colitis Diarrhea: antimicrobial associated.
• Non-steroidal toxicity (right dorsal colitis) Toxicity: non-steroidal anti-inflammatory (NSAID).
• Cyathostome infestation Cyathostomins: small strongyles.
• Infiltrative or inflammatory bowel disease Chronic inflammatory bowel disease: eosinophilic, granulomatous, lymphocytic or plasmacytic enteritis, alimentary lymphosarcoma.

Predisposing factors

General

• Hospitalization, especially with abdominal surgery and general anesthesia.
• Gastrointestinal disease.
• High ambient temperatures can increase Salmonella shedding.
• Physiologic stress (transport, illness, change in diet or management).
• Poor parasite control Parasite control programs (cyathostomiasis).
• Sandy soils (sand enteropathy Gastrointestinal: sand colic).

Specific

• Antimicrobial therapy Therapeutics: antimicrobials.
• Non-steroidal anti-inflammatory (NSAID) therapy Therapeutics: anti-inflammatory drugs.
• Proton pump inhibitors and H₂ agonists may be implicated in C. difficile infections, although strong evidence is lacking.

Pathophysiology

• Colonization of the intestinal mucosa by pathogenic bacteria (Salmonella spp Salmonella spp, Clostridium difficile Clostridium difficile, Clostridium perfringens Clostridium perfringens) leads to mucosal inflammation and injury.
• A dysbiosis is required leading to a disruption of the normal gastrointestinal flora allowing the toxigenic bacteria to proliferate.
• Clinical signs associated with colic, dehydration (hypovolemia) and SIRS/septic shock are associated with altered gastrointestinal motility (ileus to increased), hypersecretion into the lumen and the altered muscosal barrier due to inflammation.
• Neutropenia is due to sequestration and margination into intestinal villi and subsequent loss into the intestinal lumen.
• Inflammation leads to intestinal dysfunction manifested as ileus and can lead to subsequent secretory diarrhea with fluid shifting into the intestinal lumen.
• Dehydration is often severe and can lead to pre-renal azotemia and acidosis.
• In severe cases the loss of mucosal barrier function combined with suppression of the patient's immune responses can allow for the establishment of systemic infection, often seen with damage to hepatocytes following contamination of portal bloody supply and rarely fungal infections (Aspergillus Aspergillosis) within the respiratory tract.
• In the case of parasite-associated colitis Diarrhea: parasitic the emergence of L4 cyathostome larvae within the intestinal mucosa leads to potentially severe mucosal inflammation followed by dysfunction as described above as well as ongoing fibrosis of the mucosa.
• Antimicrobial therapy causes alteration of the normal colonic bacterial flora which can predispose to overgrowth of pathogenic bacteria (salmonellosis Intestine: salmonellosis, clostridial diarrhea Gastrointestinal: clostridiosis).
• Carbohydrate overload results from the ingestion of large amounts of concentrate feeds (grain) that leads to profound alterations in the chemical and bacterial composition of the colonic contents. Inflammation of the intestinal mucosa leads to increased intracolonic fluid volume and also allows increased absorption of toxic materials (endotoxin, vasoactive amines, etc) from the colonic lumen.
• The ingestion of sand while feeding leads to colonic sand accumulation Gastrointestinal: sand colic. The sand causes local irritation and inflammation, resulting in diarrhea.
• Non-steroidal anti-inflammatory toxicity Toxicity: non-steroidal anti-inflammatory (NSAID) causes mucosal injury, particularly within the right dorsal colon, subsequent severe hypoalbuminemia and often diarrhea.
• Inflammatory bowel disease Chronic inflammatory bowel disease is an immune-mediated condition wherein large numbers of inflammatory cells accumulate within the wall of the bowel (eosinophils, macrophages, lymphocytes, plasma cells). The inflammatory response causes damage to the intestinal mucosa and can lead to fluid loss into the bowel lumen but more frequently an insidious weight loss will be noted.
• Infiltrative bowel disease is a neoplastic process, most often alimentary lymphosarcoma and can present similarly to inflammatory bowel disease.

Timecourse

• Typically acute to subacute.
• Can be chronic:
  • Enteric salmonellosis.
  • Cyathostomiasis.
  • Right dorsal colitis.
  • Sand enteropathy.
  • Inflammatory/infiltrative bowel diseases.

Epidemiology

• Enteric salmonellosis and clostridial diarrhea are infectious conditions that carry an increased risk of spread in situations where large numbers of horses are at risk for colonization. Hospitalized horses are at risk for a number of reasons:
  • Stress due to surgery or general anesthesia.
  • Altered gastrointestinal function and diet.
  • Immune compromise.
  • Antimicrobial therapy.
• Horses having undergone transportation stress or other stressful experiences may also be at risk.
• Horses may shed salmonella or clostridial organisms even after they return to a clinically normal state, so care should be taken to avoid exposure of unaffected animals. This is also true during particularly hot ambient temperatures.
• Horses diagnosed with enteric salmonellosis should not be returned to the herd until a minimum of three negative fecal cultures have been obtained on normal feces, and 5 negative cultures is preferred.

Diagnosis

Treatment

Prevention

Outcomes