Equis ISSN 2398-2977

Colon: colitis

Contributor(s): Timothy Mair, Harold C McKenzie III, The Glass Horse, Jamie Prutton

Introduction

Pathogenesis

Etiology

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

Pathophysiology

  • Colonization of the intestinal mucosa by pathogenic bacteria (Salmonella spp Salmonella sppClostridium difficile Clostridium difficileClostridium 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 hepaotcytes 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

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Grønvold A M et al (2019) Fecal microbiota of horses in the clinical setting: Potential effects of penicillin and general anesthesia. Vet Microbiol 135 (3-4), 366-372 PubMed.
  • Bryan J, Marr C M, Mackenzie C J et al (2019) Detection of equine coronavirus in horses in the United Kingdom. Vet Rec 184 (4), 123 PubMed.
  • Shaw S D & Stämpfli H (2018) Diagnosis and treatment of undifferentiated and infectious acute diarrhoea in the adult horse. Vet Clin North Am Equine Pract 34 (1), 39-53 PubMed.
  • Pusterla, Nicola et al (2010) Use of quantitative real-time PCR for the detection of Salmonella spp. in faecal samples from horses at a veterinary teaching hospital. Vet J 186 (2), 252-255 VetMedResource.
  • Chapman A (2009) Acute diarrhea in hospitalized horses.Vet Clin North Am Equine Pract 25 (2), 363-380 PubMed.
  • Hassel D M, Smith P A, Nieto J E et al (2009) Di-tri-octahedral smectite for the prevention of post-operative diarrhea in equids with surgical disease of the large intestine: results of a randomized clinical trial.Vet J 182 (2), 210-214 PubMed.
  • Johns I, Tennent-Brown B et al (2009) Blood culture status in mature horses with diarrhoea: a possible association with survival. Equine Vet J 41 (2), 160-164 PubMed.
  • Ruby R, Magdesian K G & Kass P H (2009) Comparison of clinical, microbiologic, and clinicopathologic findings in horses positive and negative for Clostridium difficile infection. JAVMA 234 (6), 777-784 PubMed.
  • Granot N, Milgram J, Bdolah-Abram T, Shemesh I & Steinman A (2008) Surgical management of sand colic impactions in horses: a retrospective study of 41 cases. Aust Vet J 86 (1), 404-407 PubMed
  • Feary D J & Hassel D M (2006) Enteritis and colitis in horses. Vet Clin North Am Equine Pract 22 (2), 437-479, ix PubMed.
  • Cohen N D & Woods A M (1999) Characteristics and risk factors for failure of horses with acute diarrhoea to survive: 122 cases (1990-1996). JAVMA 214 (3), 382-390 PubMed.

Other sources of information

  • Robinson N & Sprayberry K (2009) Current Therapy in Equine Medicine 6. 6th edn. Saunders Elsevier. ISBN: 978-1416054758.


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