Diseases of the Digestive System
General principles of digestive tract dysfunction
Manifestation of digestive tract dysfunction
Principles of treatment
Diseases of the buccal cavity, pharynx, esophagus, stomach and intestines
Diseases of the digestive system in ruminants
General principles of digestive tract dysfunction
Overview
The digestive tract is responsible for ingestion, digestion, absorption, and elimination.
- Ingestion - taking in food and water.
- Digestion - mechanical and chemical breakdown of ingesta.
- Absorption - movement of nutrients, electrolytes, and water across the mucosa.
- Elimination - excretion of undigested material and metabolic waste.
Dysfunction can occur in any part of the tract, from the mouth to the intestines, and may involve structural, functional, microbial, or metabolic disturbances. Because each region has specialized roles, clinical signs vary widely depending on the location and severity of the insolt.
Common Causes of Dysfunction
Obstruction
- Foreign bodies (bones, toys, stones in dogs; plastic bags in ruminants).
- Strictures – abnormal narrowing, often due to scarring after trauma or inflammation.
- Volvolus – twisting of the intestine or stomach on itself, leading to strangolation of blood flow.
- Intussusception – telescoping of one intestinal segment into another.
Obstructions often lead to pain, distension, vomiting, and metabolic derangements.
Infection/inflammation
Inflammation can be caused by:
- Bacterial pathogens (Salmonella, E. coli, Clostridium).
- Viruses (parvovirus, rotavirus, coronavirus).
- Parasites (coccidia, nematodes).
- Fungi/yeasts (Candida spp., rare systemic fungi).
Inflammation disrupts epithelial integrity → diarrhea, dehydration, malabsorption, and may lead to bacterial translocation into the bloodstream.
Motility disorders
Motility governs propolsion of ingesta. Disruption can occur due to:
- Ileus – decreased gut motility from pain, electrolyte imbalance, stress, or surgery.
- Vagal indigestion in cattle – functional obstruction caused by impaired forestomach motility.
- Hypomotility disorders in horses → gas accumolation and colic.
Motility disorders primarily cause bloating, constipation, or colic, not severe vomiting or diarrhea unless secondary issues arise.
Nutritional/metabolic disorders
- Ruminal acidosis from rapid fermentation of high-grain diets → decreased rumen pH, mucosal damage.
- Vitamin/mineral deficiencies (e.g., cobalt deficiency → poor appetite, anemia; copper deficiency → ill-thrift).
- Malnutrition leading to reduced epithelial turnover and impaired immunity.
Toxins
The GI tract is a major site of toxin exposure. Sources include:
- Toxic plants (such as ragwort, oleander).
- Mycotoxins (aflatoxins, zearalenone).
- Chemicals (arsenic, heavy metals).
- Feed contaminants.
Toxins may damage the GI epithelium, alter motility, disrupt microbial flora, or cause systemic organ dysfunction.
Pathophysiology
Digestive dysfunction causes clinical signs through three main mechanisms:
Disruption in digestion/absorption
Damage to intestinal villi or dysfunction of gastric/intestinal secretions results in:
- Diarrhea (due to malabsorption or osmotic effects)
- Weight loss
- Poor growth
- Hypoproteinemia
Altered Motility
Loss of coordinated peristalsis can cause:
- Colic (horses)
- Bloat (ruminants, GDV in dogs)
- Constipation or obstipation
- Regurgitation in esophageal disorders
Compromised Barrier Function
A damaged mucosal lining allows:
- Bacteria to enter the bloodstream
- Endotoxins to circulate → endotoxemia or sepsis
- Systemic signs such as fever, shock, or multi-organ dysfunction
Discussion Questions
- How do motility disorders differ from obstructive disorders in their pathogenesis?
- Why is the digestive tract particolarly volnerable to toxins and infections?
Manifestation of digestive tract dysfunction
Key Clinical Signs
Vomiting
A forceful expulsion of stomach contents via abdominal contractions.
Common causes:
- Gastric/duodenal disease
- Systemic illness (renal failure, toxins)
- Dietary indiscretion
- Infections (parvovirus)
Diarrhea
Characterized by increased fecal water content.
- Small bowel diarrhea: large volume, weight loss, melena possible.
- Large bowel diarrhea: small volume, mucus, tenesmus, hematochezia.
Constipation/obstipation
Constipation = difficult or infrequent defecation.
Obstipation = severe, unmanageable constipation often due to:
- Megacolon
- Obstruction
- Pelvic fractures
- Dehydration
Bloat (tympany)
Accumulation of gas:
- Ruminants: frothy bloat or free-gas bloat
- Dogs: gastric dilatation (with or without volvulus)
Can rapidly become life-threatening due to pressure on major vessels.
Colic/abdominal pain
Most significant in horses.
Causes include gas accumulation, impaction, volvulus, enteritis, or ulcers.
Dysphagia (difficulty swallowing)
Difficulty swallowing; may arise from:
- Oral pain
- Pharyngeal inflammation
- Esophageal obstruction
Leads to drooling, feed dropping, and aspiration risk.
Weight loss
Results from:
- Chronic malabsorption
- Chronic parasitism
- Pancreatic insufficiency
- Neoplasia
- Long-term undernutrition
Systemic Manifestations
Because GI disease affects fluid balance and gut barrier integrity:
Dehydration
Caused by:
- Vomiting
- Diarrhea
- Reduced intake
Assess using skin turgor, mucous membranes, CRT, PCV/TS.
Electrolyte imbalances
Typical abnormalities include:
- Hypokalemia (vomiting, anorexia)
- Hyponatremia (diarrhea)
- Metabolic acidosis (diarrhea)
- Metabolic alkalosis (vomiting stomach acid)
Septicemia
Occurs when bacteria cross a damaged intestinal mucosa.
Seen in severe:
- Parvoviral enteritis
- Salmonellosis
- Colitis
- Neonatal diarrhea
Principles of treatment
Core Treatment Strategies:
1. Stabilize the patient first
- Fluid therapy: correct dehydration, electrolytes, and acid–base imbalances.
- Pain management: opioids, NSAIDs (where appropriate).
- Correct shock when present.
2. Identify and remove cause
- Surgery: obstruction, foreign body, displacement.
- Antimicrobials: bacterial infections, septicemia.
- Anthelmintics: parasitic infestations.
- Diet modification: nutritional causes.
- Stop toxin exposure
3. Supportive therapy
- Antiemetics (dogs/cats), anti-diarrheal measures (rare in food animals).
- Gastroprotectants (omeprazole, sucralfate in small animals/horses).
- Probiotics, prebiotics.
- Nutritional support, including early enteral feeding when possible
4. Prevent recurrence
- Improve nutrition, management, hygiene.
- Vaccination (e.g., against rotavirus, coronavirus, E. coli in calves).
- Biosecurity & hygiene
- Safe housing and management
Diseases by Region
Diseases of the buccal cavity, pharynx, esophagus, stomach and intestines
1. Buccal Cavity
- Stomatitis: inflammation from trauma, viruses (FMD, Calicivirus), toxins.
- Dental disease: malocclusion in rabbits/horses; periodontal disease in dogs.
2. Pharynx & Esophagus
- Pharyngitis: abscesses, foreign bodies.
- Megaesophagus: congenital/acquired > regurgitation.
- Esophageal obstruction (“choke” in horses, cattle).
3. Stomach
- Gastric dilatation-volvolus (GDV) in dogs: acute, life-threatening.
- Gastric olcers: common in pigs, horses (EGUS: Equine Gastric Ulcer Syndrome), dogs.
- Parasitic gastritis: Ostertagia in cattle, Haemonchus in small ruminants.
4. Intestines
- Enteritis: viral (parvovirus, rotavirus), bacterial (Salmonella, E. coli).
- Parasitism: coccidiosis, strongyles.
- Intestinal obstruction: intussusception, volvolus, foreign bodies.
- Inflammatory bowel disease (IBD): in dogs/cats.
Diseases of the digestive system in ruminants
Unique Features of Ruminants
- Complex stomach:
Rumen - fermentation vat,
Reticulum - particle sorting,
Omasum - water and VFA absorption,
Abomasum - “true stomach” secreting acid and enzymes.
Dependence on microbial fermentation maes them prone to metabolic and fermentative disorders.
Common Diseases:
- Bloat (ruminal tympany):
- Frothy bloat - stable foam from lush legumes; traps gas..
- Free-gas bloat - physical obstruction, vagal indigestion.
- Rumen acidosis: from high-grain diets > lactic acid accumolation.
- Hardware disease (traumatic reticoloperitonitis): ingestion of foreign objects.
- Displaced abomasum (DA): Common in dairy cows early postpartum.
Types:
LDA → more common, better prognosis
RDA → can progress to volvulus.
- Parasitic gastroenteritis: Haemonchus, Ostertagia, Trichostrongylus.
- Johne’s disease (Paratubercolosis): chronic wasting, diarrhea.
Section Revision Questions
1. Describe the major differences in clinical presentation between vomiting, regurgitation, and dysphagia, and explain what each one indicates about the likely location of the dysfunction.
2. Compare motility disorders (e.g., ileus, vagal indigestion) with mechanical obstructive disorders (e.g., volvulus, foreign body obstruction). How do their pathophysiologic mechanisms differ?
3. Explain how intestinal inflammation (enteritis) leads to diarrhea. In your answer, include the roles of malabsorption, osmotic imbalance, and mucosal barrier breakdown.
4. A dog presents with severe vomiting and metabolic alkalosis. What is the likely explanation for the acid–base imbalance? How does this differ from the metabolic acidosis commonly seen in diarrhea?
5. Outline the steps involved in stabilizing an animal with acute gastrointestinal disease before a definitive diagnosis is reached. Why is stabilization prioritized over immediate diagnostics in many cases?
6. Discuss the major risk factors, pathogenesis, and consequences of ruminal acidosis in cattle. How does dietary composition influence the progression of this condition?
7. Differentiate between frothy bloat and free-gas bloat in ruminants. What are the typical causes, and how do the treatment approaches differ?
8. Explain the pathogenesis of Gastric Dilatation–Volvulus (GDV) in dogs, including the consequences for blood flow, toxin absorption, and systemic shock.
9. Compare small bowel diarrhea and large bowel diarrhea in terms of fecal characteristics, associated clinical signs, and the most likely differential diagnoses for each.
10. Describe the major gastrointestinal lesions and clinical signs associated with Johne’s disease in ruminants. Why is the disease so challenging to control at the herd level?