Part 2: Diarrhea and its Pathogenesis

Part 2: Diarrhea and its Pathogenesis
By Vet. Punyaporn Kruawangmon (Doctor Pang) and Assoc. Prof. Dr. Sompote Weerakul (Ajarn Kaew)

Normally, a sloth's feces are excreted as distinct pellets, similar to deer pellets. This is classified as feces score 1 (normal). The scoring progresses as follows:

Score 2: Excreted in a pile like cow or horse dung, but with many visible pellets mixed in.
Score 3: Still in a pile, but the number of deer-like pellets is significantly reduced.
Score 4: Very few pellets remain, with a noticeable increase in liquid content.
Score 5: Unformed, mushy feces, though a few tiny pellets might still be present.
Score 6: Completely soft and mushy feces.
Score 7: Severe diarrhea with no solid form; in some cases, it becomes watery and projectile.
Compared to other animals with foregut fermentation, the primary cause of diarrhea is a diet high in starch and sugar but low in dietary fiber. (High protein and fat can also be contributing factors, but starch and sugar cause the most rapid and significant issues). Sloths fed large amounts of grains (such as corn and soybeans), fruits, and similar foods are at a high risk. Even though fresh vegetables are often recommended, relying too heavily on them can result in insufficient levels of lignin and cellulose, which they typically get from tree bark. Diet proportions must be carefully managed and evaluated using weekly fecal scores.

Starch, sugar, and digestible fiber are utilized by lactic acid bacteria in the foregut fermentation process, converting them into lactic acid. When sloths consume a diet heavy in grains and fruits, over 80% of these carbohydrates are converted into lactic acid. This overproduction lowers the pH in the gastrointestinal (GI) tract, leading to the death of beneficial microbes. This dysbiosis removes the gut's natural defense, similar to food poisoning, allowing pathogenic bacteria to overgrow and cause enteritis (intestinal inflammation).

The excess lactic acid triggers a chain reaction. Lactate-utilizing bacteria convert the lactic acid into free fatty acids (which the body can use) but also produce histamine, leading to localized GI and systemic inflammation. Additionally, the free fatty acids yield butyrate, which butyrate-utilizing bacteria also convert into histamine, perpetuating the inflammatory cycle. Another critical issue during abnormal fermentation is the increase in sulfates. Sulfate-reducing bacteria convert these into hydrogen sulfide (rotten egg gas). This toxic gas is a primary cause of severe pain in the GI tract. While defecation and flatulence can relieve this pain, standard painkillers are often ineffective. Ultimately, this entire abnormal fermentation cascade is rooted in high-energy diets loaded with continuous starch and sugar.

Clinical Signs
Initial symptoms: Straining to defecate (tenesmus), abdominal distension, and discomfort when moving or being handled. However, these are often unnoticed until fecal abnormalities appear.
Fecal changes: A reduction in uniform deer-like pellets, progressing to loose piles. This is caused by insufficient lignin and cellulose to bind the feces.
Watery and mucous diarrhea: Dysbiosis, pathogens, and increased free fatty acids lead to loose stool. The presence of mucus (produced by goblet cells to buffer the highly acidic GI tract) makes the feces look shiny.
Projectile diarrhea: Often associated with secondary bacterial infections (e.g., E. coli, Clostridium) in severe enteritis cases.
Foul odor: Feces smelling of sulfur or rotten eggs indicates hydrogen sulfide gas, which strongly correlates with severe colon pain.
Impact and Management Guidelines
Sloths mask their pain well, so a decrease in appetite is a key indicator of distress. While pain management is necessary for comfort, pain caused by hydrogen sulfide gas is difficult to alleviate until the gas is passed.

Defecation stimulation: Enemas are recommended based on the volume of feces impacted in the large intestine. Laxatives must be strictly avoided, as they cause additional pain and can rupture the bowel in cases of complete obstruction.
Prokinetics: If there is straining without defecation, distal colon stimulants may be used (the distal colon can hold up to 30% of the sloth's body weight in feces weekly).
Dietary correction: Projectile diarrhea can persist for weeks or months due to the long-lasting effects of improper diets. Correcting the diet is the most crucial step; medications are only supportive.
Electrolyte Imbalances
Projectile diarrhea causes severe electrolyte and mineral loss. Fluid shifts into the GI tract even before diarrhea visibly occurs, leading to lethargy and dangerous potassium fluctuations.

Early stage: Blood acidosis causes high potassium levels (hyperkalemia), posing a risk of cardiac arrhythmias or heart failure.
Later stage: Continuous fluid loss leads to severe potassium depletion (hypokalemia), along with low sodium and chloride levels.
Treatment: Intravenous replacement fluids or plasma-like fluids are critical, transitioning to maintenance fluids with potassium supplementation. Acidosis must be corrected concurrently (e.g., using sodium bicarbonate for organic acidosis). Oral rehydration salts (ORS) can be used for milder cases.
Nutrition and Hypoglycemia
Mild hypoglycemia can be managed by adding 5% dextrose to IV fluids. Severe cases require a 50% dextrose bolus.
Recovery food must be high in fiber and low in energy to avoid exacerbating the starch/protein issue.
Easily digestible proteins (hydrolyzed or plasma proteins) and small amounts of medium-chain triglycerides (MCTs) can be added to the recovery formula.
Improvement is indicated when defecation frequency decreases to once a week and the feces return to a deer-pellet form.
Probiotics and Medications
Microbial replacement: Probiotics are heavily relied upon and should be given twice daily. For grain-induced diarrhea, transitioning from lactic acid bacteria to yeast (or a combination) helps reduce acid accumulation and improves carbohydrate utilization.
Bacillus: Adding Bacillus strains helps prevent pathogen invasion.
Antibiotics: Veterinarians may use antibiotics initially but will taper them off to rely more on probiotics, minimizing side effects and restoring microbial balance.
Monitoring: Treatment is long-term, often lasting 1-2 months. Close monitoring via X-rays, hematology, fecal consistency, and appetite is required since clinical signs are often subtle.