NAVLE Gastrointestinal and Digestive

Ovine and Caprine Rumenitis Study Guide

Rumenitis refers to inflammation of the ruminal mucosa, most commonly occurring as a sequela to ruminal acidosis (grain overload).

Overview and Clinical Importance

Rumenitis refers to inflammation of the ruminal mucosa, most commonly occurring as a sequela to ruminal acidosis (grain overload). In sheep and goats, rumenitis represents a significant component of the parakeratosis-rumenitis-liver abscess complex and can lead to serious complications including mycotic infection, bacteremia, and liver abscesses. Understanding the pathophysiology, clinical presentation, diagnosis, and management of rumenitis is essential for NAVLE success.

Small ruminants, particularly feedlot lambs, club lambs, and dairy goats on high-concentrate diets, are at increased risk. The condition is preventable through proper dietary management and gradual diet transitions.

High-YieldRumenitis is most commonly secondary to ruminal acidosis (grain overload). Remember the cascade: excessive fermentable carbohydrates → lactic acid accumulation → decreased rumen pH → mucosal damage → secondary bacterial or fungal invasion.
Stage Pathophysiologic Events
Stage 1 Ingestion of excessive rapidly fermentable carbohydrates (grain) by unadapted animal
Stage 2 Rapid fermentation → Increased VFA production → Initial pH decrease → Streptococcus bovis proliferation
Stage 3 Increased lactic acid production → pH drops below 5.0 → Death of protozoa and gram-negative bacteria
Stage 4 S. bovis inhibited → Lactobacillus spp. predominate → Continued lactic acid production (L- and D-isomers)
Stage 5 CHEMICAL RUMENITIS: Low pH causes epithelial damage, vacuolation, erosion, ulceration of ruminal mucosa
Stage 6 Damaged mucosa → Secondary bacterial/fungal invasion → Bacteremia → Potential liver abscessation

Etiology

Rumenitis in small ruminants can result from chemical, mechanical, or infectious causes.

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