Rumenitis is usually the result of rapid intraruminal fermentation of dietary carbohydrate with subsequent production of lactic acid and increased acidity of the ruminal fluid (“grain overload”). Rations with high levels of carbohydrate are the principal cause in both dairy and feedlot cattle, but the texture of the feed and method of feeding can be modifying factors. The incidence of rumenitis in feedlot cattle is significantly higher when the cattle are transferred directly from a roughage ration to a finishing ration, and when there is poor feed bunk management. F necrophorum, alone or with other bacteria, colonizes through the area of superficial necrosis produced by the acid rumen contents. Leukotoxin may facilitate resistance to phagocytosis. Bacterial emboli from the lesions invade the hepatic portal venous system and are transported to the liver, where they can establish infectious foci of necrobacillosis that eventually develop into abscesses.