Sudden Death - Diseases

Rumen Acidosis

Other Names

Acidosis, Carbohydrate Engorgement, Carbohydrate Overload, Grain Overload, Lactic Acidosis




Rumen acidosis is most likely to occur shortly after animals consume excessive amounts of grain starch. This is most likely to occur soon after animals are introduced to pellets or when pellet feeding is re-commenced following an interruption. Rapid fermentation of starch causes high levels of lactic acid to form quickly in the rumen, killing essential gut microflora, damaging the mucosal lining, and drawing in body fluid. This leads to rumen stasis, dehydration, and diarrhoea. Severely affected animals may develop systemic acidosis, abdominal or systemic infections and laminitis. Animals may die either acutely due to overwhelming acidosis or as a result of secondary complications.

Large, strong young animals with excellent appetites are more at risk.

Clinical Signs and Diagnosis

Clinical findings and examination of feeding history and feed should raise suspicions.

Mild acidosis is more common and is associated with watery faeces accompanied by temporary inappetence. Increasing severity is evident by increased depression, dehydration, absence of ruminal movements, weak pulse, slow capillary refill, subnormal temperature, diarrhoea and colic. Animals that survive the acute illness may die within days of kidney failure, fungal rumenitis or peritonitis. Some will later develop laminitis or liver abscess.

At necropsy, the rumen is distended with pellets and fluid. Note that sloughing of the rumen mucosa is a normal postmortem change occurring within an hour of death and should not be regarded as evidence of rumenitis or excessive grain feeding unless associated with inflammatory change.

Urine test strips or specific test strips may be used to test pH of rumen fluid. Normal rumen pH is >5.9 and acidosis should be suspected if the pH is less than 5.5. Laboratory confirmation requires sections of reticulum and ventral rumen in buffered formalin for histology.

Differential diagnoses include salmonellosis, gastrointestinal accidents, enterotoxaemia and bloat.


If acidosis is suspected then high concentrate diets should be changed to increase intake of roughage. On ships this involves replacing pellets with hay or chaff. Animals should be encouraged to maintain adequate fluid intake. Animals with mild to moderate acidosis will often recover within a few days following dietary change.

Infusion of alkalinising agents (magnesium hydroxide, sodium bicarbonate) into the rumen might be considered in early cases. Administration of antibiotics may provide protection against secondary infection. Transfer of >3L and preferably 8 to 16L of rumen fluid from a healthy donor may be beneficial to reactivate the rumen and stimulate digestion and eating. Development of mycotic infection of the rumen wall may cause relapse over coming weeks and then the prognosis is grave.

Affected animals may also benefit from administration of antibiotic (procaine penicillin) to minimise the risk of complications associated with proliferation of gram positive bacteria.

Stop feeding pellets. Provide good quality hay to stimulate appetite and digestion.


Introduce animals to higher carbohydrate diets incrementally over a period of two to three weeks monitoring carefully for early signs of acidosis such as reduced appetite, reduced rumen movement and sloppy faeces.

Avoid instances where animals might be allowed to gorge on concentrate diets such as following a period of cessation or reduced feed avavilability.

Feed additives (ionophores, virginiamycin, sodium bicarbonate and sodium bentonite) may be considered in feedlot situations as aids to minimize the risk of acidosis particularly during the first few weeks of grain introduction.