Subacute ruminal acidosis

What it is

Subacute ruminal acidosis (SARA) is a fermentation disorder in which rumen pH falls below physiological values for several hours a day. It occurs when the production of volatile fatty acids from starch and sugars exceeds the rumen's capacity to absorb them and to neutralise them with saliva, whose production depends on chewing and therefore on the physically effective fibre in the ration. In field practice, a rumen fluid sample obtained by rumenocentesis with a pH of 5.5 or less is usually considered low.

Acute ruminal acidosis (grain overload) is the severe form: after sudden ingestion of a large amount of grain, Streptococcus bovis and lactobacilli proliferate, lactic acid accumulates, pH falls much further, the rumen stops and fills with fluid, and the rise in osmolality draws water from the blood. The animal develops dehydration, metabolic acidosis and chemical rumenitis, and can die quickly.

The consequences of repeated acidity are:

• Rumenitis and parakeratosis: the rumen epithelium becomes inflamed and loses its barrier function.
• Liver abscesses: rumen bacteria, mainly Fusobacterium necrophorum and Trueperella pyogenes, cross the damaged wall and reach the liver through the portal vein. An abscess that erodes the caudal vena cava can cause caudal vena cava thrombosis, with septic emboli in the lung.
• Laminitis and claw lesions: these are attributed to vasoactive substances and endotoxins released from the rumen that disturb the corium of the claw; this link is less well proven than is usually claimed (see Key studies).

Who it affects

• High-yielding dairy cows in early lactation, when they move abruptly from the dry cow ration to a concentrate-rich ration, and primiparous cows.
• Herds that feed concentrate separately in few meals, with mixed rations that cows can sort or with forage chopped too finely.
• Feedlot cattle on grain-rich diets. Acute acidosis occurs in any bovine that suddenly gains access to grain or to feeds rich in starch or sugars.

Anatomy involved

• Rumen: its mucosa is a stratified squamous epithelium with papillae that absorb volatile fatty acids. Low pH damages the papillae (rumenitis, parakeratosis), reduces motility and fibre digestion, and opens the way for bacteria.
• Liver: receives blood from the rumen through the portal vein, so it is the first filter for bacteria crossing the rumen wall and the site where abscesses form.
• Hooves: the vascular corium supports horn production. Its disturbance shows as sole haemorrhages, white line disease and sole ulcers, with lameness.

Clinical signs

• SARA: the signs are herd-level and non-specific: erratic or reduced intake, milk fat depression, looser faeces or faeces with undigested fibre and grain, less rumination, loss of body condition, more lameness and liver abscesses found at slaughter.
• Acute acidosis: anorexia, depression, ruminal atony with a fluid-filled rumen (splashing sound), foul-smelling diarrhoea, dehydration, tachycardia, ataxia, recumbency and death in severe cases. Survivors can develop mycotic rumenitis, liver abscesses or laminitis.

Diagnosis

• Rumenocentesis: puncture of the ventral sac of the rumen through the left flank to measure pH in a group of at-risk cows (in early lactation). A single sample does not diagnose an individual cow; it is interpreted at group level.
• Assessment of the ration and management: starch and effective fibre content, particle size, feed sorting at the bunk, feeding frequency, bunk space and abrupt diet changes.
• Indirect indicators: milk fat, faecal consistency, rumination time, lameness frequency and liver abscesses at slaughter; none is specific.
• Acute acidosis: history of access to grain, very low rumen fluid pH, absence of live protozoa and haemoconcentration with metabolic acidosis.

Treatment and prevention

• SARA: correct the ration and management. Enough physically effective fibre, a limit on starch, gradual adaptation to concentrate before and after calving, frequent delivery of a well-mixed ration that cannot be sorted and enough bunk space; buffers (sodium bicarbonate) and other additives help, but do not make up for poor management.
• Acute acidosis: remove the grain; in mild cases, oral alkalinising agents (magnesium oxide or hydroxide) and hay; in severe cases, intravenous fluid therapy with correction of the acidosis and emptying of the rumen by lavage or rumenotomy.
• Liver abscesses: rarely diagnosed in the live animal; in feedlots they are controlled through diet management and, in some countries, with in-feed antimicrobials, whose preventive use is increasingly restricted.
• Claw lesions: functional trimming and treatment of lesions, with good lying surfaces.
• Drug use in food animals is subject to each country's regulations and to withdrawal periods for milk and meat.

Key studies

• Garrett et al. (1999), experimental study that set up the field diagnosis. The pH of fluid obtained by rumenocentesis was 0.28 units lower than that obtained through a rumen cannula. To distinguish groups fed more or less forage, it proposed sampling 12 cows and considering the group affected if 3 or more had a pH below 5.5. It was based on few animals, but it is the criterion used in field studies.
• Kleen et al. (2013), cross-sectional study of 26 German dairy farms with 315 cows sampled by rumenocentesis. 20% of cows had a pH of 5.5 or less, and 11 of the 26 farms met the SARA criterion; these tended to be larger and to offer less lying space. Cows with low pH had poorer body condition, but there was no clear trend in lameness. It is a single measurement per cow.
• Khorrami et al. (2021), meta-analysis of published studies and of 5 of the authors' own experiments. The physically effective fibre content (particles longer than 8 mm) and the starch content of the ration were enough to predict mean rumen pH. It proposes a safe range of 15–18% of this fibre with 20–25% starch on a dry matter basis. Cows in their first and second lactation had a mean pH 0.2 units lower and twice as much time below pH 5.8 as cows with three or more parities.
• Passos et al. (2023), systematic review of the relationship between ruminal acidosis and laminitis: of 339 articles only 16 were included. There was an association between diets rich in rapidly fermented carbohydrate, acidosis and acute laminitis, mostly in short-term experimental induction protocols; two studies that induced acidosis with oligofructose did not observe clinical signs of laminitis, and the mechanism remains unclear. The widespread idea that field SARA causes chronic claw lesions is not well supported by strong studies.
• Young et al. (2026), network meta-analysis of 32 controlled studies (72,086 animals) together with a randomised trial in more than 16,000 feedlot cattle. The meta-analysis indicated that in-feed tylosin reduces liver abscesses compared with no treatment, and that withdrawing it before the end of finishing is not equally effective. In the trial, the reduction in severe abscesses with continuous tylosin was not conclusive on its own (OR 0.75; 95% CI 0.51–1.11). Two authors are linked to the feedlot industry; the data come from feedlots, not dairy cows.