URBANA, Ill. – Scientists are not sure why some cows develop the condition known as subacute ruminal acidosis, or SARA, but producers know it causes a number of minor symptoms that can create major problems.
“Subacute ruminal acidosis is what happens when the pH of the rumen – the large compartment of a cow’s stomach – gets too low,” said Josh McCann, assistant professor of animal sciences at the University of Illinois. “It’s not severe, but it’s lower than ideal. It’s difficult to detect. Because of that, we don’t have a great understanding of how it happens and what are the contributing factors.”
Left untreated, cows can develop inflammation, laminitis — a hoof issue related to lameness — or liver abscesses. Constantly fighting low-level ailments leaves cows with fewer resources to invest in milk or meat production. McCann said that leads to higher culling rates in dairies.
To learn what is happening in the rumen during subacute ruminal acidosis, McCann and his collaborators tried to induce the condition in dairy cows. They simulated the behavior of rapid feeders – cows that are most often affected by subacute ruminal acidosis. They fed those cows a restricted diet followed by a full feed. They measured rumen pH and sampled the microbial community before and six days after initiating the feeding treatments. Unfortunately the treatments did not always predict which cows developed subacute ruminal acidosis.
“Differences between animals on day six were observable on day one,” McCann said. “Bacteria in the phylum — Bacteroidetes and the genus Prevotella — were overrepresented in some cows on day one. Those were the ones that were going to get (subacute ruminal acidosis), regardless of what we fed them. These bacteria may be a marker for (subacute ruminal acidosis) or are actually contributing to it happening in some animals.”
The researchers observed that the epithelium, or lining of the rumen, also changed as a result of subacute ruminal acidosis. Within 24 hours of subacute ruminal acidosis induction, they saw genetic evidence that the epithelium was responding to the challenge. The genes for proteins holding epithelial cells together were more active as compared with healthy animals.
“The epithelium is a barrier; it’s the fence that keeps bacteria out,” McCann said. “I think our data shows that the epithelium ‘sensed’ the challenging conditions and sent the defense signal to attempt to maintain barrier function. When it fails to do that in more prolonged cases of (subacute ruminal acidosis), bacteria can enter the bloodstream to cause liver abscesses or other problems.”
Liver abscesses can be treated with antibiotics, but that’s costly. McCann said the feed-lot industry loses upward of $400 million per year due to liver abscesses stemming from subacute ruminal acidosis.
The average producer is not going to test for rumen pH, microbial community or gene expression of epithelial proteins. But the research takes a step closer to better detection and possible prevention of subacute ruminal acidosis. McCann said he hopes his research team will be able to develop a relatively inexpensive blood test for the condition. He also said he thinks a key to detection and prediction lies in understanding individual feeding behavior.
“If we can identify animals that are at risk – maybe those that vary a lot in their feed intake – we can look at some nutritional measures of prevention,’ he said. “Maybe adjusting their diet, or a targeted feed additive like a probiotic.”
The article, “Induction of subacute ruminal acidosis affects the ruminal microbiome and epithelium,” is published in Frontiers in Microbiology. The work was a collaboration with other University of Illinois animal-sciences faculty, with Phil Cardoso and Juan Loor, and with Ehsan Khafipour at the University of Manitoba. The research was supported in part by the American Jersey Cattle Association Research Foundation.
By: Lauren Quinn, University of Illinois College of Agricultural, Consumer and Environmental Sciences