Whatever label we put on it, it’s a syndrome we want to avoid. And acidosis is not just about acid chemistry. It’s really about carbohydrates, fiber, adsorption and ecology ... rumen ecology.
We all know about cattle getting into the grain bin. A barn door breaks or someone leaves the gate open; the cattle rush in and engorge themselves, each animal happily stuffing itself with 5 pounds of corn in minutes. Or, less spectacularly, a farmhand feeds too much grain to the herd every day for a couple of weeks or switches the herd from a hay diet to a high-grain diet without a sufficient adjustment period.
Then come the acidosis symptoms: sharply reduced feed intake, dehydration, sunken eyes, grinding teeth, abdominal pain, lameness, depression, coma, death. We call the veterinarian and promise to change some things, like fixing the barn door.
But if we want to understand what happens during acidosis and how to avoid it, we should first understand what happens in a rumen under normal conditions.
Ruminants – cattle, sheep, bison, elk, wildebeests and giraffes – are nutritional specialists. They are exquisitely engineered to consume and extract the maximum amount of energy from high-fiber feeds. The basic process is straightforward enough: They eat something (a beautiful grass pasture, for example) which travels down the esophagus into the rumen and then ferments.
The rumen, of course, is a huge flow-through fermentation sac containing vast populations of bacteria, protozoa and fungi.
But the rumen is not a simple septic tank; it’s an extremely complex ecological system. Its anaerobic (no oxygen) environment may contain more than 1,000 different species of microbes. Its acid-base balance is extremely important to its ecology.
Under normal high-fiber conditions, the rumen pH is 6.0 to 6.5, although this may drop slightly after extended feeding. When bacteria ferment the feed, their primary products are small molecules called volatile fatty acids (VFAs). These are acetate, propionate and butyrate, which contain two carbons, three carbons and four carbons, respectively.
In the rumen liquid, these VFAs are in their acidic form. As you can imagine, if VFAs accumulate too much in the rumen, they would cause the rumen pH to drop, i.e., become more acidic, which could cause serious problems.
But our cattle and sheep maintain a healthy rumen pH through two powerful methods: absorption and buffers. As the VFAs are produced, some are absorbed through the rumen wall into the blood, where the host animal metabolizes them for energy. In fact, that’s the primary method ruminants obtain energy from their diet – through the fermentation of feed and the absorption of the resulting VFAs.
The second method to control rumen pH is with a buffer, primarily sodium bicarbonate. No, our animals don’t rush to the feed store each day to purchase bags of sodium bicarbonate; they make it themselves. Their salivary glands synthesize bicarbonate, which flows into the rumen in the saliva. And ruminants make lots of saliva.
I’m not kidding. In a 24-hour period, sheep can produce 1 to 4 quarts of saliva. That’s impressive, but it pales compared to cattle. In 24 hours, the salivary glands of an adult cow can produce 25 to 40 gallons of saliva, especially on a high-fiber diet.
So each time these animals chew their vegetables, saliva flows into the rumen, which helps stabilize the pH. This chewing includes the periods they graze, eat hay or chew their cud, which covers most of each day.
But adding grain to the diet changes things. Grain (corn, barley, wheat, etc.) is really a package of starch, with some protein and soluble sugars and very little fiber. Starch is fermented by different bacteria. Starch and sugars also ferment much faster than fiber, with a concomitant faster increase in acid products.
Grain can shift the basic ecology of the rumen. The faster acid production from starch fermentation drives the rumen pH down to 5.5 to 6.0, which is ideal for starch-fermenting bacteria but detrimental to fiber-fermenting bacteria. The microbial population shifts to favor starch fermentation. The buffering system struggles to keep up. To complicate the issue, grain diets entail less chewing, so there is less saliva flowing into the rumen.
But the good news is: The rumen system is rather robust; it can usually handle these changes. Under good management, our grain-fed ruminants can do very well. The greater intake of high-energy feeds results in higher amounts of energy absorbed, which can increase milk production, weight gain and reproductive performance.
Even though fiber fermentation is suppressed, our grain-feeding farm systems and numerous feedyards are testimonials to how well our cattle can thrive on high-starch diets. But we need to realize we may be on thin ice: Those grain diets must be managed properly.
Here’s where things get dicey. Grain reduces the rumen pH to favor starch-fermenting bacteria. The buffering system counters the acidifying effects of starch fermentation as long as sufficient buffer comes into the rumen, primarily in the saliva. But then someone leaves a gate open and the cattle engorge themselves on grain. Then what happens?
First, the rumen experiences a burst of starch fermentation. Those starch-fermenting bacteria become happy indeed, and their numbers explode. (Recall that bacteria reproduce by binary fission, so populations can double and double again in a short period of time.) But as they quickly ferment the starch, the cascading production of VFAs begins to overwhelm the buffering capacity in the rumen.
Since there is less chewing of grain than fiber, less saliva is released. This timing is crucial. Less bicarbonate flows into the rumen while, at the same time, acid production has dramatically increased. The rumen pH begins to drop further. Then things get worse.
As the rumen pH sinks below 5.5, the rumen environment begins to favor other species of bacteria, especially the bacteria that synthesize lactate in addition to VFAs. Lactate is lactic acid, which unfortunately is a stronger acid than the VFAs. The lactic acid drives down the pH further and faster.
The lower pH now extremely favors lactate-producing bacteria, which produce even more lactate – a spiraling feedback system. The rumen pH may drop below 5.0. As the lactate crosses the rumen wall into the blood, the extra acid begins to overwhelm the blood buffering system. The plasma pH begins to fall below a critical threshold (usually below 7.4). Hemoglobin in the red blood cells loses its efficiency for carrying oxygen.
Other enzymes and cell systems begin to slow down or fail. The cow shows the classic symptoms of acidosis.
Not all animals suffering from acidosis will die. Sometimes, acidosis can be subclinical, which means the rumen pH is lower than ideal, some fiber digestibility is lost, and animal performance may be lower than expected, but the animals continue to act and eat normally.
To some extent, subclinical acidosis helps explain the nutritional phenomenon taught in schools as the Associative Effect: The addition of grain to a ration will reduce the digestibility of the fiber components of that ration.
But back on the farm, faced with clinical acidosis or the subclinical variety, now what? Well, there are scores of excellent guides and factsheets online that describe treatments, including changing the feed. And of course, we can call the veterinarian.
But knowing the background chemistry and ecology of acidosis gives us a running start about the problem. It can help us avoid calling the veterinarian in the first place or spending time online frantically searching for remedies.
This knowledge is indeed comforting and useful. But either way, I would still repair the barn door. 
Woody Lane, Ph.D., is a livestock nutritionist and forage specialist in Roseburg, Oregon. He operates an independent consulting business and teaches workshops across the U.S. and Canada. His book, From The Feed Trough: Essays and Insights on Livestock Nutrition in a Complex World, is available through Woody Lane.
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Woody Lane, Ph.D.
- Ruminant Nutritionist and Forage Specialist
- Lane Livestock Services
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