Changes

Excessive quantities of rapidly fermentable carbohydrates in the ruminant diet results in overproduction of volatile fatty acids by the rumen microflora, lowering rumen pH below its ideal range of pH 6-7. Volatile fatty acids are a normal product of rumen fermentation and are readily used by tissues as an energy source. Tissues are capable of utilising the excess volatile fatty acids (VFAs) produced from the fermentation of high levels of carbohydrate; however, the instability in rumen pH makes it difficult for these to be absorbed properly and hence put to good use. VFA are normally passively absorbed across the rumen wall via finger-like papillae. These papillae increase in length when ruminants are fed high-carbohydrate diets, presumably to enhance absorption and protect the animal from accumulation of acids in the rumen. Despite this, a diet too high in concentrates will actually impair the absorptive capacity of the rumen, and VFAs will acumulate without effective utilisation by tissues.  

Excessive quantities of rapidly fermentable carbohydrates in the ruminant diet results in overproduction of volatile fatty acids by the rumen microflora, lowering rumen pH below its ideal range of pH 6-7. Volatile fatty acids are a normal product of rumen fermentation and are readily used by tissues as an energy source. Tissues are capable of utilising the excess volatile fatty acids (VFAs) produced from the fermentation of high levels of carbohydrate; however, the instability in rumen pH makes it difficult for these to be absorbed properly and hence put to good use. VFA are normally passively absorbed across the rumen wall via finger-like papillae. These papillae increase in length when ruminants are fed high-carbohydrate diets, presumably to enhance absorption and protect the animal from accumulation of acids in the rumen. Despite this, a diet too high in concentrates will actually impair the absorptive capacity of the rumen, and VFAs will acumulate without effective utilisation by tissues.  

 

Unlike in the glandular stomachs of carnivore and ominvores, the epithelium of the rumen is not protected by a layer of mucus. so they are vulnerable to chemical damage by acids. Low ruminal pH leads to rumenitis, erosion, and ulceration of the ruminal epithelium. Once the ruminal epithelium is inflamed, bacteria may colonize the papillae and leak into the portal circulation. These bacteria may cause liver abscesses, which may eventually lead to peritonitis around the site of the abscess. If the ruminal bacteria clear the liver (or if bacteria from liver infections are released into circulation), they may colonize the lungs, heart valves, kidneys, or joints. The resulting pneumonia, endocarditis, pyelonephritis, and arthritis are often difficult to diagnose antemortem. Postmortem evaluation of these conditions in animals that are slaughtered, culled, or that died on the farm can be very beneficial.

Unfortunately, lactate production at low ruminal pH can offset gains from VFA absorption. As pH drops, lactate-synthesizing bacteria such as Streptococcus bovis begin to ferment glucose to lactate instead of VFA. This is a dangerous situation, since lactate has a much lower pKa than VFA (3.9 vs 4.8) and lactate is 5.2 times less dissociated than VFA at pH 5.0. As a result, lactate stays in the rumen longer and contributes to the downward spiral in ruminal pH.

Additional adaptive responses are invoked if lactate production begins. Lactate-utilizing bacteria, such as Megasphaera elsdenii and Selenomonas ruminantium , begin to proliferate. These beneficial bacteria convert lactate to other VFA, which are then easily protonated and absorbed. However, the turnover time of lactate utilizers is much slower than that of lactate synthesizers. Thus, this mechanism may not be invoked quickly enough to fully stabilize ruminal pH. Periods of very high ruminal pH, as during feed deprivation, may inhibit populations of lactate utilizers (which are sensitive to higher ruminal pH) and leave them more susceptible to severe ruminal acidosis.

Besides disrupting microbial balance, feed deprivation causes cattle to overeat when feed is reintroduced. This creates a double effect in lowering ruminal pH. Cycles of feed deprivation and refeeding are critical risk factors for subacute ruminal acidosis.

Low ruminal pH during subacute ruminal acidosis also reduces the number of species of bacteria in the rumen, although the metabolic activity of the bacteria that remain is very high. Protozoal populations are limited as ruminal pH approaches 5.0. When fewer species of bacteria and protozoa are present, the ruminal microflora are less stable and less able to maintain normal ruminal pH during periods of sudden dietary change. Thus, pre-existing subacute ruminal acidosis increases the risk of acute ruminal acidosis in the event of accidental ingestion of excessive amounts of grain.

 

Ruminal epithelial cells are not protected by mucus, so they are vulnerable to chemical damage by acids. Low ruminal pH leads to rumenitis, erosion, and ulceration of the ruminal epithelium. Once the ruminal epithelium is inflamed, bacteria may colonize the papillae and leak into the portal circulation. These bacteria may cause liver abscesses, which may eventually lead to peritonitis around the site of the abscess. If the ruminal bacteria clear the liver (or if bacteria from liver infections are released into circulation), they may colonize the lungs, heart valves, kidneys, or joints. The resulting pneumonia, endocarditis, pyelonephritis, and arthritis are often difficult to diagnose antemortem. Postmortem evaluation of these conditions in animals that are slaughtered, culled, or that died on the farm can be very beneficial.

Caudal vena cava syndrome can cause hemoptysis and peracute deaths due to massive pulmonary hemorrhage in affected cows. In these cases, septic emboli from liver abscesses can lead to lung infections, which ultimately invade pulmonary vessels and cause them to rupture.

Caudal vena cava syndrome can cause hemoptysis and peracute deaths due to massive pulmonary hemorrhage in affected cows. In these cases, septic emboli from liver abscesses can lead to lung infections, which ultimately invade pulmonary vessels and cause them to rupture.

Subacute ruminal acidosis has also been associated with laminitis and subsequent hoof overgrowth, sole abscesses, and sole ulcers. The severity of laminitis depends on the duration and frequency of metabolic insult. These foot problems generally do not appear until weeks or months after the initiating event. The mechanism by which subacute ruminal acidosis increases the risk of laminitis has not been fully characterized.

Subacute ruminal acidosis has also been associated with laminitis and subsequent hoof overgrowth, sole abscesses, and sole ulcers. The severity of laminitis depends on the duration and frequency of metabolic insult. These foot problems generally do not appear until weeks or months after the initiating event. The mechanism by which subacute ruminal acidosis increases the risk of laminitis has not been fully characterized.