Acidosis and the ‘hungry games’ -

For millions of years, as the result of natural selection, ruminants developed the capability to obtain the greatest part of the energy necessary to reproduce and maintain vital function by ruminal microbial fermentation.

Ruminal micro-organisms produce enzymes that degrade plant complex carbohydrates. Such biological strategy enables ruminants to eat fibrous plant materials, which cannot sustain vital functions for most single-stomach animals.

However, if high levels of animal productivity are necessary, forage alone cannot sustain efficient systems of production. Thus, it is necessary to feed ruminants with grains or co-products.

Steady and healthy ruminal fermentation is only possible if microbial population is adapted to respective dietary carbohydrates.

Thereby, abrupt dietary changes, mainly from roughage to high-concentrate diets, result in a mutualism break between rumen microbial population and host animal.

This is the initial trigger for the most- studied nutritional disorder in cattle production: ruminal acidosis.

The process of adaptation of newly received cattle is a multifactorial complex which compresses stress, behavioral, nutritional, microbiological and physiological effects along with management, feedstuff costs and logistics.

The adaptation process includes recovery of body water, establishing or improving immunity to common virus pathogens, establishing social structure in the pen and adapting microbes in the rumen to new feeds.

Nutritionists have developed several feed adaptation protocols ranging from duration and methods.

The most common approach is the step up (step wise), in which the concentrate in the feed increases in predetermined number of diets and days within diets.

Another approach is limiting the amount of feed in the final ration and slowly increasing it a few grams per day in the diet according to bunk score.

Straight to the gut
Acidosis may lead to a vast range of nutritional disorders. Loads of acid in a rumen can cause ruminal epithelial damage, which decreases short-chain fatty acid absorption, consequently resulting in less energy being available for the animal to obtain nourishment and restricting growth.

Moreover, acidosis often leads to a disruption of the rumen epithelium, resulting in bacteria gaining access to blood circulation and ultimately causing liver abscesses.

Measurements of costs regarding decreased performance related to acidosis-affected animals are often difficult because of the differences in the possible diagnoses.

Acidosis is classified as either being acute or subacute according to its intensity. Acute acidosis may result in severe diarrhea, “downers,” poor performance and often death.

Thus, it is easier to diagnose a few animals instead of a great proportion of the herd. Production costs are related directly with animal death or very poor performance in conjunction with treatment.

On the other hand, a subacute acidosis symptom is not easily detected and often leads to a larger portion of a herd being infected.

The major response by the animal to subacute acidosis is reduced feed intake with an accompanying reduction in performance.

North American feedlot nutritionists and managers estimate that the cost of subacute acidosis is between $15 to $20 per animal.

What you’re feeding
Certain types of feedstuffs provide greater chances to induce acidosis compared to others. Rate, site and extent of starch digestion are the main considerations in classifying acidosis potential with certain diet ingredients.

For example, grain type affects starch degradation. Wheat and barley are more degradable than corn and sorghum due to starch granule protection by protein or starch granule conformation.

Additionally, intensive grain processing improves starch ruminal degradation, and consequently increases the incidence of acidosis.

Likely due to higher moisture content, corn presents greater frequency in potential acidosis cases than dry rolled corn.

On the other hand, highly fermentable co-products with low starch content, such as pectin present in citrus pulp, is rapidly fermentable but does not produce lactate during its fermentation.

Ionophore antibiotics are one of most recommended classes of acidosis-preventative feed additives.

These molecules present the capability to form lipid soluble complexes with cations and mediate their transport across the lipid barrier of microbial cells. Ionophores are generally bacteriostatic and not bacteriocidal.

The mechanism of bacteriostatic activity of ionophores is related to their ability to alter the flow of cations across the cell membrane.

Target bacteria are mainly gram-positive, such as lactate-producing S. bovis and Lactobacillus spp.

In addition, ionophores, specifically monensin, cause significant reduction on bloat incidence due to decreased slime and microbial gas production by rumen microbes in a lower pH environment.

Recently, consumers’ concern about the effects of the antibiotic cross-resistance of human pathogens derived from animals fed with growth-promoting antibiotics has increased.

The use of monensin and virginiamycin as growth-promoting compounds were banned in Europe. The actual risks implicated in the adoption of these compounds are still unknown.

The general public’s safety concerns and related questions seem to be correlated more with consumer perception and political issues than scientific knowledge of the effects of the growth-promoting hormones in animals.

Still, it opens new frontiers for “natural” feed additive research development. Essential oils derived from spice plants like cinnamon, pepper and oregano are receiving special efforts due to their anti-microbial capacity and may result in altered rumen fermentation processes.

Despite being the most-studied digestive disorder in cattle, ruminal acidosis still presents blind spots. The first intriguing fact is individual susceptibility.

If one challenges animals from the same herd and similar background with a high-concentrate diet protocol, animals will present a range of acidosis symptoms, ranging from no symptoms, moderate and even severe ruminal acidosis within the same feeding period.

Genetic differences also factor in acidosis, but specific biological causes are currently unknown. The understanding of these differences can help the nutritionist to better design diets for the adaptation period.

The combination of all the research in the area of metabolic disorder creates a masterpiece of knowledge that is utilized in a sustainable way to feed millions of people.