Consequences of Disease on Nutrition

Date of publication : 4/1/2008
Source : Ontario M. of Agriculture, Food and Rural Affairs
At the 2nd Annual London Swine Conference, Dr. Gary Dial spoke eloquently about the costs, consequences and control of endemic diseases in the swine industry. He believes that "we have entered a stage in the competitive evolution of the pork industry when we are being forced to consider any technology promising an advantage either in terms of cost management or revenue enhancement".  Thankfully, genetic selection has enabled the industry to take advantage of recent, promising scientific advancements in nutrition and health so the majority of producers know how to feed pigs and manage the influences that health has on nutrient utilization.

One area not well understood, at least until recently, is how endemic diseases affect the pig. Recent research has demonstrated that endemic diseases negatively impact pig performance without causing obvious clinical signs of disease. Infectious agents induce an immune response designed to remove the offending agent from the body. In turn, the immune system induces a cascade of effects, many of them detrimental to growth, on the pig's metabolic system. Experts in this field suggest that technologies that minimize activation of the pig's immune system will enhance the rate and efficiency of growth and improve lean deposition in the carcass.

A series of experiments have been conducted investigating the effect of diseases on metabolism and immune function. These studies show that, during a health challenge, immune substances cause a metabolic response to the infection that shifts nutrients away from tissue growth to support the immune response. Even when the challenge is subclinical in nature, the effect is sufficient to disrupt normal metabolism and cause losses in performance.

Exposure of an animal to any substances, whether pathogenic or nonpathogenic, results in an immune response from the inflammatory cells in the blood and tissues. The substances that are released activate the immune system, causing reduced appetite, an increase in basal metabolic rate, a shift in how both ingested and stored nutrients are used by the body, and the possibility of a slight elevation in body temperature. However, sometimes there is no obvious sign that disease is present.

When animals are challenged by disease, protein synthesis decreases while protein breakdown increases. The balance between synthesis and breakdown shifts toward breakdown as a result of at least three things:


1. reduced feed intake - the body's supplies of amino acids are gradually consumed as the body's defenses fight the infection.

2. the immune response requires the consumption of amino acids to provide the building blocks to make immune compounds, like antibodies.
 
3. the amino acid composition of muscle does not match the amino acid needs of immune products, so the body is forced to break down a disproportionate amount of muscle to meet the amino acids needs of the immune system.


Therefore, protein losses during an immunological challenge are greater than what can be maintained by feed intake, an effect that is compounded when feed intake is reduced.

In addition to skeletal muscle, the intestinal tract may also provide a source of amino acids to mount an immune response. Research in other animals has shown that the body can initiate protein breakdown to pull nutrients from tissues having a lower priority, making them available for use by the immune system. In essence, the body will literally consume itself in the process of prioritizing resources in its fight against pathogens. In addition to effects on protein synthesis, the processes initiated by an immune challenge cause major shifts in fat metabolism. Typically, as energy is consumed during periods of immune activation, fat reserves are broken down as a source of energy to feed the immune system.

As a consequence of the metabolic and physiological effects of disease, pigs endemically infected with disease agents suffer from poorer growth performance, as reflected in reduced average daily feed intake, average daily gain, and feed efficiency. In addition, the dietary lysine requirement to maximize performance is greater for pigs that are not immune challenged compared to those that are experiencing endemic infections. Challenged pigs require supplemental lysine due, in part, to poorer digestibility (as a result of intestinal wall damage) and, to a greater extent, to an inability to efficiently deposit protein.

All pathogens that cause an immune response have the potential to disrupt metabolic processes and interfere with nutrient utilization. Dr. Dial classes diseases into 4 types (see table). He speculates that as each of the Types 1, 2 and 3 diseases is eliminated, there will be a gradual improvement in growth performance and, potentially, associated increases in carcass value. He anticipates that, as preventative and therapeutic treatments are reduced, facilities are used more efficiently, and productivity improves, costs of production will decline in tune with the elimination of each endemic disease.


Class

Observations

Examples

Type 1

* largely eliminated from herds of progressive producers
* no excuse for producers tolerating these types of infections




Actinobacillus pleuropneumonia
Swine dysentery
Pseudorabies
mange
Lice
Type 2 * producers currently under pressure, for economic reasons, to eliminate these types of infections

PRRS
Mycoplasma hyopneumonia
Type 3

* future targets for elimination
* economically important
* more difficult to eliminate from and/or keep out of herd



Salmonella cholerasuis
Ileitis
Swine influenza virus
Hemophilus parasuis
Actinobacillus suis
streptococcus suis
Type 4 * producers will be forced, by market forces and legal pressures, to eliminate
* relatively inconsequential to the pig Human pathogens
ie: Salmonella DT104


Source: Dial, G., Rademacher, C., Wiseman, B., Roker, J., and Freking, B. 2002. Costs, consequences and control of endemic diseases. Proceedings of the London Swine Conference. April 11-12, 2002.
 
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