The Interaction of Genetics, Nutrition, Management, and Infectious Agents in
Intensive Poultry Production Systems
By : F. William Pierson
Picture a Formula-one race car, the epitome of driving machines, capable of traveling at incredible speeds. All it needs for peak performance is an expert driver, expert maintenance, plenty of fuel, and a smooth track. Now picture 12,000 of them all racing around the “Old Brickyard” at 200 mph. Throw in some rain, a little moisture in the fuel mix, or a leaky master cylinder and the result can be a disaster.
In essence, that’s what we’ve done over the past 50 years, through aggressive genetic selection. We have produced a bird that is a highly specialized, finely tuned, protein producing machine capable of great performance under a narrow set of conditions e.g., the right feed, in the right environment, good immunity, and minimal exposure to disease causing agents.
But the reality is that such conditions rarely exist or they are transient at best, in most turkey growout operations. That’s why raising healthy poultry is just plain difficult. It’s also why figuring out disease problems on some farms is no longer a matter of simple cause and effect.
The purpose of this lecture is to provide an integrated view of how multiple factors can interact to produce disease. Identifying the various factors and understanding their relationship to one another is essential to solving the complex health problems which qualify as emerging infectious diseases of poultry.
GENETICS
It is clear that genetic selection for performance traits has a negative effect on immunocompetence. Chickens selected for a low antibody response to sheep red blood cells (SRBC) have higher body weights as juveniles and better feed efficiency than those selected for a high antibody response (1, 2,). Therefore it’s not surprising that birds specifically bred for high body weight have lower antibody titers to SRBC than those bred for low body weight (3). Indeed, a genetic constitution favoring performance over antibody production appears to increase susceptibility to mycoplasmal, viral, protozoal, and ectoparasitic diseases (4). It has been suggested that the basis for this effect may be a deliberate reallocation of physiologic resources towards production and away from immune function (1, 5). In such birds the standing levels of defense are lower and less “machinery” is dedicated to meeting defense needs at the time a disease challenge occurs. In essence, the bird is genetically “tooled” for growth and not biological warfare. Resources can be reallocated, but often the response may be too little, too late.
Figure 1. (see attached Powerpoint file) is a schematic representation of what happens in birds programmed for “growth”. Defenses are marginally ready in the event of a viral challenge. If the challenge is mild, the bird will manage the “invasion” with little disruption of the normal flow of resources. But if the challenge is more than standing defenses can handle, a shift in the flow of resources must occur if the bird is going to survive. This shift can be great enough to cause a reduction in growth, activity, and bacterial defenses. However, the flow towards maintenance, e.g., “keeping the boiler running”, must be uninterrupted or else death will occur. At this point, secondary bacterial infections can become a problem. Organisms like E. coli are usually waiting in the wings for a chance like this. So the battle begins on a second front. If the struggle goes on long enough, you can forget “production”. A bird in this state is just trying to survive. Ultimately, it’s a matter of how long the resources will hold out. Once the bird starts dipping into its allocation for maintence, the war is over, and the enemy doesn’t take prisoners.
Depending on the distribution of such birds in a population, the effect on a flock can be more or less devastating. Individuals near the center of the “genetic” distribution e.g., the average poult, may be able to grow and handle disease better than those at either extreme. Most of us have seen this effect first hand: the best growing birds are the first to die and the runts live forever.
NUTRITION
Nutrition has a lot to do with whether a bird will be able to handle a disease challenge. The quantity and quality of nutrients in feed as well as the pattern of feeding can affect health.
A good example of this would be the occurrence of necrotic enteritis in broiler chickens. Often feed milling operations will substitute wheat for corn because the price is better. What may seem to be a subtle change in formulation can affect the gastrointestinal tract dramatically. In response to the variation in carbohydrate, the microfloral balance within the GI tract may shift in favor of Clostridia. Toxin production associated with this overgrowth can result in the development of necrotic plaques in the mucosa.
Obviously the microbial ecology of the GI tract is more complicated than this. Theoretically, an overgrowth of one species of bacteria or its disappearence, can have a ripple effect involving a multitude of interdependent organisms, not only other bacteria but viruses, fungi, protozoa, and nematodes. An example of this type of intricate interdependence can be found in the way dietary fiber effects susceptibility to coronavirus infection in turkeys. Fiber is fermented by bacterial organisms; the bi-products of this fermentation include short chain fatty acids (SCFA’s). These SCFA’s are utilized by enterocytes as an energy source. The availability of this energy source stimulates enterocyte differentiation and maturation. As cells differentiate and mature, they express receptors necessary for coronavirus target recognition. The result is increased susceptibility to coronavirus infection.
It’s not just the addition of nutrients to the diet that can alter the response to disease. What happens when you remove feed and water for 48 hours? You will see a decrease in the relative weights of lymphoid organs e.g., bursa and thymus, (6) and an increase in the ratio of circulating heterophils to lymphocytes (7). Such changes may be the result of “perceived stress” and not necessarily a “nutritional deficiency” but this type of physiological response is associated with an increase in susceptibility to viral diseases. Normally, commercial birds would never go this long without feed in the field. But what happens when a feed delivery get messed up or when there is feed refusal due to the presence of an unpalatable substance in the feed? How long do birds go without feed and water when they are moved to new surroundings i.e., from brooder to finisher; or in the case of breeders, at the time of dark out or molting? What happens when you change from crumble to a full pellet? What happens when water is unavailable or when it is less palatable due to medications or contaminants? The bottom-line is that the bird mounts a physiologic response to cope with what is perceived as an abnormal situation. That response has short-term benefits but if there are pathogens present in the environment, it may be just the opportunity they’ve waited for.
Nutrition is important in determining what resources will be available to help withstand a disease challenge (5). Diets conducive to growth in certain selected lines of broilers actually seem to decrease their resistance to E. coli challenge (8,9) and those that contain increased levels of animal protein seem to increase resistance to E. coli. (10).
Without question, relative deficiencies in certain vitamins and minerals can have an effect on disease resistance. The term relative is important here because genetic make-up is without a doubt more important than the NRC in determining what a bird needs. Using the same old vitamin-mineral premix in the same old amounts may not be sufficient for this year’s genetic stock. For example, a relative deficiency in vitamin A may compromise immunity by allowing a premature degeneration and reduced turnover of epithelial cells which serve as one of the primary barriers to invasion by pathogenic organisms (11). Antibody responses to Salmonella (12) and Newcastle disease virus (13) are also reduced in cases of vitamin A deficiency. Likewise, diets relatively low in vitamin E and selenium can also result in epithelial degeneration (14) and decreased humoral (15) responses.
There are lots of other examples but what’s important to remember is this: that form, content, quality, and availability of nutrients including water can affect the ability of a bird to successfully respond to a disease chal.
For more information : http://courses.iddl.vt.edu/AEID_I/index.html
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