J APPL POULT RES 2007. 16:121-125
© 2007 Poultry Science Association
Informal Nutrition Symposium |
Metabolic Challenges: Past, Present, and Future
S. Leeson
Department of Animal and Poultry Science, University of Guelph, Ontario, Canada N1H 2W1
1 Corresponding author: sleeson{at}uoguelph.ca
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SUMMARY
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Metabolic disorders have been recognized for 50 yr, and yet most still affect the poultry industry. Before 1950, several disorders as described in the literature were most likely because of incomplete knowledge regarding requirements for certain vitamins and some trace elements. The first classical description of a metabolic disorder was that of cage layer fatigue, recognized in 1955. Since that time, some 15 to 20 disorders have been documented, and with few notable exceptions, none have been completely eliminated. Metabolic disorders can be categorized as chronic, which usually affect a small percentage of a flock, and acute, which invariably involve more birds but is sporadic in occurrence. When of sufficient economic significance, it may be possible to reduce the effect of a certain disorder by genetic selection. In the future, for both meat birds and layers, it is predicted that disorders related to skeletal integrity will pose limits to ever-increasing production efficiency.
Key Words: metabolic disorder • cage layer fatigue • ascites • sudden death syndrome • fatty liver hemorrhage syndrome
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DESCRIPTION OF PROBLEM
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Metabolic disorders will always be around to some degree for most poultry species. Since we assume to have identified all the nutrients required by poultry, current metabolic disorders are rarely the result of overt deficiencies or excesses of any nutrient or group of nutrients. Skeletal disorders can obviously arise due to deficiencies of key nutrients such as Ca, P, or vitamin D3 and as such cannot really be categorized as metabolic disorders. The situation of induced deficiencies, when diets are apparently adequate in the total level of all nutrients, is sometimes described as a metabolic condition. However, for the purpose of this review, with few notable exceptions, conditions that are precipitated by the deficiency of nutrients are not considered as classical metabolic disorders. Today, most disorders are precipitated by factors such as environment, feed ingredients, and, most importantly, by increased metabolism and productivity. It is in fact a testament to the poultry geneticists that we see so few metabolic disorders relative to the phenomenal increase in productivity of modern poultry strains. Today, we see male broiler chickens of 3 kg live weight at 42 d, which results from the consumption of just less than 5 kg of feed. An average daily gain of 73 g was probably not expected at the dawn of the broiler industry. Likewise, we see turkeys approaching 1 kg of live weight per week of age, whereas large commercial flocks of layers are capable of 330 eggs in 365 d. For all of these poultry species, the increased productivity has generally been accompanied by an increased liveability. Although the incidence of metabolic disorders are often negatively correlated with productivity, the balance of their occurrence today, relative to current productivity, suggests that they are not yet limiting performance.
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PAST
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Aldrovandi [1] quoted Varro (100 BC) with a very early recognition of a metabolic disorder in that "the hen should not rest on the floor to sleep in order to keep from dirtying itself with dung because when this adheres to their feet, it creates gout" (p. 92). During the early part of the 20th century, there was often reference to apparent metabolic disorders in poultry, although in hindsight, it is now obvious that these problems were precipitated by nutrient deficiencies and, most often, vitamins and minerals. Rickets, induced by vitamin D3 or macromineral deficiency, and crazy chick disease, related to the inadequacy of vitamin E, are classic examples of apparent metabolic derangements. There were also problems described which we now ascribe to toxicity, such as fluoride and V toxicity, related to phosphate contamination, and Se toxicity, caused by feeding high levels of cereals grown on Se-rich soil.
One of the first classical metabolic disorders was detailed in the 1930s and was often described as gizzard erosion. The condition is unlikely to be related to the condition seen today, because meat and fish meals were rarely added to poultry diets at that time, and so the histamine, gizzerosine, or both was not likely a factor. Ewing [2] described dried ox bile as a preventative of gizzard erosion in young chicks. Round heart was also described in the 1940s, although in Victorian times, there was reference to "egg-heart" to describe a heart lacking a defined apex. Many consider the description of cage layer fatigue (CLF) by Couch [3] as the forerunner of classic metabolic conditions afflicting birds under modern commercial conditions. The condition coincided with the housing of birds in cages, and even today, CLF is virtually unheard of in floor-reared birds. In this situation, exercise appeared to be the trigger to the Ca imbalance, although access to feed, and hence variable Ca intake, may also have been a contributing factor. The contribution of coprophagy to the nutrient supply of the bird was also raised as an issue. Even though dietary Ca levels were low in the 1950s, compared with modern standards, CLF was not usually resolved by Ca supplements, and so CLF was, and still is, a classical example of a metabolic disorder.
Titus [4] described signs for most of the vitamin and mineral deficiencies, and by this time, the potentially confounding effect of diet inadequacy was not a factor in the etiology of subsequent discussion on metabolic conditions. Table 1
details the chronology for most of the significant metabolic disorders that have afflicted poultry over the last 50 yr. The dates shown in Table 1 are not descriptive of the very first study or report on each condition; rather, they attempt to pinpoint the time when the individual conditions were more widespread and receiving attention from commercial industry and research.
It is interesting that many of the disorders listed in Table 1
are ongoing problems and have not been fully resolved. Most of these conditions are precipitated by environmental factors, although, undoubtedly, the degrees to which they affect the bird are greatly influenced by productivity. Fatty liver and kidney syndrome (Table 1) is perhaps best described as the consequence of a simple deficiency of biotin, although its onset in the early 1970s proved difficult to resolve. The condition was eventually traced to a lower-than-expected bioavailability of biotin in wheat. Fatty liver and kidney syndrome is therefore a classic example of an apparent metabolic disorder that is ingredient-specific. To some extent, oily bird syndrome is another ingredient- or ingredient class-specific problem, being related to the level and saturation of dietary fats.
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PRESENT
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Today we have 2 general types of metabolic disorders, namely those that are endemic and affect a relatively small proportion of a flock, and those that occur sporadically but usually at relatively high incidence. That they occur attests to the fact that we still do not have adequate control methods.
For broilers, most metabolic disorders are endemic, with ascites, sudden death syndrome (SDS), and skeletal deformities being the major problems. Spiking mortality in broilers is more sporadic and at this time is not likely to contribute to the general mortality in most flocks. For layers, most of the problems are sporadic, with fatty liver hemorrhagic syndrome and CLF the main concerns, although when they occur, they have a significant economic effect for individual flocks. Interestingly, these metabolic disorders in layers often recur at the same farm.
Ascites in broiler chickens is an interesting example of the effect of a metabolic condition on broilers, the interim attempts at resolving the problem, and the final relegation of its importance through genetic selection. Ascites first became problematic in countries such as Mexico and Columbia, where the altitude exacerbates the need for O2 to fuel the ever-increasing metabolic rate. It is ironic that many of these farms moved to higher elevations at the recommendation of "experts" who suggested this as a move to resolve issues with heat distress seen at lower altitudes. Although altitude, and associated lower O2 tension, contributed to ascites, the cooler nighttime temperature at these sites was probably as big a factor. Up to 30% mortality was common in male broilers, grown under such conditions in the early 1980s. Cause of death was related to hypertrophy of the heart as a result of the birds attempt to oxygenate the blood for normal metabolism. The defective heart subsequently caused inefficient drainage of the portal system, and serum leaked from the liver, causing fluid accumulation in the abdominal cavity. Death quickly occurred, because the volume of ascitic fluid diminished the tidal volume of the air sacs, which further limited the blood oxygenation. Prevention rested with limiting O2 demand, and this meant limiting growth. Feeding mash diets caused a dramatic decline in mortality, because growth rate was reduced. In fact, just a 3 to 5% decline in growth rate was all that was needed to dramatically reduce the mortality. Unfortunately, the continual genetic improvement in growth rate meant an ever-increasing O2 demand, and, at best, new management techniques had to be continually adjusted. Over time, ascites became problematic even at low altitude, and by the mid-1980s, there was a flurry of research activity to try and resolve the issue. The need to control ascites and other metabolic disorders, which by 1985 were probably responsible for the doubling of normal mortality, spurred new management practices such as light control of broilers [5] and nutritional programs to limit early growth [6]. Today, in spite of a 20% increase in growth rate compared with just 10 yr ago, ascites is no longer a major issue, because geneticists have successfully identified resistant birds and used this knowledge within their breeding programs.
Concurrent with ascites was SDS and skeletal disorders, which today account for most of the chronic losses due to metabolic disorders. It is interesting that even after 25 yr of research, we still do not have a clear picture of the etiology of SDS. It is most problematic when male birds approach heavier marketing weights. The sudden death is likely associated with electrolyte imbalance in the bird, either as chronic preconditioning or as an acute end point. Sudden death syndrome was eclipsed by studies on ascites, which was an easier disorder to study because the cause and effect were fairly well known. Today, we are still struggling to find answers to the problem of SDS. The SDS in heavy breeders also seems to relate to the electrolyte and mineral imbalance of birds, and at one time, was very much strain-specific.
Physiology of bone growth is well researched, and our ongoing issues with leg problems in broilers attest to the complexity of the problem. Specific conditions such as tibial dyschondroplasia (TD) are reproducible with diet modification, and rickets in young broilers and turkeys should be preventable considering our knowledge of Ca, P, and vitamin D3 metabolism. There is not likely to be a single underlying cause of conditions such as rickets in young turkeys. Anecdotal evidence suggests that rickets is an ever-present concern at turkey farm A, whereas farm B within the same company, using the same feed, never witnesses the condition. Likewise, the chronic occurrence of rickets has sometimes been resolved by using newer metabolites of vitamin D3, whereas other locations indicate little benefit from such diet manipulation.
Spiking mortality seems to be occurring at increasing frequency. Death of up to 1% per day at 17 to 20 d of age is associated with hypoglycemia. Rarely endemic in flocks, it occurs sporadically, and there is a suggestion that the current trend of using all-vegetable diets is perhaps a contributing factor. Our unpublished observations confirm that birds fed vegetarian diets do have lower blood glucose than birds fed animal proteins. In birds, blood glucose is regulated by glucagon rather than insulin. Serine is a precursor of glucagon, and because milk powder is rich in serine, this may be the basis for the suggestion of top dressing feed with milk powder to prevent spiking mortality. In our study, adding serine to a vegetarian diet corrected the depression in blood glucose seen because of using such diets. Interestingly, birds fed vegetarian diets plus serine (but not without) were significantly heavier than 7-d-old chicks fed conventional broiler diets. Under controlled environment conditions, using a step-down lighting program starting before 4 d of age also seems to prevent spiking mortality.
For laying hens, metabolic disorders of current concern are CLF and fatty liver hemorrhagic syndrome. As previously detailed, CLF was first described 50 yr ago and still continues to be a major issue. In many instances, it has emerged as a chronic problem afflicting a small number of birds in a flock, rather than an acute and widespread disorder as occurred in the 1950s. Today, CLF is more commonly seen at 36 to 40 wk of age, rather than at point of lay, as was initially described. For whatever reason, Ca metabolism is impaired and the bird plunders its cortical bone, thus rendering the skeleton fragile and ultimately nonfunctional. Adequate prelay nutrition is important, as is phase feeding of both Ca and P. Intake of these nutrients and vitamin D3 is difficult to optimize in pullets during their first few weeks of life, when diets designed for an intake of 95 g may be inadequate when actual feed intake is closer to 85 g per day.
We recently observed CLF in a group of individually caged Leghorns. The birds were 45 wk of age and all fed the same diet. Within a 10-d period, 5% of the birds had CLF, and the feed analyses showed adequate levels of Ca and P. The only common factor was an exceptionally high egg output for these affected birds. All these birds averaged 96% production from 25 to 45 wk of age, and all had individual clutch lengths of at least 100 eggs. One bird had a clutch length of 140 eggs (i.e., 100% production). Their sisters in adjacent cages fed the same diet and without CLF had maximum clutch lengths of 42 eggs in this period, and on average, the production was closer to 90%. These data suggest that in certain situations, CLF is correlated with exceptionally high egg output.
Fatty liver hemorrhagic syndrome is often the major cause of mortality in commercial flocks. The liver is the main site of fat synthesis in the bird, and a fatty liver is normal. In fact, a liver devoid of fat is an indication of a nonlaying bird. However, in some birds, excess fat accumulates in the liver, and this fat can oxidize, causing lethal hemorrhages. Excess fat accumulation can only be caused by a surfeit of energy relative to the needs for production and maintenance. Low-protein, high-energy diets, and those in which there is an amino acid imbalance or deficiency, can be major contributors to a fatty liver condition in layers. It is known that diets low in lipotrophic factors such as choline, Met, and vitamin B12 can result in fatty infiltration of the liver. However, these nutrients are seldom directly involved in most of the fatty liver problems reported from the field. Excessive feed intake, and, more specifically, high-energy intake, is the ultimate cause of the condition. It is well known that laying hens will overconsume energy, especially with higher-energy diets, and this is particularly true of high-producing hens. There is some information to suggest that daily fluctuations in temperature, perhaps affected by the season of the year, will stimulate hens to overconsume feed. Hence, it is important to attempt some type of feed- or energy-restriction program if feed intake appears to be excessive. Birds ultimately die from hemorrhage caused by the oxidation of the accumulated fat. Antioxidants and high levels of vitamin E are preventative.
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FUTURE
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With few exceptions, most major metabolic disorders still contribute to mortality, morbidity, or both. With the exception of SDS, our knowledge of causative factors allows some measure of control, and economics ultimately dictates the degree to which these changes to diets, feeding programs, or management scenarios are implemented. Fatty liver hemorrhagic syndrome in layers is known to be caused by a surfeit of energy and so should be controllable. The continued occurrence of this metabolic disorder attests to the imprecision of feeding and management at the farm level. We necessarily manage flocks of poultry and work on the biased assumption that all birds in a flock are reacting as per the average of our observational metrics. Obviously, this is a practical compromise, and birds at the extreme of the population norm will always be more susceptible to metabolic disorders. Likewise, the supply of nutrients to birds is less precise than the effort we spend on defining nutrient needs. We often spend considerable time and effort defining the requirement of an amino acid to the second decimal place or worry ourselves as to whether product A is 82 or 85% as efficacious as compared with product B. In reality, the practice of controlling ingredient nutrient content, feed mixing, feed separation during transportation, and variable bird intake each day probably negates such exacting science. We need to describe the nutrient content of diets as accurately as possible, but should realize that the feed supply at the farm level is not an exact science. This imprecision will always disadvantage some birds in a large flock, and so we are unlikely to ever be free of most metabolic disorders.
The underlying trigger to most metabolic disorders is high productivity. When laying hens produced 300 eggs in a year, we thought that we were approaching the practical limit. Today, 330 eggs in a 1-yr cycle are achievable. It is perhaps not too surprising that metabolic disorders are going to occur in a portion of the layer flock when normal clutch length is greater than 100 eggs. Improvements in the growth rate of broilers and turkeys continue unabated, and at some stage, we will run out of management options to grow these birds. For broilers, the limit to growth will be the maturity of the skeleton relative to bird welfare and the stresses of mechanical processing. For layers, the limit to production will be eggshell quality. Overall, my prediction is that metabolic disorders related to skeletal integrity will be our major challenge over the next 10 to 15 yr and will pose the ultimate limit to increased productivity in all areas of poultry production.
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CONCLUSIONS AND APPLICATIONS
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- There are some 15 to 20 metabolic disorders of commercial significance in the poultry industry.
- Although each disorder has unique predisposing factors, increased productivity, either as egg output or growth, is a common factor.
- Few metabolic disorders have been totally eliminated.
- Today, we have chronic disorders affecting a small proportion of most flocks or acute disorders affecting more birds within isolated flocks.
- Ascites is an example of a metabolic disorder that attained such economic significance that it precipitated action by geneticists to resolve the problem.
- In the future, metabolic disorders related to skeletal integrity will be our major concern in both egg and meat birds and will provide the limit to increased productivity.
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REFERENCES AND NOTES
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- Aldrovandi, V. 1600. The Ornithology of Ulisee Aldrovandi (1600). Vol. II, Book XIV. Translated from Latin by L. R. Lind. Univ. Oklahoma Press, Norman.
- Ewing, W. R. 1941. Handbook of Poultry Nutrition. W. R. Ewing, Upper Montclair, NJ.
- Couch, R. 1955. Cage layer fatigue. Feed Age 5:55–57.
- Titus, H. W. 1961. The Scientific Feeding of Chickens. Interstate Printers and Publishers, Danville, IL.
- Classen, H. 1991. Increasing photoperiod length provides better broiler health. Poultry Digest. June: 15.
- Zubair, K., and S. Leeson. 1996. Compensatory growth in the broiler chicken. A review. World’s Poult. Sci. J. 52:189–201.[Web of Science]
This article has been cited by other articles:
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S. Leeson
Predictions for Commercial Poultry Nutrition
J. Appl. Poult. Res.,
January 1, 2008;
17(2):
315 - 322.
[Abstract]
[Full Text]
[PDF]
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SUMMARY
DESCRIPTION OF PROBLEM
