Reducing chick mortality:

Minimizing Adipose Depletion in rheas and ostriches

 Donna Fezler

Rubber rhea Syndrome and Fading Chick Syndrome are evolutionary adaptation mechanisms resulting in death caused by the depletion of body fat in ostrich and rhea chicks.  The syndromes may be complicated by secondary bacterial, viral, or protozoan infections coinciding with the loss of body fat. 

 These birds have a metabolism that is highly dependent on their fat stores, and management techniques must strive to keep their fat stores intact.  Reducing stress is critical since the stress hormones literally release stored body fat into the bloodstream as a supposedly temporary measure.  Under chronic stress which depletes the fat stores, the chicks have a reduced ability to produce energy for heat and body functions, and the rhea chicks lose the anti-inflammatory capabilities of the body fat.  Since research on adipose in ratites is so limited, this article will focus on manipulating known factors that significantly impact adipose in other animals: 

 ·       Stress reduction

·       Consistent light-dark regime to stimulate melatonin

·       Appropriate dietary fats

·       Evaluation of environmental toxins

·       Copper levels

 A. Stress reduction

 Stress mobilizes fatty acids from depot fat and promotes bone resorption, providing phosphorus for energy to fuel whatever actions may be necessary to cope with the stressor.  This is meant to be a short term adaptation response, and all metabolic systems should reset after the stressful incident is over (1).  Chronic stress reactions occur if an animal is in poor health due to disease, inadequate diet, or improper environmental conditions (1-3).  Previously outlined management strategies for reducing stress in ostriches apply to rheas.

 Temperature is very critical to preserving the young chick’s adipose supply, and following environmental temperature guidelines appropriate for the age of the chick is essential.  Low temperatures will cause an increase in the fat burning mechanism, depleting the chick’s limited fat reserves and compromising the chick’s immune system’s ability to fight bacterial, viral, or protozoan infections. 

 High temperatures are also stressful and the birds respond by becoming anorexic.  In an attempt to reduce metabolic heat, digestion is suppressed.  However, since birds have a limited supply of stored energy, glycogen, they can rapidly become hypoglycemic (low blood sugar) from lack of food (4).  Hypoglycemia is a serious condition which can quickly kill even adult birds.  Ratites appear very susceptible to both high and low blood sugar.

 B. Melatonin: the Adaptation Hormone

 Glucocorticoids are known to induce the fight and flight response, and when this mechanism is running it puts the chicks body at “high idle”, rapidly using available fat stores.  Since fat is so critical in these birds, without a shut off switch the stress hormones initiate a suicide mechanism.  Melatonin, the chief hormone of the pineal gland in vertebrates, is widely distributed in the plant and animal kingdoms.  Melatonin has been referred to as the adaptation hormone.  Aside from the fact that melatonin is grabbing the nutritional fad spotlight, there are some salient scientific facts that may make a significant difference in consistently increasing our chick survivability.  In chickens, melatonin synthesis is rapidly and nearly completely abolished by light (5).  The lack of a constant dark period could cause reduced effects on the positive actions of the melatonin hormone, and may play a role in the immune response (6, 7).

 1.     Melatonin is a powerful antioxidant hormone produced by the pineal gland capable of scavenging the damaging free radicals that degrade cell membrane lipids. In vitro activity exceeds the activity of the antioxidants, vitamin  E and glutathione, and it has been shown to have a stimulatory effect on the production of glutathione in rats (8-11).

 2.     Melatonin affects thermoregulation.  During nighttime secretion of melatonin body temperature is decreased, supposedly as an energy conserving mechanism (12-15).  Too much light, for instance from heat lamps, could reduce the amount of melatonin being secreted and force the chicks to have a higher energy use at night than nature intended.  This could put them into an energy deficit and contribute to the increased use of body fat.

 3.     Melatonin blunts the effects of stress hormones, although it does not appear to directly affect their production or release (16-20).   Since the production of melatonin is dark dependent, darkness is critical to these birds.  In the wild the chicks are able to find darkness under the parental male’s wings, and chicks will instinctively crawl under a human’s shirt and immediately quiet down and nestle.  This behavior, which is obviously calming, may have its basis in hormonal control, specifically the stress hormones.  Even adult birds are much calmer when hooded.  Twelve hour light-twelve hour dark cycles are recommended for poultry (21) utilizing full spectrum light or natural lighting and infra-red heaters.

 C. The role of insect lipids and essential fatty acids

 Watching rhea babies is like watching little fly-catching machines.  Whether confined to the barn or out in a field, the majority of the infant’s time is spent chasing and eating insects.  In a natural, field raised situation the chicks seek flies and grasshoppers - insects that are mainly fat and protein.  Insect fat is peculiar and flies in particular have very different fats than the dietary fats available through grain based diets.  Grain based feeds contain predominantly the unsaturated fats, oleic acid (16 carbons) and linoleic acid (18 carbons).  In contrast fly fat is composed of only long-chained, very stable, saturated fats that begin at 18 carbons and progress up to 40 carbons.  In addition the insects’ body has an ample store of the enzymes necessary to readily convert the saturated fat to unsaturated fat (22, 23).  The saturated fat stored in an insect’s body is a highly stable fat that does not oxidize easily to free radicals that must be countered by the body’s antioxidant system.

Interestingly, as fall approaches and the days shorten, the bottle fly, a calliphorid, will increase their fat body content by 2.5-3 times in preparation for hibernation.  At the end of the season the rhea’s eggs decline in long chain fat content as the fly’s body increases its fat stores, so the late hatch chicks are provided the extra fat that may be necessary for improving survivability of late season chicks.  (Although a fly may be nature’s intended food in the wild, in confinement situations flies carry disease and should be controlled).

However, for the chick to utilize these insect fats, desaturase enzymes must transform the saturated fats into the more readily usable unsaturated fats.  In humans a disorder or deficiency of these desaturase enzymes appears to play a role in diseases such as cystic fibrosis, diabetes, eczema, and essential fatty acid deficiency in bottle-fed babies (24-26).  The fat in the chicks’ insect based diet is exclusively long chain fats packaged with the enzymes to transform these fats into the readily usable poly-unsaturated fats.  The young chicks’ ability to utilize dietary fat evolved around their food source.   Their bodies are designed to use a different type of fat than is generally available in a grain-based diet. The chicks may be overwhelming their bodies’ capability to synthesize the needed desaturase enzymes to properly use the nutrient fat we provide in their diets.

 D. Environmental toxins and  challenges

 Toxic chemicals are stressors to all plants and animals, requiring detoxifying systems. These substances can include drugs, fertilizers, cleaning chemicals, pesticides, and poisons.  Due to the highly reactive nature of their fat, ratites may be utilizing a fat-based detoxification  system, the lipoxygenase enzyme, to detoxify their bodies.  This process, which also produces the inflammatory leukotrienes, is a mechanism for degrading foreign substances, xenobiotics, in the body (27-29).  Xenobiotics can range from therapeutic drugs to toxic chemicals and are very efficiently broken down by the same enzyme system that also produces the inflammatory agents.  The anti-inflammatory quality of the rhea’s fat may be an evolutionary adaptation to control the side effects of the detoxification process.  When the fat runs out, and toxic stress persists, the chick may have no way to stop the inflammatory reaction.

 Do you know the chemical history of your ground?  Was it cultivated and treated with insecticides, fertilizers or herbicides?  Was it ever a feed lot?  We know that chicks raised on used soil have higher mortality rates than chicks on virgin ground.   As animals metabolize and detoxify their bodies, they excrete toxins, contaminating and concentrating the toxins in the soil.  Each succeeding year the level of toxins may increase, and without testing the soil there is no way to know.  Although old soil has been blamed for higher microbial levels, this has been conjecture, and it is equally likely the level of toxins are higher in used ground.  A soil test is recommended.

 In one study, dietary lead increased the level of the fatty acid arachidonic acid (the fat necessary to start the lipoxygenase detoxification process) in chick cells even though there was no source of arachidonic acid in the diet.  The chick must rely on its desaturase enzymes to produce the arachidonic acid from its dietary fats (30, 31).  At the time, the researchers were unable to explain why lead toxicity would produce such an inefficient change in the cell membrane.

However, arachidonic acid breaks down to the prostaglandins and leukotrienes.  In the process of going from arachidonic acid to leukotrienes the enzyme that detoxifies xenobiotics ( i.e. lead) is activated (29).  Constant exposure to lead stresses the body, forcing it to adapt by changing to a cell structure that provides the arachidonic acid needed to detoxify the lead. The end product of this system is a leukotriene inflammatory agent which would further explain the evolutionary need for an anti-inflammatory fat.

 Since both fat and bone serve as inert storage sites for toxicants, loss of adipose and bone mass can exacerbate the problem of toxins in the body, further reducing the chicks ability to survive.  In starvation or bone demineralization, there will be increased movement of the toxicants, which will be reflected by an increased plasma concentration and even intoxication in an animal previously exposed (32).

 Nitrate contamination of rural well water by chemical fertilizers, livestock and human waste, and other organic waste is a global problem causing toxicity in many species (33, 34).  In cropland areas, the nitrate levels in the water may peak seasonally when farmers are fertilizing their fields in spring and fall.  If this is a problem in your area, water nitrate levels should be closely monitored.  Your county extension agent is familiar with local groundwater conditions and variance.

 E. Copper

 Copper deficiency in ratites has been implicated as a stress factor.  The role of copper in homeostasis and adipose is varied and critical.  The one study of mineral levels in ostriches showed a wide range of copper levels and especially low levels in cases of traumatic death caused predominately by cardiac failure and skeletal disorders, and recommended that studies should be focused on copper (35). 

1.     Copper plays a role in the desaturase enzymes that enable the body to take saturated fats and turn them into biologically usable desaturated fats.  A copper deficiency can produce decreased desaturase activity, altering cell membrane structure (30, 36) and exacerbating fatty acid deficiency (37). 

2.     Copper is a critical component in the anti-oxidant superoxide dismutase.  Copper deficiency has been linked with low superoxide dismutase levels and a lessened ability of the animal to counteract free radicals with no evidence of compensation by the manganese superoxide dismutase (36, 38). 

3.     A copper deficiency caused test rats to shift from burning carbohydrates as body fuel to burning fat, reducing the amount of body fat in the animals.  The rats also had a lower rate of gain and a significantly higher daily heat production.  The copper deficient rats were not using energy efficiently, exhibiting normal dietary patterns with depressed growth rates, decreased fat and somewhat decreased body mass in a four week period (39). 

 In ratites, where fat depletion is a life-threatening situation, a copper deficiency, whether caused by insufficient dietary levels or increased demand by other body functions, can only compound the problem.

Summary

1.     Stress reduction or elimination should be the primary focus.  Perhaps the simplest, most cost effective and efficient method of providing the proper environment for the rhea chick is already on your farm:  the male rhea.  Throughout the day, the chicks will seek shelter or shade in the dark of the parental male’s wings.  These guys really know what they are doing and it is by far the easiest way to raise chicks (40). 

 2.     Melatonin production can be controlled by the light-darkness cycle.  Light regime recommendations for poultry suggest a 12 hour alternating cycle of light and dark utilizing natural or full spectrum lighting.  Infra-red heat lamps can be used with no effect on the 12 hour dark cycle. 

 3.     Essential fatty acids play a significant evolutionary role in ratite nutrition.  Further nutritional research is warranted to specifically define the chicks’ needs.

 4.     Test soil and water for toxins.

5.     Copper levels in ratites may play a significant role in chick survivability.  Indiscriminate supplementation, however, simply adds copper to the list of toxins that the chick has to excrete.  Research studies are needed to define optimal copper levels.

 6.     Although not directly impacting adipose depletion, exercise is critical  for proper growth and development.

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