Fats and essential fatty acids
Fats provide high concentrations of energy as well as supplying the bird with essential fatty acids (EFAs). The latter are required for cellular integrity and are used as the building blocks for internal chemicals. These internal chemicals, such as prostaglandins, play an important part in reproduction and inflammation. Fats also provide a carrier mechanism for the absorption of fat-soluble vitamins, such as vitamins A, D, E and K.
The primary EFA for birds is linoleic acid, as it is for mammals (Brue, 1994). The absolute dietary requirement of this fatty acid is 1% of the diet. If the diet becomes deficient in this EFA, there will be a rapid decline in cell structure. This is shown clinically by the skin becoming flaky, dry and prone to recurrent infection. Linoleic acid deficiency also leads to fluid loss through the skin, which in turn leads to polydipsia. It is, however, unlikely that any seed-eating bird will be deficient in linoleic acid, as it is widely found in sunflower seeds and safflower seeds amongst others.
Another EFA which is thought to be important for birds is alpha-linolenic acid, which is necessary for some prostaglandin and eicosanoid production.
The problem of overconsumption of fats in cage birds which are not exercising regularly is well known, and high-fat oil seeds are prime culprits for this (Figure 12.2). The same applies to under-worked raptors fed overweight laboratory rats. Female raptors are particularly prone to this after the breeding season, when large amounts of cholesterol are mobilised for yolk production. Hypercholesterolaemia is hereditary as well as dietary in raptors, but it can be reduced by regular exercising and feeding of lean, low-fat prey. Saturated animal fats provide a supply of cholesterol in excessive amounts for seed and fruit eaters, causing atherosclerosis in older parrots fed on meat and fatty foods.
Preen gland impactions have many causes but may be associated with a deficiency in EFAs and vitamins A and E (see Figure 12.3)
Carbohydrates are mainly used for rapid energy production. This is particularly important in birds, because they are in constant demand of rapid supplies of energy for their often-hyperactive and high-metabolism lives. Birds that are debilitated in some way will particularly benefit from the supply of high carbohydrate foods.
Dietary fibre does not seem to be important for cage and aviary birds, as the presence of excessive volumes of digestive contents does not make good survival sense when trying to evade predators. As raptors are carnivorous, they do not have a dietary fibre requirement either. Only a few wild birds, such as the ratites (ostriches, emus, rheas and cassowaries) and grouse have large fermenting caeca. The red grouse, e.g. lives predominantly on heather shoots for certain times of the year.
Apart from these general dietary requirements, birds, like all animals, require a variety of vitamins and minerals for a healthy diet.
Vitamins are obviously an essential part of the bird’s nutritional requirement.
These compounds are grouped together, although they are widely differing in nature, and all animals have a requirement for various numbers of these. They are categorised into:
- Fat-soluble vitamins A, D, E and K
- Water-soluble vitamins such as the B vitamin complex and vitamin C.
In cage birds and waterfowl the diet frequently contains only the vitamin A precursors, which are present as carotenoid plant pigments. In birds, the most important version of these, in terms of how much vitamin A can be produced from it, is beta-carotene (Harper & Skinner, 1998). Vitamin A is needed for a number of functions, the best known of which is maintenance of the light sensitive pigment in the retina of the eye. It is also important in the process of epithelial cell turnover and keratinisation, which is why a deficiency in vitamin A has been linked with mite infestations, such as ‘scaly face’.
Hypovitaminosis A is a commonly seen problem in companion birds, particularly parrots. This is mainly due to the very low levels of beta-carotenes present in seeds, especially in the much loved sunflower seeds, millet and peanuts. An example of the requirement for vitamin A is quoted as 40 IU per budgerigar, up to a safe maximum of 2500 IU (Harper & Skinner, 1998). The lower levels may be met by as little as 0.4 g of carrot per day, but would require 200 g of millet seed to provide the same amount – i.e. five times a budgerigar’s average weight!
If a relative deficiency in vitamin A occurs then mucus membranes become thickened. Oral and respiratory secretions dry up because of blockage of salivary and mucus glands with cellular debris. This leads to poor functioning of the ciliary mechanisms in the airways that have a role in removing foreign particles. This, combined with vitamin A’s role in immune system function, leads to respiratory and digestive tract infections (Figure 12.4). One of the most frequently seen infections, particularly in parrots fed an all-seed diet, is the fungal respiratory disease aspergillosis. Sterile pustules and cornified plaques inside the mouth are also commonly seen, with enlargement of the sublingual salivary glands.
Vitamin A is required for bone growth, for the normal function of secretary glands such as the adrenals and for normal reproductive function. On another level, coloured plumage, particularly the red and yellow, is derived from beta-carotene pigments. Therefore, birds such as the red-factor canaries will become paler in colour if they are fed a diet deficient in this vitamin precursor.
Because it is fat soluble, vitamin A can be stored in the body, primarily in the liver. The recommended minimum dietary levels are 8000–11 000 IU/kg of food offered for both Passeriformes and Psittaciformes (Scott, 1996; Kollias & Kollias, 2000).
This vitamin is primarily concerned with calcium metabolism, and vitamin D3 compound is the most active in calcium homeostasis. Plants are not effective as suppliers of this compound.
Cholecalciferol is manufactured in the bird’s skin in a process enhanced by ultraviolet light. Indoor-kept birds produce much less of this compound and this can lead to deficiencies. Exposure to just 11–45 minutes of unfiltered sunshine (glass filters out the important ultraviolet light) has been shown to prevent rickets in growing chickens (Heuser & Norris, 1929). Cholecalciferol must then be activated, first in the liver and then by the kidneys, before it becomes functional. It works with parathyroid hormone to increase reabsorption of calcium at the expense of phosphorus from the kidneys. It also increases absorption of calcium from the intestines and mobilises calcium from the bone, increasing the blood’s calcium levels.
Hypovitaminosis D3 affects with calcium metabolism and causes rickets. This is exacerbated by diets low in calcium. Typical sufferers are Psittaciformes, indoor-kept birds fed all-seed diets and raptors fed all-meat diets with no calcium supplementation. This produces well-muscled, heavy birds which have poorly mineralised bones. Radiographical evidence shows flaring of the epiphyseal plates at the ends of the long bones. The end result is bowing of the limbs, especially the tibiotarsal bones. The recommended minimum levels are 500 IU/kg of food offered for Psittaciformes and 1000 IU/kg for Passeriformes (Kollias & Kollias, 2000).
Hypervitaminosis D3 is caused by over supplementation with D3 and calcium, and leads to calcification of soft tissues, such as the medial walls of the arteries, and the kidneys. This leads to hypertension and organ failure. The recommended maximum levels are 2000 IU/kg of food offered for Psittaciformes and 2500 IU/kg for Passeriformes (Kollias & Kollias, 2000).
Vitamin compound is found in several active forms in plants. The most active is alpha-tocopherol. It has an important role in immune system function, particularly lymphocyte cell activity. Vitamin E is combined with selenium into the metalloenzyme glutathione peroxidase. This mops up the free radicals that are produced in the metabolism of dietary polyunsaturated fats, which would otherwise cause cellular damage.
Hypovitaminosis E produces a condition known as ‘white muscle disease’ in which damage occurs to the muscle bundles and their myoglobin content, leading to pale-coloured muscles and muscle weakness. In addition, birds deficient in vitamin E, such as cockatiels may be more susceptible to the protozoal gut parasite Giardia spp. and may pass undigested whole seeds in their droppings.
Hypovitaminosis E may occur due to a reduction in fat metabolism or absorption, as can occur with small intestinal, pancreatic or biliary diseases. It may also occur because of a lack of green plant material in the diet, as this is the main source of vitamin E. Vitamin E deficiency may also occur in birds fed on diets high in polyunsaturated fatty acids, such as fish-eating raptors fed oily fish like tuna. These diets rapidly deplete vitamin E reserves in metabolising the polyunsaturated fats.
Hypervitaminosis E is extremely rare. The recommended minimum level is 50 ppm for both Passeriformes and Psittaciformes (Kollias & Kollias, 2000).
Because vitamin K is produced by bacteria normally present in the gut, it is very difficult to get a true deficiency, although absorption will be reduced when fat digestion/absorption is reduced as in, e.g. biliary or pancreatic disease.
The consumption of warfarin- and coumarin-derived compounds (such as those found in plants like sweet clovers) can increase the demand for clotting factors. It can also be a problem for raptors that have eaten prey that has been killed by these rodenticides. The deficiency produced causes internal and external haemorrhage, but vitamin K also functions in calcium/phosphorous metabolism in the bones and this may also be affected. The recommended minimum level for raptors, Passeriformes and Psittaciformes is 1 ppm (Wallach & Cooper, 1982).
Vitamin B1 (thiamine)
Thiamine is found widely in plant and animal tissues alike. It is concerned with a number of cellular functions, one of which involves the integrity of the central nervous system.
Hypovitaminosis B1 is uncommon. The most likely cause is the presence of enzymes called thiaminases in the diet, which destroy thiamine. A source of thiaminases is raw saltwater fish, which may be fed to some raptors, such as sea-eagles and ospreys. However, there are thiamine antagonists present in foods such as blackberries, beetroot, coffee, chocolate and tea. When a deficiency occurs, neurological signs such as opisthotonus, weakness and head tremors appear. In addition, the fungal infection aspergillosis is a common sequel to B1 deficiency. The recommended minimum levels for raptors, Psittaciformes and Passeriformes are 4 ppm (Kollias & Kollias, 2000) or 5 g of usable vitamin B1 per day for raptors (Wallach & Cooper, 1982).
Vitamin B2 (riboflavin)
Vitamin B2 is present in particularly small amounts in seeds, and so deficiency is primarily seen in seed-eating birds. Hypovitaminosis B2 causes growth retardation and curled toe paralysis in chicks. This is due to its function in cartilage, collagenous and nerve cell tissue growth. Birds can be supplemented using commercial powder supplements or simple brewer’s yeast. The recommended minimum levels for Psittaciformes and Passeriformes are 6 ppm (Kollias & Kollias, 2000), for game birds 3.6 mg/kg and waterfowl (Austic & Cole, 1971) 4 mg/kg of feed offered (Scott & Norris, 1965).
Niacin is found widely in many foods, but the form that occurs in plants has a low availability to the bird. It is used in many cellular metabolic processes.
Birds fed a high proportion of one type of seed, such as waterfowl overfed on sweetcorn, can become deficient. This results in retarded growth, poor feather quality and scaly dermatitis on the legs and feet. Intertarsal joint deformities can occur in the larger waterfowl. The recommended minimum requirements are 50 ppm for Passeriformes and Psittaciformes (Kollias & Kollias, 2000) or 55–70 mg/kg of feed in general (Wallach & Cooper, 1982).
Vitamin B6 (pyridoxine)
Any deficiency of pyridoxine will result in retarded growth, hyperexcitability, convulsions, twisted neck and polyneuritis, although a deficiency is rarely seen. Recommended minimum levels are 6 ppm in Passeriformes and Psittaciformes (Kollias & Kollias, 2000) or 2.6–3 mg/kg of feed for game birds (Scott & Norris, 1965).
Pantothenic acid is found widely in plants and animals and so deficiency rarely occurs. When it does occur in birds, signs include crusting of the feet, eyelids and commissures of the beak, poor feather growth and general epidermal desquamation. The recommended minimum levels are 20 ppm for Passeriformes and Psittaciformes (Kollias & Kollias, 2000) or 35.2 mg/kg of feed in ducks (Scott & Norris, 1965).
True deficiencies are rare due to gut bacterial production. Deficiencies produce a range of signs, including exfoliative dermatitis and gangrenous toes. The recommended minimum requirements are 0.25 ppm for Passeriformes and Psittaciformes (Kollias & Kollias, 2000) or 0.09–0.15 mg/kg of feed in waterfowl (Wallach & Cooper, 1982).
Folic acid deficiency leads to severely impaired cell division. This can lead to a number of problems, such as failure of hen birds’ reproductive tract development, a macrocytic anaemia due to failure of red blood cell maturation and immune system cellular dysfunction.
Folic acid is needed to form uric acid, the waste product of protein metabolism in birds. Therefore, a relative deficiency of folic acid may occur in some individuals fed a very high protein diet. In addition, some foods, such as cabbage and other brassicas, as well as oranges beans and peas, contain folic acid inhibitors. The use of trimethoprim sulphonamide drugs may also reduce gut bacterial folic acid production. The recommended minimum requirements are 1.5 ppm for Passeriformes and Psittaciformes (Kollias & Kollias, 2000) or 1.25 mg/kg of feed (Scott & Norris, 1965).
Vitamin B12 is produced by intestinal bacteria so deficiency is uncommon, although it may occur after prolonged antibiotic medication. Vitamin B12 is required for many metabolic pathways and neurological function and a deficiency may cause a knock-on deficiency in folic acid. It will cause slow growth, muscular dystrophy in the legs, poor hatching rates and high mortality rates in young birds, as well as hatching deformities. The recommended minimum requirements are for 0.01 ppm in Passeriformes and Psittaciformes (Kollias & Kollias, 2000) or 0.009–0.25 mg/kg of feed offered (Wallach & Cooper, 1982).
Choline may be synthesised in the body, but not in enough quantities for the growing bird. Because of their interactions, the need for choline is dependent on levels of folic acid and vitamin B12. Excess dietary protein increases choline requirements, as does a diet high in fats. Deficiencies cause retarded growth, disrupted fat metabolism, fatty liver damage and perosis (slipping of the Achilles tendon off the intertarsal joint groove). The recommended minimum requirements are 1500 ppm for Passeriformes and Psittaciformes (Kollias & Kollias, 2000) or 1300–1900 mg/kg of feed offered (Wallach & Cooper, 1982).
There are only a few wild birds that have a direct need for vitamin C. These include the red-vented bulbul (Pycnonotus cafer) and the willow ptarmigan/red grouse (Lagopus lagopus) as well as the crimson sun-conure, a form of parrot. Birds in general do not need vitamin C in their diets as it can be produced from glucose in the liver. If a bird is suffering from liver disease, therefore, it may require a dietary source of vitamin C.
Vitamin C is needed for the formation of elastic fibres and connective tissues and is an excellent anti-oxidant similar to vitamin E. Deficiency leads to scurvy in which there is poor wound healing, increased bleeding due to capillary wall fragility and bone weakness.
Vitamin C also increases gut absorption of some minerals, such as iron. This may be important for chronically anaemic patients, but can be a danger for softbills, such as the mynah and toucan families, as these birds are prone to liver damage from excessive dietary uptake of iron.
There are two main groups of minerals:
Macro-minerals (such as calcium and phosphorus) are present in large amounts in the body. Micro-minerals or trace elements (such as manganese, iron and cobalt) are all necessary for normal bodily function, but are needed in far lower quantities.
The active form of calcium in the body is the ionic, double-charged molecule Ca2+. Lowered levels of this form lead to hyperexcitability, fitting and death. This can occur even though the overall body reserves of calcium are normal.
Calcium levels in the body are controlled by vitamin D3, parathyroid hormone and calcitonin working in opposition to each other. The ratio of calcium to phosphorus is particularly important – as one increases, the other decreases and vice versa. A ratio of 2:1 calcium to phosphorus is desirable in food for growing birds and 1.5:1 for adults. In periods of high egg laying though, to keep pace with the output of calcium into the shells, a ratio of 10:1 may be needed (Brue, 1994). A known deficiency problem occurs in many birds fed an all-seed diet due to the lack of calcium in such a diet and the presence of phytates (phosphorus containing compounds) which bind calcium in the gut and prevent absorption. This is particularly a problem in African Grey Parrots (Psittacus erithacus), which may present with collapse or seizures due to low blood calcium levels. Excessive calcium in the diet (>1%), however, reduces the use of proteins, fats, phosphorus, manganese, zinc, iron and iodine and combined with a high level of vitamin D3 may lead to calcification of soft tissue structures.
Phosphorus, like calcium, is used in bones. It is also used in the storage of energy as adenosine triphosphate (ATP), and as a part of the structure of cell membranes. Levels of phosphorus are controlled in the body as for calcium, the two being in equal and opposite equilibrium with each other. Nutritional secondary hyperparathyroidism may occur when dietary phosphorus exceeds calcium, and this can lead to progressive bone demineralisation and renal damage due to high circulating levels of parathyroid hormone.
High dietary phosphorus, particularly as phytates, will reduce the amount of calcium which can be absorbed from the gut, as it forms complexes with the calcium present there. This can be a big problem in cage birds which are predominantly seed eaters, as cereals are high in phosphorus and low in calcium. It may also be a problem for raptors fed pure meat with no calcium/bone supplement.
Most of the magnesium in the body is found in the bone matrix. However, it is also essential for phosphorus transfer in the formation of ATP, and cell membranes in soft tissues such as the liver. Most magnesium is absorbed in the small intestine, and is affected by large amounts of calcium in the diet, which will reduce magnesium absorption. The recommended minimum levels are 600 ppm (Kollias & Kollias, 2000) or 475–550 mg/kg of feed (Wallach & Cooper, 1982).
Sodium is the main extracellular, positively charged ion and regulates the body’s acid–base balance and osmotic potential. Along with potassium, it is responsible for nerve signals and impulses.
A true dietary deficiency (hyponatraemia) is rare, but may occur due to chronic diarrhoea or renal disease. These disrupt the osmotic potential gradient in the kidneys leading to further water loss and dehydration. Excessive levels of sodium in the diet (greater than ten times recommended levels) lead to poor feathering, polyuria, hypertension, oedema and death. Minimum levels are quoted as 5–10 mg/kg of feed offered (Wallach & Cooper, 1982) or around 0.12% of the diet offered (Kollias & Kollias, 2000).
As with mammals, potassium is the major intracellular positive ion. It is essential in maintaining membrane potentials and it is the principal intracellular cation affecting acid–base reactions and osmotic pressure. Rarely is there a dietary deficiency, but, severe stress may cause potassium deficiency, hypokalaemia. This is caused by an increased kidney excretion of potassium due to an elevation in plasma proteins which is often seen at times of stress. This can lead to cardiac dysrhythmias, muscle spasticity and neurological dysfunction.
Potassium is present in high amounts in certain fruits such as bananas. It is controlled in the body in equilibrium with sodium under the influence of the adrenal hormone aldosterone, which promotes sodium retention and potassium excretion. The recommended minimal level is 0.4–1.1 mg/kg (Scott & Norris, 1965).
This mineral is the major extracellular negative ion. It is responsible for maintaining acid–base balances in conjunction with sodium and potassium. Deficiencies are rare due to its combination with sodium in the diet as salt.
Micro-minerals (trace elements)
Iron is required for the formation of the oxygen-binding centre of the haemoglobin molecule. Absorption from the gut is normally relatively poor as the body is very good at recycling its iron levels from old red blood cells.
Certain species have a greater ability to absorb iron from the small intestine. The mynah and toucan/toucanet families are examples. This ability may become a problem when diets rich in iron are presented to these species. For example, rodents and day-old chicks may be fed to toucans, and so occasionally are various brands of dog or monkey biscuits. In addition, vitamin C increases iron absorption by converting the iron into the more easily absorbed ferrous (Fe2+) state. This can lead to a condition known as haemochromatosis, where the liver becomes fatally overloaded with absorbed iron. The recommended minimum requirement for Passeriformes and Psittaciformes is 80 ppm, but for toucans and mynahs a maximum of 60 ppm, or less than 160 mg/kg of feed, is recommended (Worrell, 1991). Dietary deficiencies rarely occur. However, ground foraging species reared on impervious surfaces such as wire or concrete have suffered iron deficiency. This is because soil consumption, which occurs during ground feeding, is another source of iron.
Copper is used for haemoglobin synthesis, collagen synthesis and the maintenance of the nervous system.
Deficiencies occur, as with iron, in some ground feeding species like pheasants and other game birds, reared on surfaces such as concrete where soil consumption during the foraging process does not occur. Signs include chronic anaemia with general weakness, limb deformities and hyperexcitability. The recommended minimum requirements are 8 ppm for Passeriformes and Psittaciformes, and 4 ppm for Galliformes (Wallach & Cooper, 1982).
This is a vital trace element for wound healing and tissue formation, forming part of a number of enzymes.
Deficiencies can occur in young, rapidly growing birds fed on plant material high in phytates such as cabbage, wheat bran and beans. This is because, as with calcium, the phytates bind zinc and prevent its absorption from the gut. In addition, high dietary calcium itself decreases zinc uptake. Deficiencies cause retarded growth, poor feathering, enlarged intertarsal joints and slipped Achilles tendon (perosis). The minimum recommended requirement is 50 ppm for Passeriformes and Psittaciformes (Kollias & Kollias, 2000).
Manganese is primarily found in plant materials but is often present in unavailable forms. Efficient bile salt production is required for its absorption, so birds with hepatic and biliary dysfunction are most at risk of a deficiency.
Manganese is necessary for normal bone structure; hence deficiencies are most commonly manifested by the swelling and flattening of the lateral condyles of the intertarsal joint, allowing the Achilles tendon to slip out of the groove created for it (a condition known as perosis). In addition, the tibiotarsus and tarsometatarsus may exhibit lateral rotation. Young may be born with retracted beaks and shortened long bones. The recommended minimum requirement is 55–60 mg/kg of feed (Wallach & Cooper, 1982).
The sole function of iodine is in thyroid hormone synthesis. Deficiencies cause goitre, and produce effects such as reduced growth, stunting and neurological problems. It is a relatively common finding in budgerigars fed on an all-seed diet without additional supplementation. They adopt a classic, hunched posture on the perch because the enlarged thyroid gland constricts the tracheal lumen. They may also be seen to regurgitate seed from the crop. Goitre is one of the differential diagnoses in a vomiting budgerigar. Levels of 4 mg per budgerigar per week prevent goitre from developing (Blackmore, 1963).
Its functions are similar to vitamin E, as it is found in the enzyme glutathione peroxidase. If there is a general deficiency in both selenium and vitamin E, a condition known as exudative diathesis will occur. This is when the smaller, subcutaneous blood vessels become damaged and leakier. Fluid then moves rapidly out into the subcutaneous spaces and oedema forms over the neck, wings and breast. This is often followed by stunted growth, limb weakness and death.
The selenium content of plants is dependent on where they were grown and the levels of selenium in the soil. The recommended minimum requirement is 0.1 ppm for Passeriformes and Psittaciformes (Kollias & Kollias, 2000).
Examples of food types for Psittaciformes and Passeriformes
As a rough example of food types suitable for commonly kept cage and aviary birds, please examine the list given below.
Rape seed, millet, canary seed, hemp and linseed are useful for smaller species such as finches, canaries, budgerigars and cockatiels.
Safflower, sunflower and pumpkin seeds are useful for larger parrots but beware of addiction to sunflower seeds!
Almonds, walnuts, Brazil nuts and hazel nuts are useful for larger parrots, but be careful of addiction to peanuts and Aspergillus spp. toxin poisoning. Peanuts and pine nuts may also be fed. Nuts are high in calories.
A wide variety of fruits are useful foods. Examples include apple, pear, melon, mango, papaya, pomegranate, guava, apricot, peach, nectarine, oranges and bananas. Grapes and kiwi fruit should be fed sparingly due to their high sugar content, which can cause diarrhoea. Oranges should also only be fed in small amounts, since excess can cause gastric upset, and they should not be fed to toucans and mynah birds due to their high vitamin C content and iron absorption facilitation.
Broccoli, watercress and wild rocket are good sources of vitamin A and calcium. Other good vegetables include Swiss chard, kale, sweet pepper, carrot, beetroot, boiled potato, peas, mung beans (particularly sprouted ones), cauliflower, tomato and sweetcorn.
Do not feed avocados as these cause severe fatty liver damage in birds. Lories, lorikeets and hummingbirds are all nectar feeders and so require a specialised artificial syrup food. Many are commercially produced. They may also take very ripe fruits, and enjoy eating the pollen from flowers.
Specific nutritional requirements
Nutritional requirements for growth
The egg is a perfect capsule of nutrients providing all that is needed for the developing embryo. The hen must be fed a balanced diet to ensure that she has the nutrients available to instil into the egg. If she is fed a poor or deficient diet then the egg may not be fertile. It could also undergo:
- Early embryonic death (EED). This is often signalled by a blood ring left in the yolk, which suggests a vitamin A deficiency.
- Retarded embryonic development (RED). This is often associated with vitamin B deficiencies.
- Embryonic deformities, which may be seen with manganese, zinc or other trace element deficiencies.
Hatching occurs after the developing chick has absorbed the external yolk sac, and the chick must then be supplied within 3–4 days with high levels of energy and protein for the growth phase. The remaining internal yolk sac supply will last that long.
When feathers are produced, a huge demand for protein occurs, as feathers are made of keratin, a protein, and will eventually make up one-tenth of the bird’s weight. In addition, there will be several feather changes during the first 2 years of life, as juvenile down plumage is replaced by adult plumage. Young birds also have a much larger requirement for calcium and vitamin D3 for developing bones. On average, sexual maturity for the larger parrots, such as African grey parrots, macaws and cockatoos, is not reached until 2–4 years of age, so this growth phase may be prolonged.
If, during this growth phase, disease or low environmental temperatures are introduced, energy is diverted to immune system function and heat supply. This results in less energy for growth and in slowing of the growth rate. This may be reversed in later periods of growth, assuming no permanent damage has been caused. The obvious side-effect of this, though, is that adult weights are achieved at a later age. If a retarded bird is supplied with excess nutritional levels after this period of leanness, a compensatory growth spurt may occur and the chick appears to grow more rapidly than other birds of that age group.
For all of this growth to occur, it has been estimated that minimum energy requirements for small Psittaciformes and Passeriformes are five times that of adults. Young chicks nearly double their weights over 48 hours, and require a protein level of 15–20%, as opposed to an adult’s protein need of 10–14% (Harper & Skinner, 1998). Commercial and home-prepared diets for chicks are usually preformulated mashes with this level of protein, eggs and dairy products which have a good broad spectrum of amino acids supplementation and 20% protein levels.
Excessive protein supplementation may be equally damaging. Levels greater than 25% of diet have been shown to lead to behavioural problems, and claw, beak and skeletal deformities, particularly if combined with a lack of calcium. Levels of 0.6–1.2% of the diet as calcium have been quoted for chick growth (Brue, 1994) with a calcium:phosphorus ratio of 2:1 maintained.
Nutritional requirements for breeding
These requirements include those needed for egg production as well as for courtship behaviour. The requirements for egg production are high, with large volumes needed of fats for the yolk, calcium for the shell and proteins for the albumen (egg white). As egg production commences, the hen bird will increase the volume of food consumed, so removing the need to increase the energy concentration of the diet being offered. It is, however, essential that the diet offered is a balanced one, with increased protein content, particularly from methionine and cystine (the sulphur containing amino acids) and lysine.
In addition, a moderate increase in the amount of calcium and vitamin D3 offered (an increase of 0.35% of the adult maintenance requirement for calcium) is needed, so that levels approach 1% of diet (Harper & Skinner, 1998). This not only helps to ensure proper calcification of eggshells and the developing embryo, but also to prevent egg-binding in the hen. This is when poor calcium reserves lead to low calcium blood levels, weakness, uterine muscular paresis, egg retention, shock and death.
Other compounds which, if supplied above the minimum daily requirements mentioned earlier, help with egg production, include vitamins A, B12, riboflavin and the mineral zinc. In addition, it is useful for improved hatching rate, to increase the levels of the B vitamins biotin, folic acid, pantothenic acid, riboflavin (B2) and pyridoxine (B6), as well as vitamin E, iron, copper, zinc and manganese to above the minimum daily requirements.
Nutritional requirements for the older birds
As with cats and dogs, the aim is to provide a diet of high digestibility whilst reducing slightly the protein, sodium and phosphorus levels. This preserves renal function and prevents hypertension.
In addition, lowering cholesterol and unsaturated fat levels is important, as atherosclerosis is common in older birds. The levels of vitamins A, E, thiamine (B1), B12, and pyridoxine (B6), the mineral zinc, amino acid lysine and fatty acid linoleic acid should also be slightly increased to ensure that any decrease in digestive function and age-related cellular damage is contained.
Special nutritional requirements for debilitated birds
Extra nutritional support for debilitated and diseased birds is vital and plays an essential role in ensuring recovery of the avian patient after disease or debility. Enteral nutrition is currently the most usual method of supporting the debilitated patient, with parenteral (intravenous) nutrition still being in its infancy in avian therapeutics.
First, fluid requirements should be assessed, as any animal will succumb to dehydration long before starvation. The reader is referred to chapter 14 for a more detailed discussion of this topic.
Second, energy requirements should be estimated. These can be calculated roughly from the MER by multiplication as follows:
Starvation = 0.5 × MER
Trauma = 1.5 × MER
Sepsis = 2.5 × MER
Burns = 3–4 × MER
From these crude estimations, a rough idea of the levels of nutrition demanded and the energy concentration of the diet can be derived.
Third, protein requirements should be evaluated, as debilitation will increase amino acid and protein turnover. This may be through the increased use of proteins in the immune system response, or for repair of damaged tissue or simply after using tissue proteins as an energy source.
Birds with liver disease
Birds affected by hepatic dysfunction should be fed a diet which reduces liver use by decreasing its need to convert body tissues into blood glucose, and decreasing its need to break down the waste products of excess protein metabolism. Therefore birds should be fed a diet high in digestible carbohydrates, such as boiled rice, pasta or potatoes, for energy and sugars. Protein sources should be of a high biological value (high in essential amino acids) such as those found in whole eggs. This is in an attempt to keep to a minimum the overall amount of protein fed, particularly purine-producing proteins such as are found in fish, meat, etc. These protein sources lead to the greater build-up of waste products of protein digestion, which the liver then has to detoxify and eliminate via the kidneys. The feeding of frequent, small meals is also advisable for liver disease patients, as is the addition of vitamin B supplements to the diet.
Birds with renal disease
Like the liver, the kidney is responsible for eliminating the waste products of protein metabolism (Figure 12.5). It is therefore important in renal disease to reduce protein levels, and ensure that the protein sources provided have a high biological value.