1.5% of a birds body weight is made up of calcium which represents the most predominant mineral in the body being located mainly in the skeletal system.
PETRA ZSIVANOVITS MRCVS and NEIL FORBES FRCVS
Great Western Exotic Vets
Unit 10 Berkshire House, County Park,
Shrivenham Road, Swindon, SN1
Physiological functions:
Calcium is involved in blood coagulation, transmission of nerve impulses, the permeability and excitability of cell membranes, activation of enzyme systems, glandular secretion, muscle contraction, calcification of eggshells and contraction of the uterus during egg laying.
Low blood calcium levels result in hyperexcitability due to a decrease in electrical resistance and an increase in membrane permeability of nerve tissue to sodium and potassium.
Normal blood calcium levels range from 2.0 to 2.8 mmol/L.1 Calcium levels vary considerably between species.
For budgerigars a range of 1.6 – 2.54 mmol/L has been described,
for African grey parrots 2.10 – 2.59mmol/L,
for amazons 1.87 – 2.42mmol/L,
for macaws 1.70 – 2.47 mmol/L,
for cockatoos 2.2-2.7 mg/dl, and
for canaries of 1.27 – 3.34 mmol/L.2
However when considering normal blood calcium levels, one should first consider what is really normal for that species. There is an argument that the normal blood values of a given species are those extracted from free flying individuals, living in their natural environment, given the freedom to feed and exercise as nature alone dictates.
However could we really expect our caged feathered friends blood to match up to their wild cousins.
So many caged birds are fed such a poor diet (often for a period of decades), that ‘so called’ normal values may well include values which were in fact from birds on a long term deficient diet.
The consequence of this is that one includes into a normal range, the values for birds which are actually far from normal.
More over these so called normal ranges do not take account of normal physiological elevations which occur immediately prior to and during egg laying as well as other naturally induced fluctuations.
In the blood there are three different forms of calcium:
– Ionised calcium which is the physiologically active form.
– A further one-third of plasma calcium is protein-bound (mainly to albumin) and
– The residual small volume is chelated calcium bound to phosphate or citrate.
The total blood calcium concentration needs to be interpreted together with the plasma protein level, (especially albumin), as a low blood albumin level (hypoalbuminaenia) reduces the protein-bound calcium fraction and results in an 2 over-all decreased calcium concentration although the biological active ionised calcium fraction (which is what the metabolism relies on) is not effected.
Over 95% of eggshell is composed of calcium carbonate.3,4 When considering blood calcium levels it is important to remember that lipaemia (fat in the blood) can falsely elevate blood calcium levels. Glucocorticoid therapy will decrease total calcium concentration by increasing urinary excretion and decreasing intestinal absorption of calcium. Additionally, increased calcium concentrations have been reported with dietary excesses of vitamin D3, osteolytic bone tumours and dehydration. ‘
Calcium is absorbed in the upper small intestine. Calcium enters the mucosal membranes (lining of the gut wall) via a diffusion-type process and is then secreted into the blood with help of an active transport system involving a calcium-binding protein. This system is regulated by the active metabolite of vitamin D3 (in response to low plasma calcium levels). There is also some absorption in the lower small intestine through passive diffusion.
The absorption is increased by high-protein diets and acidification of the intestines while components such as phytate (in cereal grains), oxalates (in spinach, rhubarb and related vegetation) and phosphates (high in pulses and meat) decrease absorption of calcium due to formation of complexes.
Insoluble calcium salts are formed in the presence of high concentrations of free fatty acids (often found in very high-fat diets – e.g. sunflower or peanut based diets) or because of impairment of fat digestion. Additionally, calcium is ‘recycled’ in the avian kidney. More than 98% of initially excreted calcium is reabsorbed back into the blood stream from the urine. This reabsorptive process operates close to maximum efficiency.
Calcium metabolism is predominantly regulated by two hormones and one vitamin that closely interact with each other if there are changes in the blood calcium level. The paired parathyroid glands (one or two pairs depending on species varieties) secrete parathyroid hormone in response to a lowered blood calcium level. Levels of parathyroid hormone in the blood are normally extremely low.
However parathyroid hormone is elevated during the process of eggshell calcification. Parathyroid hormone initiates an increase of the tubular reabsorption in the kidneys, which leads to decreased calcium excretion, whilst at the same time vitamin D3 aids calcium reabsorption from bone as well as increased calcium absorption from the gut.
So blood calcium level is elevated by increasing levels of parathyroid hormone and vitamin D3.
Not only does parathyroid hormone increase the blood calcium level but it also influences the secretion of phosphate from the kidney, thereby decreasing the blood phosphate level. This is important as the metabolism of calcium:phosphorus:and Vitamin D3 are all inextricably linked. Although one may refer to a bird as being calcium deficient, in reality it is an imbalance of Ca:P:D3.
Prior to egg laying additional bone is laid down in the middle of the upper leg and wing bones (medullary bone) forming a reserve to be called upon at this time of exceptional calcium requirement. During the egg-lying cycle, parathyroid hormone controls the reabsorption of this medullary bone to meet the raised calcium requirements of eggshell production.
Furthermore, parathyroid and prolactin hormones enhance the synthesis of the key calcium-regulating hormone 1,25 dihydrocholecalciferol (an activated form of vitamin D3).
It is also considered that 3 female hormones (oestrogens) which rise prior to egg laying, cause a fall in blood calcium which also triggers the production of more 1,25 dihydrocholecalciferol. The increase in parathyroid hormone level leads to an increased blood calcium level in less then ten minutes.
Vitamin D3 is converted into the active form 1,25 dihydrocholecalciferol in three steps, which take place in the skin under the influence of sunlight or ultraviolet light, the liver and the kidneys.
Apart from increasing blood calcium and decreasing blood phosphorous levels the main function of vitamin D3 is to increase intestinal absorption of calcium and phosphorous. This increase in intestinal calcium absorption, commences after sexual maturity and peaks during eggshell. The activity of this enzyme is oestrogen (female hormone) dependent.
As in all homeostatic mechanisms in the body, where there is one key to turn on a process, the body also requires one to turn it off. Calcitonin is a hormone, which is secreted by ultimobranchial glands, which are located behind the parathyroid glands. An increase in blood calcium level results in an increase secretion of calcitonin, which in turn reduces calcium reaborption from bone.
As mentioned above at the centre of calcium metabolism is the so-called calcium to phosphorous ratio, which is based on the amount of phosphorous available to the bird as opposed to the total phosphorous content of the diet.
During bone growth, most species require ratios of approximately 1.5:1 to 2:1 in order to maintain normal serum calcium values. Ratios of 2:1 ratios are required to achieve maximum bone density.
Reproductively active psittacine birds should be offered a diet with a calcium to phosphorous ratio between 1:1 and 2:1 in order to prevent excessive calcium mobilisation from the bones. Field experience with formulated diets suggests that approximately 1% calcium in dietary dry matter is sufficient for reproduction in psittacine birds.
Indeed if there is more than 1% dietary calcium, eggshells maybe excessively thick, which may lead to reduced weight (water) loss during incubation and hatching difficulties.
Different reports of the widest tolerable ratio vary from between 0.5:1 and 2.5:1 to between 0.8:1 and 3.0:1, with ratios over 3.3:1 producing rickets and leg abnormalities. The more unbalanced dietary Ca:P levels are, the more important becomes the correct vitamin D3 levels.8
Most available commercial seeds are extremely calcium deficient often with totally unsuitable calcium to phosphorous ratio:
Sweet corn = 1:32
Pumpkin = 1:27
Muscle meat has a ratio of 1:20
Milo = 1:14
Oats = 1:8
Safflower = 1:8
Peanut = 1:7
Sunflower seed = 1:6
Millet = 1:6
Pine nuts = 1:4
It is therefore evident that carnivorous birds fed an all-meat diet (rather than a mixed meat and bone, (i.e. whole carcass diet) are particularly at risk, but so also are psittacines fed on seed based diets with poor Ca:P ratios.9 4
Birds fed on unbalanced diets typically suffer from malnutrition, leading to diseases such as mouth or respiratory infections, central nervous signs (e.g. seizures, fits or weakness).
As pointed out above, diets that contain predominantly seeds are deficient in calcium. Strangely many pet parrot owners when questioned in the surgery as to their birds diet, proudly exclaim they are on a ‘premium’ diet. This typically comprises sunflower seeds with added dried fruit, chilli peppers etc..
However when you question the same owner as to what the bird actually eats, (rather than what it is offered), the response is usually ‘just the sunflower seed’. On occasions the owner qualifies the diet eaten by stating that the bird also eats lost of fruit and vegetable.
However when one considers that seed is at least 90% dry matter, whilst fruit and vegetable is 85 – 90% water, the bird would actually need to eat 6 -9 times the volume of fruit or vegetable as seed for them to consume the same amount of each food type in comparable dry mater terms.
The calcium content of some seed fed to psittacine birds has been analysed as follows:
Sweet corn 0.2 mg/dl dry matter,
Proso millet 0.1 mg/dl dry matter
Oat groats 0.8 mg/dl dry matter
Peanuts 0.6 mg/dl dry matter
Pumpkin/squash 0.5 mg/dl dry matter
Safflower 0.8 mg/dl dry matter
Sunflower 1.2 mg/dl dry matter
Wheat 0.6 mg/dl dry matter.6
Fruits and most vegetables also have a low calcium content. Most seed diets contain excessive levels of fat and may be deficient in vitamins A, D3, E, B12 and K1, plus the B vitamins (riboflavin, pantothenic acid, niacin, biotin, choline), and the minerals and trace elements (iodine, iron, copper, manganese, selenium, sodium, calcium, zinc) and some essential amino acids such as lysine and methionine.
Studies about the composition of seeds with and without hull show that the calcium content is halved when the hulls are removed.
In feeding a seed diet one has to consider that most seeds found in mixtures sold for caged psittacines birds are foreign to the experience of their free-living relatives.
Additionally, nutrient intake from selfselecting diets based on mixtures of seeds are highly unpredictable, possibly limiting an already deficient diet even further. As mentioned above, high-fat seeds such as sunflower and safflower may interfere with calcium uptake from the intestine.
Alternatively, excess levels of calcium can precipitate deficiencies of magnesium, iron, iodine, zinc and manganese if these are only marginally supplied.
Calcium supplementation can be offered in form of calcium syrup or powder.
Any supplement added as a coating to the outside of seed is largely lost when hulls are removed and powdered supplements commonly separate from the food that is eaten if the food is not moistened. Food with naturally high levels of calcium are bone, cheese or yoghurt.
There is a difference between grit and crushed shells. Grit is composed of minute stones and commonly contains silicate and sandstone. Crushed shell is almost entirely composed of limestone (calcium carbonate) and is readily digested by acids in the proventriculus.
Therefore, crushed shells provide a source of calcium, whilst grits main effect is in aiding the mechanical breakdown of dietary plant material. Whilst previously keepers have considered that psittacine birds should be 5 given additional grit on a regular basis, we now know that grit taken up as a youngster will last birds for years and no further grit is required.
During the reproductive cycle there are physiological phenomena, which are related to changes in calcium metabolism.
A few days before ovulating, calcium blood levels can increase up to 7.5mmol/L in psittacine birds (oestrogen-induced hypercalcaemia).12 This increase in blood calcium, with deposition in the medulla of thigh and upper wing bones (femur and humerus) will occur even when birds are on a calcium deficient diet.
The rise in calcium is caused by an increase in the protein-bound calcium, secondary to the oestrogen-induced transport of yolk proteins to the ovary as calcium complexes. The concentration of ionised calcium (the active calcium actually used by metabolism) remains constant.
The calcium is derived from an increased efficiency of intestinal absorption. Reproductively active psittacines have a selective preference for foods rich in calcium.
Their consumption of calcium increases daily during the pre-laying and during the early stages of shell calcification, so long of course as they can gain access to additional dietary calcium. Furthermore, renal calcium excretion decreases during shell formation. 12,13 Vitamin D3 synthesis in the kidney and liver is stimulated by oestrogens, prolactin and parathyroid hormone.13
Although oestrogens and testosterone induce formation of medullary bone matrix regardless of the calcium intake or the vitamin D3 status of the bird, it has been shown that the bone only becomes fully mineralised when both vitamin D3 and the sex steroids are present.
This medullary bone fills the cavity of long bones. The skeleton may increase in weight by up to 25% during the prelaying period. These bone changes are readily evident on radiography at this stage of the reproductive cycle. The calcium is later reabsorbed by osteolytic activity and deposited in the eggshell as calcium carbonate, while the phosphorous is excreted from the body.
Nearly 10% or more of total body calcium is needed for the deposition of each eggshell.1 Approximately 30-40% of eggshell calcium is derived from medullary bone, if calcium concentration in the food is below 2%. Conversely if the dietary calcium concentration is 3.6% the entire calcium demands can be provided from intestinal absorption14, rather than medullary bone reabsorption.
As much of the eggshell is formed during the night, when generally no calcium is consumed and when the calcium content of the digestive tract is gradually decreasing, medullary bone may be considered as the primary source of shell calcium during the latter hours of darkness.
It doesn’t take a rocket scientists to calculate the possible effects of repeated egg laying by a hen which is on a deficient diet. In time either her skeleton will become depleted or she will lay calcium deficient eggs (leading to deficient chicks at hatching) or both.
In contrast to the physiological phenomena described above there are several pathological conditions which influence or cause hypercalcaemia (excess blood calcium) or hypocalcaemia (deficiency of blood calcium).
In non-laying female and male budgerigars, a phenomenon can occur which resembles physiologic bone marrow ossification (polyostotic hyperostosis), but involves mainly humerus and femur in budgerigars, whilst physiologically it is predominantly the femur and tibiotarsus which are normally affected.
The birds can show apathy, inco-ordination, increased thirst and urination, abdominal distension, 6 weakness, paresis or paralysis of one or both legs.
In some studies the phenomena is seen in association with tumours of the ovary, testicle, which supports the theory that the condition may be a pathological exacerbation of a normal physiologic phenomena triggered by excessive blood oestrogen levels (as are often produced by gonadal tumours).
However, other reports describe that affected hens have normal ovaries and no evidence of hormone-secreting tumours or other hormone related disease. Impaired liver function (often linked to a high fat diet – e.g. sunflower, peanut or millet – causing a fatty liver condition) has been suggested as a possible reason as the liver is responsible for removing oestrogens from the blood.15
Many problems that arise in hatching psittacine chicks can be related to calcium imbalance. Female birds, which are deficient in vitamin D3 or calcium, can lay softshelled or thin-shelled eggs that are more prone to cracking during incubation, or may suffer delay in actually producing the egg due to reduced oviduct muscle activity. If the embryo might not have received enough vitamin D3 in the egg for proper mobilization of eggshell calcium, there is a high risk of embryonic death.16 Malnutrition during the neonatal rearing period is a particular risk. Whilst many adult birds will cope with a marginally deficient diet, a young fast growing chick will certainly be effected. Orthopaedic problems such as leg deformities and toe malposition are most commonly caused by nutritional deficiencies during the rearing period (especially of vitamin D3 and calcium). Indeed these are the problems which we most commonly experience in practice.
Secondary nutritional hyperparathyroidism occurs as a result of a calcium-deficient diet has been reported as a common problem in birds. In this condition there is only a limited absorption of calcium from the diet, leading to an increase in parathyroid gland size as the parathyroid attempts to maintain normal blood calcium levels.
High levels of phosphorous or low levels of vitamin D3 in the diet exacerbate the condition (as stated before it is the Ca:P:Vit D3 ratio which is all important, rather than the calcium alone).
Clinical signs include hypocalcaemia (low blood calcium), frequently leading to seizures, weakness, muscle cramps, increased thirst, loss of appetite, regurgitation, decreased egg production, production of soft-shelled eggs, egg binding and fragile (brittle) bones leading to pathologic fractures.
Secondary hyperparathyroidism may also occur due to kidney disease. In severe long term kidney disease, the last step in converting vitamin D3 into the active metabolite is restricted. As a result the intestinal absorption of calcium is reduced.
The condition should be treated with calcium and vitamin D3 supplementation by mouth as well as calcium direct into the blood stream, (depending of the severity of the signs). Furthermore, the birds should be weaned over to a balanced, quality formulated diet.
Metabolic bone disease in birds occurs as two forms: rickets which is found in growing animals whilst osteomalacia (osteodystrophy) occurs in mature birds.
Rickets is characterised by an inadequate dietary intake of calcium, phosphorous and vitamin D3 or improper calcium to phosphorous ratio, which results in an enlargement of the parathyroid glands and nutritional secondary hyperparathyroidism.
The result is that the bones which grow by way of cartilagenous extensions of the long bones, prior to mineralisation of the cartilage, fail to mineralise. The cartilagenous ‘growth plate’ becomes widened and a deviation or distortion may arise, most commonly affecting the bones which bare pressure or weight. The 7 disease is most commonly seen in hand-reared psittacine birds.
Bone deformities develop throughout the skeleton, particularly in the distal (bottom of the) tibiotarus, the femoral head and the ribs. Effected nestlings are often found in a characteristic sitting position with spread legs.
The skeletal bones and beak become soft and pliable. The deformation of the ribs can lead to breathing distress demonstrated as an increased rate or effort in breathing. Birds that are effected by osteomalacia show enlarged parathyroid glands and hence have an increased osteoclastic activity (ie the bird is breaking down more of its own bone in an attempt to maintain an adequate blood calcium level), this can result in complete demineralisation of medullary bone, then progressing to affect cortical bone in severe cases. In birds the replacement of the resorbed bone by fibrous tissue (osteodystrophia fibrosa) is not common. As bones become more demineralised, spontaneous pathological fractures occur. These fractures effect demineralised bones with thin cortices (the outer wall of the bone) and are termed ‘greenstick fractures’.
The terminology is earnt as these bones are soft and bendable, flexing and resetting in a manner similar to a green twig on a tree. Bones most commonly affected are the ribs, vertebrae, tibiotarsus, tarsometatarsus and femur.
In raptors and particularly in African grey parrots in the age range two to five years, a so-called hypocalcaemia syndrome has been described.18,19,20 Clinical signs are incoordination, imbalance (such as falling off the perch – often interpreted as weakness), convulsions and seizures. Indeed this is the commonest cause of central nervous disease in African grey parrots.
The bird is often hypersensitive to noise or movement. Notable is the fact that in African grey parrots there is no demineralisation of the skeleton to maintain normal calcium levels.
At post mortem, the parathyroid glands of the affected parrots appear normal, in other words the AGP body appears to make less effort to maintain its normal blood calcium value. Treatment of this condition comprises the administration of parenteral calcium gluconate applications and calcium and vitamin D3 dietary supplementation.
Affected birds typically respond within minutes of treatment. It has been postulated that a virus infection may effect the parathyroid glands also that oxy or chlor-tetracycline (antibiotic) medication may precipitate clinical disease by chelating (binding and inactivating) some of the normally available blood calcium.
Research has shown that African grey parrots have significantly lower calcium, albumin and total protein concentrations compared to Amazon parrots, which may account for why they are the species most commonly affected by this condition.
Serum calcium levels are below 1.5 mmol/L and can even be as low as 0.6 mmo/L.21 There are theories postulated that these birds are not able to mobilise body bone calcium stores (which indeed would be the case if insufficient parathyroid hormone was being produced).
Deficiency in parathyroid hormone is suggested as the commonest cause of low blood calcium levels. Vitamin A deficiency may also play a role as a deficiency of vitamin A inhibits osteoclast activity and hence prevents mobilisation of calcium from bone.10 The condition has also been described in Amazon parrots and conures.22
Erythremic myelosis in conures (Haemorrhagic conure syndrome) has been described in Blue-crowned conures, Peach-fronted conures, Orange-fronted conures and Patagonian conures.23 A viral aetiology (retrovirus) has been suggested, but has not yet been proven. Calcium deficiencies together with dietary lack of vitamin K and other nutrients are believed to trigger the disease by possibly altering normal clotting mechanisms.
Nose bleeds, breathing difficulties, severe weakness, intermittent increase in urination and diarrhoea and occasionally ataxia are possible clinical 8 signs. Blood biochemistry shows decreased total protein and blood calcium deficiency.
At post mortem, multiple lung haemorrhage, development of pseudocysts in the pectoral muscles and pericarditis are seen. All therapeutic regimes (injectable vitamin K, vitamin D3, calcium and antibiotics) have been unsuccessful. Administration of calcium can prolong a bird’s life and may stabilise the patient’s condition.
Hypervitaminosis D3 (>4-10 million IU/kg diet or 3% of dietary calcium) causes abnormal calcification of the kidney tubules and arteries as well as calcium deposition in and around the internal organs affecting mainly the liver, proventriculus and ventriculus, intestines, heart and blood vessels.
It is possible that additional effects of excessive blood calcium levels may be the deposit of uric acid in the kidney, visceral gout, renal gout and decreased food intake.
Cockatiels seem to be particularly sensitive to high calcium or high calcium and vitamin D3 levels in the diet. Young macaws may also be more susceptible to hypervitaminosis D3.24
Signs of vitamin D3 deficiency parallel those of calcium deficiency, as in effect each causes failure of the same calcium metabolism system. Adult females may show thin-shelled or soft-shelled eggs, decreased egg production and poor hatchability. Seizuring or leg weakness may occur due to pathologic bone fractures.
In neonates fractures and bent bones are particularly common. Low levels of calcium in the diet, particularly if associated with high levels of phosphorous (as found in meat, pulses, brazil and peanuts, pumpkin seeds, safflower, sunflower) will precipitate the clinical signs associated with hypovitaminosis D3. Vitamin D3 deficiency may be due to low dietary levels, malabsorption, failure of the processes of synthesis either in liver or kidneys or under conditions of inadequate exposure to ultraviolet light.
Ultra violet light is provided with full spectrum lighting or by natural unfiltered sun light.
Once light has passed through a window any beneficial UV light will have been removed. Evidently parrots (including African greys) were designed to live in a natural out door situation and not enclosed away from the sun light.
Gout is the deposition of uric acid crystals on body organs (visceral gout), in joints (articular gout) or in the ureters (renal constipation).
High dietary levels of protein, calcium, hypervitaminosis D3, poor kidney response, dehydration, cold weather and other stress factors work in concert to interfere with the kidney’s ability to adequately excrete uric acid.
In birds with renal disorder or gout, calcium, phosphorous, magnesium, sodium and vitamin D3 levels should be reduced to avoid kidney mineralisation.
Deficiencies of minerals such as calcium, zinc, selenium, manganese and magnesium may be associated with brittle, frayed feathers and itchy skin. There may be alterations in colour or discolouration of feathers. The plumage can appear dull with a lack of sheen. Symmetric feather loss and moulting disorders can occur.25,26
Another condition that occurs in fast growing larger waterfowl is the rotation of the distal wing tip (beyond the carpus – i.e. wrist) due to heavy, blood-filled, developing flight feathers being supported by non-rigid, inadequately mineralised, growing bones.
The result is that the primary flight feathers stick out when the wing is folded at rest to the body (giving rise to the colloquial term angle wing or aeroplane wing). The cause is multi-factorial.
Contributing factors may be of genetic origin or related to incubation and hatching problems or malnutrition. Rapid growth due to excessive 9 levels of protein and energy and low levels of calcium, calcium and phosphorous imbalance, and hypovitaminosis D may all inter react.27. The condition has also been described in some psittacine birds such as budgerigars, macaws, and conures 26
Perosis: A primary or secondary lack of manganese, caused by an excess of calcium, (which may bind manganese), and a deficiency of choline in the diet are considered responsible for a disease called perosis.
Affected birds show thickened hocks together with bending deformities of the tibiotarsus and tarsometatarsus, resulting in the luxation of the achilles tendon and rotation of the inter-tarsal joint. This condition is seen in galliformes, in waterfowl and in ratites but there are no reports about psittacine birds suffering by perosis so far.
Practical Consequences
Whenever possible allow parrots access to unfiltered day light (at least 45 minutes each day), or alternatively provide UV light by means of full spectrum bulbs. Such bulbs should be within 0.5m of the bird’s favourite perch, must be kept clean and should be changed every 6 months.
A correct dietary calcium to phosphorus ration (1.5:1 to 2:1) is essential. Foods high in phosphorus should be minimised (i.e. meat, pulses, brazil and peanuts, pumpkin seeds, safflower, sunflower). Foods with a correct Ca:P ratio should be encouraged (blackberries, citrus fruits).
Whilst there may be some controversy about allowing parrots to eat (well cooked) chicken bones, it certainly is beneficial from a calcium metabolism point of view.
The author would suggest that parrots be offered one well cooked chicken drum stick with all meat removed, once a month. Such bones should be hung up to prevent them from swallowing the whole bone, but so that they can bite the soft parts of the bone from around the joint.
Unless a high quality pelleted diet is fed, it is almost certain that you will need to provide a Ca + vitamin D3 supplement, in a form which is actually consumed and is biologically active.
The provision of adequate levels of Vitamin A is important not only for calcium metabolism but also for the prevention of respiratory and mouth infections.
Vitamin A is found at high levels in the following foods ( in the level of decreasing concentration: apricot, tomato, peach, pumpkin, plum, carrot, red peppers, sweet corn, citrus fruit, green peppers).
Food supplements can be excellent if they are actually consumed at the manufacturers recommended level. Keepers should never use more than one supplement, as over supplementation can certainly cause significant disease (see vitamin D3 toxicosis above).
Years ago a survey was conducted which demonstrated that 75% of all sick parrots were suffering from a nutritional deficiency which was in part responsible for their disease condition, sadly little has changed.
As eloquently described by Rosemary Low in Parrots Issue 44, a diet should be varied and balanced. This may be achieved by feeding some seeds, together with sprouted seeds and fresh fruit and vegetables. Even the latter diet does require the addition of a suitable vitamin and mineral supplement.
Such diets need to be prepared fresh daily with particular attention to hygiene. This is certainly the authors preferred method for parrot breeders or enthusiasts with numbers of parrots who are able to spend a considerable amount of time about their birds on a daily basis.
How 10 ever we are great believers in not asking a keeper to do something which for them is not practical as inevitably it will not be achieved. Breeders not only have the time to prepare a mixed soft food diet, but also they have many mouths to feed.
The cost factor alone is the reason why few parrot breeders feed a pelleted diet. However for the average pet parrot owner, making a fresh wet diet daily is equally in practical. The cost of feeding a pelleted diet for a single bird is a small price to pay for a healthy bird.
There is no reason why a pelleted diet should not be supplemented with fruit or vegetable, so long as the fruit or vegetable is in itself nutritionally balanced.
REFERENCES:
1. Canny CJ and Pollock CG (2000): Avian endocrinology. In: Manual of avian medicine, Olsen GH
and Orosz SE (eds), Mosby, Inc., St. Louis, Missouri, 313-358.
2. Scope A (1999): Diagnose- Klinisch-chemische Untersuchungen. In: Kompendium der
Ziervögelkrankheiten, Kaleta EF and Krautwald-Junghanns ME (eds), Schlütersche GmbH and Co.
KG, Hannover, 92-96.
3. Hochleithner Mb (1991): Möglichkeiten der chemischen Blutuntersuchung beim Wild- und
Ziervogel (Possible approaches to haematochemical investigations in wild and pet birds).
Verhandlungsbericht des 33. Internationalen Symposiums über die Erkrankungen der Zoo- und
Wildtiere, 153-160.
4. Roudybush TE, Grau CR (1991): Calcium requirements for egg laying in cockatiels. Am Fed Avic
Watchbird, 18(1), 10-13.
5. Goldstein DL and Skadhauge E (2000): Renal and extrarenal regulation of body fluid compostion.
In: Whittow (ed), Sturkie’s Avian Physiology, Academic Press, Florida, 265-298.
6. Ullrey DE, Allen ME and Baer DJ (1991): Formulated diets versus seed mixtures for psittacines.
Journal of Nutrition, 121(11 Suppl), 193-205.
7. Brue RN (1994): Nutrition. In Richie BW, Harrison GJ, Harrison LR (eds): Avian medicine:
Principles and applications, Lake Worth, Fla, Wingers, 63-95.
8. Roudybush T (1986): Growth, signs of deficiency and weanig in cockatiels fed deficient diets. Proc
Assoc Avian Vet, 330-340.
9. Brue RN (1980): Nutritional deficiencies of seed diets. Nutritional lecture series handout. Kaytee
Products.
10. Rosskopf WJ, Woerpel RW and Lane R (1985): The hypocalcemic syndrome in African greys: An
up-dated clinical viewpoint with current recommendations for treatment. Proc Assoc Avian Vet,
129-131.
11. Johnson AL (1986): Reproduction in the female and reproduction in the male. In Sturckie PK, (ed):
Avian physiology, New York, 1986, Springer-Verlag, 403-451.
12. Elaroussi MA (1993): Adaption of the kidney during reproduction, Poultry Sci, 72(8), 1548-1556.
13. Maierl J, König HE and Liebich HG (2001): Skelett und Skelettmuskultur. In: Anatomie und
Propädeutik des Geflügels, König HE and Liebich HG (eds), SchattauerVerlagsgesellschaft mbH,
Stuttgart, 9-16.
14. Johnson AL (2000): Reproduction in the femal. In: Whittow (ed), Sturkie’s Avian Physiology,
Academic Press, Florida, 569-596.
15. Joyner KL (1994): Theriogenology. In Richie BW, Harrison GJ, Harrison LR (eds): Avian medicine:
Principles and applications, Lake Worth, Fla, Wingers, 748-786.
16. Olsen GH (2000): Embryologic considerations. In: Manual of avian medicine, Olsen GH and Orosz
SE (eds), Mosby, Inc., St. Louis, Missouri, 189-212.
17. Orosz SE (2000): Diagnostic work-up plan. In: Manual of avian medicine, Olsen GH and Orosz SE
(eds), Mosby, Inc., St. Louis, Missouri, 1-16.
18. Hochleithner M (1989): Convulsions in African grey parrots (Psittacus erythacus) in connection
with hypocalcaemia. Five selected cases. Proc Europ Symp Avian Med and Surg. 44-52.
19. Hochleithner M (1989): Convulsions in African grey parrots. Proc Assoc Avian Vet, 78-81.
20. McDonald JL (1988): Hypocalcemic seizures in African grey parrots. Can Vet J, 29(11), 928-930.
21. Lumeij JT (1990): Relation of plasma calcium to total protein and albaumin in African grey
(Psittacus erythcus) and Amazons (Amazona spp.) parrots. Avian Pathol, 19, 661-667.
22. Rosskopf WJ, Woerpel RW and Lane R (1985): The hypocalcemia syndrome in African greys: An
up-dated report. Avian/Exotic Prac, 2(1), 22-25.
23. Rosskopf WJ, Woerpel RW and Lane R (1984): Erythremic myelosis in conures, the
‘Haemorrhagic conure syndrome’- a preliminary report. Proc Intl Conf Avian Med, 213-228.
24. Takeshita K (1985): Hypervitaminosis D in baby macaws. Proceed Assoc Avian Vet, 341-345.
25. Krautwald-Junghanns ME (1999): Nichtinfektiöse Erkrankungen von Gefieder und Haut. In:
Kompendium der Ziervögelkrankheiten, Kaleta EF and Krautwald-Junghanns ME (eds),
Schlütersche GmbH and Co. KG, Hanover, 126-139.
26. Coles BH, Krautwald-Junghanns ME (1998): Self-Assessment picture tests in veterinary medicine,
avian medicine, Mosby, Inc, St. Louis, Missouri, 148-149.
27. Fowler ME (1978): Miscellaneous water birds. In: Fowler ME (ed): Zoo and Wild Animal Medicine.
Philadelphia, WB Saunders Co, 211-217.
Conversion of a Parrot (“Seed Junkie”) from Seed to a Pelleted Diet
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