| Color Key | |
| Important key words or phrases. | |
| Important concepts or main ideas. | |
1. Learning Objectives and Review
1.1. Learning Objectives
- Know the specific deficiencies/excesses present in an all seed diet for a psittacine bird
- Be able to make recommendations for a general balanced psittacine diet
- Understand the consequences of Vitamin A deficiency in both pet birds and poultry and its clinical implications
- Be able to recognize the clinical presentation of Vitamin E/Selenium deficiency in pet birds and poultry
- Understand the husbandry practices that might lead to a calcium and vitamin D imbalance in a variety of bird species
- Understand the husbandry practices that might lead to obesity in a pet bird and its potential negative health impacts
1.2. Review
Review the Exotic and Wild Animal Nutrition notes presented in the 1st Year Feeds and Feeding course for basic information on avian nutrition.
 |
2. Introduction
In our attempt to keep birds in captivity, clearly we will not be able to provide them with the identical diet which the birds naturally find in the wild. Herein lies the problem: even with the best intentions and significant scientific investigation (not yet performed with many birds), we still manage to miss a few critical points. This inherent pitfall is demonstrated by the errors of formulation seen even in the well researched field of dog and cat nutrition (e.g. taurine).
With birds, there is admittedly very little information available. Most nutritional diseases are identified retrospectively. In addition, many problems arise through the ignorance of the pet owner resulting from the unfortunate lack of information provided to them when they purchase their pet.
The most common mistake is seen with the parakeet owner who is led to believe that the bird can survive on commerical parakeet seed for its entire life. This has come to pass because some parakeets do live to a "ripe old age" consuming only commercial parakeet seed. This phenomenon is indisputable. However we know seeds alone do not provide a complete and balanced diet as we have already discussed and in practice we see some recurring problems.
In poultry, barring unusual circumstances where the feed has been improperly formulated, stored, or administered, commercial rations practically eliminate the occurrence of nutritional disease in poultry. The following nutritional diseases are most likely to occur in backyard flocks where the owners are feeding on an ad hoc basis.
3. Review of Basic Pet Bird Nutrition
3.1. Seed based diets
"Seed only" diets are still the most common diets fed to pet birds. Many commercially available seed mixtures mislead the client with claims of "fortified", "complete", etc. Seed diets are deficient in: calcium, vitamin A, iodine, and some essential amino acids. Two classes of seeds are seen in these mixtures: starch seeds and fat or oil seeds. Starch seeds provide carbohydrates for energy but contain less protein. Fat or oil seeds contain lipids as energy and provide more protein.
 |
3.2. Pelleted/formulated diets
Very recently, in the last 5-10 years, there has been an explosion of pelleted, extruded, or completely formulated diets. There is as yet no real standard by which to measure their quality. However, research is ongoing by these feed companies in order to capture the bird food market.
The only major problems identified with these formulated diets so far are those of acceptability or palatability and the ease with which the birds can be converted to the new " foreign" food. Feeding a pelleted diet is the surest method of delivering an adequate diet to a pet bird.
3.3. Supplementary foods
Many birds are fed seed and/or pelleted diets, but are supplemented with "table food" or fresh foodstuffs. In general this is a good practice because it helps to balance what might otherwise be an inadequate diet, and it provides variety and enrichment for the bird. Fresh fruits and vegetables, meats, dairy products, pasta and other low fat "human foods" are healthy and well accepted by many birds. A supplementary calcium source can be provided by dairy products, cuttlebone, oyster shell, alfalfa sprouts, or a human calcium supplement. Many different prepared vitamin and mineral supplements are available for birds.
 |
 |
The optimal diet should include a combination of all: seeds, pellets, and fresh foods.
3.4. Dietary no-nos
If left to their own devices or through inappropriate encouragement by their owners, birds, like the rest of us, will develop a taste for certain things which are not good for them. Examples include the old favorite chocolate and other sweets, alcohol, fatty foods such as toast with butter, pizza only diet, and of course the standard peanuts and sunflower only diet. In addition surprisingly, excessive amounts of egg can produce hypercholesterolemia, arteriosclerosis, and stroke just as it does in humans.
There is still some controversy over the feeding of grit or gravel to parakeets and other psittacine birds. Since psittacines hull their seeds before eating them, they appear not to require grit for grinding their food in the gizzard unlike the gallinaceous birds which swallow their food whole. At most it is felt that they require one or two grains per month! Consequently, grit is not routinely recommended for any psittacine birds. Owners should be told to avoid grit, especially products containing charcoal as a digestive aid. Excessive consumption of grit can result in life threatening gastrointestinal impaction.
4. Nutritional Diseases
| Common Nutritional Diseases of Poultry | Common Nutritional Diseases of Pet Birds |
| Vitamin A deficiency | Vitamin A deficiency |
| Vitamin D3 deficiency | Calcium imbalance (deficiency) |
| Vitamin E Deficiency | Vitamin E/Selenium deficiency |
| Perosis | Iodine deficiency |
| Curled toe paralysis | Obesity |
4.1. Vitamin A deficiency
4.1.1. Pet birds
Hypovitaminosis A is undoubtedly the most common nutritional deficiency seen in pet birds. It is usually the result of an all or mostly seed diet without fresh fruits and vegetables. As stated previously, seeds are nearly devoid of Vitamin A.
| Foods high in vitamin A |
| Broccoli |
| Yellow corn |
| Carrots |
| Cantaloupe |
| Collared Greens |
| Peaches |
For more suggested foods see Table of Nutrient Content of Some Fruits and Vegetables in the Appendix.
4.1.1.1. Clinical signs
The profound clinical manifestation of Vitamin A deficiency is (as in other animals), squamous metaplasia of epithelium. Changes are most often seen in the upper respiratory tract, but can also be encountered in the rest of the respiratory tract, the GI tract, urinary tract, etc. Squamous metaplasia of these highly glandular tissues results in keratin buildup and obstruction of salivary glands, nasal sinuses, the trachea, kidney tubules, etc. This may result in sterile or infected abscess formation, and decreased clearance of normal bacterial flora and increased susceptibility to disease. Vitamin A deficiency also may affect feather quality. Vitamin A toxicity is rare but may occur with over-supplementation.
4.1.1.2. Diagnosis
Diagnosis of vitamin A deficiency is usually made based on history of a deficient diet and clinical signs such as the blunted or absent choanal papillae, keratin abscess, etc. Biopsies are rarely done for purely diagnostic purposes, however should be performed in conjunction with surgical removal or curettage of obstructive lesions.
 |
 Periorbital swelling in an African Grey
parrot
|
4.1.1.3. Treatment and Prevention
Treatment for vitamin A deficiency includes supplementation of Vitamin A by injection and orally by correcting the diet and adding a vitamin supplement. The secondary manifestations of the disease also have to be dealt with often requiring treatment of opportunistic infection, abscesses, etc. as well as surgical removal of sterile keratin masses which are interfering with normal function.
Prevention through appropriate dietary management is the key to maintaining good health and avoiding this disease.
4.1.2. Poultry
Deficiencies in vitamin A are most likely to occur in chicks under 7 weeks of age. Since a large amount of vitamin A is stored in the egg yolk, this supplies the newly hatched chick with adequate amounts for the first few weeks of life. Laying hens deficient in vitamin A will often produce chicks that show vitamin A deficiency in addition to signs of deficiency in the hen. In certain instances laying hens experience vitamin A deficiency because of increased demands for nutrient associated with egg production.
 |
4.1.2.1. Clinical signs
- Pale comb and wattles
- Reddened and swollen conjunctiva with watery or scaly ocular exudate.
- Swollen or exudative infra-orbital sinuses.
- Nasal exudate may be present suggesting an upper respiratory tract infection.
- Reduced rate of growth in young birds
- The normal yellow color of the shanks and feet may be pale or absent.
- Laying hens show decreased egg production when deficiency has been present for several months.
4.1.2.2. Diagnosis
Diagnosis is made based on Microscopic lesions associated with vitamin A deficiency consisting of hyperkeratosis of esophageal mucosa in addition to squamous metaplasia of tracheal and esophageal glands. Squamous metaplasia is also present in nasal turbinate epithelium. A concurrent infection of capillariasis may exacerbate vitamin A deficiency since these worms utilized host stores of vitamin A. A careful analysis of the diet is the best way to make the diagnosis of vitamin A deficiency.
Differential diagnoses: infectious coryza of chickens, infectious sinusitis of turkeys and wet pox
4.2. Vitamin D3, Calcium and Phosphorous Imbalances
4.2.1. Pet birds
Absolute dietary deficiency of calcium is very common in pet birds. All seed diets contain very little calcium, and contain quite a bit of phosphorus. The calcium to phosphorus ratio can range from 1:7 to 1:37.
This disease is most acute and life threatening when seen as 'Hypocalcemia syndrome in African Grey parrots'. This specific syndrome will be discussed later under metabolic diseases.
4.2.1.1. Clinical signs
Symptoms of calcium deficiency in most psittacines includes rickets in young growing birds, osteopenia, pathologic fractures, generalized weakness, tetany, unthriftiness, and egg-binding.
4.2.1.2. Diagnosis
The diagnosis is based on clinical signs, dietary history, radiographs, and sometimes with the aid of serum calcium levels.
4.2.1.3. Treatment
Treatment of tetany, generalized weakness or egg binding with corresponding abnormally low serum calcium levels requires administration of parenteral calcium and may constitute an emergency situation. In general however, treatment of chronic calcium deficiency merely requires dietary correction, and administration of oral calcium with or without concurrent administration of vitamin D. Prevention of this problem is clearly the optimal alternative and is accomplished through correct dietary management.
| Sources of Dietary Calcium | |
| Cuttlebone | Dairy products |
| Oyster shell | Commercial diet |
| Fresh vegetables | Mineral supplement |
For more suggested foods see Table of Nutrient Content of Some Fruits and Vegetables in the Appendix.
4.2.2. Poultry
(Rickets, Caged layer fatigue, Osteoporosis)
Although an exclusive deficiency of vitamin D can theoretically occur, this nutrient is almost always complicated with deficiencies of calcium and phosphorous. It is important to remember that all birds, including poultry, require the D3 form of vitamin D. The D2 form is nutritionally inert. Laying hens are especially vulnerable to deficiencies of vitamin D3, calcium and phosphorus because of the high demand for these nutrients required for egg production.
 Rickets and growth plate abnormalities seen in
poultry
|
4.2.2.1. Clinical signs in poultry
- Growing birds are lame or reluctant to move or walk with a stiff-legged gait.
- The hocks may show variable swelling.
- Beading or swelling of the rib costochondral junctions and soft, easily bending bones (rickets). These signs are only seen in young growing animals.
- Laying hens may show a reluctance to move (caged layer fatigue). In some instances they develop fractures of thoracic vertebrae, wing and leg bones. S-shaped deviations in the cartilaginous portion on the keel may be palpated.
4.2.2.2. Diagnosis
Diagnosis is based on careful examination of the diet regarding the levels of vitamin D3, calcium and phosphorus. Recommendations suggest 500 IU of vitamin D3 per pound of feed. Gross and microscopic lesions are specific for deficiency states of vitamin D3, calcium and phosphorus but from a practical standpoint it is virtually impossible to state with certainty which of these three nutrients are absent. Soft, rubbery bones and beaks, beaded ribs, broken long bones and vertebrae and enlarged parathyroid glands are all suggestive of deficiency with vitamin D3, calcium and phosphorous.
Note: some references state that only calcium deficiency will result in parathyroid hyperplasia and that deficiency in phosphorous will not cause this lesion.
4.2.3. Wild birds
Metabolic bone disease is a commonly seen in young raptors that are kept in captivity and fed only skeletal meat. This occurs when bids are not fed whole prey, which includes bone as a source of calcium and phosphorus. Clinical signs of metabolic bone disease involve similar signs seen in poultry including rickets, pathologic fractures, and a soft bills. Occasionally this syndrome is also seen in free-living birds, particularly young crows. The etiology in free-living birds is not clearly understood but may involve inappropriate food choices by parent birds (garbage scavenging), or environmental contaminants interfering with normal calcium metabolism.
4.3. Vitamin E/Selenium deficiency
Vitamin E or selenium deficiency can result in "White muscle disease", muscular dystrophy, encephalomalacia, exudative diathesis or "crazy chick disease". This syndrome can be seen in any animal and is commonly seen in captive waterfowl, chickens and less often in psittacines (most often in cockatiels).
Oil soluble Vitamin E is needed as an antioxidant to protect against peroxidative damage. It neutralizes free radicals which attack cell membranes. Selenium is a cofactor for glutathione peroxidase which performs a similar function.
 Vitamin E deficiency in waterfowl
|
A deficiency may develop due to a lack of sulfur amino acid (cystine and methionine), due to competition with other fat soluble vitamins (over-supplementation with cod liver oil as a source of vitamin A), or with rancid fats in foods such as dog food. Conditions which produce intestinal malabsorption (giardiasis) may also result in insufficient absorption of Vitamin E.
| Dietary Sources of Vitamin E |
| Vegetable oils |
| Seed oils (especially wheat germ oil) |
| Green leafy vegetables |
| Eggs |
4.3.1. Pet birds
4.3.2. Poultry
Three distinct patterns of disease are seen in chickens with vitamin E deficiency: encephalomalacia (crazy chick disease), muscular dystrophy and exudative diathesis. Baby chicks, turkey poults and ducklings all show similar signs of disease with vitamin E deficiency. Almost every case of vitamin E deficiency is associated with diets that are high in polyunsaturated fats (cod liver oil and soy bean oil). Diets contaminated with rancid fat can also lead to vitamin E deficiency.
 Encephalomalacia in a chick
|
4.3.2.1. Clinical signs
- Encephalomalacia
- Signs are usually seen in 2 - 4 week old chicks
- Ataxia, loss of balance, and opisthotonos.
- Muscular dystrophy
- White streaks in pectoral and leg muscles
- In turkey poults the gizzard smooth muscle will sometimes show white streaks.
- Exudative diathesis
- Red/black or blue/black, gelatinous subcutaneous edema in the ventral abdominal and thoracic region.
- Similar changes are sometimes present in the intermandibular space and periorbital region.
- Birds with extensive edema may have difficulty walking and stand with legs apart.
4.3.2.2. Diagnosis
Diagnosis involves recognition of clinical signs and examination of the feed. Storage time and temperature of the feed is an important consideration in establishing a diagnosis of vitamin E deficiency. Examination of the ration usually reveals rancid feed or inadequate levels of vitamin E and/or selenium.
Differential diagnosis should include the following: Encephalomalacia clinically resembles avian encephalomyelitis. Exudative diathesis can resemble gangrenous dermatitis due to cutaneous Cl. perfringens infection. Subcutaneous crepitation and gas formation is usually present in gangrenous dermatitis but it is not seen in exudative diathesis. Gangrenous dermatitis is a sequela of immunosuppression from a previous infection with infectious bursal disease virus.
4.4. Angular Limb Deformities
(Perosis,Slipped tendon disease, Chondrodystrophy, Curled toe paralysis)
Perosis is a condition of 4-12 week old chickens, turkeys and pen-reared pheasants and quail. It may also be seen in other rapidly growing birds such as ratites, cranes, waterfowl, etc. This condition occurs as the result of lateral slippage of the gastrocnemius (Achilles) tendon at the tibiotarsal (hock) joint due to a generalized disorder of long bone growth plates resulting in impaired linear growth. Normal bone mineralization is maintained. The tendon is also histologically normal, however there is an enlargement of the hock joints and a secondary varus or valgus deformity of the lower leg. The etiology of perosis is complex and associated with a deficiency or imbalance in dietary manganese, choline, biotin, folic acid, niacin, pyridoxine (vitamin B6) and zinc. Curled toe paralysis is a nutritional problem of chicks associated with a deficiency in riboflavin (vitamin B2). Natural occurrence of this condition is rare.
 |
4.4.1. Clinical signs
- Birds are seldom observed with perosis until there is displacement of the tarsus.
- Unilateral lameness results with hopping on the unaffected leg.
- The condition can be bilateral..
- Affected joints are usually swollen.
4.4.2. Diagnosis
Diagnosis is usually based on clinical signs and gross lesions. Analysis of the ration usually reveals that there is a deficiency of manganese, but the other ingredients listed above must also be considered.
Differential diagnosis should include Mycoplasma infections and reovirus which can produce lesions in the hock joints of chicken and turkeys resembling perosis. Tendon displacement does not usually occur with either of these conditions.
4.5. Iodine responsive goiter
(Parakeets, canaries, pigeons)
 |
Hyperplasia of the thyroid gland occurs frequently in budgies due to apparent iodine deficiency. Insufficient iodine reduces the production of T3 and T4 resulting in an increased production TSH and hyperplasia of the thyroid. The gland may grow from 1.5 mg to 1000 mg in mass!
The disease state is produced by the anatomic effect of a mass occupying lesion at the thoracic inlet.
4.5.1. Clinical signs
Clinical signs include dyspnea, change of voice (pressure on the trachea) and/or regurgitation or difficulty swallowing (pressure on the esophagus)
4.6. Obesity, Fatty Liver Syndrome
Obesity is a very common problem seen in pet birds. It often occurs in malnourished birds that are fed primarily a sunflower/peanut diet. Sunflower seeds contain from 25-47% fat, 24% protein, and are deficient in many vitamins; the Ca:P ratio is 1:7. If dietary causes are not obvious, hypothyroidism should be ruled out and treated accordingly.
4.6.1. Clinical signs
In budgerigars and cockatiels we often see multiple well organized lipomas in association with this disease. Amazons usually will present with obvious obesity, exercise intolerance, lethargy, and a palpably enlarged liver (radiographs confirm). In any animal a life threatening toxemia from hepatic lipidosis may develop during starvation or fasting initiated by some other disease process. Animals experiencing acute toxemia will present with anorexia, depression, dyspnea, ataxia and occasionally vomiting.
 |
4.6.2. Diagnosis
Diagnosis is based on history, clinical signs, physical examination, radiographs, and serum biochemistry results (AST, TG, cholesterol, and bile acids). A liver biopsy would confirm the disease, but is rarely performed.
4.6.3. Treatment
Treatment in a subclinical situation (obesity) involves dietary management and increased exercise. Pelleted weight loss diets are available, or the owner can feed the suggested "natural" low fat diet:
Treatment of acute toxemia requires nutritional and fluid support, including a high quality low protein, high carbohydrate diet (suggested tube feeding formula: 1 cup baby oatmeal, 1 tablespoon Nutrical, warm water to the right consistency, or prepared diet - "Carbofuel"), and lactulose to help reduce blood ammonia levels. Total parenteral nutrition may be indicated if available and practical.
5. Ancillary Material
5.1. Readings
5.1.1. Texts and Articles
Altman, Robert B., et al. Avian Medicine and Surgery. Philadelphia. W.B. Saunders Co., 1997. Chapter 30.
Bourke, Ann M. Vitamin A toxicity in conures. Newsletter of the Association of Avian Veterinarians, Dec. 1996-Feb. 1997.
De Voe, Ryan S., Maureen Trogdon and Keven Flammer. Preliminary assessment of the effect of diet and -carnitine supplementation on lipoma size and bodyweight in budgerigars. Journal of Avian Medicine and Surgery, 18 (1) : 12-18.
Donoghue, Susan. Clinical nutrition of companion birds. Journal of Avian Medicine and Surgery, Vol. 11(4), 1997, pp. 228-246.
Klasing, Kirk C. Comparative Avian Nutrition. CAB International, 1998.
LaBonde, Jerry. Obesity in pet birds. Proceedings of the 1992 Annual conference of the AAV, New Orleans, Louisiana, September 1-5, 1992, pp.72-77.
Murphy, Joel. Psittacine fatty liver syndrome. Proceedings of the 1992 Annual conference of the AAV, New Orleans, Louisiana, September 1-5, 1992, pp. 78-82.
Ritchie, Branson W., et al. Avian Medicine: Principles and Application. Lake Worth, Fla., c1994: Chapter 31.
Tufts OCW material is licensed under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported License.
Legal NoticesPrivacy