4.1.1. Seed based diets vs. pelleted diets

• Seed diets are deficient in: calcium, vitamin A, iodine, and some essential amino acids

• Feeding a pelleted diet is the surest method of delivering an adequate diet to a pet bird, but palatability and boredom may be problematic

• The optimal diet should include a combination of all: seeds, pellets, and fresh foods.

• For a good illustrated discussion about seeds in the diet please take a look at the Zupreem client education handout on nutrition. (Note: The Exotic service does not specially recommend Zupreem pellets over other pellets)

• Supplementary foods such as fresh fruits and vegetables are healthy and well accepted by many birds. Supplemental calcium sources are highly recommended (cuttlebone, oyster shell, etc.)

• Foods to avoid are: chocolate, alcohol, high fat foods, avocado, and girt or gravel supplements. ANY PROCESSED HUMAN FOOD!!

• A good basic nutritional plan is to have the bird on pellets to 80% and other fresh veggies or fruits to 20%

4.2.1. Vitamin A deficiency

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.

For more suggested foods see Table of Nutrient Content of Some Fruits and Vegetables in the Appendix.

4.2.2. Calcium/phosphorus imbalances

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’ discussed below.

4.2.3. Vitamin E deficiency

4.2.4. 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.

4.2.5. 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 investigated (blood work not reliable for dx.) and treated accordingly.

5.1.1. Psittacine Hepatitis Complex

The clinical appearance of hepatitis in birds is fairly consistent regardless of the etiology. Clinical signs in pet birds include: Anorexia, vomiting/regurgitation, diarrhea, change in color of feces (bright green, yellow) and often urates as well (green or yellow biliary pigments). There is never jaundice since birds do not produce billirubin in significant number to cause jaundice. Birds may appear dyspneic from an enlarged liver or ascites producing a mass effect in the coelom. Neurologic signs may also be present with hepatoencephalopathy.

Approach to diagnosis should include history, physical exam (enlarged liver, ascites), CBC, blood chemistry (including bile acids, AST) and radiographs.

Differential diagnosis for psittacine hepatitis should include the viral diseases (herpesvirus, polyomavirus, adenovirus, reovirus) plus: bacterial hepatitis (mycobacteria,salmonella,other gram negative bacteria), parasitic hepatitis (coccidia, trematodes),chlamydiosis, toxic hepatitis (aflatoxins, lead), and hepatic lipidosis (very common).

General treatment of viral hepatitis involves isolating affected birds and providing supportive care, including: fluid therapy, nutritional support, lactulose, and antibiotics for primary or secondary bacterial infections. Aviary management with identification of chronic subclinical carriers, etc. may be very difficult, but will be crucial. Vaccination for viral causes will become more important in the future.

5.1.2. Viral hepatitis in psittacine birds

Hepatitis in pet birds is a common clinical condition caused by several different viruses. There are 4 main viruses known to be responsible for this condition. Three of the four main psittacine hepatitis viruses and chicken adenovirus are characterized by the presence of inclusion bodies:

5.1.3. Psittacine Herpesvirus Hepatitis (Pachecos Disease)

Psittacine herpesvirus was first described by Pacheco and Bier in 1930-31 as a disease in Brazilian parrots = “Pachecos disease”.

All psittacines are susceptible to this virus to a variable degree. There is often very high mortality in flock outbreaks. A report of an outbreak in a flock of 75 mixed psittacines resulted in 24 animals dead in 19 days! This is a devastating disease.

5.1.4. Polyomavirus

The family of papovaviruses includes cutaneous papillomaviruses and polyomaviruses commonly known to cause “budgerigar fledgling disease,” a form of “French molt“. Polyomaviruses cause feather dystrophy as well as classic hepatitis including intranuclear basophilic inclusions in the liver, spleen, kidney and many other tissues. Hydropericardium may also be seen along with an enlarged heart, enlarged pale congested liver with multiple pinpoint foci, and congested kidneys.

The disease chiefly effects young birds, budgies, lovebirds and other larger psittacines, but also may affect adults. This virus is also an important disease in finches. However, it is now felt that different strains of the virus are involved in finches, budgies, and larger psittacines and that these strains should not cross infect these groups. Polyomavirus in larger psittacines has become a very important and increasingly more common cause of fatal hepatitis in young birds across the country. These birds are nearly always captive bred birds which has made this recent phenomenon of great concern to American breeders.

5.1.5. Psittacine Beak and Feather Disease

Psittacine beak and feather disease virus occurs in both wild and captive psittacines. It was first described in the mid-70’s in wild sulfur-crested cockatoos in Australia. It is considered a cause of the syndrome called French molt, along with polyomavirus infection in budgies. It has since been described in 42 psittacine species including: black and white cockatoos, lovebirds, budgies, African Gray parrots, Amazon parrots, Lorikeets and others. Similar viruses in non-psittacines have been reported in pigeons and doves, canaries and finches, geese, and a black-backed gull.

The virus itself is very small; 20 nm. Current classification puts this virus in the family Circoviridae, along with porcine circovirus and chicken anemia virus.

5.1.6. Proventricular Dilatation Syndrome

Very recently, the etiology of Psittacine proventricular dilatation syndrome, also known as lymphoplasmacytic ganglioneuritis and encephalomyelitis, neuropathic gastric dilatation, and “Macaw Wasting disease” has been provisionally determined to be a new bornavirus (see the article in Virology Journal ).

This disease is classically seen in Macaws, but has more recently been consistently reported in cockatoos, conures, amazons, african greys, etc. In the last 10 years it has been described in over 50 different species including sporadic reports in some non-psittacine wild birds. It is consider to be 100% fatal but a few long term survivors exist. It is unclear if these birds should be considered shedders.

5.1.7. Other important viruses

• Avian paramyxovirus or Newcastle Disease

• Adenovirus

• Reovirus – new outbreak in Budgies

• Psittacine Pox

5.2.1. Spontaneous bacterial enteritis in psittacines

Bacterial enteritis is often a spontaneous stress associated disease. Stress factors such as transport/relocation, introduction of a new bird in the household, heavy molting, breeding/egg-laying, and weaning are all capable of initiating diarrhea. Many times however, the stress factor or initiating cause remains elusive.

The most common pathogens involved in psittacine bacterial enteritis are:

• E. coli

• Klebsiella

• Salmonella

• Pasteurella

• Pseudomonas

• Aeromonas

• Citrobacter (also in Finches).

Other less common organisms include:

• Enterobacter

• Proteus

• Serratia

• Mycobacterium

• Chlamydophila

• Candida

• Aspergillus.

5.2.2. Spontaneous bacterial respiratory disease in psittacines

As with bacterial enteritis, bacterial respiratory disease is also often a stress associated phenomenon, including environmental stress (cold). Bacterial disease also commonly develops secondarily to an underlying Vitamin A deficiency.

The most common pathogens involved in psittacine bacterial respiratory diseases are:

• Klebsiella

• E. coli

• Enterobacter

• Pseudomonas

• Pasteurella

• Mycoplasma

Others encountered include:

• Salmonella

• Proteus

• Serratia

• Hemophilus

• Actinobacillus

• Chlamydia

• Aspergillus

5.2.3. Mycobacteriosis

• M. avium primarily involved

• GI/liver focus, similar to Johne’s disease in cattle

• M. TB also possible, contracted from human REPORTABLE

5.3.1. Characteristics of the disease in psittacines

The disease in psittacine birds will vary greatly depending on the virulence of the organism and the immune system of the individual bird. The incubation period is from 3 days to several weeks.

5.3.2. Diagnosis

Suspicion of a diagnosis of psittacosis in a parrot species initially is based on details of the history, clinical signs, radiographs, CBC, chemistry panel, cloacal and choanal cultures. An attempt is made to rule out other diseases. Conclusive diagnosis usually requires one or more of the following techniques:

5.3.3. Treatment options

Tetracyclines (tetracycline, chlortetracycline, oxytetracycline, and doxycycline) and related compounds have historically been recommended. They are very effective but work only during the active dividing stage of the organism. For this reason, prolonged therapy for 45 days is required. Even after successful treatment, you can never GUARANTEE a bird FREE of the organism!

Chlortetracycline has been the classical government approved therapeutic option. It is one of the few drugs approved for use in birds by the FDA. The goal is to achieve > 1 mg/ml blood concentration for 45 days. The recommendations require giving treated food for larger birds at 5-10 mg chlortet/g food (1%CTC) as the sole food supply. Budgies and finches should receive 0.5 mg/g of food. Food must contain < 7% calcium. Treatment through the drinking water is not acceptable.

Doxycycline is now accepted by the government as the antibiotic of choice for treatment of this disease. Doxycycline comes in an oral form, an IV form and an IM form that lasts 5-6 days. The long acting form is only available from Europe and can be obtained through import (contact the FDA, phone 240-276-9200). One logical regimen would be to start with an injection of doxycycline or oxytetracycline and follow with individual oral dosing, followed by medicated feed if acceptable. LA-200 (Oxytetracycline) injection can also be used at 100 mg/kg IM every 3 days.

Refer to the Compendium on Chlamydia for up to date information.

Other effective antibiotics such as the fluoroquinolones are most likely very effective against this organism. Azithromycin has been recently released for use in humans and is effective in treating human chlamydia. However these agents have not been tested sufficiently in birds to prescribe a regimen.

Vaccines have been in the works for more than 40 years. There are MANY PROBLEMS with this methodology!! A new approach using recombinant technology is currently underway at Louisiana State.

5.3.4. Public health concerns – the disease in people.

Before the advent of antibiotics, psittacosis infection resulted in a 20% mortality rate in people. The discovery of tetracyclines has changed that considerably. It is now recognized as an important occupational hazard in the poultry and pet bird industries.

The disease in humans has an incubation period of 5-14 days. Clinical signs of fever, cough, headache, weakness, fatigue, chills, myalgia, also nausea, vomiting, anorexia, photophobia, and chest pain may occur. Splenomegaly may also be present. Diagnosis is made with thoracic radiographs and confirmed through serology. The classical appearance is of single or bilateral dependant lobar infiltrates. In people the differential diagnosis includes mycoplasmal pneumonia, Q fever (Coxiella), systemic fungal disease, TB, influenza, Legionnaires disease, tularemia, and bacterial pneumonia.

Treatment in people includes the administration of 500 mg tetracycline q6h PO x 7-10 days. The patient usually responds in 2 days. Other antibiotics such as erythromycin, tylosin, penicillin, and most recently azithromycin have also been shown to be effective. Following infection only short term immunity develops: a person can be reinfected within months!!

It is important for the veterinarian to advise alerting their physician if a bird in the household is diagnosed with Chlamydiosis.

5.4.1. Candidiasis in pet bird species

Candidiasis is most important in young unweaned birds. It is often referred to as “sour crop“. It most often develops secondary to a crop motility disorder, antibiotic therapy, and/or systemic disease. One should routinely use antifungal agents when using antibiotics in baby birds. Candidiasis is also seen in older birds on chronic antibiotic therapy or with immunosuppressive conditions (e.g. Beak and Feather ds.).

Clinical signs in pet birds usually include anorexia, weight loss, regurgitation and crop stasis. Diagnosis is based on clinical signs and demonstration of the organism on cytology and/or culture of a crop wash, pharyngeal swab, or fecal smear. Budding yeast will be seen as strongly Gram (+) with a gram stain.

Principles of treatment dictate that one must resolve the underlying disorder, not just treat the fungal infection. Effective drugs for candidiasis include: Nystatin, ketoconazole, itraconazole and fluconazole.

Macrorhabdus ornithogaster

Avian gastric yeast is an enteric fungal disease seen in budgies, other psittacines, canaries, finches, turkeys, quails, ducks, geese, ibis and ostriches producing chronic wasting and eventual death. The organism was originally classified as a giant bacteria called “megabacteria” and very recently confirmed as a fungi. The organism is thought to colonize the proventriculus, elevating the pH and altering the physiology of the stomach disrupting the thick, acellular koilin layer found in this portion of the avian GI tract. Malabsorption/maldigestion results in a wasting syndrome.

Koilin is a carbohydrate-protein complex secreted by the mucosal glands and surface epithelium of the ventriculus. This material hardens in the upper and middle layer of the secretion as a result of exposure to hydrochloric acid secreted by the proventriculus. In the absence of normal HCl secretion, the koilin layer does not form properly.

The organism is Gram positive and can easily be seen on gram stain preparations of feces, or a proventricular wash. They are very long (1 x 90 mm), very difficult to culture, and resistant to all known antibiotics. Treatment with acidification of the GI tract (vinegar, grapefruit juice) and the antifungal agent amphotericin B orally (100 mg/kg PO) has been effective in some cases. Spontaneous recovery has also been reported but prognosis may be very poor. It can be routinely seen during PM exams of many budgerigars as an incidental finding.

5.4.3. Aspergillosis

Aspergillosis is a serious condition usually associated with stress, chronic malnutrition, chronic disease and/or immunosuppression. It is most often seen in wild birds, but can be seen in chronically ill captive psittacines.

• Most often involves respiratory tract (air sacculitis, granulomatous pneumonia, rhinitis), but may invade other organ systems

• Clinical signs include weakness, anorexia, weight loss, dyspnea/exercise intolerance, +/- nasal discharge ; May see sudden death

• Diagnosis is complicated – radiographic evidence only at very advanced stage of the disease ; laparoscopy, serology/protein electrophoresis and cytology/culture

• Therapy challenging – prognosis guarded

   

  • Itraconazole is often used with varied success. DO NOT use this drug in African Grey parrots, it is TOXIC.

  • Lamisil appears to be well tolerated by all birds and shows some good success.

6.1.1. Lead poisoning

This is the most common toxic disease of pet birds, and is very prevalent in the Northeast. Lead poisoning is also seen in wild birds, especially waterfowl. It often involves an insidious course with chronic exposure. The acute disease is more easily recognized.

6.1.2. Zinc toxicosis

(New wire disease)

Zinc toxicosis is the second most commonly encountered heavy metal poisoning seen in pet birds. Zinc is present in the environment on galvanized metal objects, such as cage wire or clips used to assemble cages. Birds housed in such cages or with access to galvanized materials can ingest enough zinc to become affected.

6.1.3. Other common toxins

• Teflon toxicity

   

  • Burnt Teflon (PTFE) produces toxic gas

  • Respiratory emergency, usually fatal

  • Start supportive treatment immediately (mannitol or furosemide)

• Pesticides

• Poisonous plants (see document in Supplementary Material folder) – MANY

• Miscellaneous household toxins – Items reported include: alcohol, nicotine, hexachlorophene (soaps), ethylene glycol, motor oils, match heads, carpet cleaners, and scented deodorizing candles (Glade) among many others.

6.2.1. Hypocalcemia of African Grey parrots

The etiology of this phenomenon is not well understood, however one can usually document a dietary deficiency of calcium, and/or an excess of phosphorus. One can often demonstrate a high fat diet (sunflower!!) also which may be precipitating Ca soaps and lowering serum calcium. It would appear that the calcium/phosphorus metabolism in African Grey parrots is different than that of other birds and mammals. These birds seem to have a difficult time mobilizing calcium from extravascular sources (such as bone). It may be that they require more UVB than other parrots (see references below). Most birds, mammals and reptiles will readily use up bone stores before they allow hypocalcemia to occur (metabolic bone disease). These unique parrots however develop hypocalcemia usually without developing metabolic bone disease.

6.2.2. Diabetes mellitus

Diabetes mellitus does occur in avian species with relative frequency. It is most often reported in budgerigars, toucans, and ducks, but can occur in any species (recent report in red-tailed hawk and a broad-wing hawk). The pathophysiology of this disease is different in non-meat-eating birds than in most mammals. It is felt that glucose metabolism in these birds is much more dependant on glucagon concentration than on insulin levels. Diabetes is often a problem of an increase in glucagon, rather than a decrease in insulin. Histologically, there are many more alpha cells in the pancreatic islets than beta cells. In meat eating birds, the pancreas resembles the mammal’s pancreas.

6.2.3. Other Common Metabolic Diseases

• Gout (see also more discussion in Raptor Medicine notes)

   

  • Hyperuricemia, high protein diet or renal failure

  • Visceral gout – Common end stage disease

  • Articular gout – most often in small birds, particularly budgies. Uric acid crystals are deposited in joints of the legs and wings causing severe pain, swelling and inflammation. A genetic reason for the prevalence of gout in budgies has been proposed. Renal failure cannot always be demonstrated.

• Hemochromatosis (see Pigeon and Passerine lecture)

   

  • Not a common disease of psittacines

  • Seen in captive mynah birds and toucans

6.3.1. Chronic egg laying

Chronic egg laying is a common problem in several species of companion birds, especially the cockatiel. It is characterized by an individual hen laying repeated clutches, or continuing to lay beyond the normal clutch size, often without end! It occurs without the presence of a mate. Causes are likely hormonal and environmental, however attempts to manipulate environmental conditions often fail in controlling this problem. Consequences of chronic egg-laying are exhaustion, calcium depletion, egg-binding (see below), coelomitis, salpingitis, etc. Occasionally a bird will spontaneously stop laying, but will usually start up again with a prolonged egg-laying period in the following winter or spring.

Treatment for chronic egg-laying should include attempts to manipulate the environment: altering the photoperiod, removing nest sites, perceived mates, etc. Hormonal treatments have included medroxyprogesterone acetate (Depo-provera), levonorgestrel, HCG and most recently leuprolide acetate (Lupron) a synthetic analog of GnRH. Lupron has been the most effective and the safest therapy to date. To prevent seasonal recurrence and avoid repeated hormonal therapy surgical hysterectomy is recommended as a permanent cure. This surgical procedure (spay) can be risky but should be offered in case medical management does not prove to be successful.

6.3.2. Egg binding

Egg binding in pet birds is most often a result of hypocalcemia resulting from either a nutritional deficiency or protracted egg-laying and an excessive drain of calcium for egg shell production. The lack of available calcium during the laying process results in primary uterine inertia and the birds inability to contract and expel the egg.

Other causes include chronic egg-laying, vitamin A deficiency, environmental stresses, poor physical condition on the hen, young hen (first clutch), large egg, or an anatomical abnormality. There may also be a genetic predisposition for egg-binding. This condition is most commonly seen in budgies, cockatiels, and finches, but can be seen in any female laying bird.

6.4.1. Subcutaneous and intra-coelomic lipoma

This is one of the most frequently observed neoplasms in pet birds. Some studies suggest that this tumor has a 40% incidence in parakeets. Whether this observation is the result of genetic influence or just the popularity of pet parakeets is unclear. Other species commonly associated with this tumor are cockatoos and Amazon parrots. Obesity and advancing age probably play some role in this tumor as is the case in dogs and horses. Based on information gleaned from mammals, it is probably wise to not surgically remove a lipoma unless it has grown to a size to be uncomfortable to the bird.

This is common on the skin of the eyelids and junction of the beak and face. Parakeets, Amazon and African gray parrots are some of the species commonly affected. Canaries are affected to a lesser degree. Internal papillomatosis has a predilection for the cloaca and intestinal tract in some pet birds species (cloacal papilloma). As in mammals, these tumors are suspected to be caused by viruses, although none have been isolated. Recent evidence suggests that a herpes virus may be responsible for internal papillomas in pet birds.

This is one of the more common malignant neoplasms diagnosed in pet birds. The subcutis of the wing, leg, junction of the beak and face, neck and sternum are regions commonly affected. Species most often involved are: parakeets, cockatoos, parrots and macaws.

6.4.4. Squamous cell carcinoma

This is seen on the skin of the head in birds but is also seen in other locations. It is sometimes seen in a setting of chronic feather pulling (self trauma). The role of ultraviolet rays and carcinogenic agents is probably the same in birds and mammals.

This is the most common kidney tumor in pet birds. In this instance also the budgerigar seems to be over-represented. The peculiar anatomic relationship of the kidney, lumbosacral plexus and spinal cord often result in a bird with this tumor clinically presenting with unilateral paresis or paralysis. Additionally, the prognosis for this tumor is poor because of the difficulty in performing surgery in this region.

6.4.6. Testicular Neoplasia

Sertoli cell tumors and seminomas are commonly seen in parakeets, clinical signs similar to renal tumors (unilateral lameness)

6.4.7. Lymphosarcoma

This has been diagnosed in a number of pet and wild bird species with the tumors occurring in many different locations. The liver and spleen are the two common locations in the abdominal cavity but lymphomas have also been seen in the periorbital region. Although retroviruses are a likely etiologic candidate for this tumor, relatively little is known about the etiology of this tumor in comparison to the wealth of information on this form of neoplasia in chickens.