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Author: Gretchen Kaufman, DVM
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OCW Zoological Medicine 2008
Psittacine Medicine (2008)
G. Kaufman, DVM
Cummings School of Veterinary Medicine at Tufts University

1. Learning Objectives and Review

This section pulls together the main diseases and health issues of psittacines, representing the major group of birds seen in pet bird veterinary practice. Color coded topics indicate learning objectives that the student should become familiar with. Cases will be presented in class to illustrate these topics.

Please review the parrot conservation section from the Introduction to Zoological Medicine course to better understand the context for these wild birds.

2. Introduction

2.1. Psittacine Taxonomy

Most pet birds fall into the Psittaciforme group general known as parrots and including: amazon parrots, macaws, conures, cockatoos, cockatiels, budgerigars, love birds, etc. A great review of psittacine taxonomy previously published by Dr. Brian Speer can be found in the Appendix.

The Parrot Lexicon is also a great reference with pictures as is the University of Michigan site.

See additional images in Psittacine Folder

Don't forget to test yourself with the Pet Bird Species Identification

2.2. Anatomic Features

Psittacines are highly adapted to survival their wild environment. Specific characteristics include

  • Hooked beak for manipulating food

  • Hard/strong keratinized beak for cracking open food objects: nuts and seeds

  • Amazing feet!

  • Crop

  • Most are sexually monomorphic

    • Parakeets have different colors oft eh cere (males have blue, females have a brown cere)

Parrot
Parrot

3. Husbandry

Please review the materials presented in Clinical Skills regarding husbandry, restraint and general care of pet birds. There are many pitfalls in husbandry that result in clinical disease, including:

  • Poor caging materials - metal cages utilizing galvanized wire or soldered joints containing zinc may produce life threatening zinc toxicosis

  • Sand paper covered perches - originally designed to keep nails short, end up producing abrasions on feet and can result in pododermititis

  • Free-flighted birds accessing :

    • lead paint (lead toxicosis)

    • poisonous household plants (rare)

    • smashing into windows etc. causing trauma

    • flying into boiling water on a stove

Thermal burns after flying into a pot of boiling water
Thermal burns after flying into a pot of boiling water

4. Nutrition and Nutritional Disorders

4.1. Review of Basic Pet Bird Nutrition

Also review the Exotic and Wild Animal Nutrition notes presented in the 1st Year Feeds and Feeding course for basic information on avian nutrition.

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. Important Nutritional Diseases of Psittacines

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.

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.

4.2.1.1. 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.

4.2.1.2. 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.

Sterile abscess
Sterile abscess

Periorbital swelling in an African Grey parrot (Hypovitaminosis A)
Periorbital swelling in an African Grey parrot (Hypovitaminosis A)

4.2.1.3. 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.

4.2.2. 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.

4.2.2.1. 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.

4.2.2.2. Diagnosis

The diagnosis is based on clinical signs, dietary history, radiographs, and sometimes with the aid of serum calcium levels.

4.2.2.3. 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.

4.2.3. Vitamin E deficiency

4.2.3.1. Clinical signs

Clinical signs include paralysis, muscle weakness, ataxia, and sudden death

4.2.3.2. Diagnosis

Diagnosis is based on ruling out other causes of the clinical signs above. Pathologic findings include muscle necrosis/fibrosis, fragility of red blood cells with vascular leakage, and demyelination and neuronal degeneration in the central nervous system.

4.2.3.3. Treatment

Treatment includes parenteral injections of Vitamin E/Selenium, and oral supplementation using vitamin E capsules or wheat germ oil. Clearly correction of the underlying cause, if known, is desirable.

4.2.4. Iodine responsive goiter

(Parakeets, canaries, pigeons)

Budgerigar
Budgerigar

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.

4.2.4.1. Clinical signs

Clinical signs include dyspnea, change of voice(pressure on the trachea) and/or regurgitation or difficulty swallowing(pressure on the esophagus)

4.2.4.2. Diagnosis

Diagnosis is based on history, rule outs, and clinical signs. Mild hypothyroidism may also be present. It is often a difficult diagnosis to make since the mass is rarely palpable or radiographically evident.

4.2.4.3. Treatment

Treatment includes dietary supplementation with iodine (Lugol's iodine solution), or a special formulated vitamin with iodine. Thyroxine supplementation is not necessary.

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.

4.2.5.1. 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.

Amazon parrot
Amazon parrot

4.2.5.2. 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 and can easily be performed in combination with an endoscopic exam of the coelomic cavity.

4.2.5.3. 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:

Psittacine Low Fat Diet

Sweet potatoes (cooked)

Fresh vegetables

Sprouts

Fresh fruits (apple, apricot,cantaloupe)

Lean meats (cooked)

Hard cooked eggs (occasional)

Low fat breads

Cooked pasta, rice

Plain low fat yogurt

Vitamin supplement (very important
if not getting pelleted 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. Infectious Diseases

Infectious diseases are common and very important in avian medicine. Many psittacine diseases are highly contagious and can sweep through a collection of birds very quickly. Some of these are carried asymptomatically for many years, causing disease or an outbreak of disease long after the initial exposure. Acutely infected animals will deteriorate quickly, often times before a final diagnosis is determined. The avian veterinarian needs to respond quickly to these situations, often covering several possible etiologies at the same time.

The following are the most important infectious diseases of psittacines. Follow the links for in depth descriptions.

5.1. Viral Diseases

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:

Inclusion Body Hepatitis

Herpesvirus

Focal hepatic and splenic necrosis
Intranuclear, eosinophilic inclusions

Papovavirus

Multiple pinpoint hepatic foci
Intranuclear basophilic inclusions

Adenovirus

Diffuse hepatic necrosis
Intranuclear basophilic inclusions

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.

5.1.3.1. Clinical signs

Initially one may see sudden death without any clinical signs. However, signs that do consistently appear include anorexia, depression, and yellow mustard diarrheic feces.

5.1.3.2. Diagnosis

Diagnosis can be made based on clinical signs of hepatitis and epidemiological evidence of exposure (see below). Due to the peracute nature of this disease, necropsy of a dead bird often leads to diagnosis of a flock problem. Classic pathologic features include intranuclear eosinophilic inclusions and focal hepatic (and splenic) necrosis. Blood tests are useful, but are only positive in the viremic phase.

pacheco - A gross photo and H & E photomicrograph of the liver of a conure with Pacheco's disease, or psittacine herpesvirus hepatitis
pacheco - A gross photo and H & E photomicrograph of the liver of a conure with Pacheco's disease, or psittacine herpesvirus hepatitis

5.1.3.3. Treatment

Although supportive care is the primary treatment available, sick birds rarely respond. Quarantine of sick birds is essential! A flock can be treated with Acyclovir for a minimum of 7 days. Birds that are already sick often do not respond. There was a vaccine (killed) available for this disease. However, due to some serious problems with the adjuvant in the vaccine it has been withdrawn.

5.1.3.4. Epidemiology

The epidemiology of this disease can make it difficult to manage. Classically, asymptomatic carriers have been shown to be the culprit in outbreaks. These carriers may incubate the disease for up to 2 years before shedding it. Historically Patagonian and Nanday conures have been implicated, although other birds may serve as carriers. Infection is spread initially by asymptomatic carriers but may be disseminated through human caretakers. It is felt that various forms of stress induce shedding of the virus in the feces. There is at present no sure way to identify carrier birds, or even birds that are responsible for an outbreak. In one study of 70 psittacines (mostly African Grey parrots and amazons), 30 were seropositive without any signs of disease! Amazons, cockatoos and macaws are very sensitive and often do not survive infection. Recovered birds may have lifelong immunity (low serum titer) but should be considered carriers for life.

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.

5.1.4.1. Clinical signs

Clinical signs will vary with species and age of the bird. Poor/abnormal feather growth is seen most commonly in budgies. Other birds develop subcutaneous hemorrhages, depression, anorexia, weight loss, decreased crop motility, regurgitation, diarrhea, dehydration, dyspnea, ataxia/paresis/paralysis, polyuria, or peracutedeath.

5.1.4.2. Diagnosis

Diagnosis can be made based on antibody tests (virus neutralization), and a PCR test detecting antigen in feces and blood, and/or on post-mortem. It is recommended that both blood and cloacal swabs be submitted for testing in an aviary situation, preferably in serial sample submissions. The PCR test can also be performed on environmental samples (swabs of cages, rooms, bowls, etc.) to detect presence of the virus

Polyoma - Acute hepatic necrosis seen with polyomavirus infection
Polyoma - Acute hepatic necrosis seen with polyomavirus infection

5.1.4.3. Treatment/Epidemiology

Treatment is symptomatic. Management of affected animals is critical in controlling or eliminating the disease in a flock situation. Vaccination is available to assist in managing this devastating disease and is recommended in aviary settings and for young birds leaving the aviary. Identification of the source of infection is very important. Recovered adults and parent birds may be implicated as subclinical carriers. Birds with persistently high titers (FA virus neutralization test) are probably carriers. Recent studies on budgies have shown that seropositive birds under the age of 2 years, including nestlings, are responsible for transmitting the disease. Removal of these birds from the breeding flock will eliminate the spread of infection to subsequent generations. Non-carriers achieve only short-lived titers. Virus may persist in the environment for a long period of time. The incubation period is felt to be 2 weeks or greater.

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.

5.1.5.1. Clinical signs

Clinical signs include the appearance of "dirty" feathers followed by abnormal molts with abnormally shaped feathers (retained sheaths, hemorrhage, short clubbed feathers, deformed and curled feathers) and outright alopecia. In later stages we see necrosis of the beak and palatine area and epiglottis. The virus causes epidermal necrosis, but also infects both the bursa and thymus (atrophy and necrosis) resulting in various levels of immunosuppression. There appear to be various stages of the disease: not all birds will develop all stages and result in death. Rare cases of spontaneous recovery/remission have been seen. Lovebirds may harbor the virus for years without clinical signs.

5.1.5.2. Diagnosis

Diagnosis is based on biopsy of affected feather follicles (pulling blood feather) or utilization of a DNA probe on white blood cells. The latter test has recently been introduced and may be able to identify very early stages of the disease, before clinical signs develop and help identify carrier birds. On the biopsy or at necropsy, basophilic intracytoplasmic and intranuclear inclusions may be seen in epithelial cells and macrophages. The DNA probe can also be used on necropsy specimens to detect virus in various tissues including the bursa and thymus.

PBFD - Normal cockatoo on left, affected bird on the right
PBFD - Normal cockatoo on left, affected bird on the right

5.1.5.3. Treatment

Symptomatic treatment is essential in managing chronically affected birds. This includes regular beak grooming and monitoring closely for secondary infections due to immunosuppression.

5.1.5.4. Epidemiology

The degree of infection may depend greatly on the age that the bird first acquires the infection: Chicks <7 days old are the most susceptible. At this age the bursa is very sensitive, becomes infected and then proceeds to disseminate the virus throughout the body. When these birds become fledglings between 3-12 weeks of age they will begin to develop clinical signs: 80-100% abnormal feathers within 1 weeks time. Conversely, one may see minimal feather dystrophy, but acute death in 1-2 weeks.

Older birds develop chronic disease: chronic feather dystrophy with or without beak necrosis. There have been some reports of 10, 15, and 20 year old birds first showing signs. Because of this, it is thought that the incubation period may be extremely long. However, most birds affected are <3 years of age, and most birds die within 6-12 months of development of feather signs. Death may result from advanced neurologic disease or from secondary infections, presumably as a result of immunosuppression.

Virus may be recovered from feces, crop secretions, feather dust and white blood cells. It may be very stable in the environment. Horizontal transmission is important. Vertical transmission studies are ongoing. Maternal antibody has been shown to exist. A vaccine is in development (University of Georgia), but has not been released to the market.

This disease has come under very good control in recent years in companion birds, mostly through diligence by captive breeders. A new disturbing series of outbreaks has been recently described in lories in several locations. It is thought that the infection in lories represents a new or different strain of the 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.

5.1.6.1. Clinical signs

Clinical signs include weight loss, maldigestion, and regurgitation. CNS signs may develop in very late stages of the disease.

5.1.6.2. Diagnosis

Radiographs usually demonstrate a grossly dilated proventriculus with or without contrast upper GI radiography. 40% of positive cases can be diagnosed with a full thickness crop biopsy, showing characteristic lesions(i.e. ganglioneuritis). Other cases can only be positively diagnosed with a full thickness proventricular biopsy. However this procedure is significantly more risky and is not commonly performed. Histology shows lymphocytic myenteric ganglioneuritis in the walls of the proventriculus, ventriculus and sometimes the rest of the GI tract. Leiomyositis, smooth muscle degeneration, and sometimes nonsuppurative encephalomyelitis may also be identified at necropsy.

Rule-outs for a dilated proventriculus include infectious problem (incl. fungal gastritis), heavy metals toxicosis, and gastric foreign body obstruction.

5.1.6.3. Treatment

There is no specific treatment other than management of the chronically ill patient, supportive care for malnutrition/maldigestion and weight loss. This disease is highly fatal especially if CNS are noted. A recent protocol using celecoxib at 10 mg/kg P.O. once daily. for 2-3 months has shown significant improvement in clinical birds.

5.1.7. Other important viruses

  • Avian paramyxovirus or Newcastle Disease

  • Adenovirus

  • Reovirus - new outbreak in Budgies

  • Psittacine Pox

5.2. Bacterial Diseases

Normal flora of the psittacine respiratory and gastrointestinal tracts - Understanding the normal flora of the bird you are treating, whether it be a psittacine, a passerine, anseriform, raptor, etc. is important in interpreting culture results and in designing appropriate therapies. Bacterial diseases are common in pet birds and often involve relatively normal flora or environmental pathogens which develop into disease in response to stress and immunosuppression. Psittacine normal flora is primarily Gram +.

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.

5.2.1.1. Clinical signs

Clinical signs of bacterial enteritis include diarrhea, dehydration, anorexia, weight loss, septicemia, and occasionally sudden death.

5.2.1.2. Diagnosis

The diagnosis is based on history, clinical signs, fecal gram stain and cloacal culture and sensitivity. The fecal gram stain is used as an in-house quick screen test to determine whether an excessive number of gram negative organisms (>10%, usually of one type) are demonstrable in the feces.

Important differential diagnosis includes dietary indiscretion, and hepatitis, particularly Chlamydiosis.

Fecal gram stain from a normal psittacine bird
Fecal gram stain from a normal psittacine bird

5.2.1.3. Treatment

Treatment for bacterial enteritis requires the use of appropriate antibiotics and fluidtherapy, ideally based on culture and sensitivity.

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

5.2.2.1. Clinical signs

Clinical signs of respiratory disease may include sneezing, nasal discharge, dyspnea, lethargy, anorexia, exercise intolerance, wasting and rarely coughing. The clinical signs will vary according to the location of the infection, from the sinuses (upper respiratory), to the airsacs, or the lungs themselves.

5.2.2.2. Diagnosis

The diagnosis is based on clinical sign, choanal culture and sensitivity, and radiographs. Radiographs are extremely important in locating and characterizing the infection. Important differential diagnosis includes viral respiratory diseases (Amazon tracheitis virus), chlamydia, toxic inhalants(Teflon, smoke), allergies, fungal disease and dyspnea caused by abdominal distention (non-respiratory cause).

5.2.2.3. Treatment

Treatment necessarily involves the use of appropriate antibiotics, delivered in various formsincluding local application, systemic administration and nebulization. Adjunctive therapies include fluid therapy, Vitamin A therapy, andO2 therapy if necessary.

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. Chlamydiosis

(Chlamydiosis, ornithosis, psittacosis, parrot fever)

Chlamydiosis is the most important zoonotic disease of psittacines. It is endemic to the US and in the wild population. Veterinarians have an obligation to be able to recognize the signs of chlamydiosis, give accurate counsel to their clients regarding this disease, and actively participate in public health regulations regarding reporting and treatment of psittacine patients. REPORTABLE

Family Chlamydiaceae

Genus Chlamydia

Chlamydia trachomatis

Human ocular and venereal infections

Chlamydia suis

Swine

Chlamydia muridarum sp.nov.

hamsters and mice

Genus Chlamydophila

Chlamydophilapsittaci

6 avian serovars and 2 mammalian serovars: birds, humans, separate serovars for pigeons, turkeys

Chlamydophila pneumoniae

humans, horses, koalas, other mammals

Chlamydophila pecorum

mammals, incl. koalas

Chlamydophila felis

Cats

Chlamydophila caviae

Guinea pigs

Chlamydophila abortus

ruminants

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.

5.3.1.1. Acute disease

Birds may present with upper respiratory signs (conjunctivitis/sinusitis/rhinitis are often seen in cockatiels), air sacculitis, dyspnea, and/or anorexia, vomiting, diarrhea, lethargy, dehydration, with bright green feces (hepatitis). It can also involve the CNS at late stages of the disease.

5.3.1.2. Chronic disease

Usually represented by a sickly unthrifty bird with repeated episodes of illness. Poor feather coat, repeated episodes of "colds" and chronic diarrhea are common signs.

5.3.1.3. Asymptomatic chronic carrier

Birds often appear absolutely normal with no signs of disease whatsoever. These birds may become acutely ill when stressed, but more likely will shed the organism intermittently when placed under stress and resulting in infection of other birds and humans in the immediate environment. Cockatiels are thought to be one of the most common asymptomatic carriers of C. psittaci.

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:

5.3.2.1. Culture

This process is expensive and time consuming, although extremely valuable. Positive retrieval of the organism for culture requires active shedding of the organism by the animal at the time the swab is taken. This is unreliable, unless the subject is ill at the time. Positive culture, however is irrefutable proof of infection.

5.3.2.2. Serology

Direct complement fixation

Detects IgG, gold standard, some false (-) results occur early in infection and also in budgies, cockatiels and Af. Greys

Elementary body agglutination

Detects IgM (early stages). Very quick but not very sensitive. Usually done as a screen or in conjunction with other tests (University of Miami ).

Indirect immunofluorescence assay

Detects primarily IgG, relatively sensitive and specific, false (-) results in early stages (University of Miami ).

5.3.2.3. Feces/tissue antigen capture tests

IDEIA, chalmydiazyme, CELISA, IMAGEN and other human products designed to detect chlamydia trachomatis have been used to detect chlamydophila psittaci antigen in birds using swabs from respiratory tract or feces. They depend on large numbers of organisms in the sample and, of course, active shedding of the organism. There is also much cross reactivity with bacteria in fecal samples (false +). Takes only 20 minutes, used by many clinics as a bench top screening test.

5.3.2.4. PCR test

PCR test for chlamydial DNA has recently become available. This test is reported to be more sensitive and specific than those listed above. Problems with sample handling can effect test results. Animals that are not currently shedding will be missed. Doxycycline interferes with PCR as the pathogen will not be shed about 20 hours after start of treatment. . This test is currently available from Research Associates Laboratories , Texas A&M , and University of Miami .

5.3.2.5. Interpretation of antemortem chlamydia tests

The following points should be taken into consideration when interpreting results of antibody or antigen tests.

  • Antibody is relatively short lived and quite variable, therefore chronic carriers may not be picked up at all.

  • A positive test usually implies recent infection/exposure.

  • Paired titer may be necessary in the very early acute phase (too early for antibody to have developed).

  • False positives and negatives may occur with all the tests for a variety of reasons (e.g. some birds such as cockatiels don't produce IgM with chlamydial infections

  • Use of paired titers and multiple tests plus protein electrophoresis (University of Miami) to help refine the diagnosis is often useful.

  • Single test results using the above techniques may be confusing or misleading.

New tests are being perfected all the time. The ultimate test would be able to detect the chronic carrier bird, and detect small amounts of antigen, and/or low titers.

5.3.2.6. Post Mortem Diagnosis

  • Precautions must be observed when autopsies are performed on birds suspected of chlamydiosis. The entire bird should be thoroughly soaked with detergent and water to minimize feather dust and dander aerosols. A surgical face mask should be worn by all those involved in the autopsy.

  • Gross lesions are variable but usually always associated with a diffuse fibrinous serositis involving the air sacs, abdominal serosa (liver, spleen, intestine and mesentery) and pericardium.

  • In some instances tan/yellow, less than 1 mm diameter foci may be seen in the spleen or liver. These represent focal necrosis.

  • Direct imprints of air sac swabs, liver and spleen are the best post mortem diagnostic specimens to establish the diagnosis of avian chlamydiosis. Wright-Geimsa stain is the most effective for demonstrating the intracellular elementary bodies. Monoclonal FA reagents are also available. These tests will give an immediate diagnosis. Isolation can take 48 hrs. to 3 weeks!! Machiavello's and Casteneda's stains have also been recommended for demonstrating the organisms in formalin fixed, paraffin embedded tissues.

Chlamydia - Direct imprint from air sac with DifQuik stain showing an initial body
Chlamydia - Direct imprint from air sac with DifQuik stain showing an initial body

Direct imprint from air sac with DifQuik stain showing an initial body.

5.3.2.7. Postmortem Differential Diagnosis

The gross lesions of avian chlamydiosis are impossible to differentiate from Mycoplasma gallisepticum infection in turkeys.

Fowl cholera, influenza and aspergillosis can also resemble the gross lesions of avian chlamydiosis.

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. Fungal Diseases

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.

An oral plaque in a young pigeon, possible candidiasis
An oral plaque in a young pigeon, possible candidiasis

5.4.2. Avian gastric yeast

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.

Gastric yeast - Avian gastric yeast on a fecal gram stain
Gastric yeast - Avian gastric yeast on a fecal gram stain

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.

5.5. Parasitic Diseases

Parasitic diseases are unusual in pet psittacines except in animals kept in flocks out doors (breeders, collections).

  • Knemidokoptes mites

    • Most often seen in budgies

    • Lesions visible on the cere/beak

    • Responds well to ivermectin (be careful not to overdose with 1% solution - dilute with propylene glycol if needed)

  • Giardiasis

    • Easily treatable with metronidazole

scaly face
scaly face

6. Noninfectious Diseases/Disorders

6.1. Toxic Diseases

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.

Common Household Sources of Lead

Leadshot

Lead based paint

Contaminated water supply

Curtain weights

Bird toys with lead weights

Bells with lead clappers

Costume jewelry

Plaster containing lead

Putty, caulking, and solder

Galvanized wire/Hardware cloth

Glazed ceramics

Mirror backs

Leaded stained glass

Batteries

Linoleum

Champagne and wine bottle foils

6.1.1.1. Clinical signs

Clinical signs of lead poisoning can be quite variable and include: anorexia, diarrhea or GI stasis, vomiting, PU/PD with hematuria (Amazons), muscle weakness, paralysis, ataxia, blindness, seizures, and death.

6.1.1.2. Diagnosis

The diagnosis is based on history, clinical signs, radiographs, CBC (mild anemia), blood lead levels (suspect at 20 mg/dl or 0.2 PPM, diagnostic at 40+ mg/dl for most birds). Quik bench top test kits are available. One can also measure protoporphyrin and ALAD (delta-aminoleulonic acid dehydrase) levels. At necropsy tissue lead levels should be measured on kidney and liver samples.

6.1.1.3. Treatment

Treatment for lead poisoning (often begun before laboratory test results are known) includes elimination of the source of the lead via cathartics, intestinal chelators(MgS04,) peanut butter (bulking agent,) or surgery, and chemotherapy to bind and aid elimination of systemic lead.

CaEDTA

CaEDTA acts to bind lead in the serum. Bone and tissue levels will equilibrate with serum levels and gradually be decreased. CaEDTA is very poorly absorbed from the GI tract and must be given parenterally unless one is trying to chelate intestinal lead. It is felt to be highly nephrotoxic in mammals (as is the lead), but this has not been demonstrated in birds. CaEDTA should be used with care in renal compromised patients. Some recommend the course of therapy as 5 days on and 5 days off chelation to avoid renal toxicity.

Succimer (Chemet)

meso-2,3-dimercaptosuccinic acid

This is a new compound which is being used in pet birds. It has been developed for use in children with chronic lead poisoning. It is an orally administered chelating compound and can be used on a long term basis. A dose of 30 mg/kg orally twice daily has been recommended. Higher doses have been shown to cause toxicity and death, especially in cockatiels. In acute cases succimer can be used in combination with a single dose of CaEDTA.

Penicillamine

Penicillamine may be another option to parenteral CaEDTA therapy. However some violent GI reactions have been seen with the use of this agent. Penicillamine is orally administered, orally absorbed, but not as good a chelator as CaEDTA but is often used in combination with CaEDTA.

The prognosis for recovery is good if treatment is begun before severe neurologic disturbances are evident. The prognosis is guarded once neurologic signs have developed.

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.

6.1.2.1. Clinical Signs

Clinical signs are very similar to those seen with lead poisoning and include: PU/PD, GI problems, decreased fertility, weight loss, weakness, ataxia, anemia, cyanosis, hyperglycemia, seizures and death.

6.1.2.2. Diagnosis

Diagnosis is made based on history, clinical signs, radiographs and serum concentrations of zinc (R/O lead). Serum levels above 2 ppm are diagnostic. Tissue levels of zinc, particularly in the pancreas, are useful in making a postmortem diagnosis. Zinc toxicity usually has a less favorable prognosis than lead toxicity.

6.1.2.3. Treatment

Treatment is similar to lead poisoning. CaEDTA is used primarily for chelation. Removal of any remaining zinc wire in the GI tract is also important. Support and monitoring of renal function, GI function and anemia are important during the treatment period.

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. Metabolic Diseases

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.

6.2.1.1. Clinical signs

The affected bird is most often recognized in an acute phase, but the disease can be chronic. Acute clinical signs include weakness, falling off the perch, poor feather condition, and occasionally tetany and/or seizures.

6.2.1.2. Diagnosis

The diagnosis is based on clinical signs, signalment, and ionized calcium levels < 1.0 mg/dl (normals are > 1 -1.5 mg/dl). Total serum calcium is not a reliable factor to diagnose this disease. Radiographs are usually not useful in making a diagnosis since these birds are not osteopenic. Postmortem lesions include enlarged parathyroid glands with significant degeneration.

6.2.1.3. Treatment

Treatment involves injections of calcium in the acute phase, followed by oral supplementation, perhaps for life. One should also make sure there is an adequate source of Vitamin D3 available. The exposure to full spectrum light (including UVB) is a must for long term management. Refer to the following article for a good discussion of this specific syndrome: The Effect of UV-B Lighting Supplementation in African Grey Parrots , by Michael Standford.

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.

6.2.2.1. Clinical signs

Clinical signs of diabetes are what one would expect.

  • Polyuria

  • Polydipsia

  • Polyphagia

  • Weight loss (usually)

6.2.2.2. Diagnosis

Diagnostic tests include blood glucose, and urine glucose determinations. Insulin/glucagon ratios can also be measured and will definitively prove the diagnosis. Serum glucose levels will often be greater than 800 mg/dl.

6.2.2.3. Treatment

Treatment consists of regular administration of insulin (NPH usually recommended), however, the response is often poor as one might expect. The overall prognosis is guarded.

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.

Uric acid crystals
Uric acid crystals

Articular gout in a budgie
Articular gout in a budgie

  • Hemochromatosis (see Pigeon and Passerine lecture)

    • Not a common disease of psittacines

    • Seen in captive mynah birds and toucans

6.3. Reproductive Disorders

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.

Egg binding
Egg binding

6.3.2.1. Clinical signs

Clinical signs of egg-binding include straining, fluffed and slumped posture, lethargy, anorexia, abdominal swelling (palpable egg?), and occasionally prolapse of the uterus.

6.3.2.2. Diagnosis

The diagnosis is based on history, clinical signs, palpation, and the radiographic evidence of an egg in the abdomen.

6.3.2.3. Treatment

Therapy for egg-binding includes providing a moist warm environment, calcium, oxytocin, Vitamin A injections, treatment for shock if indicated, manual assistance, evacuation of the egg, and rarely surgical intervention.

6.4. Neoplastic Diseases

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.

Lipoma
Lipoma

6.4.2. Papillomatosis

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.

Esophageal papillomas in a macaw
Esophageal papillomas in a macaw

Cloacal papilloma in an Amazon
Cloacal papilloma in an Amazon

6.4.3. Cutaneous fibrosarcoma

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.

Fibrosarcoma at the commissure of the beak in a budgie
Fibrosarcoma at the commissure of the beak in a budgie

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.

Squamous cell carcinoma on the neck of an Amazon
Squamous cell carcinoma on the neck of an Amazon

6.4.5. Renal cell carcinoma

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.

Cutaneous lymphoma
Cutaneous lymphoma

6.5. Dermatologic Diseases

  • Feather/skin disorders

    • Folliculitis, dermatitis (bacterial, fungal)

    • Malnutrition (esp. Vitamin A)

    • Liver disease

    • Intestinal irritation (Giardia)

    • Viral diseases (Beak and Feather, Polyomavirus)

    • Endocrine disorders

    • Diagnosis through history and comprehensive testing

    • Treat underlying cause

  • Behavioral feather picking

    • R/O above disorders (this is quite expensive)

    • Treat as behavioral problem - environmental enrichment

    • Behavioral modification drugs such as clomipramine or Prozac may be used

6.6. Trauma

Traumatic injuries are not uncommon and may include the following:

  • Broken blood feather

  • Fracture or injury secondary in association with leg band

  • Flying into ceiling fan

  • Getting caught/slammed in a door

  • 'Night fright' (cockatiels fall off their perch in total darkness)

  • Cage mate trauma

  • Self-mutilation

Trauma
Trauma

7. References and Resources

7.1. Professional Organizations

Association of Avian Veterinarians (AAV) http://www.aav.org/

American Association of Zoo Veterinarians http://www.aazv.org/

7.2. Websites

Parrot Lexicon http://www.parrot-lexicon.com/

Veterinary Information Network: http://vin.com/

7.3. Diagnostics and vaccine products mentioned in the text

Polyomavirus and PBFD PCR. Research Associates Laboratory, Inc., 100 TechneCenter, Suite 101, Milford, OH 45150)

Avian Polyomavirus Killed Vaccine. Biomune Co. 8906 Rosehill Road, Lenexa,KS 66215

Psittacine Pox Vaccine. Maine Biological Labs Inc., Waterville, ME 04901)

7.4. Journals

Journal of Avian Medicine and Surgery

Avian Diseases

Exotic DVM Magazine http://www.exoticdvm.com/

7.5. Texts and Articles

Veterinary Clinics of North America, Exotic Animal Medicine series. WB Saunders, Co.

Altman, Robert B., et al. Avian Medicine and Surgery. Philadelphia. W.B. Saunders Co., 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), 2004 : 12-18.

Denver, Mary C., et al. Comparison of two heavy metal chelators for treatment of lead toxicosis in cockatiels. AJVR , vol. 61 (8), 2000: 935-940.

Donoghue, Susan. Clinical nutrition of companion birds. Journal of Avian Medicine and Surgery, Vol. 11(4), 1997, pp. 228-246.

Eidson, Millicent. Psittacosis/avian chlamydiosis. JAVMA, v.221 (12), 2002: 1710-1712.

Fudge, AM (ed). Laboratory Medicine Avian and Exotic Pets. Philadelphia, PA : Saunders, 2000:99-110.

Gallerstein, Gary A. The Complete Pet Bird Owner's Handbook, 3rd Rev ed. Avian Publications, 2003. Available from Amazon.com.

Harcourt-Brown, Nigel and John Chitty. BSAVA Manual of Psittacine Birds. 2nd ed. Gloucester, UK : British Small Animal Veterinary Association, 2005.

Hoogesteijn, Almira L., et al. Oral treatment of avian lead intoxication with meso-2,3-dimercaptosuccinic acid. Journal of Zoo and Wildlife Medicine 34 (1), 2003: 82-87.

Gregory, Christopher R., et al. Proventricular dilatation disease : a viral epornitic. Proceedings of the 1997 Annual Conference of the Association of Avian Veterinarians, Reno, Nevada, September 1997, pp. 43-52.

Grund, Christian, et al. Serological studies on persistent aPMV-1 infection associated with PDD. Proceedings of the Annual Conference of the Association of Avian Veterinarians, New Orleans, LA, 1999:19-23.

Harrison, Gregg J. and Teresa L. Lightfoot. Clinical Avian Medicine. Palm Beach, FL : Spix Pub., c2006.

Holz, Peter, et al. Suspected zinc toxicosis as a cause of sudden death in orange-bellied parrots (Neophema chrysogaster). Journal of Avian Medicine and Surgery, 14 (1), 2000: 37-41.

Kearns, K.S. Avian Mycobacteriosis. In Recent Advances in Avian Infectious Diseases, K.S. Kearns and B. Loudis (eds.). http://www.ivis.org

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.

Olsen, Glenn H., and Susan E. Orosz. Manual of Avian Medicine. Mosby, 2000. Available through Barnes and Noble. (This text is used in the Advanced Avian Elective.)

Phalen, David N. Viremia, virus shedding, and antibody response during natural avian polyomavirus infection in parrots. JAVMA, Vol 217 (1), 2000: 32-36.

Reed, Holly H. Circovirus in lories and lorikeets. Proceedings of the AAZV and IAAAM Joint Conference, 2000: 317-321.

Rosskopf, Walter J., et al. Successful treatment of avian tuberculosis in pet psittacines. Proceedings of the 1991 Annual Conference of the AAV, Chicago, Illinois, September 23-28, 1991, pp.238-251.

Stanford, Michael. The effect of UV-B lighting supplementation in African Grey Parrots. Exotic DVM, 6.3, 2004: 29-32.

Stanford, M. Calcium metabolism In: Clinical Avian Medicine, Harrison G.J. and Lightfoot T.L. (Eds.), available on IVIS, 2006.

Topor, Suzanne V. The control and prevention of avian polyomavirus infection. Journal of Avian Medicine and Surgery, 13(3), 1999:157-159.

Tully, Thomas N, Lawton, Martin P.C., and Dorestein, Gerry M. (ed.) Avian Medicine. Boston : Butterworth Heinemann, 2000.