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Parrots and related species

Members of the parrot family are the most common avian pet and, therefore, the most likely to be presented to the veterinarian. Table 8-1 shows the most commonly encountered species.

Consultation and handling

Psychologically, most pet birds are little different from their wild ancestors—the veterinary surgeon constitutes a potential predator, so the bird is likely to exhibit a flight or fight response when handled. Exceptions to this are hand-reared parrots (or imprinted raptors and owls). However, in extremis, birds vary in their susceptibility to stress, and while some, such as the larger psittacines, can be handled relatively safely, others, such as canaries, carry a greater risk.

A great many captive-bred, hand-reared birds can be superficially examined while perched on the owner or on a freestanding perch, thereby minimizing stress. If care and patience are used, then auscultation of the lungs and air sacs, plus some assessment of body condition, can be achieved in this way.

It is important to weigh parrots at every consultation (Fig. 8-1); tame birds can be accurately weighed using a small perch designed to fit onto standard weighing scales.

Aggressive birds, or birds unused to handling, may need to be “toweled” in order to examine them. Use a large towel that will cover most of the bird. Drop or place it over the bird such that the head is covered and the bird cannot see your hands. With one hand, grab the bird's head or neck from behind so that there is control of the beak, and use the other hand to gather up the rest of the bird into the towel. Do not in any way compress the sternum, as this will seriously compromise the bird's breathing.

Birds will attempt to mask signs of illness and so may not exhibit clinical signs until a disease course is quite advanced. It is important to observe the bird from a distance for several minutes prior to handling, as a relaxed bird is more likely to show signs of ill health.

Important nonspecific clinical signs in parrots

• Heavy lidded/dark periorbital coloring

• Fluffed up/feather plucking

• Abnormal or absent feeding/drinking behavior

• Polydipsia/polyuria

• Lethargy

• Abnormal activity

• Change from normal perching activity or on floor of cage

• Abnormal profile

• Abnormal breathing action

• Abnormal vocalization

• Tail-bobbing. A sign of dyspnea. Respiratory rates of psittacines are high, but a recovery time exceeding 3 min would be considered abnormal.

• Regurgitation

From Malley (1996).

259

Table 8-1 ¾rrots and related species: Key facts
African grey parrot Blue-fronted Amazon parrot Blue and gold macaw Moluccan cockatoo Peach-faced lovebird Cockatiel Budgerigar
Average life span (years) 50-70 40-50+ 50-80+ 50+ 10+ 10-20+ 4-13
Weight (g) 300-400 320-460 950-1175 640-1025 50-61 80-90 45-50 (60+ for large show budgerigars)
Sexing DNA or surgical sexing DNA or surgical sexing DNA or surgical sexing DNA or surgical sexing. Also males have black irides, females have reddish brown. DNA sexing The small, ventral (true) tail feathers (not the overlying longer remiges) are barred in females (hard to assess in Lutinos).
The red-orange color of the cheek patches is more pronounced in males.
Cere is blue and smooth in males; brown and rough in females. Young blue mutation females may have a pastel-blue cere.
Estimating age Young chamber such as an incubator, and supply oxygen as close to the bird's head as possible.

3. Allow the bird a few minutes to relax in this warm, high-oxygen environment before continuing with the examination.

4. If it is imperative to handle the bird, warn the owner first that although you must do this, there is a chance of losing the bird. If necessary ask the owner to sign a consent form.

5. Handle the bird either with your hands or with a towel. Never use gloves or gauntlets. With larger psittacines, if necessary, have an assistant grip the head firmly from behind if you are concerned about being bitten. Do not grip around or otherwise compress the sternum as this will compromise respiration.

6. Consider either sedation or inducing anesthesia by masking the bird down with isoflurane or sevoflurane for a more detailed examination. For those birds with respiratory or cardiovascular compromise, the relative risks and benefits of anesthesia need to be considered.

Avian core body temperature often exceeds 40.5° C, and birds have a large surface area rela­tive to body mass, which means that they must expend a great deal of energy in thermal homeostasis. Feathers act as an insulative layer but do not grow back as readily as mammalian fur, so as few as possible should be removed, should surgery be indicated.

Heat loss and, therefore, energy conservation can be reduced by placing the bird close to a heat source—vivarium heat mats are ideal for this. Place a towel or similar over the mat to prevent burns and protect the mat from fluids. Young chicks are unable to thermoregulate, so they must be maintained in an incubator.

Fluid therapy

Birds are primarily uricotelic which, as in reptiles, predisposes them to gout-related problems. Blood volume is between 4.4 and 8.3 mL/100 g body weight in chickens. In some species, it can be as high as 14 mL/100 g.

Dehydration

1. Most critically ill birds should be assumed to be 5% to 10% dehydrated.

2. Increased skin turgor over the foot or upper eyelid, collapse or poor filling of the ulnar vein, sunken or glazed eyes, dry and tacky mucous membranes, tachycardia, depression, and red or wrinkled skin in psittacine neonates all indicate dehydration.

3. The daily maintenance water requirement for psittacine birds is around 50 mL/kg per day, with that of passerines and young birds being much higher.

4. A 500-g (0.5-kg) bird with 10% (0.1) dehydration, therefore, requires (0.5 ? 0.1) liters = 0.05 L = 50 mL fluid. As in other species, which fluids are given depends on the reason for giving fluids. Half of the fluid deficit should be replaced within the first 12 to 24 hours. The remaining 50% is divided over the following 48 hours, to be given alongside the daily maintenance.

Fluid administration

• Per cloaca. Water can be absorbed from the cloaca (and naturally from material refluxed into the colon), so this can be used as route for rehydrating with small volumes when there is a risk of aspiration pneumonia (Table 8-2).

• Oral fluids are usually given by crop tube. Not suitable for birds that are regurgitating, recumbent, or fitting.

• Intravenous. Birds can tolerate fluid replacement rates of up to 10 mL/kg given in a bolus, if given slowly over 5 to 7 minutes. Sites include the right jugular vein, brachial vein (Fig. 8-2), and the medial metatarsal vein. Intravenous catheters are difficult to maintain in birds, so bolus administration is preferred. Isotonic solutions should be administered slowly at a rate of 10 to 15 mL/kg. A “shock” dose of 90 mL/kg can be used if large volumes are needed rapidly. Suggested individual bolus volumes are listed in Table 8-3.

Table 8-2 Parrots and related species: Cloacal fluid administration
Species Suggested volumes for cloacal administration (mL)
Budgerigar 0.5
Cockatiel 1
Amazon 4
Macaw 6-7

Table 8-3 Parrots and related species: Suggested individual bolus volumes
Species Bolus volume (mL)
Budgerigar 1-2
Cockatiel 2-3
Conure 4-6
Amazon 8-10
Macaw 15-25

Fig. 8-2. Placement of an intravenous catheter into the brachial vein of a cockatoo. Use a collar if it is to be kept in place for several days.

• Subcutaneous fluids can be given into the interscapular area (not caudal neck to avoid the cervicocephalic air sac) or the inguinal region. Small volumes (5 to 10 mL/kg) should be given at each site, and absorption may be poor.

• Intraosseous. Distal ulna and proximal tibiotarsus. Strict asepsis and anesthesia. All types of fluids, including blood transfusions. Do not administer very acidic, alkaline, or hypertonic solutions IO without diluting them first.

Choice of parenteral fluids

• Crystalloids. Only 25% of a crystalloid solution remains in the peripheral vasculature 30 minutes after administration. Hartmann’s solution contains lactate that is converted to bicarbonate by the liver and so may help correct acidosis but is contraindicated with hypernatremia.

• Hypertonic saline solution at 3% to 7.5% will help to correct circulatory collapse by triggering fluid shifts from the interstitial space into the circulation, followed quickly by isotonic solutions to prevent tissue dehydration. Do not use hypertonic solutions if cranial hemorrhages are suspected.

• Colloids. Bolus administration of hetastarch at 10 to 15 mL/kg IV t.i.d. for up to 4 treatments may be safe and effective for hypoproteinemia.

• Oxyglobin can be given at a dose rate of up to 15 mLzkg IV or IO.

• Whole blood. Birds are tolerant of anemia, but a transfusion should be considered if the PCV falls below 15.0 L/L. Use blood from the same or similar species; blood groups have been only poorly investigated.

Nutritional supplementation

If the bird is eating normally, then supply its usual diet. For short-term management, recovery diets commercially available for dogs and cats (nonmilk-based) may be crop-tubed for car­nivorous, insectivorous, or omnivorous birds. Dextrose can be given orally, by subcutaneous injection up to 2.5%, or IV. It is a metabolic acidifying agent and may be contraindicated in cases of metabolic acidosis. Note that most birds are diurnal and will not feed in the dark. For parrots, hand-rearing formula can be used.

Wing clipping of pet parrots

A badly clipped bird is not only at increased risk of damage to itself, but such clipping may also predispose to feather-picking and self-mutilation. Wing clipping can be controversial, but the major justification for wing clipping is that it facilitates the necessary interaction between a pet parrot and the other family members, allowing the bird to become involved with, and behave as, part of the family (or “flock”) rather than being confined to its cage. However, the ideal would be that the bird is left fully flighted and controlled verbally, using commands such as “step up,” “step down,” “leave,” and “no.”

Wing clipping

1. Both wings should be clipped, allowing the bird to maintain its balance.

2. It is the primary flight feathers that allow lift, and it is these that should be trimmed such that the cut end is tucked beneath the coverts.

3. Developing “pin” feathers should not be cut as these will hemorrhage; instead leave alone and leave a feather alongside it or on either side for support to prevent accidental damage.

Microchipping

1. Microchips are placed into the left pectoral musculature.

2. Occasionally hemorrhage may occur, but usually digital pressure is sufficient for hemostasis.

3. Microchips inserted SC, although potentially less traumatic, are readily palpable and are subject to removal and fraud.

Analgesia

Table 8-4 Parrots and related species: Analgesic doses
Analgesic Dose
Butorphanol 0.5-4.0 mg/kg IM every 2-4 hr
Carprofen 1.0-4.0 mg/kg SC or PO b.i.d.
Ketoprofen 1.0-5.0 mg/kg IM b.i.d. or t.i.d.
Meloxicam 0.1-0.5 mg/kg SC or PO s.i.d.
Morphine 0.1-3.0 mg/kg IV

Sedation

• Midazolam 0.5 to 3.0 mg/kg IM or intranasal

• Diazepam 0.2 to 2.0 mg/kg intranasal. IM administration likely to be irritant with delayed absorption (Mans 2014)

• Butorphanol 1.0 to 3.0 mg/kg IM or intranasal

• Midazolam 1 to 2 mg/kg plus butorphanol 1 to 2 mg/kg IM if heavier sedation is required. Macaws usually require this combination to gain adequate sedation for clinical procedures (Mans 2014).

• Benzodiazepines can be reversed by flumazenil at 0.01 to 0.1 mg/kg PO.

Anesthesia

From a practical point of view, induction and maintenance with gaseous anesthesia are of choice. Atropine can be given as premedication at 0.05 to 0.1 mg/kg SC. This reduces mucus and counters bradycardia from vagal stimulation during surgery.

Gaseous anesthetic protocol

1. Hold the bird's head into a mask or place into an induction chamber. Isoflurane offers a rapid induction and recovery (as does sevoflurane).

2. Intubate (uncuffed endotracheal tube) whenever possible.

3. During anesthesia, regularly give positive-pressure ventilation to reduce risk of CO2 buildup in the abdominal air sacs.

4. Main sources of heat loss are the extremities (especially the feet) and the air sacs. Wrap the feet with silver foil and maintain the bird on an external heat source.

5. If using halothane, start at low concentrations (0.5% to 1.0%) and gradually increase to 3.0% to 4.0%. Induction at high concentrations can lead to dangerously high levels of halothane present in posterior air sacs. Attempts to resuscitate bird by flushing through with oxygen or manual ventilation will only force this reservoir of halothane through the lungs, further increasing blood concentrations.

Parenteral anesthesia

1. Always weigh the bird accurately before using parenteral anesthesia, and always intubate and maintain on oxygen whenever possible.

2. A range of anesthetic protocols are available from the literature. The ones the author has used include:

a. Ketamine at 5 to 30 mg/kg IV or IM. No analgesic effect. Avoid birds with potential liver/kidney complications.

b. Ketamine 5 mg/kg plus xylazine 0.25 to 1.0 mg/kg IV or IM

c. Ketamine 5 to 20 mg/kg plus midazolam 0.25 mg/kg IV or IM. This gives good sedation, muscle relaxation, and recovery.

d. Ketamine 3 to 6 mg/kg plus medetomidine 25-100 gg/kg IV or IM

e. Both medetomidine and xylazine can be reversed with atipamezole at 5 ? medetomidine dose.

Air sac perfusion anesthesia

Avian respiratory anatomy means that the trachea can be “bypassed” by insertion of a suitable cannula into one of the caudal air sacs (abdominal or caudal thoracic) for delivery of oxygen and anesthetic gases. This technique is suitable for oral or tracheal obstructions or if surgery is required at or around the oral cavity. Glottal or tracheal foreign bodies or other obstruc­tions will usually give their presence away by producing a whistling sound during the respira­tory cycle. These birds are extremely liable to sudden death. The main priority is to establish a patent airway as quickly as possible, therefore the need to anesthetize and insert an air sac tube.

Air sac perfusion anesthesia technique

1. Use soft tube with holes in walls.

2. Use a 4-mm-diameter tube for a 350-g bird, increasing pro rata.

3. A left lateral approach is used with the left leg extended cranially and a small incision made behind the last rib and ventral to the flexor cruis medialis muscle (Fig. 8-3).

4. A small pair of hemostats can then be used to enter the coelom in a craniomedial direction, which will provide access to the caudal thoracic air sac.

5. A tube is then secured in place with a suture and attached to the anesthetic machine. Note: A higher airflow rate (>50% above normal) will be required to maintain anesthesia this way.

6. The tube can be left in situ for 1 to 3 weeks.

Fig. 8-3. Anatomical markers for the placement of an air sac tube.

Recovery

• Keep quiet.

• Wrap wings gently in towel/paper toweling to reduce injury from flapping.

• Keep warm, preferably mid-20s° C.

• Recovery must be fast from anesthetic—birds under 100 g should be eating within 30 minutes.

Cardiopulmonary resuscitation

1. Can use doxapram at 5 to 7 mg/kg IM or sublingually.

2. Intubate if not already done.

3. Intermittent positive-pressure ventilation once every 5 seconds.

4. If in cardiac arrest, begin rapid chest compressions.

5. Give epinephrine at 0.5 to 1.0 mL/kg of 1:1000 intrathecal, intracardiac, IO, or intraperitoneal.

Skin disorders

Avian skin is very thin, with the epidermis only up to 10 cells thick in feathered areas. There are few cutaneous glands:

1. Uropygial gland. Not present in all species (e.g., Amazon parrots and Pionus parrots). When present, it lies dorsally near the tip of the tail. There can be up to 18 orifices depending on the species. Usually bare except for a tuft of down feathers known as uropygial wick. Secretes a lipoid sebaceous secretion—sebum—that is water repellent. It also helps to keep plumage supple and smooth, contains vitamin D3 precursors, has antibacterial and antifungal properties, and enhances feather coloration. However, most sebum is produced from epidermal cells that contain keratin-bound phospholipids that coat the skin and feathers.

2. Small wax-secreting glands are present in the external wall of the auditory meatus.

3. There are mucus-secreting vent glands.

4. There are no sweat glands.

Commensal bacterial numbers on the skin of birds are considered to be lower than those found on mammals. Yeasts are infrequent commensals. Malassezia is not isolated from normal or self-mutilating birds (Preziosi et al 2006); in the same study, Candida albicans was isolated but significance was unclear.

Feathers serve a number of functions, including insulation, protection from trauma, acces­sories to flight, species recognition patterns, and display. There are several types and sub­groups of feathers.

Feather types

1. Contour feathers are divided into:

a. Flight feathers

i. Remiges (carried on the wing)

(1) Primary—borne on the manus

(2) Secondary—borne on the antibrachium

ii. Retrices (carried on the tail)

b. Body feathers

c. Coverts—cover the bases of the retrices or remiges

d. Ear coverts—screen the external opening of the ear and improve hearing

2. Other feathers include down feathers, filoplumes, bristles, and semi-plumes. Various intermediate forms of feathers will be encountered. Powder feathers usually structured like down feathers, occasionally semi-plumes, and contours shed a fine white powder of keratin onto contour feathers to provide waterproofing. Particularly obvious in African grey parrots and cockatoos.

Signs of skin disease

Pruritus

• Flies

• Hippoboscids (flat flies/louse flies) occasionally encountered, especially with aviary birds. Can transmit hemoparasites such as Haemoproteus and Leukocytozoon, as well as transferring mites and lice among individuals.

• Lice: Can reach significant numbers on debilitated birds

• Ticks: Occasionally on new imports. Sudden death associated with tick attachment to head. Suggested etiologies include hypersensitivity reactions, toxin injection, or a tickborne infection. Can also transmit other diseases such as haemoprotozoan parasites, Borrelia spp., and louping ill

• Red mite (Dermanyssus avium) and other species

• Northern fowl mite (Ornithonyssus spp.)

• Feather mites: Found between the barbs on the ventral surfaces of feathers. Often niche specific so in the budgerigar, Protolichus lunula is found on the wing and tail feathers, whereas Dubininia melopsittaci occurs on the smaller body feathers.

• Quill mites: Live inside quills

• Sarcoptid mites present on the feather shafts may be encountered occasionally. Treat as above.

• Quill wall mites

• Skin mites

• Epidermoptid mites

• Knemidocoptid mites. Common is Knemidocoptes pilae (scaly face/scaly leg)

• Harpirhynchid mites: Attach to feather bases. May induce hyperkeratotic epidermal cysts

• Cheyletiellid mites: Rare

• Polyfolliculitis: Common in lovebirds. Multiple feathers arise from single feather follicle.

Fig. 8-4. Stress lines in the primary and secondary flight feathers in an African grey parrot. Note also the abnormal red pigmentation.

Ulceration/folliculitis

• Erysipelas

• Staphylococcus

• Aspergillus

Feather damage, pathology, and loss

• “Stress” lines (see “Findings on Clinical Examination” below and Fig. 8-4)

• Dystrophic feathers sometimes occur secondary to folliculitis.

• Polyomavirus (papovavirus): Usually presents in chicks but is carried asymptomatically by adults. Signs include a distended abdomen, lack of or malformed down feathers, multifocal follicular and feather pulp hemorrhages, and retarded growth of tail and contour feathers (infected budgie chicks may be referred to as “walkers”). There may be a urate-soaked vent because the virus also infects the liver and the kidneys. Also slow weight gain, slow emptying crop, and vomiting. This virus is responsible for budgerigar fledgling disease, which usually is rapidly fatal.

• Psittacine beak and feather disease (PBFD, circovirus; Fig. 8-5). Usually affects birds younger than age 3 years. Signs include loss of feathers, decrease in down feathers on flanks, retained pin feathers, short clubbed feathers, and deformed feathers. Beak may change in color, grow abnormally, and become necrotic, beginning with a palatine crust in the maxillary beak. Secondary bacterial infections make the condition worse. Older, chronically infected African grey parrots may produce red feathers in abnormal position such as the covert feathers (Fig. 8-6).

Diet

• In macaws especially, thinning of the feathers and retention of keratin sheaths of pin feathers, in particular the flight and tail feathers, is linked to poor diet.

Fig. 8-5. Psittacine beak and feather disease in a sulfur-crested cockatoo.

• Unsupplemented seed diets are deficient in minerals, sulfurous amino acids, and vitamins; birds on unsupplemented diets show increased feather replacement intervals (Wolf et al 2003) and may exhibit old, tattered feathers.

Self-trauma

• Secondary to ectoparasites

• Hand-reared parrots may never learn the normal species-specific methods of preening.

• Grossly abnormal feathers in budgerigars—called feather dusters or chrysanthemum disease—are a genetically recessive condition.

• Chewing at extremities; can be secondary to topical irritations

Scaling and crusting

• Papillomavirus: Reported in Timneh African grey parrots. Proliferative cutaneous lesions seen on head, especially eyelids, beak commissure, and skin contiguous with lower beak

• Herpesvirus: Described in cockatoos and macaws as dry proliferative lesions on the toes that are limited to extremities; not life-threatening

• Hyperkeratosis of the plantar surfaces of the feet—hypovitaminosis A (see Nutritional Disorders)

Erosions and ulceration

• Neoplasia (squamous cell carcinoma; Klaphake et al 2006)

Fig. 8-6. Abnormal red pigmentation in an African grey parrot with psittacine beak and feather disease.

Nodules and nonhealing wounds

• Avian pox virus (skin pox)

• Wartlike lesions of the skin. Yellowish nodules form on the beak, eyelids, and other areas of the skin that disintegrate and discharge a serosanguineous fluid. The areas then scab over. When present on the feet, lesions may occlude distal vasculature, resulting in tissue necrosis of the lower extremities. Note: Can occur in a diphtheritic form or a septicemic form.

• Staphylococcus may occasionally be encountered as a cause of dermatitis. More often it is isolated as a secondary invader in bumblefoot.

• Candidiasis has been seen as focal raised lesions as well as more generalized ulcerations. Head lesions have been reported in eclectus parrots, Amazon parrots, and cockatiels. Aspergillus lesions, Trichosporon asahii, and dermatophytosis are occasionally encountered.

• Feather cysts: Secondary to follicle damage; the developing feather is unable to emerge and forms a large, cystlike structure.

• Cryptococcosis (Berrocal 2004)

• Mycobacteria (Ferrer et al 1997)

• Bumblefoot: Typically chronic infection and abscessation of the feet, especially the plantar surfaces. Often due to staphylococci or streptococci.

Changes in pigmentation

• Erysipelothrix infections may cause an erythema of the skin in an acute infection with sudden death.

Fig. 8-7. Prepatagial chronic ulcerative dermatitis in an African grey parrot.

Chronic ulcerative dermatitis (CUD)

• Usually associated with chronic conditions such as mycobacteriosis, tumors, abscesses, or xanthomas. Poor nutrition may also contribute. Four main presentations are:

• Prepatagial CUD: Wing web area. Possibly linked to Giardia or hypovitaminosis E. Usually very pruritic and painful. Patagium may also be affected. Commonly seen in chronic self-mutilating African greys (Fig. 8-7)

• Proventer CUD: Keel area; common in African greys and large Amazons. Secondary to trauma following hard landings. Bruises or splits forming ulcers.

• Postventer CUD: Between cloaca and tail. Possibly similar etiology to proventer CUD. Poor nutrition also implicated

• Squamous cell carcinoma (Klaphake et al 2006)

• Ectoparasites (see “Pruritus” above)

Alopecia

• Pruritic (self-mutilation) versus nonpruritic. PBFD is provisionally differentiated from self-inflicted trauma in single birds as feathers on head also affected; normally bird cannot reach these to self-damage.

Neoplasia

• Lipomas (Fig. 8-8), fibrosarcomas, liposarcomas, and squamous cell carcinomas are some of the more common skin neoplasms reported in birds. Xanthomas are common, especially in budgerigars. These are nonneoplastic yellowish nodules or plaques caused

Fig. 8-8. Lipoma in a budgerigar.

by an accumulation of cholesterol and fats. Can be ulcerative. Often found over an area of pathology such as a lipoma.

Allergies

• There is a strong suggestion that allergies may be the cause of skin disease in some cases, especially in Old World psittacines.

Findings on clinical examination

• Observe bird in cage or at rest on owner. Assess if it show signs of a typical sick bird—ruffled, fluffed up feathers, sleepiness, and tail “pumping.” Is it pruritic?

• Assess the surroundings. Are feces normal? Stress or sudden influx of fruit may trigger very loose feces.

• Handle the bird:

• Examine nares, beak, eyes, and buccal cavity, including choana. Look particularly for signs of vitamin A deficiency (see Nutritional Disorders).

• Examine skin; note signs of inflammation, hyperkeratosis, ulceration, and trauma.

• Assess feather quality:

• Stress lines—lines visible on the vanes of the feather that denote areas of poor quality of the barbs. Thought to be linked to release of endogenous corticosteroid.

Fig. 8-9. Anesthesia of a cockatoo for further skin investigation.

• Frayed, dirty, or matted feathers: Inappropriate size caging may cause repeated damaged to the retrices of those birds with long tails such as parakeets and macaws.

• Abnormal feather coloration may result from nutritional deficiencies, hepatopathies, or PBFD.

• Examine for parasites:

• Pluck one or two feathers for examination under a light microscope for ectoparasites and feather pulp examination.

• Examine uropygial (preen) gland, cloaca, and feet.

• Auscultate heart, lungs, and air sacs.

• Palpate abdomen.

• Anesthesia may be required with birds difficult to handle safely (Fig. 8-9).

Investigations

1. Routine hematology and biochemistry

a. Zinc and lead levels may be appropriate to investigate low-grade heavy metal poisoning. Collect samples for zinc in either heparin or plain tube (without gel as this may contain zinc). Although blood levels can be indicative of zinc toxicity, there is no absolute correlation between blood zinc levels and clinical signs. As a general rule, if zinc levels are >32 to 50 pmol/L and there are consistent clinical signs (see Neurologic Disorders and Gastrointestinal Tract Disorders), then zinc toxicity should be suspected. Significant zinc levels are often accompanied by an absolute or relative monocytosis.

2. Aseptic collection of samples for bacteriology/mycology

3. Cytology

4. Radiography: A standing view using horizontal beam is useful for detecting metallic foreign bodies in the conscious bird; otherwise lateral and ventrodorsal views, under general anesthesia (GA), are required for meaningful radiography.

5. Endoscopy

6. Serology for PBFD, polyomavirus, Aspergillus antigen, and Chlamydophila antigen should be taken if thought necessary.

7. Fresh fecal samples for parasitic examination; look for Giardia, nematode eggs, etc. Smears can be dried and stained.

8. Bulk fecal samples (collected over 3 to 5 days) can be submitted for Chlamydophila polymerase chain reaction (PCR).

9. Diagnostic imaging, including radiography and endoscopy

10. Biopsy

a. Note: Eosinophilic dermatitis linked to Trichosporon asahii infection.

Management

• Optimize diet: Consider converting to pelleted foods, using multivitamin supplements, reducing seed intake, and increasing fruit consumption where appropriate.

• Where there is significant feather loss, consider supplementary heating to counter loss of insulation.

• Covering broad-spectrum antibiotics may be useful if there are obvious skin lesions.

• If pruritic, consider analgesia—meloxicam (Metacam) oral suspension at 0.1 mg/kg body weight b.i.d. Do not use steroids.

• Collars

• Collars are inherently very stressful to parrots; they interfere with normal feeding (many parrots transfer their food to their mouth with a foot), flight, climbing, and crop function. They are heavy relative to the weight of the bird and generally alienate the bird from its immediate surroundings. They also do not address any underlying cause or pathology, and if these are not addressed then feather plucking/self- mutilation may resume when the collar is removed.

• Therefore, collars should be used judiciously and on a case-by-case basis.

• If possible, hospitalize the parrot for 24 to 48 hours to enable the bird to get used to the collar, as well as allowing any minor adjustments and reassessments to be made.

• A collar should be removed only after the bird has been clinically well for a reasonable period of time, as it is likely that, as in other species, abnormal or triggering sensations will persist for some time following the clinical resolution of lesions. Early removal often results in repeat damage.

TreatmentZspecific therapy

• Ectoparasites

• Ticks: Treat with ivermectin or fipronil. Remove ticks manually where possible.

• Red mite and other species

- Ivermectin at 0.2 mg/kg PO, SC, or IM. Repeat monthly as required

- Light dusting with pyrethrin powder

- Treat environment in case of red mite; painting woodwork may “seal in” mites.

• Feather mites

- Cis-permethrin powder

- Fipronil spray applied to cotton wool; beware hypothermia in small birds due to evaporation of carrier.

- Treat quill mites, sarcoptid mites, and quill wall mites as for feather mites.

• Knemidocoptid mites (e.g., Knemidocoptes pilae):

- Ivermectin at 0.2 mg/kg PO, SC, or IM. A small drop may be applied topically over the jugular vein or onto the back of the neck and seems to work well. Injection is not recommended in birds weighing Polyomavirus: In some countries such as the United States, vaccination may be available. The virus may persist in the environment for some time, so testing with PCR should be undertaken.

• Bumblefoot: Usually requires surgical intervention; bird may need supportive dressing on affected foot to prevent reinfection of surgical site. If the condition is unilateral, be aware of pressure sores and other sequelae affecting the good leg due to bird shifting weight onto it.

The self-mutilating parrot

Self-mutilation, like stereotypies, is a form of abnormal repetitive behavior exhibited in captive parrots. Often psychological in origin, the alternative of an underlying causal disease should not be ruled out, either as differential diagnoses or as contributing factors. Epidemio­logic evidence (Garner et al 2005) points toward there being an inherited susceptibility, an increased incidence in females, and a link to certain stressful environmental conditions. There are no “quick fixes,” and investigation is often prolonged and expensive. A methodical and holistic approach is required. This should take into account the background of the bird, its environment, its disease status, and its psychological well-being.

Background

• Species

• Most common in African grey parrots and cockatoos (Cacatua spp.—Jayson et al 2014).

• Macaws and cockatiels often begin with the wings and legs.

• Amazon parrots and Moluccan cockatoos tend to mutilate skin rather than feathers.

• African greys will denude all areas of skin from neck down.

• Captive-bred/hand-reared (CBHR) or wild-caught? Wild-caught individuals may be more prone to parasitic or psychological causes, while nutritional causes may be more common in CBHR birds. Hand-reared parrots may never learn the normal, species­specific methods of preening.

• Single or with others? If with others, are any of them showing similar signs?

• House bird or aviary? Again parasites are more common in aviary than living rooms. If aviary, are others affected? Positioning the cage next to a wall is associated with increased risk of feather plucking (Jayson et al 2014).

• Is the parrot a recent introduction/acquisition of unknown clinical history, or a long-standing pet of known clinical history that has not been exposed to any new birds? Note: Even long-standing pets can be at risk of "new bird” problems if introduced or exposed to other birds it has not previously been with (e.g., if the owner buys another bird or the parrot is boarded at the local pet shop). Length of ownership also increases the risk of feather plucking (Jayson et al 2014).

• How long has the bird been self-mutilating?

• Is it constant or recurrent, and if recurrent, is it associated with anything (time of year, owner holidays, perceived periods of sexual activity)? Does it occur at a particular time of day?

• Was there an apparent initial trigger? Building work? New dog/child/partner? Birds not used to change may not tolerate it well.

• Does the bird self-mutilate when owner is present? Or when absent? Self-mutilation is associated with owners who have one or more holidays per year (Jayson et al 2014). If seen, how does bird behave while self-mutilating? Does it appear pruritic, vocalize or scream, or even interrupt a favored activity to self-mutilate?

• Try to find out what the bird's normal demeanor is. Is the bird normally relaxed, fearful, aggressive?

• How has the self-mutilation progressed? Where did the bird start plucking and how did it progress?

• How does the owner respond? In some psychological cases the noisy excitable response of the owner can become a reward for this behavior!

Environmental

Lighting

• Photoperiod: Many of the birds kept as pets are equatorial in origin and so are physiologically attuned for a 12-hour day/night cycle. African grey parrots exposed to longer than 12 hours of darkness are more likely to feather pluck (Jayson et al 2014).

• Intensity: The majority of psittacines are open scrub (budgerigars) or high canopy (parrots) species that are exposed to high-intensity sunlight. This would include UV light that may act as a natural antiparasiticide, bactericide, and fungicide.

• Spectrum: UV lighting in particular may be important with vitamin D3 synthesis from precursors excreted by the uropygial gland. In mammals vitamin D is important for normal skin function, and this may also be the case in birds.

Diet

• Seed-based diets are inappropriate for sole, long-term maintenance of many psittacines. Fat and hence energy levels are too high and protein levels relatively low and of poor quality. They are also low in vitamin levels.

• Attempt to wean onto newer pelleted diets. This can be difficult to do, plus anecdotally there seem to be occasional behavioral reactions to colorings used. Otherwise some basic research may be needed to ascertain suitable foods.

Water

• Amazons, African greys, and many others are from humid, tropical rainforest areas. A daily dowsing with water and consequent necessary preening may encourage normal feather and skin integrity. Daily spraying with lukewarm water or access to a bath is appreciated by many birds.

Environmental toxins

• Zinc, often from galvanized caging or cheap metallic toys: Blood levels can be indicative of zinc toxicity, but as with lead, there is no absolute correlation between blood zinc levels and clinical signs. As a general rule, if zinc levels are >32.0 to 50.0 pmol/L and there are consistent clinical signs (see Neurologic Disorders and Gastrointestinal Tract Disorders), then zinc toxicity should be suspected. Significant levels often accompanied by an absolute or relative monocytosis. Feather plucking can be associated with chronic low-grade zinc toxicity; gut problems may be seen as toxicity and can cause gut stasis. Acute poisonings can damage liver and kidneys, causing vomiting, polyuria, and hematuria. Consider radiography to look for metallic foreign bodies in the gizzard.

• Other heavy metals such as lead, copper, and iron may cause similar signs.

Treatment for zinc toxicity

• Sodium calcium edetate at 35 mg/kg IM b.i.d. for 5 days, stop for 3 to 4 days, and then repeat. Continue until zinc levels fall.

• Dimercaptosuccinic acid (DMSA) at 30 mg/kg PO b.i.d. for 10 days or 5 days per week for 3 to 5 weeks

• Penicillamine at 55 mg/kg PO b.i.d. for 7 to 14 days

• Tobacco smoke: May predispose to brittle feather production, as may an excessively dry atmosphere

• Toys: Psittacines are gregarious creatures. Most live as a pair within a flock and are constantly interacting with their flock members. All single psittacines should have a toy “friend” that they can feed, huddle up to, beat up, and generally completely dominate. Other toys should be rotated or changed with great frequency. Particularly useful toys are:

• Wooden objects, as these can be systematically destroyed, exercising the beak and claws, and occupying valuable time

• Toys into which food can be placed and with which the parrot must work to obtain its food

Findings on clinical examination

• Note if the condition is symmetrical. Self-mutilation due to psychological causes is often not symmetrical in early stages.

• Handle the bird:

• Examine nares, beak, eyes, and buccal cavity, including choana. Look particularly for signs of vitamin A deficiency.

• Examine skin; note signs of inflammation, hyperkeratosis, ulceration, trauma, and seborrhea.

• Assess feather quality:

• Stress lines—lines visible on the vanes of the feather that denote areas of poor quality of the barbs—may indicate that a significant stressor has happened to the bird at a crucial point in the development of that feather. This may have been a disease or nutritional deficiency.

• Frayed, dirty, or matted feathers: Inappropriate size caging may cause repeated damage to the retrices of those birds with long tails such as parakeets and macaws.

• Abnormal coloration may result from nutritional deficiencies, hepatopathies, or PBFD.

• Examine for parasites:

• Pluck one or two feathers for examination under a light microscope for ectoparasites and feather pulp examination.

• Feather scoring:

• This allows a structured approach to defining and monitoring the extent of the self-mutilation. A final score is arrived at and noted, allowing an objective view of improvement or deterioration to be assessed. Feather scoring may prove difficult with a recalcitrant bird and should GA be needed (e.g., for radiography), this would provide an ideal opportunity to assess this (Fig. 8-10).

Investigations

1. A general blood screen is highly recommended. Especially interested in WBC count and differential, liver and kidney biochemistry, and zinc levels.

2. Blood samples for PBFD or polyomavirus PCR

3. Chlamydophila serology

4. Fresh fecal samples for parasitic examination; look for Giardia, nematode eggs, etc.

5. Bulk fecal samples (collected over 3 to 5 days) can be submitted for Chlamydophila PCR.

6. Diagnostic imaging, including radiography and endoscopy

7. Aseptic collection of samples for bacteriology/mycology

8. Biopsy

Pathological causes of self-mutilation

Refer to Skin Disorders.

Otherwise significant conditions include:

• Chlamydophilosis

• Staphylococcus has been linked to feather-picking in a budgerigar and feather loss in an unspecified psittacine (Hermans et al 2000).

Fig. 8-10. Feather scoring system. From Meehan et al 2003a.

• Aspergillus

• Avian bornavirus (proventricular dilatation disease, PDD)

• Other diseases, including hepatopathies and renal disease

• Endocrinologic

• Hypothyroidism—rare (see Endocrine Disorders)

• Sex hormone disturbances: Self-mutilation can be associated with seasonal changes or sexual activity. May pick at leggings. It is normal in many species to remove a patch of feathers ventrally at nesting time to form the brood patch whereby eggs can be kept warm. Consider measuring serum estrogen or androstenedione levels. Possible sex predisposition toward females.

Psychological causes of self-mutilation

• Frequently overdiagnosed. Should only be considered when other etiologies have been reasonably eliminated.

• True cause not yet elucidated. Adverse environmental stimuli likely to be involved in many cases (see Garner et al 2005); may in some cases be linked to commercial bird-rearing techniques and practices that nestling parrots are exposed to at a time of neurologic development with high psychological sensitivity and receptivity

• Suggested manifestations include:

• Attention seeking: Abnormal behavior is reinforced by the owner paying attention when bird self-mutilates.

• Displacement behavior: In the wild stressful situations can be avoided by flying off. In captivity this may not be an option, and so fear/aggression may be channeled into exaggerated “normal” behavior such as preening.

• Boredom, including the concept of time budgets: In the wild, a parrot will spend a significant amount of time flying to and from roosts and food sources, interacting with flock mates, avoiding predators, and so on. In captivity this time void can be filled by extending other normal behavioral repertoires that it can undertake, such as eating (especially Amazon parrots) or preening.

• Separation anxiety: The high intelligence of parrots suggests that this could be quite common.

• Obsessive-compulsive disorders: Akin to stereotypic disorders—bird will stop favored activity just to pluck.

Psychotropic drugs

These should not be considered a first line of action; their use should be considered once a physical or environmental problem has been reasonably ruled out or addressed. Suggested medications include:

1. Amitriptyline at 1.0 to 5.0 mg/kg PO b.i.d.

2. Doxepin at 0.6 mg/kg IM or IV daily 0.5-2 mg/kg PO every 12 hours, or 2 drops of 5.0 mg/kg solution per 30 mL drinking water

3. Fluoxetine at 0.4 mg/kg PO daily

4. Haloperidol at 0.1 to 0.4 mg/kg PO daily

a. Alternatively, dilute 3.0 mg into 1 L of fresh drinking water, offered fresh daily; increase the dose progressively by double dosing every 2 weeks until a dose of 12.0 mg/L is achieved.

b. Continue treatment for at least 3 to 4 months before gradually withdrawing over a period of time.

c. May induce Parkinson-like tremors, which disappear when drug is withdrawn

d. Haloperidol works reasonably well with self-mutilating birds; behavior of the bird is likely to alter for the better long before feather improvements are seen.

Management

1. Correct diet. Ideally change to pelleted foods. At the very least, begin supplementation with multivitamin and/or calcium (if appropriate).

2. Address any environmental issues such as photoperiod, irritants such as smoking, and so on.

3. Remove any metallic objects from the cage.

4. Consider environmental enrichment techniques (more/different toys; companion of same species if no risk of infection, etc). If left alone for long periods, consider leaving radio or TV on. Birds naturally inhabit noisy environments—silence usually means there is a predator about. Environmental enrichment (including provision of a conspecific companion) has been found to be beneficial in birds displaying both self-mutilation (van Hoek and King 1997) and stereotypies (Meehan et al 2003b, Meehan et al 2004).

5. If pruritic, consider analgesia—meloxicam at 0.2 mg/kg PO, IM body weight once daily.

6. Attend to any obvious wounds. Application of topical amorphous hydrogel dressings (e.g., IntraSite Gel, Smith and Nephew Healthcare Ltd) encourages secondary healing.

7. Where there is significant feather loss, consider supplementary heating to counter loss of insulation.

8. Undertake specific treatment regimens as results of tests dictate.

9. Avoid the use of collars unless absolutely necessary. May stress bird and interfere with normal behavior, including feeding and crop function.

10. Basic training—“Step up,” “Step down,” “No,” and “Stay”—can be useful in both interacting with the bird in a controlled manner and filling in valuable time. The ideal is to establish a parent-child or leader-follower relationship rather than a partner­partner one.

11. Do not forget the owners. They are likely to be embarrassed at the state of the bird and feel guilty if they have been feeding their bird the wrong food or if some other managemental deficit is identified, but you need them on board for what is liable to be a prolonged haul. They must be encouraged not to lose heart, as improvement may take some time.

Upper respiratory tract disorders

Nasal tract

Cere color in budgerigars is a secondary sexual characteristic; in most sexually mature males it is a smooth, bright blue structure, while in most females it has a rougher texture and is brown in color. Young female light blue birds may have a pastel blue cere, leading to incorrect sexing; these darken to a more normal female-type cere with maturity. Gonadal tumors may secrete inappropriate sex hormones that can lead to a change in cere color of adult birds.

Rhinitis

Viral

• Paramyxovirus (see Lower Respiratory Tract Disorders)

• Influenza A (orthomyxovirus—see Lower Respiratory Tract Disorders)

Bacterial

• Chlamydophilosis

• Mycoplasmosis

• Other bacteria

Fig.8-11. Blocked nares in an African grey parrot.

Fungal

• Aspergillus

• Candida (see “Treatment” in Lower Respiratory Tract Disorders)

Dietary

• Hypovitaminosis A (see Nutritional Disorders)

Neoplasia

Other noninfectious problems

• Choanal atresia

• Allergies

• Rhinoliths—require surgical removal followed by antibiotic cover; often linked to hypovitaminosis A (Fig. 8-11)

Investigations

1. Radiography

2. Rhinogram

3. Routine hematology and biochemistry

4. Culture and sensitivity

5. Endoscopy of choana

6. Biopsy

Sinusitis

• Typically presents as swelling of the infraorbital sinus

• For possible etiologies, see “Rhinitis” above and Lower Respiratory Tract Disorders.

• Bacterial

• Mycobacterium spp.

• Mycoplasmal

• Fungal

• Papillomas

• Sunken eye sinusitis: Collapse of the outer delineating skin due to negative pressure in the infraorbital sinus, which results from blockage of normal connecting diverticuli. Should return to normal when sinus problem is resolved.

• Neoplasia

• Teratoma (Diaz-Figueroa et al 2005)

• Thymoma (Diaz-Figueroa et al 2004)

Treatment

• Appropriate antibiosis

• Flushing of the infraorbital sinus, followed by culture and sensitivity plus cytology as appropriate

• Surgical removal of inspissated material

Lower respiratory tract disorders

Viral

• Paramyxovirus

• Avian pox virus (diphtheritic form)

• Amazon tracheitis virus (herpesvirus)

• Orthoreovirus

• Influenza A (orthomyxovirus)

• Adenovirus—interstitial pneumonia

• PDD—secondary aspiration and inhalation pneumonia

Bacterial

• Mycoplasma spp.

• Chlamydophilosis—primarily C. psittaci, but other serotypes occasionally encountered

• Escherichia coli

• Pseudomonas spp.

• Bordetella avium

• Mycobacterium avium

• Others

Fungal

• Aspergillosis

• Cryptococcosis

Protozoal

• Sarcocystis falculata (Coccidia)

Parasitic

• Tracheal mites Sternostoma tracheacolum (in small parakeets and cockatiels)

• Air sac worms (e.g., filarid nematodes)

• Cyathostoma and Syngamus spp. (rare)

Dietary

• Hypovitaminosis A

• Squamous metaplasia of the respiratory tract predisposes to respiratory infections.

Neoplasia

• Glottal neoplasia

• Hemangiosarcoma (Hanley et al 2005)

• Hepatic neoplasia or other coelomic mass

Other noninfectious problems

• Tracheal foreign body—seed husk a common finding in cockatiels

• Polytetrafluoroethane (PTFE) toxicity from overheating of Teflon

• Inhalation of other fumes from fires

• Abdominal disease (e.g., neoplasia, hemocoelom, yolk serositis)

• Hypothyroidism (goiter) in budgerigars on a seed-only diet

• Air sac rupture (usually pathological)

• Cigarette smoke

• Creosote

• Anemia

• Allergic, asthmalike conditions

• Chronic pulmonary interstitial fibrosis (CPIF), especially in older Amazon parrots (Zandvliet et al 2001). Preexisting pulmonary damage or allergies may contribute to the etiology of CPIF.

• Cardiovascular disease (see Cardiovascular and Hematologic Disorders)

Findings on clinical examination

• Dyspnea and tachypnea—can be very severe

• Open-mouthed breathing

• Change in voice—may cease "talking"

• Sneezing

• Head swinging and neck stretching. Forward-leaning and extended neck strongly suggests tracheal obstruction.

• Coughing occasionally encountered, but is uncommon. Beware parrots that imitate their owner's cough.

• Tail-pumping

• Increased recovery time/exercise intolerance

• Increased inspiratory sounds often associated with upper respiratory tract disease.

• Increased expiratory sounds often associated with lower respiratory tract disease.

• Abdomen may be distended (fluid, neoplasia, hemorrhage).

• Subcutaneous air-filled swelling; may vary in size (ruptured air sac)

• Yellow urates and peracute death common with Sarcocystis. Old World parrots are especially susceptible.

Investigations

1. Radiography

a. Ventrodorsal view is best for detecting abnormalities of the lungs and air sacs.

b. Distension of abdominal air sacs indicates upper respiratory obstruction (e.g., tracheal fungal granuloma or seed husk).

Table 8-5 Parrots and related species: Chlamydophila serology

Result of Chlamydophila serology Interpretation
Negative (no antibodies to C. psittaci) May not have seroconverted. Retest in 7-10 days in acutely ill birds.
Weak positive Suspicious, but interpretation may depend on species tested and test used. May also reflect previous exposure.
Strong positive Highly indicative of infection, especially if accompanied by consistent clinical signs.

2. Fluoroscopy

3. Routine hematology and biochemistry

a. Very high heterophil count (15 to 40 ? 109/L) indicative of aspergillosis

b. High PCV: 0.55 to 0.74 L/L in chronic pulmonary interstitial hyperplasia. Also often have a respiratory acidosis with a pH of 7.16 to 7.3 (normal, 7.35 ± 0.08), hypoxemia: PO2 of 33.69 to 52.77 (normal, 49.46 ± 7.62), and hypercapnia: PCO2 of 48.77 to 80.08 (normal, 37.92 ± 4.23) (figures from Zandvliet et al 2001)

c. High aspartate transaminase (AST) and creatine kinase (CK), often with Saraxystis

4. Serology for Sarcocystis, Aspergillus, and Chlamydophila—ideally investigate with repeat sampling to assess rising titer, but screening tests may also be useful (Table 8-5)

5. Hemagglutination inhibition tests and ELISAs may be of benefit in detecting influenza A.

6. Culture and sensitivity

a. Tracheal lavage; needs GA

7. Cytology

8. Endoscopic biopsy

9. Endoscopy

a. Endoscopic examination of trachea and syrinx

b. Air sacs and lungs (high-risk procedure)

10. Transillumination of trachea in small psittacines may reveal mites or nematodes (rare).

a. Mite or nematode eggs may be detected in feces or sputum microscopic examination.

11. Fecal samples

a. Chlamydophila PCR

b. Modified Ziehl-Neelsen staining of fecal samples or PCR for mycobacteriosis

Management

1. Reduce stress as much as possible. Placing bird in a darkened room may help.

2. Covering broad-spectrum antibiosis; may be given by nebulization

3. Provide oxygen support.

4. Nutritional support

5. Placement of a tube into a caudal air sac to allow normal breathing in cases of tracheal blockage

6. Bronchodilators (e.g., aminophylline 4.0 mg/kg PO or IM b.i.d.)

7. Mucolytics (e.g., bromhexine at 3.0 to 6.0 mg/kg IM or 6.5 mg/L fresh drinking water daily)

TreatmentZspecific therapy

• Foreign body

• Remove if possible; may require endoscopy or tracheotomy

• Emphysema

• Physical tapping and draining of air from emphysematous lesions. May need to be repeated. If necessary, place a stent if it fails to resolve quickly.

• Viral diseases

• Provide supportive treatment and covering antibiosis.

• Amazon tracheitis virus: Acyclovir at 10 to 40 mg/kg IV or SC t.i.d.

• Influenza: Provide covering antibiosis. Potentially a zoonosis and reverse zoonosis, so avoid contact with infected people.

• Paramyxovirus: Supportive treatment. Paramyxovirus A (Newcastle disease) is notifiable in the UK.

• Chlamydophilosis

• Enrofloxacin at 5.0 mg/kg IM daily or 12.5 mg into 100 mL drinking water fresh daily

• Doxycycline

- Doxycycline hyclate intravenous human preparation given 60 to 100 mg/kg IM every 5 to 7 days for 45 days

- Doxycycline hyclate as an in-water powdered medication: Use deionized water. However, Flammer et al (2003) found that drinking water with 400 mg of doxycycline/L over a 14-day period failed to maintain therapeutic plasma doxycycline concentrations.

- In the same study, hulled seed coated with sunflower oil and doxycycline powder to a concentration of 300 mg of doxycycline hyclate/kg maintained therapeutic plasma doxycycline concentrations for 42 days without notable adverse effects.

- Note: Birds may be intermittent excreters, so at least 3 consecutive negative samples should be achieved before ceasing treatment.

• Bacteria: Appropriate antibiosis

• Mycobacteriosis

• Potential zoonosis. Consider euthanasia.

• Two suggested treatment regimens (Rupiper et al 2000) are:

- Ethambutol (200 mg), isoniazid (200 mg), and rifampin (300 mg) all crushed together and mixed with 10 mL of a simple syrup. This is administered daily according to Table 8-6.

- Combination therapy of ethambutol (10 mg/kg PO b.i.d.), streptomycin

(30 mg/kg IM b.i.d.), and rifampin (15 mg/kg PO b.i.d.)

Table 8-6 Parrots and related species: Volumes required for suggested treatment regime of Mycobacteriosis
Bird weight (g) Volume of mixture (mL)
rule, if zinc levels are >32 to 50 pmol/L and there are consistent clinical signs (see also Neurologic Disorders and Gastrointestinal Tract Disorders), then zinc toxicity should be suspected. Significant levels are often accompanied by an absolute or relative monocytosis.

• Radiography (Figs. 8-14 and 8-15)

• Standing radiograph for ingested metallic particles

• Contrast radiography of old, discharging tongue lesions to investigate presence of possible foreign body

• Ileus may indicate an enteritis, heavy-metal toxicity or PDD (Fig. 8-16)

• Endoscopy

• Creamy-yellow lesions in the crop and/or esophagus suggest trichomoniasis. Take grab biopsy and look at wet prep under microscope.

• Ultrasonography

• Fluoroscopy

Management

1. Supportive treatment, including fluids (see Nursing Care)

2. For proventriculitis, consider:

a. Metoclopramide at 0.2 to 0.5 mg/kg IM or PO b.i.d.or t.i.d.

b. Cimetidine at 5 mg/kg PO b.i.d.

c. Gavage with activated charcoal

Fig. 8-14. Diagram of radiographic anatomy of a psittacine (lateral view).

Fig. 8-15. Diagram of radiographic anatomy of a psittacine (ventrodorsal view).

Fig. 8-16. Radiograph of a young African grey parrot with ileus.

TreatmentZspecific therapy

• Trichomonas

• Metronidazole at 50 mg/kg PO every 12 hours for 3 doses; alternatively 30 mg/kg PO

b. i.d. for 5 to 7 days (Girling 2004)

• Candida

• Nystatin at 300,000 IU/kg PO b.i.d. for 10 days

• Amphoteriin B at 1 mg/kg PO b.i.d.

• Sour crop: Flush with warmed saline solution. May need to be done under GA; consider intubation and packing of the choana prior to flushing.

• Megabacteriosis (Macrorhabdus ornithogaster)

• Amphotericin B at 1 mL/kg PO of 100 mg/mL suspension b.i.d.; for budgerigars

0.5 mg/bird b.i.d. until organism is eliminated.

• Ketoconazole at 10 mg/kg b.i.d. PO.

• Laceration of the tongue may require suturing.

• Foreign body: Remove either via the oral cavity or surgery (ingluviotomy). If flushing out crop, do so under GA, intubated with head held down and choana packed to reduce risk of aspiration.

• Zinc or other heavy-metal toxicity

• Sodium calcium edetate at 35 mg/kg IM b.i.d. for 5 days, stop for 3 to 4 days, then repeat. Continue until zinc levels fall.

• DMSA at 30 mg/kg PO b.i.d. for 10 days or 5 days a week for 3 to 5 weeks

• Penicillamine at 55 mg/kg PO b.i.d. for 7 to 14 days

• Avian bornavirus (PDD—see Gastrointestinal Tract Disorders)

• Crop fistula in hand-reared psittacines: These may require surgical debridement and closure (two layered). Etiology is due to being fed on food that is too hot.

• Crop stasis due to dilute preparation: Increasing the concentration of the food mix to 20% to 30% dry matter will often rectify this problem.

• Ingluvoliths: Removal via the oral route or break down into smaller particles using warmed saline (Girling 2004)

• Goiter

• Supplement with iodine. A stock solution of 2 mL of strong Lugol's iodine solution in 30 mL water is prepared; 1 drop of this is added to 250 mL drinking water daily for treatment and 2 to 3 times weekly for prevention.

Assessment of droppings

Normally, there are both fecal and urinary portions to a bird dropping. The fecal part should be dark and well formed; the urinary part should contain white crystals of uric acid plus a small amount of liquid urine. However, fecal consistency reflects diet and, therefore, varies according to species, from small, hard droppings in budgerigars to liquid “squirts” in lori­keets. Therefore, birds presenting with diarrhea should have their feces closely examined to differentiate genuine loss of fecal consistency from polyuria.

Assessment of avian droppings

Fecal portion

• The fecal portion may be small or absent if:

• Bird is anorexic.

• Cloacoliths or other obstructions are present.

• May be poorly formed—genuine diarrhea (Fig. 8-17)

• May be abnormally colored:

• Blood may be present.

• Certain highly pigmented fruits may do this.

• May contain abnormalities such as:

• Undigested seeds

• Worm eggs or protozoal cysts (on microscopic examination)

Urinary portion

• May be dry if:

• Bird is on an all-seed diet (e.g., budgerigar).

• May have a high water content if:

• Bird is on a high water content diet (e.g., fruit or vegetables).

• The bird is polydipsic.

• If the bird is polyuric, always collect a sample and check for glucose, blood, and protein.

• May be abnormally colored:

• Light to dark green may indicate liver disease due to high biliverdin levels.

• Greenish to a bronze color may indicate liver disease but can also occur after trauma.

Fig. 8-17. Genuine diarrhea in a parrot. Note the loss of fecal consistency.

Always collect a fresh sample.

• Microscopic examination of a wet preparation will often pick up protozoa and worm eggs.

• Fecal flotation for protozoal oocyst counts

• Gram stain: The normal gut flora of psittacines should be predominantly gram-positive.

A Gram stain should highlight changes in the bacterial flora, including yeast overgrowths.

• Swab for bacterial culture and sensitivity if appropriate.

Differential diagnosis for gastrointestinal disorders

Viral

• Avian bornavirus (PDD—formerly known as macaw wasting disease; can affect a variety of psittacines) (Staeheli et al 2010)

• Paramyxovirus

• Chronic paramyxovirus infection can cause cloacal dilatation.

• Papillomatosis (a possible herpesvirus)

• Orthoreovirus and orthoreovirus-like agent (budgerigars)

• Pacheco disease

• Polyomavirus

• Rotavirus

• Picornavirus

• Adenovirus

Bacterial

• Hepatitis, proventriculitis, enteritis due to:

• E. coli

• Klebsiella spp.

• Pseudomonas spp.

• Salmonellosis

• Yersinia pseudotuberculosis

• Chlamydophilosis (psittacosis)

• Mycobacterium avium (avian tuberculosis)

• Clostridia

• Clostridium colinum and C. perfringens in lories (Pizarro et al 2005)

• Megacolon secondary to C. tertium

Fungal

• Candida

• Megabacteriosis (Macrorhabdus ornithogaster)

• Mucormycosis

Protozoal

• Giardia

• Spironucleus (Philbey et al 2002)

Parasitic

• Uncommon in psittacines, but ground-feeding Australian parakeets are particularly at risk

• Nematodes

• Ascarids (especially Ascaris platycerci and Ascaridia hermaphrodite) and Porrocaecum spp.

• Capillaria

• Thelazia and Oxyspirura spp.

• Spiruroids: Proventricular worms (e.g., Geopetitia, Dispharynx, Habronema, and

Tetrameres spp.)

• Cestodes (e.g., Raillietina spp.)

Dietary

• Dietary indiscretion

Neoplasia

• Gastric carcinoma

• Gastric adenoma

• Papilloma (papillomatosis—see “Viral” above).

Other noninfectious problems

• Calcinosis circumscripta (deep granuloma in tongue)

• Proventricular ulceration

• Proventricular impaction

• Foreign body

• Sloughed koilin due to ventriculitis

• Dysplastic koilin

• Intussusception

• Cloacal prolapse

• Megacloaca

• Cloacal impaction

Findings on clinical examination

• Weight loss

• Vague signs of ill health (e.g., cessation of talking)

• Passing undigested seeds in feces (PDD)

• Melena (ulceration, severe enteritis)

• Hemorrhagic feces (Pacheco disease)

• Neurologic signs (PDD, paramyxovirus)

• Vent soiled with accumulated feces

• Budgerigars: Usually due to obesity (cannot clean themselves) or herniation of abdominal musculature

• Central American parrots (e.g., Amazons, macaws, and hawk-headed parrots): Likely to be papillomatosis. This affects the cloaca, but also the oral cavity and proximal gastrointestinal tract.

• Yellow-green diarrhea, wasting, and death (spironucleosis)

• Wide range of clinical signs, including gastrointestinal and respiratory, may be seen with systemic bacterial infections such as Salmonella and Yersinia. Occasionally neurologic signs may be seen with Salmonella.

• Green diarrhea, dyspnea, and sneezing (chlamydophilosis)

• Weight loss (Mycobacterium avium); may also exhibit slow-growing masses

• Cloacal tissue visibly protruding from vent (cloacal prolapse)

• Physiologic enlargement of the cloaca in reproductively active Vasa parrots (Coracopis vasa) and lesser Vasa parrot (C. nigra)

• Sudden death (Clostridial infection); may be linked to stress triggers

• Sudden, mass deaths in budgerigars (orthoreovirus-like agents)

Investigations

1. Routine hematology and biochemistry

2. Serology and PCR (crop swab) for avian bornavirus

3. Samples for culture and sensitivity

a. Fecal examination

b. Gram stain

c. Modified Ziehl-Neelsen staining for mycobacteriosis

d. Wet preparation/flotation for worm eggs/protozoa (Fig. 8-18)

e. Abundant motile trophozoites (Spironucleus)

4. Proventricular wash for proventricular worm eggs

Raillietina Prosthogonimus Syngamus trachea

Fig. 8-18. Diagram showing some eggs of intestinal parasites of psittacines (not drawn to scale).

5. Fine-needle aspirate/staining/cytology of any abnormal masses (including staining for mycobacteria)

6. Radiography (including contrast studies)

a. Dilated crop, proventriculus, gizzard, and gut (PDD, severe enteritis)

b. Contrast studies for PDD, proventricular ulceration, foreign body

c. Dilated cloaca (megacloaca)

7. Fluoroscopy

8. Chlamydophila PCR; ideally take three samples from each bird: conjunctiva, choana and feces; serology for Chlamydophila

9. Mycobacterium avium PCR on feces/suspect material

10. PCR for Pacheco disease and polyomavirus

11. ELISA and virus neutralizing tests for orthoretroviral infection: isolation of orthoreovirus from feces, biopsy samples, ascitic fluid, or respiratory secretions

12. Endoscopy

13. Ultrasonography

14. Biopsy

a. Full-thickness crop wall, including large blood vessel for PPD will allow diagnosis in 75% of cases (Gregory et al 1996). Biopsy of proventriculus is a more difficult operation and carries a higher risk. Biopsy has now been superseded by serologic and PCR testing for avian bornavirus.

15. Postmortem of affected birds

a. Yersinia: a degree of hepatomegaly; patchy discoloration of the liver and in more advanced cases; miliary lesions in liver, kidneys, and spleen

Management

1. Supportive management, including covering antibiosis

2. Fluid therapy

TreatmentZspecific therapy

• Pacheco disease—see Hepatic Disorders

• Orthoreoviral infection: supportive treatment: New World species often respond well, but Old World species carry a poorer prognosis

• Other viral diseases

• Symptomatic and supportive treatment only

• Parasites

• Birds in outside aviaries should be wormed twice yearly (avoid breeding season) or have fecal screens every 6 months. All new birds should be wormed during quarantine.

• Suitable treatments include fenbendazole at 50 mg/kg PO as a once-only dose, or water-soluble avermectins (e.g., moxidectin 0.1% added to drinking water at 20 mg/L for 48 hours). Note: Fenbendazole may be toxic to cockatiels (Lloyd 2003).

• Capillaria: Infection is direct, but intermediate stages can be carried by earthworms, so remove fecal material regularly and prevent access to soil. Treat with fenbendazole at 50 mg/kg by crop tube; this may need repeating every 2 weeks until the bird is clear.

• Ascaridia and Porrocaecum spp.: The life cycle is direct, although earthworms may act as transport hosts.

• Thelazia and Oxyspirura spp.: Carried by intermediate arthropod host

• Proventricular worms (e.g., Geopetitia, Dispharynx, Habronema, and Tetrameres spp.): Indirect life cycle using insect intermediate hosts

• Cestodes: Single dose of praziquantel at 8 to 10 mg/kg PO

• Giardia

• Metronidazole at 20 mg/kg PO b.i.d.

• Spironucleus

• Metronidazole as above

• Dimetridazole failed to work (Philbey 2002)

• Candida and mucormycosis

• Nystatin at 300,000 IU/kg PO b.i.d. for 10 days

• Amphotericin B at 1 mg/kg PO b.i.d.

• Avian bornavirus (PDD): Poor response to treatment but some individuals recover. Treatment should include:

• Broad-spectrum antibiosis (e.g., enrofloxacin at 5 to 20 mg/kg PO daily, co-trimoxazole at 30 mg/kg PO b.i.d.)

• Motility modifiers (e.g., cisapride at 1.0 mg/kg PO b.i.d.; metoclopramide 0.5 mg/kg PO, IM, or IV BID-TID)

• The use of cyclooxygenase-2 (COX-2) inhibitors such as celecoxib (Celebrex, Pfizer) at 10 mg/kg PO daily appears to be beneficial in some cases, but their use should be considered carefully; meloxicam (another COX-2 inhibitor) appeared to exacerbate clinical signs of PDD in experimentally infected cockatiels (Hoppes et al 2013).

• Keep in-contact birds in strict isolation, although horizontal transmission to immunocompetent, fully fledged birds appears poor (Rubbenstroth et al 2014).

• Institute good hygiene, ventilation, and other good management.

• Immediate and thorough investigation of any sick or dead birds

• Probably an isolation period of 2 to 3 years without any fresh incidence of PDD is needed before declaring an aviary free of the disease (Doneley et al 2007).

• Obesity in budgerigars: Consider supplementing with L-carnitine (1000 mg/kg food).

• Abdominal herniation in budgerigars will often require surgery to remove excess abdominal musculature.

• Papillomatosis: Surgical removal of papillomas from cloaca and oral cavity if causing problems. Infected birds often subsequently develop neoplasia of the pancreas, and bile duct carcinoma has been reported in affected Amazon parrots.

• Salmonella: Antibiotics based on culture and sensitivity findings

• Autogenous vaccination can clear carriers (Harcourt-Brown 1986). Two doses are given 2 weeks apart; each dose consists of 1.0 mL PO and 0.5 mL SC.

• Other bacterial infections: Appropriate antibiosis

• Yersinia: Prevent access of wild birds and rodents to aviaries and food stocks.

• Clostridial infections: Metronidazole at 20 mg/kg PO b.i.d.

• Macrorhabdus ornithogaster—see “Differential Diagnoses for Vomiting/Regurgitation/ Dysphagia”

• Mycobacterium avium: Potential zoonosis, so recommend euthanasia. For suggested treatment protocols, see under Lower Respiratory Tract Disorders.

• Chlamydophilosis (see Lower Respiratory Tract Disorders)

• Proventricular ulceration

• Cimetidine at 5 mg/kg PO b.i.d.

• Address underlying factors, including possible secondary bacterial and fungal ulceration.

• Proventricular impaction

• Flush with warm saline either via mouth or via ingluviotomy incision.

• If fails may need to undertake a proventriculotomy.

• Cloacal prolapse: Requires cloacopexy

• A pursestring suture may provide temporary alleviation of the condition, but cloacopexy should give more permanent results.

• Investigate the possibility of underlying predisposing factors (e.g., cloactitis, etc.).

• If linked to reproductive activity, see Reproductive Disorders.

• Megacloaca: Cloacal reduction surgery (Graham et al 2004)

• Cloacal impaction: Requires manual removal, usually under an anesthetic.

• Covering antibiotics; investigate and deal with underlying factors

Nutritional disorders

Nutrition

The diet of most psittacine birds is very poor compared with their comparable diet in the wild. Nutritional problems arise by two means:

1. Provision of inappropriate food

2. Selectivity of the bird (Werquin et al 2005)

These apply especially to a sunflower-seed-based diet.

Disorders

• Incorrect protein levels

• In cockatiels, the optimum protein level for growth and weaning is around 20% crude protein, but:

- 5% causes severe stunting followed by 100% mortality.

- 10% to 15% leads to stunting and some mortality.

- 25% gives good weight gain but also behavioral problems such as aggression.

- 35% gives paradoxical poor growth and aggression.

• Hypervitaminosis A: Excessively high levels of vitamin A have been associated with cataract formation and bone abnormalities. High levels of carotenoids can cause a yellowing discoloration of skin and fat.

• Hypovitaminosis A: Hyperkeratosis and squamous metaplasia of epithelia, including the pharynx, respiratory tract, and occasionally renal tubules. Often there are sterile white plaques visible in oral mucosa and blunting or loss of the choanal papillae. Rhinitis (and occasionally rhinoliths) and blepharitis are common. Sneezing may occur, and there is a predisposition toward respiratory infections. In severe cases, metaplasia of the renal tubules can result in visceral gout. Hyperkeratosis of the plantar surfaces of the feet is seen.

• Hypervitaminosis D3: Can result in calcification of viscera, especially the kidneys, triggering a visceral gout

• Metabolic bone disease: This is often a hypovitaminosis D3 combined with a hypocalcemia and hyperphosphatemia. In particular, African grey parrots appear to have difficulty in mobilizing skeletal calcium reserves. Such birds often present with a hypocalcemic tetany—wings fluttering violently in apparent “fits.” Such birds often have high parathormone levels, low 25-hydroxycholecalciferol levels, and low serum ionized and nonionized calcium levels.

Fig. 8-19. Hypocalcemia in an African grey parrot. Note the three-point stance, using the beak to aid support.

Clinical signs of metabolic bone disease in birds

• General weakness (Fig. 8-19)

• Pathological fractures and/or bending of bones

• Rickets

• Paralysis

• Tetany

• Dystocia

• Low clutch size, thin- or soft-shelled eggs, and low hatchability. (Egg-laying hens may have an episode of acute hypocalcemia that can result in partial paresis and perhaps egg-binding.)

• Polydipsia/polyuria occasionally seen due to increased phosphorus turnover, triggering a diuresis.

• Birds, especially the young, with bone and joint deformities, might be deficient in both calcium and vitamin D3.

• Hypovitaminosis E: Affected birds may become lethargic and show coordination and equilibrium problems. Complete paralysis can occur. Other signs include white muscle disease. If the gizzard is affected, then undigested seed may be passed. Splayed legs and edema of the neck, wings, and breast may be seen. Reproductive problems can be encountered, including infertility and low hatchability due to weakness in the pipping muscle of the chick.

• Hypovitaminosis K: Can occur with coccidiostats and long-term antibiosis that destroys the normal gut flora. Failure to produce vitamin K leads to blood-clotting problems, which can present as excessive hemorrhage.

• Riboflavin (vitamin B2): However, adult hens deficient in vitamin B2 develop fatty livers and elongated flight feathers and have low egg production and low hatchability In chicks the signs are weakness and diarrhea, inward curling toes, and depigmented feathers (achromatosis) in cockatiels.

• Pantothenic acid: Cockatiels raised on a diet deficient in pantothenic acid fail to grow contour feathers on the chest and back and die at age 3 weeks. Other signs include dermatitis on the face and feet, decreased growth, decreased feathering, and incoordination.

• Biotin: Deficiencies can occur due to ingested mycotoxins in the diet affecting biotin uptake; signs as for pantothenic acid

• Folic acid: Genuine deficiencies can occur with long-term antibiosis. Signs include anemia, immunosuppression, poor egg production, low hatchability, and stunting of chicks, often accompanied by deformation of upper beaks.

• Vitamin B12: Deficiencies are rare but include anemia, poor feathering, reduced growth, reduced food intake, nervous disorders, gizzard erosions, and fatty accumulations in the heart, liver, and kidneys.

• Choline: Deficiencies include poor growth of young birds, fatty liver syndrome in adults, and calcification of soft tissues. Cockatiels on a low-choline diet exhibited unpigmented wing and tail feathers but no calcification.

• Iodine: In budgerigars linked to goiter formation (see “Differential Diagnoses for Vomiting/Regurgitation/Dysphagia” in Gastrointestinal Tract Disorders)

• Hypocalcemia: Often combined with hypovitaminosis D3 (see “Metabolic Bone Disease” above)

• Obesity: Common in Amazon parrots, Galah cockatoos, cockatiels, and budgerigars. Subcutaneous fat deposits may be visible, and there is infiltration of internal organs with fatty tissue. May give rise to atherosclerosis and sequelae (e.g., cerebrovascular accidents)

• Hepatic lipidosis: Obesity; lethargy, depression, and anorexia. Neurologic signs may be seen, consistent with hepatic encephalopathy. Urates may be yellow or green.

• Atherosclerosis (see Cardiovascular and Hematologic Disorders)

• Hemochromatosis (iron storage disease): Hepatomegaly is rare.

Investigations

1. Hematology and biochemistry

a. Hepatic lipidosis may show an increased lactate dehydrogenase, AST, triglycerides, and bile acids.

b. Blood levels for calcium (including ionized calcium), phosphorus, magnesium (see Table 8-7)

c. Vitamin D3 (blood 25-hydroxycholecalciferol levels >50 nmol/L)

Table 8-7 Blood calcium, phosphorus and magnesium levels in two parrots species.
Parameter Hispaniolan parrot (Amazona ventralis) African grey parrot (Psittacus erithacus)
Calcium/mmol/L 2.20-2.60 2.05-5.05
(2.20-2.58)* (2.03-2.7)
Ionized calcium/mmol/L 0.96-1.22f
Phosphorus/mmol/L 0.58-1.42 0.81-1.91
(0.58-1.23) (0.78-1.71)
Ca: P ratio 2.62-5.39 1.81-3.77
(2.62-5.39) (1.67-3.50)
Magnesium/mmol/L 0.74-1.27 0.82-1.4
(0.82-1.07) (0.82-1.07)
*Note: Range in parentheses excludes egg-laying females.

TFrom Shaw 2013.

From de Carvalho 2009.

d. Vitamin A levels (retinol 0.471 ± 0.209 pg/mL—Torregrossa et al 2005)

e. Vitamin E levels (α-tocopherol 13.5 ± 6.60 pg/mL)

2. Radiography

a. Hepatomegaly (hepatic lipidosis, neoplasia)

b. Hypervitaminosis D3: Calcification of the kidneys

c. Skeletal abnormalities: Pathological fractures, healed fractures, bone deformities, osteomalacia (metabolic bone disease)

3. Liver biopsy

4. Dietary analysis

Management

1. Dietary imbalances often predispose to secondary pathogen invasion, so covering antibiosis should be considered. Aim to switch to a more healthy diet, which, depending on the species, should consist of:

a. Exchanging seed mix for a good proprietary pelleted food (e.g., Harrison's Bird Foods)

b. Enhancing the diet by increasing the consumption of colored vegetable such as sweet peppers and noncitrus fruits

c. Using appropriate vitamin and mineral supplements

d. Sprouting seeds help to convert some of the fat into carbohydrate.

e. Altering diets can be time consuming. Many parrots are seriously neophobic and are reluctant to eat novel substances.

2. Milk thistle (Silybum marianum) is hepatoprotectant. Dose at 4 to 15 mg/kg PO b.i.d. or t.i.d. (Wade 2004).

3. Provide exposure to UVB light—especially important for African grey parrots.

TreatmentZspecific therapy

• Hepatic lipidosis

• Poor prognosis

• Provision of interosseous fluids (Hartmann's), diet high in nutrients (include fructose, biotin, choline, and lactulose), and broad-spectrum antibiotic therapy may be useful.

• Consider L-carnitine (see “Obesity” below)

• Hypovitaminosis A

• Injectable vitamin A at 5000 IU/kg once daily for 2 weeks. Then adopt maintenance rate of 5000 IU daily PO or feed colored vegetables such as carrots and peppers.

• Metabolic bone disease

• Hypocalcemia: Calcium gluconate 10% at 100 to 200 mg/kg (1 to 2 mL/kg) IM daily or 50 to 100 mg/kg by slow IV

• Supplement with vitamin D3 at 5000 IU/kg daily, as well as calcium

• Some cases may need magnesium supplementation (see de Carvalho 2009).

• Provide access to full-spectrum lighting with an ultraviolet B component (e.g., sunshine or commercially available lighting) to allow natural endogenous vitamin D3 production.

• Hypervitaminosis D3

• In some cases, clinical signs regress when vitamin D3 levels are returned to normal. Macaws particularly seem to be susceptible to high vitamin D3 levels, and it is recommended that vitamin D3 levels should not be higher than 2000 IU/kg of a parrot's diet (with a gross energy diet range of 3200 to 4200 kcal/kg).

• Vitamin E

• Works synergistically with selenium and can be given as a combined (such as Vitesel, Norbrook (UK)) at 0.01 mL/kg IM every 7 to 14 days

• Other hypovitaminoses: Supplement with appropriate vitamin preparations. Complete revision of diet recommended.

• Iodine: Supplement with iodine (see “Differential Diagnosis for Vomiting/Regurgitation/ Dysphagia”).

• Hemochromatosis: Select low-iron diet. May be linked to chronic inflammatory conditions.

• Obesity: In budgerigars, L-carnitine at 1000 mg/kg food has been effective in inducing weight loss, along with shrinkage of lipomas.

Hepatic disorders

Note: Psittacines lack a gallbladder.

Viral

• Pacheco disease (herpesvirus)

• Polyomavirus

• Adenovirus

Bacterial

• Bacterial hepatitis

• Chlamydophilosis

• Yersinia pseudotuberculosis

• Mycobacteriosis

Fungal

• Aflatoxicosis

Nutritional

• Hemochromatosis

• Hepatic lipidosis

Neoplasia

• Hepatic tumors

• Lymphoma (likely linked to retrovirus infection—see Cardiovascular and Hematologic Disorders)

Other noninfectious problems

• Cirrhosis

• Steroid hepatopathy (iatrogenic)

• Amyloidosis

Findings on clinical examination

• Unwell bird, fluffed-up appearance

• Anorexia

• Polydipsia/polyuria

• Very green or yellow appearance of feces

• Ascites (secondary to portal hypertension)

• Respiratory signs (ascites/chlamydophilosis)

• Multifocal follicular and feather pulp hemorrhages (polyomavirus)

Investigations

1. Radiography

a. Hepatomegaly (Pacheco disease, neoplasia, hemochromatosis)

b. Ascites

2. Routine hematology and biochemistry

a. Liver enzymes raised; AST is not liver specific, but raised AST plus bile acid levels indicate liver disease; raised AST plus CK suggests muscle injury. In end-stage liver disease, plasma liver enzyme levels may be normal or low.

3. Culture and sensitivity

4. Coelomic tap (culture and sensitivity, cytology)

5. Fecal or cloacal swab for Pacheco disease PCR

6. Endoscopy

a. Hepatomegaly, splenomegaly, renal enlargement

7. Ultrasonography

a. Hepatomegaly (Pacheco disease)

8. Biopsy

Management

1. Supportive therapy, including fluids

2. Lactulose at 0.5 mL/kg PO b.i.d.

3. Milk thistle (Silybum marianum) is hepatoprotectant. Dose at 4 to 15 mg/kg PO b.i.d. or t.i.d. (Wade 2004).

TreatmentZspecific therapy

• Pacheco disease is usually rapidly fatal. Try acyclovir at 80 mg/kg PO t.i.d. for 7 to 10 days or 40 mg/kg IV or SC t.i.d. (cited in Girling 2003)

• Hemochromatosis (see “Nutritional Disorders")

• Hepatic lipidosis (see “Nutritional Disorders")

Splenic disorders

• Chlamydophilosis (see Lower Respiratory Tract Disorders)

• Lymphoma (see Cardiovascular and Hematologic Disorders)

Cardiovascular and hematologic disorders

Where possible, auscultate tame birds while at rest on a perch or the owner, as stressed birds exhibit such high heart rates that meaningful auscultation is difficult. Any abnormal heart rate or rhythm is likely to be associated with heart disease or a more systemic illness.

Viral

• Polyoma virus—hydropericardium

• Avian bornavirus (PDD)—myocarditis

Bacterial

• Valvular endocarditis—can be thrombotic

• Bacterial infiltration

• Pericarditis

• Chronic systemic lung disease

Fungal

• Pericarditis

• Chronic systemic lung disease

Protozoal

• Haemoproteus

• Leucocytozoon

• Akiba spp.

• Plasmodium

Nutritional

• Fat accumulation (lipomatosis cordis)

• Atherosclerosis (especially Amazons and African greys)

Neoplasia

• Lymphoma/lymphosarcoma

Other noninfectious problems

• Chronic pulmonary interstitial fibrosis, especially in older Amazon parrots (Zandvliet et al 2001)—very commonly causes right ventricular enlargement (see Respiratory Tract Disorders)

• Right ventricular enlargement also from other causes of systemic lung disease (e.g., chronic mycosis)

• Pericardial effusion with or without ascites

• Ventricular hypertrophy or dilatation

• Myxomatous degeneration of atrioventricular valve (Oglesbee and Lehmkuhl 2001)

• Calcification of the blood vessels

• Lack of exercise (plus poor diet)

• Avocado toxicity—hydropericardium

• Urate deposits in the aorta

• Congenita

Findings on clinical examination

• Exercise intolerance

• Apparent respiratory signs

• Auscultation: Arrhythmias and altered heart sounds (e.g., murmurs)

• Vomiting and wasting (Leucocytozoon)

• Concomitant signs such as ascites, pulmonary disease, and air sacculitis

• Neurologic signs—typically cerebrovascular accidents secondary to atherosclerosis

Investigations

1. Radiography

a. Normal radiographic heart parameters (Table 8-8)

b. Liver enlargement

Table 8-8 Parrots and related species: Normal radiographic heart parameters
Ratio of cardiac silhouette width to: (%)
Sternum length (measured on the bird)

Width of thorax (measured on ventrodorsal radiograph)

Width of coracoid (measured on ventrodorsal radiograph)

35-41

51-61

545-672

From Straub et al (2002).

bgcolor=white>Cholesterol
Table 8-9 Parrots and related species: Blood cholesterol levels
Species Triglycerides (mmol/L)
(mmol/L)
Bavelaar et al* Polo et alt Bavelaar et al* Polo et alt
Palm cockatoo 3.6 ± 0.5 1.2 ± 0.5
(2.8-4.2) (0.8-1.9)
Long-billed cockatoo 5.65-6.33 0.79-1.78
Amazon (yellow-headed 7.46-9.65 7.1 ± 2.5 1.7-2.86 1.6 ± 0.4
Amazon) parrot (4.3-10.9) (1.1-2.1)
Blue and gold macaw 4.2-4.77 4.2 ± 0.9 0.35-0.52 1.2 ± 0.7
(3.1-6.7) (0.4-2.5)
Scarlet macaw 5.0-5.3 4.1 ± 1.1 0.38-0.66 1.0 ± 0.3
(2.3-6.4) (0.5-1.6)
Red fan parrot 4.09-4.54 0.35-0.38
African grey parrot 8.38 ± 2.57

(5.31-18.62)*

* Values from Bavelaar et al (2005). + Values from Polo et al (1998). tBavelaar & Beynen (2003).

2. Routine hematology and biochemistry

a. Increased blood cholesterol levels are a major risk factor for atherosclerosis (Table 8-9).

3. Cytology (blood smears for hemoparasites)

4. Blood culture and sensitivity

5. ECG

a. Sinus rhythm normal.

b. Sinus arrhythmias and second-degree heart block considered physiologic in birds

c. Partial fusion of P and T waves (P on T phenomenon) can be normal, especially in females.

d. Isoflurane anesthesia may increase heart rate.

e. Normal ECG values after Casares et al (2000) and Musulin and Adin (2006) (Table 8-10)

6. Endoscopy

7. Biopsy (liver, kidney, pectoral muscles)

8. Ultrasonography

9. Echocardiography/Doppler

Table 8-10 Parrots and related species: Normal lead II ECGs
Variable Hyacinth macaw Green wing macaw African grey parrot
Body weight (g) 1331 ±149 1214 ± 173
Heart rate (beats/min) 283 ± 65 280 ± 97
Electrical axis (degrees) -101 (81-109) -98 (86-131)
P duration (sec) 0.02 (0.015-0.025) 0.018 (0.015-0.025) 0.012-0.018
P amplitude (mV) 0.3 (0.19-0.4) 0.2 (0.075-0.3) 0.25-0.55
QRS duration (sec) 0.02 (0.015-0.025) 0.02 (0.013-0.025) 0.010-0.016
QRS amplitude (mV) 0.65 (0.35-1.0) 0.5 (0.35-0.85)
R amplitude (mV) 0.045 (0.04-0.08) 0.05 (0.02-0.2) 0.0-0.2
T duration (sec) 0.05 (0.035-0.075) 0.045 (0.035-0.05)
T amplitude (mV) 0.3 (0.1-0.7) 0.25 (0.1-0.45) 0.18-0.60
PR interval (sec) 0.055 (0.05-0.075) 0.05 (0.04-0.07) 0.040-0.055
QT interval (sec) 0.085 (0.08-0.1) 0.09 (0.08-0.11) 0.048-0.070
ST segment amplitude (mV) 0.1 (0.05-0.15) 0.1 (0.05-0.15) 0.90-0.20

Table 8-11 Normal values of some psittacine cardiac anatomy
Values for myocardium of left free wall Sternal length (%)
Mean apical myocardium 2.3-2.85
Mean middle left myocardium 8.3-8.7
Mean basal myocardium thickness 7.9-9.0
From Krautwald-Junghanns et al (2004).

Management

1. Reduce stress as much as possible (e.g., remove affected birds from breeding programs).

2. Identify and treat underlying problems (e.g., chronic lung disease).

3. Improve diet.

TreatmentZspecific therapy

• NSAIDs (e.g., meloxicam at 0.2 mg/kg PO, IM body weight once daily) may be useful for chronic pulmonary interstitial fibrosis.

• Heart disease: Once a diagnosis is achieved, drug regimens may be adapted from mammalian treatments. Examples would be:

• Enalapril at 1.0 to 2.5 mg/kg PO daily or b.i.d. (Pees et al 2006)

• Furosemide at 0.15 mg/kg IM daily

• Digoxin at 0.05 mg/kg PO daily

• Haemoproteus: Often considered asymptomatic and self-limiting, but can be a contributing factor to anemia if present. Treat with chloroquine at 250 mg per 120 mL drinking water for 14 days. Avoid ceratopogonid vectors.

• Plasmodium

• Primaquine at 0.75 to 1.0 mg/kg PO once only, combined with an initial loading dose of chloroquine at 25 mg/kg, reducing this to 15 mg/kg at 12, 24, and

48 hours

• Leukocytozoon: May be asymptomatic, but can be fatal, with acute hepatitis, renal tubular necrosis, and myocardial hemorrhage. Chronic cases may present with wasting and vomiting. Treat as for Plasmodium. Avoid exposure to vectors such as blackflies (Simulium spp.) or Culicoides/hippoboscids.

• Lymphoma/lymphosarcoma

• Treatment is speculative and more modern regimens may be more appropriate. However, the following chemotherapeutic drugs have been used in cockatoos (France 1993):

- Prednisolone at 25 mg/m2 PO daily

- Asparaginase at 400 lU/kg IM every 7 days. Premedicate with diphenhydramine at 2 mg/kg IO once only.

- Cyclophosphamide at 200 mg/m2 IO every 7 days

- Doxorubicin at 30 mg/m2 IO every 2 days. Premedicate with diphenhydramine at

2 mg/kg IO once only.

- Vincristine sulfate at 0.75 mg/m2 IO every 7 days for 3 weeks

• Atherosclerosis

• Treat symptomatically.

• Linked to deficiency of n-3 polyunsaturated fatty acids, especially α-linolenic acid (Bavelaar et al 2005); supplement by feeding commercial diets and small seeds (e.g., flax seeds).

Musculoskeletal disorders

Viral

• PBFD

• Retroviral infection (renal/gonadal tumors)

Bacterial

• Renal infections can spread to the adjacent lumbosacral plexus.

• Septic arthritis

• Osteomyelitis

Nutritional

• Metabolic bone disease (see Nutritional Disorders)

Neoplasia

• Renal tumor (possibly due to retroviral infection)

• Gonadal tumor (especially budgerigars; possibly due to retroviral infection)

• Osteosarcoma

Other noninfectious problems

• Articular gout

• Limb bone fracture—tibiotarsal fractures are particularly common

• Spinal trauma

• Identification ring too tight (especially closed rings)

• Developmental problems of chicks

• Juvenile osteodystrophy

• Metabolic or systemic problems (e.g., cardiovascular disease, hypoglycemia, hypocalcemia, and anemia)

Findings on clinical examination

• Weakness, ataxia

• Unwillingness or inability to move

• Leg paralysis—may be unilateral or bilateral

• Limb deformities, including rotation around joints

• Flight disorders—see “Differential Diagnoses for Loss of Flight”

Investigations

1. Radiography

a. Radiograph not only the affected limb, but also the whole body, especially if there is obvious muscle wastage.

b. Contrast studies (e.g., with barium) to assess for displacement of gut by intracoelomic masses. Note: Reproductively active females store excess calcium as deposits at the femur. These should not be mistaken for pathological exostoses.

2. Routine hematology and biochemistry

a. Will need to differentiate from systemic or metabolic disorders

3. Culture and sensitivity

4. Endoscopy

5. Ultrasonography

Management

1. Supportive treatment, including covering antibiosis

2. Hospitalizing weakened birds on soft surfaces (e.g., towels) to reduce the risk of trauma

TreatmentZspecific therapy

• Renal infection: Appropriate antibiosis

• Fractures: Stabilization by external or internal fixation (Fig. 8-20). In small psittacines conservative management, including analgesia, may be more appropriate for femoral fractures.

• Identification ring too tight: Remove under GA.

• Neoplasia: Treatment rarely viable

• Osteosarcoma: Treatment has been attempted with doxorubicin at 60 mg/m2 IV diluted with saline every 30 days (Doolan 1994).

• Juvenile osteodystrophy

• In very young chicks, developmental problems such as valgus deformities (splay leg) can be corrected by hobbling the legs together before the skeleton becomes reasonably calcified. This should be done at no more than age 5 days. Older chicks may require surgical correction once the bones have sufficiently calcified to withstand such surgery.

• Reassess hand-rearing conditions, as these often reflect a poor rearing environment. Harcourt-Brown (2004) finds that dusky parrot chicks (Pionus fuscus) remain in the

Fig. 8-20. Combined internal and external fixation repair of a fractured tιbιotarsus.

nest until day 53; the presence of several chicks in such a combined space may mutually support their growing skeletons, and premature exercise may lead to pathological deformity of the long bones.

Differential diagnoses for loss of flight

Viral

• Polyomavirus

• PBFD

Bacterial

• Pathological fracture (from osteomyelitis)

Fungal

• Pathological fracture (from osteomyelitis)

Neoplasia

• Pathological fracture

Other noninfectious problems

• Cardiovascular disease

• Respiratory disease

• Neurologic disease

• Systemic disease (weakness)

• Fractured coracoid bone

• Other flight bone fractures (e.g., humerus)

• Damage to the leading edge of the wing (propatagium)

• Prepatagial cutaneous ulcerative disease—commonly seen in chronic self-mutilating African greys; too painful to extend wings (see Skin Disorders)

Findings on clinical examination

• Unable to fly

• Flight feathers absent or abnormal

- Young budgerigars—polyomavirus

- Older psittacines—PBFD

- Self-mutilation

• Flight feathers normal—consider traumatic injuries, etc.

• One wing may be held lower than the other.

• Obvious traumatic injury (i.e., swelling, compound fracture). Check especially the wing tips.

• Nonpainful, immobile swelling (i.e., old, healed fracture)

Investigations

1. Radiography

2. Routine hematology and biochemistry

3. Culture and sensitivity

4. Endoscopy

5. Ultrasonography

TreatmentZspecific therapy

• Propatagial damage: Make sure that the tendon that supports the leading edge of the propatagium—the tendon of musculis tensor propatagialis longa—is repaired if severed.

• Prepatagial CUD—see Skin Disorders

• Fracture repair where feasible.

Systemic disorders

Some conditions present with a variety of clinical signs that may be quite nonspecific. In some cases, this results from immunosuppression, leading to secondary invasion of a variety of pathogens or because of multiorgan involvement.

Viral

• PBFD—especially young African grey parrots

• Retrovirus (leukosis/sarcoma viruses)

Bacterial

• Staphylococcus aureus (Hermans et al 2000)

• Chlamydophilosis

Fungal

• Aspergillosis (see Lower Respiratory Tract Disorders)

• Penicillinosis (Lanteri et al 2011)

Protozoal

• Sarcocystis

Nutritional

• See Nutritional Disorders

Neoplasia

• Infiltrative neoplasia secondary to retrovirus infection; any organ can be affected (Girling 2003)

Other noninfectious problems

• Amyloidosis

• Iatrogenic steroid prescription

Findings on clinical examination

• Generalized ill health

• Nonspecific clinical signs

• Weight loss

• Anorexia

• Sudden death

• Obvious neoplasia

Investigations

1. Radiography

2. Routine hematology and biochemistry

a. Young birds with PDFD often profoundly leukopenic

3. Serology (Sarcocystis, Chlamydophila)

4. Cytology

5. Culture and sensitivity

6. Chlamydophila PCR

7. Endoscopy

8. Ultrasonography

9. Biopsy

TreatmentZspecific therapy

• PBFD

• Experimentally, avian interferon has been used to aid elimination of PBFD in viremic, young African grey parrots (Stanford 2003). The dose used was 1,000,000 units of avian γ-interferon IM daily for 90 days. Mammalian (feline) interferon was found to be unsatisfactory.

• Note: PBFD infection is oral, with virus entering via the bursa of Fabricius, which in psittacines can take over 18 to 20 months for normal involution to occur (Schmidt 1997). Any bird testing positive should be immediately quarantined and retested 60 to 90 days later to assess degree of immunity (Girling 2003). Immune birds will not be viremic and so will test negative.

• Steroids: Gradually wean off steroids. Always use antibiotic and antifungal medications in conjunction with steroids to counter the marked immunosuppressive effects of exogenous steroids.

• Penicillinosis—as for aspergillosis

• Sarcocystis (see Lower Respiratory Tract Disorders)

Neurologic disorders

Viral

• Paramyxovirus

• Avian bornavirus (PDD)

• Pacheco disease

• Adenovirus—budgerigars

• West Nile virus (flavivirus)

Bacterial

• Chlamydophilosis

• Bacterial meningitis

Fungal

• Fungal meningitis

Protozoal

• Sarcocystis

Parasitic

• Cerebrospinal angiostrongyliasis due to nematode larvae of Angiostrongylus cantonensis (Monks et al 2005)

Dietary

• Hypocalcemia/hypovitaminosis D3 (African grey parrots especially)

• Hypoglycemia

Neoplasia

Other noninfectious problems

• Zinc toxicity

• Other heavy-metal poisoning (e.g., lead)

• Other toxicities

• Fractures

• Renal disease, including neoplasia (see “Differential Diagnosis of Polydipsia/Polyuria” in Endocrine Disorders)

• Other neoplasia

• Idiopathic epilepsy

• Hepatic encephalopathy (severe liver disease)

• Cerebrovascular accidents (atherosclerosis)

• Head trauma (e.g., flying into windows)

Findings on clinical examination

• Weight loss

• Depression

• Torticollis and head tilt

• Ataxia; unable to balance or support itself; may continually hang onto cage bars with beak for support

• Collapse

• Tremors and seizures

• Gastrointestinal signs (undigested seeds, loose droppings) suggestive of paramyxovirus

Investigations

1. Radiography

a. Standing radiographs in the conscious bird for detection of ingested heavy metals

2. Routine hematology and biochemistry

a. Serum calcium, zinc, and lead. Alternatively, hepatic lead and zinc concentrations can be assessed from biopsy; these are thought to be much more reliable.

b. Blood levels can be indicative of zinc toxicity, but as with lead, there is no absolute correlation between blood zinc levels and clinical signs. As a general rule, if zinc levels are >32 to 50 pmol/L and there are consistent clinical signs (see Neurologic Disorders and Gastrointestinal Tract Disorders), then zinc toxicity should be suspected.

c. Blood lead levels Hypothyroidism

• Adrenal disease

Findings on clinical examination

• Polydipsia/polyuria (pituitary gland adenoma)

Investigations

1. Radiography

2. Routine hematology and biochemistry

a. Adrenal disease not reported in psittacines

b. Corticosterone, not cortisol, is responsive to ACTH stimulation.

c. Experimental ACTH stimulation gave the results shown in Table 8-12 (Zenoble et al 1985).

d. Serum thyroid hormone levels (nonmolting birds—see Table 8-13)

Table 8-12 Parrots and related species: Experimental ACTH stimulation
Corticosterone concentrations (mg/dL) before ACTH administration Corticosterone concentrations (mg/dL) 90 min after ACTH administration
Red-Iored Amazon 1.06 4.86
Blue-fronted Amazon 2.09 10.58
African grey parrot 2.33 4.69

Table 8-13 Parrots and related species: Serum thyroid hormone levels (nonmolting birds)
Species T4 concentration
nmol/L μg∕dL
Range Mean Range Mean
African grey parrot (Psittacus erithacus) 2.02-5.06 3.18 0.16-0.39 0.25
Moluccan cockatoos (Cacatua moluccensis) 2.04-6.29 4.66 0.16-0.49 0.36
Blue and gold macaws (Ara ararauna) 2.02-4.85 3.36 0.16-0.38 0.26
Umbrella cockatoos (Cacatua alba) 2.86-5.96 4.61 0.22-0.46 0.36
Yellow-headed Amazon (Amazona oratrix) 2.49-7.68 5.05 0.19-0.60 0.39
Blue-fronted Amazon (Amazo-na aestiva) 3.17-142 23.8 0.25-11.0 1.85
Lovebirds (Agapornis spp.) 0.2-4.3
Adapted from Greenacre et al (2001).

3. Culture and sensitivity

4. Endoscopy

5. Biopsy/necropsy

6. Ultrasonography

TreatmentZspecific therapy

• Hypothyroidism: L-thyroxine at 0.02 mg/kg PO daily or b.i.d.

• Goiter in budgerigars: See Respiratory Tract Disorders

Differential diagnosis of polydipsiaZpolyuria

Viral

• Paramyxovirus

• Avian influenza

• Adenovirus

• Herpesvirus

Bacterial

• Pancreatitis

• Pyelonephritis

Fungal

Protozoal

• Encephalitozoon hellem

Nutritional

• Hypovitaminosis A

• Hypocalcemia

Neoplasia

• Renal tubules

Other noninfectious problems

• Renal disease/gout

• Diabetes mellitus

• Hepatitis

• Heavy-metal poisoning, especially zinc

• Amyloidosis (renal; hepatic)

• Trauma

• Physiologic—egg laying

Findings on clinical examination

(See also “Assessment of Droppings” in Gastrointestinal Tract Disorders)

• Weight loss

• Weakness

• Polydipsia and accompanying polyuria

• Marked wetting of the bottom of the cage

• Hematuria (especially with heavy metal poisoning)

• Urate fraction may have a strong "fishy" smell common in the white cockatoos with renal disease (Stockdale 2004).

• Large, pale-colored droppings suggest pancreatic damage.

• Unilateral or bilateral lameness caused by pressure of renal tumors on adjacent lumbosacral plexus

• White uric acid tophi may be visible under the skin of the legs and feet. Joints may be swollen (articular gout).

• Neurologic signs (e.g., ataxia, generalized tremors)

Investigations

1. Hematology and biochemistry

a. Uric acid is secreted by the proximal tubule of the avian kidney and so is not dependent on glomerular filtration rate, so blood uric acids levels may only rise in chronic renal disease. It may also crystallize out as gout tophi in the kidneys (renal gout) or other organs (visceral gout), which again may limit otherwise high blood uric acid levels. Most waste nitrogen is excreted as uric acid, not urea, so urea levels tend to be low. There may be a rise in phosphorus and a change in the calcium to phosphorus ratio (see Table 8-7); therefore, need to assess multiple values (i.e., uric acid, urea, creatinine, calcium, and phosphorus) to assess renal disease

b. Biochemistry for hepatic disease

c. Blood glucose: Normal range cockatiel, 12.76 to 24.4 mmol/L; diabetic birds, >55.5 mmol/L

d. Plasma glucagon to insulin ratio 5 to 10 times higher than in mammals.

2. Urinalysis

a. Glycosuria and/or ketonuria suggestive of diabetes mellitus but may indicate mixing of feces with urine.

b. Microscopy: WBCs or renal casts suggest urinary tract disease.

3. Radiography

a. Plain and contrast (IV pyelogram with iohexol)

4. Endoscopy and biopsy

a. On endoscopy (or postmortem) uric acid may be seen deposited on certain viscera such as the pericardium or the serosal surface of the liver.

5. Cloacal swabs

a. Bacteriology: Culture and sensitivity

b. Encephalitozoon hellem (special staining required)

Management

• Supportive treatment, including fluid therapy (see “Differential Diagnosis of Gastrointestinal Disorders”)

TreatmentZspecific therapy

• Anabolic steroids (e.g., nandrolone 1 mg/kg SC) may be of some benefit. Note: Some birds react badly to such oily injections.

• Benazepril at Egg peritonitis (coelomitis)

Nutritional

• Hypocalcemia (see Nutritional Disorders)

Neoplasia

• Oviductal adenocarcinoma

Other noninfectious problems

• Dystocia (egg-binding)

• Cloacal prolapse (see Gastrointestinal Tract Disorders)

• Intracoelomic mass

• Skeletal abnormality

• Oviductal torsion

• Superovulation/excessive egg production—especially cockatiels

• Egg peritonitis (sterile)

Findings on clinical examination

• Bird may be depressed, slightly dyspneic.

• A coelomic mass may be palpable.

• Partial leg paralysis

• History of multiple egg production

• Distended, fluid-filed coelom; dyspnea (egg serositis)

Investigations

1. Hematology and biochemistry: Serum calcium (including ionized calcium)

2. Radiography

3. Ultrasonography

4. Examination under GA

5. Coelomic tap and aspiration (midline)

a. Cytology

b. Culture and sensitivity

6. Endoscopy

Management

1. Place bird somewhere darkened, warm, and of high humidity.

2. Give calcium and/or vitamin D3 supplementation.

3. Deslorelin implants (a GnRH agonist) will give temporary ovarian shutdown for up to

6 months, although times and efficacy may vary between species.

TreatmentZspecific therapy

• Dystocia (egg-binding)

• Calcium supplementation: 100 to 500 mg of calcium PO in cases of hypocalcemia

• Oxytocin 1 to 5 IU/kg IM. Use judiciously as this can have a marked effect on blood pressure.

• Dinoprost (Lutalyse) 20 to 100 pg/kg IM as a single dose

• Apply prostaglandin E2 gel to the cloaca to stimulate contractions.

• Under GA, the egg may be manipulated out.

• If the egg is thin-shelled, aspiration of the contents through the abdominal wall with a syringe and hypodermic needle will allow collapse of the egg and its subsequent delivery.

• Superovulation

• Medroxyprogesterone acetate to inhibit ovulation at 10 mg/kg IM; titrate dose as precisely as possible because overdose likely to trigger severe polydipsia/polyuria

• Leuprolide, as a single injection, to give a dose of 52 to 156 pg/kg; reversibly inhibits egg-laying in cockatiels for up to 31 days

• Surgical ovariectomy

• Egg serositis

• Abdominocentesis to alleviate dyspnea

• Antibiotics and NSAIDs to reduce inflammation

• Surgery for abdominal lavage

Growth and weaning

Psittacines (and many passerines) have altricial young and display a characteristic growth curve. This curve rises rapidly to a peak body weight just before the time of weaning and then falls slightly to the weaning weight before continuing up to the eventual adult weight.

Cockatiels younger than 1 week are unable to mobilize body tissues in the face of deficien­cies, and cockatiel chicks subjected to a low-protein diet fail to lose weight, maintaining their weight until death. Because of the expected growth curve, and this failure to lose weight in spite of nutritional problems, daily weighing is strongly recommended to monitor the chick's condition. Chicks should typically gain about 17% body weight daily in the first 7 days; all chicks should have doubled their body weight by day 7.

Psittacine chicks are ectothermic on hatching. Correct environmental temperatures are as follows:

Correct environmental temperatures for chicks

1. Newly hatched: 33.3° to 34.4° C

2. Unfeathered: 32.2° to 33.3° C

3. Partially feathered: 29.4° to 32.2° C

4. Fully feathered: 23.9° to 26.7° C

5. Weaned: 20.0° to 23.9° C

• Retained yolk sac

• Often accompanies umbilical infection

• Debridement of infected material and antibiosis

• Aspiration of yolk sac material

• Surgical resection of yolk sac

• Failure to gain weight—many possible problems, but likely to be bacterial or fungal (Candida) infection

• Start on nystatin at 300,000 IU∕kg PO b.i.d. for 10 days and a broad-spectrum antibiotic

• May need crop tubing; switch from normal hand-rearing formula to a rehydrating/ critical care formulation. This will need to be given more frequently to maintain the energy input that the chick requires. After 24 hours, begin to introduce the hand­rearing formula back into the diet over a period or 2 to 3 days.

• Reassess environmental conditions.

• Crop diseases of chicks (see “Differential Diagnosis for Vomiting∕Regurgitation∕ Dysphagia” in Gastrointestinal Tract Disorders)

• Hepatic lipidosis—chicks fed on a too high-fat diet

• Respiratory distress

• Hepatomegaly

• Reduce intake of food; reduce fat content of food; add lactulose to diet

• Parenteral fluid administration

• Hepatic hematoma

• Usually following trauma (e.g., dropping the chick)

• Often hepatic lipidosis concurrent (enlarged, friable liver)

• Supportive treatment; poor prognosis

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