Clinical signs include anorexia, depression, diarrhea, biliverdinuria, obesity, poor feathering, overgrown beak and nails,
pigment changes in feathers, abnormal molt, pruritis, dyspnea, abdominal enlargement, polyuria and polydipsia. Seizures, ataxia
and muscle tremors may occur if the liver function is significantly impaired.
The diagnosis of liver disease is based upon physical examination, hematology, plasma biochemistries (elevated liver enzymes
and bile acids) and radiology. Definitive diagnosis of hepatic lipidosis requires a liver biopsy. Every attempt should be
made to determine the exact cause of hepatic lipidosis when it occurs.
Treatment requires placing the bird on a low-fat diet such as a commercial pelleted diet supplemented with small amounts of
fresh fruits and vegetables. Excessive carbohydrates should be avoided. Patients that are depressed or exhibiting neurologic
symptoms may benefit from the use of lactulose (0.3-0.7ml/kg q 8-12h) (Cephulac, Marion Merrell Dow, Inc., 9300 Ward Pky,
Kansas City, MO 64114). Birds in critical condition should receive appropriate symptomatic therapy.
Goiter is reported most often in budgerigars and is characterized by regurgitation, dyspnea, increased respiratory noise ("chirp"
or wheeze on expiration), crop distension and even circulatory compromise.
Dietary iodine deficiency leads to diffuse enlargement of the thyroid gland with excessive colloid. The enlarged gland may
then displace the trachea, delay or prevent passage of food from the crop to the thoracic esophagus and stomach or even compress
the heart and great vessels.
The diagnosis of goiter is based upon dietary history, clinical signs, physical examination, radiology and response to iodine
supplementation. Affected birds may be treated with a 0.3% Lugol's solution in the drinking water (1 drop per 20 ml water)
as the sole source of water. The water mixture is provided daily for the first week, three times weekly during the second
week then once weekly. Patients that are dyspneic should receive supplemental oxygen as well as sodium iodide (20%) IM once
daily for three to five days. If there is no response to therapy during that time the diagnosis should be re-evaluated. Placing
the bird on a commercial formulated diet may prevent goiter.
Hypocalcemic syndrome of African Grey parrots
The exact etiology of this syndrome in African Grey parrots is unknown, however, it is suspected that diets with an inappropriate
Ca2+: P ratio (seed diets) or diets with marginal calcium, vitamin A, vitamin D3 or phosphorus levels may contribute to the development of this disease. Other proposed etiologies include decreased levels
of PTH or an inability to effectively mobilize calcium from bone due to reduced osteoclast numbers in some African grey parrots.
The disease is typically seen in young African grey parrots (2-5 years old). Clinical signs include incoordination, weakness,
falling from perches, seizures, collapse, opisthotonus and tetany. The diagnosis is based upon signalment, history, physical
examination, plasma chemistry values (serum calcium levels less than 8.0 mg/dl) and response to parenteral calcium administration. Ionized calcium levels should be performed in order to better evaluate
total body calcium. Demineralization of the skeleton to maintain normal calcium levels does not occur in this syndrome.
Parenteral administration of calcium gluconate (50-100 mg/kg IV slowly or IM diluted) (Vedco, Inc., 5503 Corporate Dr., St.
Joseph, MO 64507 USA) is the treatment of choice and will often control seizures. Diazepam (0.5-1.0 mg/kg q 8-12 or as needed)
(Valium, Roche Laboratories, 340 Kingsland St., Nutley, NJ 07110, USA) may also be required to control seizures. Long-term
therapy involves placing the patient on a proper diet if the bird is not already on one and administration of calcium glubionate
(25-150 mg/kg PO q 12h) (Neo-Calglucon, Rugby Laboratories, Inc., 2725 Northwoods Pkwy, Norcross, GA, USA) or calcium gluconate
(1 ml/30ml drinking water) in addition to vitamin A/D3 supplementation. Vitamin A, D3 and E formulations should not be used in patients eating a formulated diet. Lifelong calcium and vitamin supplementation
may be required. Follow-up examinations should evaluate plasma calcium concentrations to assess the effectiveness of treatment.
Additional follow-ups after several months of therapy may also be needed.