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1. Learning Objectives
- Be familiar with the toxic and metabolic disorders presented in this section
- Know the clinical presentation, diagnosis and treatment options for lead poisoning in birds
- Understand the pathogenesis and clinical presentation of gout in birds
- Know the clinical presentation, diagnosis and treatment options for hypocalcemia in African Grey parrots
- Know the clinical presentation, diagnosis and treatment options for hemochromatosis in target bird species
2. Toxic Diseases
2.1. Lead poisoning
This is the most common toxic disease of pet birds, and is very prevalent in the Northeast. Lead poisoning is also seen in wild birds, especially waterfowl. It often involves an insidious course with chronic exposure. The acute disease is more easily recognized.
2.1.1. Clinical signs
Clinical signs of lead poisoning can be quite variable and include: anorexia, diarrhea or GI stasis, vomiting, PU/PD with hematuria (Amazons), muscle weakness, paralysis, ataxia, blindness, seizures, and death.
2.1.2. Diagnosis
The diagnosis is based on history, clinical signs, radiographs, CBC (mild anemia), blood lead levels (suspect at 20 mg/dl, diagnostic at 40+ mg/dl for most birds). One can also measure protoporphyrin and ALAD (delta-aminoleulonic acid dehydrase) levels. At necropsy tissue lead levels should be measured on kidney and liver samples.
2.1.3. Treatment
Treatment for lead poisoning (often begun before laboratory test results are known) includes elimination of the source of the lead via cathartics, intestinal chelators (MgS04,) peanut butter (bulking agent,) or surgery, and chemotherapy to bind and aid elimination of systemic lead.
2.1.3.1. CaEDTA
CaEDTA acts to bind lead in the serum. Bone and tissue levels will equilibrate with serum levels and gradually be decreased. CaEDTA is very poorly absorbed from the GI tract and must be given parenterally unless one is trying to chelate intestinal lead. It is felt to be highly nephrotoxic in mammals (as is the lead), but this has not been demonstrated in birds. CaEDTA should be used with care in renal compromised patients. Some recommend the course of therapy as 5 days on and 5 days off chelation to avoid renal toxicity.
2.1.3.2. Succimer (Chemet)
meso-2,3-dimercaptosuccinic acid
This is a new compound which is being used in pet birds. It has been developed for use in children with chronic lead poisoning. It is an orally administered chelating compound and can be used on a long term basis. A dose of 30 mg/kg orally twice daily has been recommended. Higher doses have been shown to cause toxicity and death, especially in cockatiels. In acute cases succimer can be used in combination with a single dose of CaEDTA.
The prognosis for recovery is good if treatment is begun before severe neurologic disturbances are evident. The prognosis is guarded once neurologic signs have developed.
2.2. Zinc toxicosis
(New wire disease)
Zinc toxicosis is the second most commonly encountered heavy metal poisoning seen in pet birds. Zinc is present in the environment on galvanized metal objects, such as cage wire or clips used to assemble cages. Birds housed in such cages or with access to galvanized materials can ingest enough zinc to become affected.
2.2.1. Clinical Signs
Clinical signs are very similar to those seen with lead poisoning and include: PU/PD, GI problems, decreased fertility, weight loss, weakness, ataxia, anemia, cyanosis, hyperglycemia, seizures and death.
2.3. Organophosphate toxicity
(also carbamates)
Organophosphate (OP) poisoning is considered primarily a disease of wild birds exposed to environmental organophosphates. This occurs through agricultural spraying and through amplification in prey species (raptors). Pet birds may also be exposed to garden pesticides, flea collars, no pest strips (canaries especially sensitive), etc.
2.3.1. Clinical signs
Clinical signs of OP toxicity include: lethargy, generalized weakness, bradycardia, paralysis, and seizures. A delayed neuropathy has been described in Amazon parrots that my present as an ascending paralysis 7 to 21 days after exposure.
2.3.2. Diagnosis
Diagnosis is based on clinical signs, history of access to the toxin, and organophosphate/cholinesterase activity measurements. At post mortem decreased brain cholinesterase levels and organophosphate levels in the fresh liver can be assayed. In clinical antemortem cases, one may be able to measure decreased serum cholinesterase levels. Serum OP levels can also be done ($90).
2.3.3. Treatment
Treatment for OP toxicity includes supportive care and administration of atropine at doses of 5 mg/kg up to 20 mg/kg. An immediate response is usually seen. Repeat doses of atropine as needed. The atropine has a short half-life, and the OP has a long one. The administration of 2-PAM should only be done in the 1st 24 hrs. (need to know when exposure occurred).
2.4. Botulinum Toxicity
(Limberneck)
Botulism is one of the most important diseases of wild waterfowl. Every year there are multiple mass die-offs in the mid-west and Western US and in other places around the world.
Classical Type C botulinum toxin is produced by Clostridium botulinum bacteria growing under favorable conditions in the environment. This bacteria grows best in an anaerobic environment (shallow lakes) where there is organic material present (often dead carcasses) and high temperatures (late summer/fall). As the carcass decays further, maggots will colonize and proliferate, ingest the bacteria + toxin and attract waterfowl which ingest the maggots, the toxin, and in turn succumb and perpetuate the cycle. A single toxin laden maggot can kill a duck. This toxin most commonly affects: waterfowl, shorebirds, colonial waterbirds, and others.
Type E toxin has been shown to affect gulls, loons, and others. It has recently been reported in the Great Lakes region.
2.4.1. Clinical signs
The neurotoxin causes progressive flaccid paralysis producing signs of weakness, difficulty/inability to walk or fly, and "limberneck" in long necked waterfowl. Many of these birds drown because they cannot pick their heads up out of the water. Others will die from asphyxiation, dehydration, electrolyte imbalances, or predation.
2.4.2. Diagnosis
Definitive diagnosis is made through demonstration of the toxin in serum, stomach contents, or tissues.
2.4.3. Treatment
Animals with mild signs, usually a presumptive diagnosis, can be treated with supportive care as they metabolize the toxin. Antitoxin can be used, but must be given early on to be effective as is often not readily available.
See Supplemental Readings more information on recent outbreaks. Also refer to the NWHC site for general information http://wildlifedisease.nbii.gov/wildlifeDiseases/av_botulism/av_botulism.html.
2.5. Teflon toxicity
(Polytetrafluoroethylene)
The toxic fumes from a burning Teflon pan with little or nothing in the pan produces lethal gases of polytetrafluoroethylene. This substance is also contained in some spray starches. The clinical signs include acute respiratory distress, panic and rapid death: the bird rarely makes it to the vet. The pathology findings include: air sacculitis, pulmonary congestion, hemorrhagic pneumonitis, and necrotizing pneumonitis.
There is essentially no treatment, since the bird never reaches the doctor in time. Clearly preventative education is the only way to avoid this devastating event.
2.6. Poisonous Plant Ingestion
| Plants Reported to be Toxic in Pet Birds | ||
| Amaryllis | Hemlock | Mountain laurel |
| Avocado | Horse-chestnut | Narcissus |
| Azalea | Hyacinth | Nightshade |
| Bird of paradise | Hydrangea | Oleander |
| Black locust | Iris | Philodendron |
| Boxwood | Jack-in-the-pulpit | Pokeweed |
| Buttercup | Jerusalem cherry | Poinsettia |
| Caladium | Jimsonwood | Potato shoots |
| Castor bean | Juniper | Privet |
| Cherry | Lantana | Rhododendron |
| Clematis | Larkspur | Rhubarb |
| Cowslip | Lily-of-the-valley | Rosary pea |
| Daphne | Lobelia | Skunk cabbage |
| Datura | Marijuana | Snowdrop |
| Diffenbachia | Mistletoe | Tobacco |
| Elephants ear | Mock orange | Virginia creeper |
| English ivy | Monkshood | Wisteria |
| Foxglove | Morning glory | Yew |
Avocado toxicity has been reported in cockatiels and canaries. It has also been experimentally induced in canaries and budgies. Most budgies and 1 canary died 24-48 hrs. later! Clinical signs involve acute respiratory distress. Pathologic lesions include subcutaneous edema and hydropericardium.
2.7. Aflatoxicosis
Aflatoxin is a toxin produced by molds in food, usually Aspergillus spp.. The toxin can be found on many foodstuffs including peanuts and seeds/grains (most commonly), sprouts, cheese, bread, beans, and even meat. The disease is commonly seen in poultry but is being recognized more frequently in pet birds.
Aflatoxins primarily produce hepatotoxicity, immunosuppression, and clotting disturbances. The diagnosis is made most often at postmortem with typical hepatic histopathologic lesions. Rarely is diagnosis verified through chemical analysis. Clinically, this disease should be suspected in cases of acute hepatitis when infectious causes have been ruled out.
2.8. Miscellaneous household toxins
Beware of the free-ranging pet bird! Also beware of the free-ranging 4 year old. Items reported include: alcohol, nicotine, hexachlorophene (soaps), ethylene glycol, motor oils, match heads, carpet cleaners, and scented deodorizing candles (Glade).
3. Metabolic Diseases
3.1. Gout
Uric acid metabolism is at the root of the pathophysiology of the disease "gout". In birds, uric acid is the main byproduct of protein catabolism (vs. urea in mammals). Uric acid is produced primarily in the liver, and actively secreted by the proximal tubules of the kidney. Hyperuricemia and subsequently gout will occur when the ability of the kidney to process the amount of uric acid produced is inadequate. Hyperuricemia results in the precipitation of uric acid in the form of sodium urate crystals in various places in the body.
3.1.1. Visceral gout
Visceral gout is seen in many birds with renal failure. Uric acid crystals are deposited in or on the tissues of many internal organs such as the kidney and the heart. Causes of visceral gout are many, including severe dehydration, high protein diet (especially in young birds), vitamin A deficiency (squamous metaplasia of renal tubules), and renal failure for whatever reason (including aminoglycoside therapy).
 Visceral gout in a raptor
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3.1.2. Articular gout
Articular gout, on the other hand is seen most often in small birds, particularly budgies. Uric acid crystals are deposited in joints of the legs and wings causing severe pain, swelling and inflammation. A genetic reason for the prevalence of gout in budgies has been proposed. Renal failure cannot always be demonstrated.
 Joint aspirate showing uric acid crystals
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The treatments available for gout are not very promising. Early stages of nutritionally induced gout have been reversed with probenecid (promotes uric acid excretion), and colchicine (anti-inflammatory) for up to 10 weeks, in association with a low protein diet. Treatment of either articular or visceral gout with allopurinol has only been able to partially halt the progression of the disease and does not reverse the condition (eventually fatal if it progresses). Euthanasia should be considered in cases of advanced articular gout in budgies, due to the pain involved.
 Articular gout in budgie
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3.2. Diabetes Mellitis
Diabetes mellitis does occur in avian species with relative frequency. It is most often reported in budgerigars, toucans, and ducks, but can occur in any species (recent report in red-tailed hawk and a broad-wing hawk). The pathophysiology of this disease is different in non-meat-eating birds than in most mammals. It is felt that glucose metabolism in these birds is much more dependant on glucagon concentration than on insulin levels. Diabetes is often a problem of an increase in glucagon, rather than a decrease in insulin. Histologically, there are many more alpha cells in the pancreatic islets than beta cells. In meat eating birds, the pancreas resembles the mammal's pancreas.
3.2.1. Clinical signs
Clinical signs of diabetes are what one would expect.
- Polyuria
- Polydipsia
- Polyphagia
- Weight loss (usually)
3.3. Hypocalcemia of African Grey Parrots
The etiology of this phenomenon is not well understood, however one can usually document a dietary deficiency of calcium, and/or an excess of phosphorus. One can often demonstrate a high fat diet (sunflower!!) also which may be precipitating Ca soaps and lowering serum calcium. It would appear that the calcium/phosphorus metabolism in African Grey parrots is different than that of other birds and mammals. These birds seem to have a difficult time mobilizing calcium from extravascular sources (such as bone). Most birds, mammals and reptiles will readily use up bone stores before they allow hypocalcemia to occur (metabolic bone disease). These unique parrots however develop hypocalcemia without developing metabolic bone disease.
3.3.1. Clinical signs
The affected bird is most often recognized in an acute phase, but the disease can be chronic. Acute clinical signs include weakness, falling off the perch, poor feather condition, and occasionally tetany and/or seizures.
3.3.2. Diagnosis
The diagnosis is based on clinical signs, signalment, and serum calcium levels < 7.0 (normals are 8-13 mg/dl). Radiographs are usually not useful in making a diagnosis since these birds are not osteopenic. Postmortem lesions include enlarged parathyroid glands with significant degeneration.
3.4. Hemochromatosis
Hemochromatosis is the iron storage disease of mynah birds, birds of paradise, starlings, quetzals, ramphastids (toucans) and occasionally other birds. The etiology is uncertain, controversial and still under investigation. Proposed causes include a genetic defect in iron absorption or metabolism, or a dietary cause. In some species there appears to be an extremely efficient intestinal iron absorption mechanism: birds of paradise absorb 90% of dietary iron, humans only 10%. Further examination of the natural environment of these birds may reveal a dietary driven evolutionary adaptation to allow increased intestinal absorption of iron. This research is ongoing but supports this hypothesis (see references).
The disease results in an abnormal accumulation of iron pigments in hepatocytes (and other tissues such as myocardium, lung, kidneys, etc.), hepatic fibrosis, hepatomegaly, ascites resulting in severe abdominal distention, dyspnea, anorexia, and finally death.
3.4.1. Clinical signs
Birds usually present cachectic, in severe respiratory distress with pronounced ascites. Ramphastids (toucans) often have very vague signs and may not develop ascites.
3.4.2. Diagnosis
Diagnosis is made based on signalment, clinical signs, radiographs and liver biopsy (total serum iron concentration is not considered diagnostic).
3.4.3. Treatment
Treatment includes abdominocentesis to relieve pressure (one time emergency only), diuretics, steroids, and phlebotomy (1% body weight in ml, once weekly) and dietary management. The use of deferoxamine, an iron chelating agent used in people, may be helpful and can be used on a chronic basis. The prognosis is always guarded.
3.4.4. Prevention
Prevention of this disease in susceptible species has been most successfully accomplished through feeding low iron diets. This is critically important for maintenance of these birds in captivity. However since the true etiology is not known, the total efficacy of this technique is still in question.
4. Ancillary Material
4.1. Readings
4.1.1. Texts and articles
Altman, Robert B., et al. Avian Medicine and Surgery. Philadelphia. W.B. Saunders Co., 1997. Chapter 28, 32, 35.
Altman, Robert B., and Alan H. Kirmayer. Diabetes mellitus in the avian species. Journal of the American Animal Hospital Association, July/August, Vol 12, 1976, pp. 531-537.
Cornelissen, Hans, R. Ducatelle, and S. Roels. Successful treatment of a Channel-billed Toucan (Ramphastos vitellinus) with iron storage disease by chelation therapy. Journal of Avian Medicine and Surgery, 9 (2), 1995, pp. 131-137.
Denver, Mary C., Lisa A. Tell, and Francis D. Galey. Comparison of oral and parenteral heavy metal chelators for the treatment of lead toxicosis in cockatiels (Nymphicus hollandicus). Proceedings of the AAZV and AAWV Joint Conference, 1998: 147.
Drews, Amber, Sharon P. Redrobe, and Janet C. Patterson-Kane. Successful reduction of hepatocellular hemosiderin content by dietary modification in Toco Toucans (Ramphastos toco) with iron-storage disease. Journal of Avian Medicine and Surgery, 18 (2), 2004 : 101-105.
Hargis, A.M., et al. Avocado intoxication in caged birds. JAVMA, Vol 194 (1), 1989, pp. 64-66.
Holz, Peter, et al. Suspected zinc toxicosis as a cause of sudden death in orange-bellied parrots (Neophema chrysogaster). Journal of Avian Medicine and Surgery, 14 (1), 2000: 37-41.
Hoogesteijn, Almira L., et al. Oral treatment of avian lead intoxication with meso-2,3-dimercaptosuccinic acid. Journal of Zoo and Wildlife Medicine 34 (1), 2003: 82-87.
LaBonde, Jerry. Pet avian toxicology. 1988 Proceedings of the Annual Meeting of the Association of Avian Veterinarians, Houston, Texas, September, 1988, pp. 159-174.
McDonald, Scott E. Lead poisoning in psittacine birds. In Kirk, Robert W. Current Veterinary Therapy IX. Philadelphia: W.B. Saunders Co.,c1986. pp. 713-718.
Murphy, Joel. Diabetes in Toucans. Proceedings of the 1992 Annual Conference of the Association of Avian Veterinarians, New Orleans, Louisiana, September 1-5, 1992, pp. 165-170.
Otten, Benjamin A. Toucans in Belize: implications of diet on hemochromatosis. Proceedings of the 1997 Annual Conference of the Association of Avian Veterinarians, Reno, Nevada, September, 1997, pp. 105-107.
Otten, Benjamin A., Orosz, Susan E., Auge, Shannon, Frazier, Donita L. Mineral Content of Food Items Commonly Ingested by Keel-Billed Toucans (Ramphastos sulfuratus) Journal of Avian Medicine and Surgery 2001 15: 194-196
Ritchie, Branson W., et al. Avian Medicine: Principles and Application. Lake Worth, Fla., c1994: Chapter 24, 37.
Ryan, C.P., et al. Diabetes mellitus and islet cell carcinoma in a parakeet. Journal of the American Animal Hospital Association, Jan/Feb, Vol. 18, 1982, pp. 139-142.
Sheppard, Christine, and Ellen Dierenfeld. Iron storage disease in birds: speculation on etiology and implications for captive husbandry. Journal of Avian Medicine and Surgery, 16 (3), 2002: 192-197
Stanford, Michael. The effect of UV-B lighting supplementation in African Grey Parrots. Exotic DVM, 6.3, 2004: 29-32.
Worell, Amy. Phlebotomy for treatment of hemochromatosis in two sulfur-breasted toucans. Proceedings of the 1991 Annual Conference of the AAV, Chicago, Illinois, September 23-28, 1991, pp.9-14.
Worell, Amy. Serum iron levels in Ramphastids. Proceedings of the 1991 Annual Conference of the AAV, Chicago, Illinois, September 23-28, 1991, pp.120-130.
Worell, Amy. Further investigations in rhamphastids concerning hemochromatosis. Proceedings of the 1993 Annual Conference of the AAV, Nashville, TN, August 31-September 4, 1993, pp. 98-107.
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