Chelating agents are substances that can form multiple bonds with metal ions. They are used to treat metal poisoning in both humans and animals, including birds. Metal toxicity is a common problem faced by pet birds and wild birds, especially those living in urban environments. Sources of toxic metal exposure include lead paint, zinc coated aviary wire, metal jewelry, and environmental pollution. Chelating agents work by binding to metals and enhancing their excretion from the body. This prevents the heavy metals from accumulating and causing health issues. Some common chelating agents used in avian medicine include calcium EDTA, dimercaprol, and D-penicillamine. Choosing the right chelating agent requires an understanding of the type of metal toxicity, administration route, side effects, and overall safety. With proper treatment, chelation therapy can effectively resolve metal poisonings in birds.
Common sources of metal toxicity in birds
Birds face several sources of toxic metal exposure that can lead to poisoning:
Lead
– Old lead paint in older homes and buildings where birds are kept can chip and be ingested. Lead poisoning is common in Amazon parrots and cockatoos housed in environments with lead paint.
– Game meat or carcasses containing lead shot can be eaten by raptors and scavengers, leading to plumbism.
– Weighted or leaded perches have caused lead toxicity in caged birds.
Zinc
– Galvanized hardware cloth and wire in aviaries can contain zinc. Birds chewing on this material ingest the zinc coating.
– Galvanized metal water containers can leach zinc into drinking water.
– Pennies minted after 1982 are made of zinc and are a source if ingested.
Other metals
– Metal jewelry, chains, bells, and clasps can release nickel, copper, or other metals.
– Old soldered cages constructed with lead-tin containing solder.
– Environmental pollution from mining, smelting, battery recycling, electronics recycling, and industrial processes.
Secondary toxicity
– Eating prey or carrion containing lead shot or sinkers.
– Eating fish from lead-contaminated waters.
– Rodenticides containing bromethalin can cause secondary zinc toxicity.
Health effects of metal toxicity
Ingested heavy metals exert toxic effects on multiple organs:
– Lead: neurologic deficits, weakness, seizures, blindness, abnormal behavior changes, anemia, impaired growth and development.
– Zinc: stomach and intestinal issues like vomiting, diarrhea, gastric ulcers, pancreatic necrosis and damage. Hemolysis.
– Iron: liver disease, diabetes, arthritis, heart problems.
– Copper: liver cirrhosis, brain damage, kidney failure, gastrointestinal distress.
– Nickel: skin dermatitis, hypersensitivity reactions, asthma attacks.
– Cadmium: kidney dysfunction, fractures from osteomalacia and osteoporosis, anemia, liver disease.
Target organs
Certain metals tend to accumulate in and damage specific tissues and organs:
– Lead: bones and central nervous system
– Zinc: pancreas
– Iron: liver
– Copper: liver and brain
– Cadmium: kidneys and bones
Effects in young birds
Metal toxicosis early in a bird’s development can cause:
– Impaired growth
– Feather abnormalities
– Skeletal deformities
– Neurologic abnormalities
– Increased infection susceptibility
– Higher mortality rates
Prompt chelation is essential to minimize permanent damage.
Diagnosing metal toxicity
Metal poisonings are diagnosed through:
Clinical signs
Symptoms pointing to possible metal toxicity include:
– Feather damaging behavior
– Neurologic signs like seizures, ataxia, head tilt, blindness
– Weight loss, poor growth
– Green urates or biliverdinuria
– Anemia unresponsive to iron supplements
– Frequent infections
– Vomiting, diarrhea
– Egg shell abnormalities, reduced hatchability
Radiography
X-rays may reveal:
– Increased bone opacity indicating lead accumulation
– Gastrointestinal metal objects
Endoscopy and biopsy
Performing endoscopy and biopsy of organs can aid diagnosis by revealing:
– Ulceration
– Necrosis
– Abnormal tissue mineralization
Blood or feather testing
Lab tests on blood or feathers can quantify elevated levels of lead, zinc, iron, copper, and other metals. Testing can identify excess circulating levels or high accumulation in tissues. However, many birds have normal blood levels and abnormal tissue concentrations.
Other laboratory tests
– packed cell volume for anemia
– plasma biochemical profile
– bile or fecal metal quantitation
– urinalysis and urine heavy metal levels
Chelating agents used in birds
Several chelating drugs are used for treating metal toxicosis in birds:
Calcium EDTA
Calcium EDTA is the most common metal chelator used in birds. It has a high affinity for binding to lead, zinc, manganese, and other metals. EDTA does not enter cells well so it mostly chelates bloodstream and extracellular metals.
Advantages:
– Safe and effective for lead and zinc toxicity
– Low toxicity potential
– Inexpensive
Disadvantages:
– Primarily binds extracellular metals
– May not remove intracellular stores
– Increased loss of calcium, zinc, copper
Succimer (DMSA)
Succimer (meso-2,3-dimercaptosuccinic acid) is lipophilic so it can enter cells. It mobilizes intracellular lead from soft tissues. It is the primary chelator for lead in the central nervous system.
Advantages:
– Removes intracellular lead
– Low toxicity
Disadvantages:
– Minimal effect on blood lead levels
– Requires more frequent dosing
D-Penicillamine
D-Penicillamine is used most often for copper toxicosis in birds. It forms stable complexes with copper, lead, mercury, zinc, and other metals.
Advantages:
– Effective copper chelator
– Mobilizes renal copper stores
Disadvantages:
– Toxic effects include bone marrow suppression, kidney injury
– Hypersensitivity reactions possible
– Less safe in debilitated birds
Other agents
– Dimercaprol (BAL): For arsenic, gold, or lead poisoning. Toxic.
– Deferoxamine: For acute iron poisoning. Expensive.
– Polythiol resins: Used orally for mercury, cadmium, zinc, copper. Requires repeated doses.
Chelation protocol
The chelation protocol depends on the metal involved, severity, and bird species:
Initial stabilization
– Treat dehydration and electrolyte abnormalities. Give fluids if indicated.
– Address any seizures or neurologic issues.
– Remove metal object if present in GI tract.
Chelating agent
– Choose chelator based on metal (lead, zinc, copper etc), chronicity, and bird health status.
– Administer calcium EDTA for most cases. Succimer added if nervous system signs.
– Use dose and frequency best suited for bird size and condition.
Supportive care
– Nutritional support: Correct anemia and malnutrition. Assist feed if needed.
– Antibiotics if secondary infections present.
– GI protectants if vomiting or diarrhea.
– Monitor for side effects like renal injury or bone marrow suppression.
Monitor response
– Serial blood levels to ensure decrease in circulating metals.
– Radiographs to assess metal objects in GI tract.
– Monitor resolution of clinical signs.
Ongoing prevention
– Identify and remove source of metal exposure.
– Repeat chelation or EDTA doses if needed for total body burden reduction.
– Test related birds if shared enclosure.
– Environmental testing and remediation if pollution source.
How chelating agents work
Chelating medications work through several mechanisms:
Binding metals
Chelators form multiple bonds with metals through sulfur, oxygen, or nitrogen donor atoms. This allows a single molecule of chelator to bind with a single metal ion.
Enhanced excretion
By binding metals, chelators prevent reabsorption and increase urinary and fecal elimination. The metal-chelate complexes are more water soluble for renal excretion.
Mobilization and redistribution
Some lipophilic chelators can penetrate cells and tissues to reach stored intracellular metals. They mobilize tissue stores for redistribution to the bloodstream where they can be excreted.
Decreased organ damage
Chelation lowers circulating toxic metal levels. This reduces further accumulation in body organs and subsequent damage to their structure and function.
Competitive binding
Some chelators compete with and replace essential metals like zinc and copper that are displaced by heavy metals in tissue binding sites.
Safety and side effects
Potential adverse effects of chelating agents include:
Removal of essential elements
Aggressive chelation can decrease levels of essential metals like zinc, copper, iron, manganese, and calcium. Supplementation may be needed.
Bone marrow suppression
Depression of bone marrow activity and blood cell lines can occasionally occur, especially with D-penicillamine.
Renal damage
Chelated metal complexes are cleared by the kidneys. Impaired renal function can result from high circulating levels.
Neurologic effects
Rapid redistribution of lead stores with EDTA can cause neuroexcitation and even seizures in some cases.
Hypersensitivity
Allergic reactions including dermatitis and asthma are possible but uncommon. Oral administration reduces this risk.
Contraindications
Situations when chelation may not be advised or requires caution:
– Marked anemia – Can be exacerbated by chelator effects.
– Severe kidney compromise – Reduced excretory ability, higher toxicity risk.
– Preexisting low mineral levels – Increased depletion may occur.
– Very high blood lead concentrations – At levels above 100 ug/dL, chelation may dangerously mobilize stores.
– Advanced debilitation – Increased toxicity sensitivity due to compromised health status.
Chelation in lead toxicosis
Lead poisoning is one of the most common indications for chelation therapy in birds. Key aspects of treatment include:
Chelating agents
– Calcium EDTA, given IM or PO, is first-line for lead. It promptly lowers blood lead.
– DMSA (succimer) is added for central nervous system signs since EDTA has limited brain penetration.
COURSE of therapy
– Perform serial lead levels to assess reductions and guide duration.
– Continue chelation until blood lead normalizes, for 1-4 weeks typically.
– Average treatment course is 7-10 days for most birds.
Monitoring
– Measure blood lead weekly. Expect rapid reduction with EDTA.
– Perform serial radiographs to follow metallic lead objects in GI tract.
– Monitor blood cell counts if using higher dose chelation.
Supportive care
– Remove lead source and prevent re-exposure.
– Address seizures. Avoid prophylaxis if levels dropping.
– Fluids, nutritional support.
– Treat secondary infections.
Prevention
– Yearly screening for at-risk birds.
– Avoid lead sources – lead paint, toys, weighted perches.
– House in lead-free enclosure after treatment.
Chelation in zinc toxicosis
Zinc toxicity also commonly warrant chelation therapy:
Chelating agents
– Calcium EDTA most effective and safest for zinc poisonings.
– Penicillamine alternatively used but higher toxicity.
COURSE of therapy
– Treat until clinical recovery and zinc levels normalize, around 5-14 days.
– Pancreatic necrosis can prolong treatment to 6+ weeks.
Monitoring
– Measure blood and urinary zinc levels weekly.
– Radiographs to follow metal objects if ingestion occurred.
– Monitor for pancreatitis through serial plasma biochemistries.
Supportive care
– Correct dehydration and electrolyte imbalances.
– Antacids or coating agents if evidence of GI ulcers.
– Assist feeding if severe nausea, gastropathy present.
– Antibiotics if secondary infections develop.
Prevention
– Remove or substitute galvanized metal products in the environment.
– Avoid pennies, zinc toys if inclined to ingest non-food objects.
Conclusion
Chelation drugs are critical tools for treating heavy metal toxicosis in birds. Agents like EDTA, DMSA, and D-penicillamine work by binding to metals in the body and enhancing their elimination through urine and feces. This prevents ongoing accumulation in tissues that can lead to severe multi-organ damage. Chelation is used most often for lead, zinc, copper, and iron poisonings. The choice of drug depends on the metal involved, severity of illness, patient health status, and side effect risks. With appropriate, judicious administration guided by monitoring clinical signs and metal levels, chelation can be life-saving therapy for metal poisonings in avian patients. Identifying and eliminating the source of exposure is also key for resolving current toxicity and preventing future recurrence.