Avian Toxicology Flashcards
How can newly galvanized wire be treated to remove zinc deposits?
Wash in vinegar
What is the toxic agent of teflon?
Polytetrafluroeythylene
Describe the absorption and metabolism of lead?
What factors affect the absorption of lead? What anatomic sites allow for absorption?
What dietary items may inhance or decrease lead absorption?
Where does lead bind to in circulation?
What are the three storage compartments for lead?
How is lead deposited within the avian egg?
How is lead excreted?
Lead:
- Captive and household birds may ingest lead from leaded paints, caulking, solder, or linoleum
- Solubilized in acidic environment of proventriculus and ventriculus à absorbed in SI
- raptors - pH 1 = faster absorption
- psittacines, granivorous birds – pH 2-4
- absorption - organolead >> lead salts > metallic lead
- absorption affected by diet:
- cracked corn >> “soft” diets
- high fiber > low fiber
- calcium rich diet reduced morbidity and mortality
- inhaled lead absorbed from lungs
- lead embedded in tissues – not absorbed unless inflammation present
- lead in joints absorbed due to acidity
- 90% bound to RBC then distributed
- 3 compartments:
- Bone – 94%
- Soft tissues – 2%
- Blood and highly vascular tissues – 4%
- Eggs accumulate lead in their shells (highest concentration), yolk, and albumen
- The lowest concentration of lead is found in skeletal muscle
- Majority of ingested lead is excreted in the feces without being absorbed
- Absorbed lead filtered across glomeruli and can accumulate in renal tubular epithelium
- Chelating agents will enhance the urinary excretion of lead
What are the clinical signs and effects of lead toxicity?
How does acute lead toxicosis differ from chronic lead toxicosis?
What are three clinicopathologic effects of lead toxicity?
How is lead toxicity diagnosed?
How is it treated? Compare and contrast the various chelators.
Which chelator is associated with significant adverse effects?
- Clinical signs and effects:
- Anemia
- impairs gastroenteric motility
- cerebral edema
- progressive demyelination of peripheral nerves
- impairs neurotransmission
- immunosuppression
- Acute vs chronic
- Acute - anorexia, lethargy, bile-green diarrhea, discolored urates, altered voice (dysphonia), respiratory distress, blindness, muscle weakness that progresses to paresis/paralysis, seizures, coma, and death
- Chronic - weight loss, impaction of gizzard and/or proventriculus
- Clin path - heterophilia, hypochromic regenerative anemia, cytoplasmic vacuolization of red cells, basophilic stippling of red cells, hypoproteinemia, elevations in lactic dehydrogenase, aspartate transaminase, creatine phosphokinase, and uric acid
- Definitive test – blood lead level, cannot rule out with rads
- Treatment – decontaminate, chelate, supportive care
- Remove from GI first as chelators enhance absorption of lead
- Chelators
- CaEDTA – best chelator for bone
- D-penacillamine
- BAL (Dimercaprol)
- Crosses BBB but nephrotoxic and painful on injection
- DMSA – chelates brain and soft tissues, not bone, does not chelate zinc
Lead toxicity damages what cell resulting in neuropathy?
Schwann cells
Myelin sheath damage & vascular endothelial damage results in neural edema
Zinc toxicity commonly results from ingestion of what substances?
What are the clinical effects of lead toxicity in birds?
What is the tissue of choice for assessing zinc toxicosis?
What is the chelator of choice?
Zinc
- Ingested from carpentry hardware (nuts and bolts), U.S. pennies minted after 1982, and galvanized items (fence clips)
- objects in stomach/gizzard corroded by low pH and enter blood
- Effects:
- damages RBC’s, hemolysis and renal failure secondary to hemoglobinuria
- GI irritation causing GI signs
- Signs - pallor, weakness, ataxia, paresis or paralysis of the legs, anemia, diarrhea, weight loss, and death
- Pancreas - tissue of choice for assessment of zinc toxicosis in birds
- Tx – decontaminate, supportive care, chelation
- CaEDTA is the chelator of choice for zinc in avian species
What is the mechanism of teflon toxicity?
What is the chemical that causes the damage?
What clinical signs are commonly present?
How is this treated?
What is the prognosis?
Damage to type 1 pneumocytes, capillary endothelial cells
Congested wet lungs with pulmonary edema and hemorrhage
Terio Ch 32 - Psittaciformes
Polytetrafluoroethylene (Teflon)
- inert nonstick coating used on cookware and heat bulbs
- fumes sensitize the myocardium, causing arrhythmias, pulmonary congestion, and cardiac failure
- On necropsy, hemorrhagic and edematous lungs are the most common findings
- Signs - off their perch, uncoordinated, open mouth breathing, have respiratory rales, and will tail bob with each respiratory effort
- Treatment - humidified oxygen, diuretics to reduce pulmonary edema, nonsteroidal anti-inflammatory drugs, broad-spectrum antibiotics, and supportive care
- Most birds get respiratory signs and die
How is carbon monoxide produce?
What is the mechanism of its toxicity?
What are the clinical signs of birds with carbon monoxide toxicosis?
How is it treated?
What is the prognosis?
Carbon Monoxide
- produced by inefficient combustion of carbon-based fuels (wood, coal, petroleum, natural gas)
- toxic to all species but bird more susceptible -high respiratory and metabolic rates
- MOA - competes with oxygen for binding to hemoglobin
- Signs - dyspnea, ataxia, rapid depression, coma, respiratory paralysis, and death
- Bright red blood
- Anoxic brain damage can be permanent
- Tx – hyperbaric O2 chamber (gold standard), oxygen therapy, intubate and ventilate
- Prognosis – guarded
What is the mechanism of action of anticoagluant rodenticide toxicity?
What are the vitamin K dependent factors?
What clottting factors do birds lack?
What are the differences between first and second generation anticoagulant rodenticides? Give some examples of each.
What are the typical clinical signs?
How is this toxicity treated?
Anticoagulants
- MOA - inhibiting 1,2,3-vitamin K epoxide reductase, causing loss of vitamin K regeneration
- Vitamin K depletion and inhibition of coagulation synthesis
- vitamin K–dependent factors – 2, 7, 9, 10
- Birds lack factors 9 and 12
- both the tissue factor pathway (extrinsic) and the amplification or contact pathway (intrinsic) function in avian coagulation are affected
- 1st generation anticoagulants - require frequent, multiple feedings by rodents to produce toxicosis
- coumarin, warfarin, and indandione
- 2nd generation anticoagulants - much longer biological half-life than 1st generation
- Can persist for at least 6 months in liver and tissues
- brodifacoum, bromadiolone
- Signs - pale MM and anemia, weak, lethargic, subcutaneous ecchymoses, bleed profusely from superficial wounds
- Diagnosis – clinical signs
- Post-mortem - massive internal hemorrhage, lack of a postmortem heart blood clot
- Plasma, stomach contents, or liver checked for anti-coagulants
- Tx – decontamination, activated charcoal and evacuation
- Vitamin K IM then PO x 3wks
- Whole blood transfusion – replace clotting factors and RBC’s
What are hydrocarbons?
Where do they originate?
How do oil spills affect birds?
How are affected birds treated?
Petroleum distillates à hydrocarbons
- Examples of hydrocarbons - volatile compounds like gasoline and mineral spirits to solid waxes
- absorbed by inhalation, by ingestion, or dermally
- Volatile compounds absorbed quickly
- Oils slowly absorbed
- Distribute to fatty tissues à neurotoxicity
- Oil spills
- Destroys waterproofing and insulation on feathers
- reproductive, endocrine, and hematopoietic effects and osmoregulatory alterations
- Tx – dermal decontamination until can’t smell on feathers, can use corn starch temporarily to absorb oil until stable
- Do not lavage – risk of aspiration
- Oxygen, ventilation, antibiotics, bronchodilators as needed
What birds are commonly affected by barbituate toxicity?
What are the typical clinical signs?
Is there a seasonality to these cases?
How is this treated?
Barbituates
- lipophilic and stable compounds and can persist in the dead carcass for up to several weeks or longer
- onset – few hours post ingestion
- signs – weak, difficulty flying, walking, or standing, collapse, respiratory effort affected, may become comatose and die
- Tx – ventilation as needed, repeated activated charcoal administration (long half life)
Barbiturates
- Pentobarbital poisoning
- VETERINARY PRODUCT. Euthanized animal carcasses are consumed (burial is interfered with; landfill)
- Bald and golden eagles. Raptors have a low tolerance for barbituates.
- 17 cases in the US
- Winter and early spring for the 7 cases.
- Proximity to a carcass. Sedated, drowsy, decr heart and resp rate .Signs of struggling are not likely (as with other toxins)
- No lesions. Ingesta in upper GI as with other acute toxins. Maybe you’ll recognize the ingesta as a domestic animal.
- Liver and upper GI contents for barbituate levels. Blood too.
- Regulate carcass disposal
- None
What NSAID is particularly toxic to vultures?
How are these birds exposed?
What are the typical clinical signs and lesions?
Diclofenac (vultures)
- NSAID
- Vultures - became severely depressed ~24hrs postexposure, became comatose, and died ~48hrs postexposure
- Acute renal failure and visceral gout
- Longer half life in vultures
- Fowler 7 has a review on this topic
What is the cause of Avian vacuolar myelinopathy?
What plant species is this associated with?
What is the mechanism of the toxicity?
Is there a seasonality to this toxicity?
Avian vacuolar myelinopathy
- neurologic disease linked to cyanobacteria
- mortality in bald eagles, great horned owls, American coots, killdeer, and waterfowl (mallards, ring-necked ducks, buffleheads, and Canada geese) in SE USA
- Hydrilla verticillata (Hydrocharitaceae) and an associated epiphytic cyanobacterial species (order Stigonematales)
- cyanobacteria - produces neurotoxic amino acid b-N-methylamino-L-alanine (BMAA)
- overactivation of neuroexcitatory glutamate receptors
- Signs - ataxic and unable to walk, swim, or fly
- <1wk post exposure
- Seen late fall early winter
- Necropsy – no gross lesions, histo - diffuse spongy symmetrical vacuolation and degeneration in white matter of brain and spinal cord
- optic tectum - most severely affected
- No treatment, some recover with supportive care
What is the toxic principle of Avocado?
What lesions does it cause?
What are the associated clinical signs?
How is this toxicity treated?
Avocado (persea Americana)
- R antimere of persin – causes myocardial necrosis in birds
- Persin found in fruits, leaves (most toxic), seeds
- 24 to 96 hours after ingestion – myocardial insufficiency
- Signs – agitation, feather plucking, lethargy, respiratory distress, edema, cyanosis, cough, death
- Caged birds - more sensitive
- Chickens and turkeys - more resistant
- Dx – history of exposure and signs, no specific test
- Tx – oxygen, diuretics, antiarrhythmic drugs as needed
Aflatoxins are produced by what fungus?
What is the most common and most toxic aflatoxin?
What birds are commonly affected? Any other animals?
Where is this toxin commonly identified?
Is there a seasonality to it?
What are the clincial signs and lesions?
How is it diagnosed?
Is it a human health issue?
Aflatoxin
- Aspergillus sp found in grains. Toxins named B1, B2, G1, G2. Become more toxic after ingestion. B1 most common, most toxic. Associate with ground nuts and corn.
- Domestic ducklings. Affects trout, other wild animals (mammals as well). Birds more susceptible than mammals.
- U.S. usually, but the fungus lives world-wide.
- Fall/winter.
- Depression, lethargy, blindness, inability to fly, tremors, wing flapping.
- Variable. Hepatomegaly. Hemorrhagic fluid in coelom. GI hemorrhage. Chronic: fibrous liver, poss tumors.
- Measure aflatoxin levels in tissue. Measure in food.
- None unless you eat the birds.
What birds are most commonly affected by algal toxins adn cyanobacterial blooms?
What are the typical signs for domoic acid intoxication? How does it vary by species?
What are the cyanobacterial organisms?
What is the mechanism of microcystins and nodularins? What about anatoxins? What species are affected by this?
What organism produces domoic acid? What is its mechanism of toxiciy? What species are affected?
What organism produces saxitoxin? What birds are affected?
What organism produces brevetoxin? What is its toxin type? What birds are commonly affected?
How are these intoxications controlled?
Are these human health issues?
Algal Toxins
- Red tide toxins, phycotoxins, cyanobacterial blooms
- Dinoflagellates and cyanobacteria produce toxins: domoic acid, saxitoxin (paralytic shellfish poisoning-PSP), brevitoxin and cyanobacterial toxins (anatoxins, nodularins, microcystins)
- Birds and mammals. Pelicans, cormorants most recently. Neurotoxins mostly, cyano=hepato toxin and neuro.
- World-wide
- None.
- Vary by toxin. Domoic: pelicans serious neuro, cormorants were just easily handled.
- None.
- Difficult. Circumstantial. Test upper GI contents for toxin. Organisms from bloom.
- Decreasing nitrogen and phosphorus in waterways.
- Saltwater: brevi/domoic. Freshwater: cyanotoxin. Bloom may cause O2 depletion and sun depletion, rather than toxin
- Humans can ingest it and get ill. Skin irritation, possible inhalation problem.
