| Color Key | |
| Important key words or phrases. | |
| Important concepts or main ideas. | |
OCW Zoological Medicine 2008
Waterfowl and Raptor Medicine (2008)
F. Tseng, DVM
Cummings School of Veterinary Medicine at Tufts University
1. Learning Objectives and Review
This section pulls together the main diseases and health issues of wild and captive waterfowl and raptors. In addition some specific captive husbandry, management and rehabilitation issues will be introduced. Color coded topics indicate learning objectives that the student should become familiar with. Cases will be presented in class to illustrate these topics.
2. Waterfowl
2.1. Waterfowl Taxonomy
Order Anseriformes - Anatidae | |
Anatinae - true ducks | |
Tadornini |
shelducks |
Cairnini |
perching ducks [spur-winged geese, muscovy, wood duck] |
Anatini |
dabblers [mallards, etc.] |
Aythyini |
pochards & allies [scaup, etc.] |
Mergini |
eiders, scoters, mergansers, etc. |
Oxyurini |
stiff-tailed ducks |
Meranettini |
torrent ducks |
Anserinae | |
Cygnini |
swans |
Anserini |
geese |
Dendrocygnini |
whistling ducks |
2.1.1. Taldorini (Shellducks and allies)
Anatomically somewhere between true geese and ducks
Long necks and legs
Some are sexually dimorphic
Old World ducks
2.1.2. Cairnini (perching ducks)
Muscovy, mandarins, wood ducks etc.
Surface feeders
Nest in holes in trees
2.1.3. Anatini (dabblers)
Mallards, teal, shovelers, pintails and many others
Dabble in shallow water for food
Often upend when feeding
2.1.4. Aythyini (pochards and allies)
Found worldwide
All freshwater, except scaup
Bodies are short and rounded
2.1.5. Mergini
Mergansers, scoters, goldeneyes
Inhabit fresh and seawater
Typically hole nesters
Eat shellfish and crustaceans
Mergansers have pointed beaks with toothlike projections
2.1.6. Somateriini (eiders)
Found in open sea and coastal waters
Eider down used to line nests
Males have conspicuous plumage during breeding season
2.1.7. Oxyurini (stiff tailed ducks)
Ruddy ducks
Stiff tail used as a rudder
Large feet, difficulty walking on land
Nest on floating platforms
2.1.8. Merganettini (torrent ducks)
Three species
Western South America
Live in fast flowing rivers
Swim and dive in rapids
Sexually dimorphic
2.1.9. Cygnini (swans)
Mute, trumpeter, tundra, whistling swans
Long lived
Sexually monomorphic
Pair for life
2.1.10. Anserini (geese)
Canada, brant, snow geese, others
Adapted for living on land
Long centrally placed legs
Long necks, honking calls
Social nature
Feed primarily by grazing
Good swimmers
2.1.11. Dendrocygnini (whistling ducks)
Tropical waterfowl
Tree ducks
Live and nest in or near trees
Longer legs and more upright stance than other groups of ducks
Gregarious, pair for life
2.2. Anatomy

Sexing: phallus of males
Male ducks have sex specific modifications of the syrinx and trachea

Geese and swans molt once a year, ducks twice a year
Post breeding "eclipse" (postnuptial molt) - unable to fly during molt
Highly modified and sensitive beak for seeking and processing different food sources
Webbed feet: anisodactyl/palmate, 3 digits forward, one in back (often vestigial)
Presence of crop variable
Large cecae
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Grit present in large, thick-walled ventriculus, especially in granivores
Mechanical digestion takes place in the ventriculus


2.3. Handling and restraint
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Chief defenses are beaks, wings, and feet
Can pinch with beaks
Large geese and swans will use wings to fend off attackers
Grasp neck just below head with one hand
Place other arm around and under body, hold to handlers body
2.4. Captive management
![]() Duck Pond
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![]() seabirds
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For indoor hospitalization,
Provide a dry, warm enclosure with non-slip flooring
Keep quiet, dimly lit
Try to move outdoors if held longer than 48 hours
Provide access to water and padded flooring
Feed high quality ground waterfowl pellets, lots of greens, e.g. duckweed
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Domestic waterfowl
Selected for size, growth rate, carcass quality, egg production
Not easily stressed
House indoors at night
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Ornamental waterfowl
Commonly pinioned or kept in netted pens to prevent escape
Need access to stream or pond
Easily stressed
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Water quality very important
Flow through vs. filtration systems needed to deal with effluent
Routine demudding necessary
Reed beds can act as purifiers
Sea ducks and diving birds require deep water that is ice-free in winter
Dabblers require an expanse of shallow water's edge to be able to swim and get out on land
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Construction of ponds and natural vegetation
Stone or concrete often used, watch for foot problems
Vegetation should not be too dense, can lead to crop impactions
Certain parasites overwinter on grass so periodic deworming may be necessary
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Animal density dependent on species compatability
Most waterfowl are gregarious
Some seabirds, e.g. loons and grebes, don't do well housed together
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Breeding considerations
Success in captivity dependent on health of animals as well as simulating natural habitat in captivity
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Preventing escapes and predation
Fencing works for some species
Traps and/or bait boxes may be needed to catch predators
Netting for aerial predators, e.g. hawks

2.5. General care
2.5.1. Quarantine
Start collection with juvenile birds reared on fresh, uncontaminated pasture
Physical exams, treat with appropriate anthelmintics, routine bloodwork, serology for M. avium and other infectious diseases
Minimum six week quarantine
2.5.2. Pinioning vs. fully enclosed caging
Pinioning is amputation of the distal phalanx of one wing (removal of MC3 and 4)

Prevents primary feather development
Carried out at 2-3 days of age with minimal problems
More difficult and traumatic when older
2.6. Nutrition
Wide diversity of natural food habits
2.6.1. Commercially prepared diets
Waterfowl starter (19-22% protein) for first 2-3 weeks of life
Waterfowl grower (12-17% protein) up to 4-6 months of age
Waterfowl breeder (17-18% protein) for the period prior to and running throughout laying
Waterfowl maintenance (up to 14% protein) for general non-breeding use
Game bird, trout, sea duck chow
Avoid medicated poultry feed!
Supplement with greens, grit, and oyster shell especially in young birds

2.6.2. Nutritional diseases
2.6.2.1. Angular limb deformities
Perosis or slipped tendon (bandylegs) is a condition characterized by enlargement of the hock, bending deformities of the tarsal bones and medial luxation of the Achilles tendon
May attempt to repair surgically
Angel wing is caused by the weight of the growing flight feathers placing excess stress on the weak muscles of the carpal joint
Attempts to correct angel wing with bandaging are often unsuccessful
Seen in rapidly growing young
May be due to diet too high in protein, too low in calcium, manganese or Vitamin D
Poor flooring substrate contributes to development of perosis
Correct by increasing greens, decreasing commercial diet, supplement with calcium and phosphorus, correct caging
2.6.2.2. Thiamin deficiency in fish-eaters
From feeding frozen fish without B1 supplementation
Defrosting of fish leads to activation of thiaminase
Clinical signs are neurologic - ataxia, weakness, opisthotonus
Responds well to treatment with up to 20 mg/kg thiamin IM weekly
2.6.2.3. Vitamin E deficiency
Young growing ducks fed "old" feed or inappropriate feed
Diet with rancid fat, requiring more antioxidant activity, leads to low vitamin E levels
May result in encephalomalacia, exudative diathesis, reproductive abnormalities
Muscle degeneration, capture myopathy have also been linked with vitamin E deficiency
Steatitis has been seen in piscivores fed high fat content fish in captivity and in great blue herons from the wild


2.7. Infectious disease transmission
Exchange of disease between wild and domestic populations through:
Direct contact
Environmental contamination
Vectors
2.8. Viral diseases
2.8.1. Duck viral enteritis
(Duck plague, DVE)
This is an acute, herpes virus disease of wild and domestic anseriformes (ducks, geese and swans). Wild ducks are the natural host and often transmit disease to domestic and captive breeds. There is marked variation in the susceptibility and mortality of this disease in wild duck species. Massive outbreaks are sometimes seen in waterfowl with hundreds of birds affected. It is most often seen in nonmigratory waterfowl. Duck plague herpes virus can remain latent in the trigeminal ganglion of carrier animals similar to other herpes virus. Shedding through fecal/oral discharge or active disease is produced during periods of stress. This disease is REPORTABLE.
2.8.1.1. Clinical Signs
Acute (sudden death), hemorrhagic disease, massive outbreaks
Serous and mucoid occulonasal discharge with diarrhea and occasional CNS signs
Anorexia, weakness and ataxia with photophobia and pasted eyelids.
The ground where sick birds have rested is often blood-stained.
Penile prolapse
2.8.1.2. Diagnosis
Hemorrhages in liver, pancreas, intestinal mucosa, lungs and kidneys are the typical gross lesions.
Hemorrhage into body cavities may also occur.
The esophageal-proventricular junction often shows a localized region of mucosal hemorrhage.
Annular bands of hemorrhage are sometimes seen in the small intestine that correspond with the GALT.
Crusty plaques are sometimes found on esophageal, cecal and rectal mucosa.
Intranuclear, eosinophilic inclusions typical of herpes virus disease can usually be found associated with necrotic foci in the liver and mucosal epithelial cells.
Vasculitis is also a common microscopic lesion.
Fowl cholera is an important differential diagnosis to consider in an outbreak of duck plague. A Gram stain of peripheral blood from a bird infected with P. multocida will always show many bipolar, gram negative rods.
2.8.1.3. Differential diagnosis
Duck Viral Hepatitis
Erysipelas
2.8.1.4. Prevention
MLV vaccine available for domestic ducks. Some birds survive infection and become carriers
2.8.2. Duck viral hepatitis - picornavirus
Picorna virus
Primarily in Pekin ducklings - rapid onset of 100% mortality
Lethargy, CNS signs, death
Adult mallards act as transport hosts
Muscovy ducks are resistant
Vaccination of breeding females may help to limit infection
2.8.3. Goose viral hepatitis
Parvovirus
Not yet known in US
Ataxia, diarrhea, coryza
Affects goslings < 30 days of age
Diagnosed with virus isolation
Vaccinate breeding birds to limit infection
2.8.4. Avian influenza (fowl plague)
Orthomyxovirus
Domestic turkeys and ducks at risk (H5N1 strain is considered pathogenic)
Migratory waterfowl may be the viral source (fecal-oral)
Mortality previously considered low in waterfowl but recent events in China (2005) indicate that the virus may have mutated to become virulent in waterfowl species (See more on this in Avian Influenza readings and links and Conservation Medicine Challenges)
Conflicts arise between poultry industry and waterbird conservation efforts
2.8.5. Newcastle Disease Virus (NDV) - paramyxovirus 1

Has been seen in large outbreaks involving double crested cormorants in the Great Lakes
Mostly nestlings and subadults affected
Clinical signs include torticollis, ataxia, tremors, paresis, and clenched toes
Highly contagious
Shed in feces
REPORTABLE
2.8.6. Poxvirus

Avipoxvirus group
Songbirds, gamebirds, marine birds are most susceptible
Mosquitoes are common vectors
Wartlike nodules on featherless areas of the body (feet, legs, base of the beak, eye margin)
Cutaneous form is self-limiting and birds can recover if able to feed
Internal form of disease (wet pox) is primarily a problem of domestic fowl
Emerging disease - reason unclear
2.8.7. Reticuloendotheliosis
Avian type C retrovirus
Also known as duck infectious anemia
Can cause splenic necrosis
Infection with REV renders ducks partially resistant to Plasmodium infection
2.8.8. Adenoviruses
Upper respiratory disease with tracheitis
Seen in domestic goslings
Basophilic intranuclear inclusion bodies seen on cytology of infected tissues
2.9. Bacterial diseases
2.9.1. Avian cholera - Pasteurella multocida
Many taxa of birds affected with varying susceptibilities - waterfowl and coots are very sensitive to infection
Environmental contamination from diseased birds is the primary source of infection
Ingestion most common route of infection
CNS, GI signs, acute death, hemorrhagic lesions are frequently seen on necropsy
Control with early detection, carcass collection and incineration, habitat management
Concerns raised about biological costs due to large numbers of birds that die during outbreaks
Four major geographic foci - CA, OR, TX, NE
2004 outbreaks in ruddy ducks in CA and cormorants in South Africa. Read more at Outbreak of avian cholera in cormorants - South Africa (2004). ProMED-mail 20040106.0059. <http://www.promedmail.org>. Accessed December 2008.
2.9.2. Riemerella anatipestifer
Infectious serositis, fibrinous air sacculitis, pericarditis seen on necropsy
Septicemic disease of young domestic ducklings
Also seen in young swans and geese in the wild
GI, respiratory, CNS signs
Differential diagnosis Salmonella, colisepticemia, Newcastle?
2.9.3. Botulism (limberneck)

Western duck sickness, alkali poisoning
Paralytic, often fatal disease
C. botulinum toxin, type C in waterfowl, Type E in loons and gulls
One of most important diseases of migratory birds
Summer/fall incidence when ambient temperatures are high and bodies of water become more alkaline
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Carcass-maggot cycle
Toxin production takes place in decaying animal carcasses
Flies deposit eggs on carcasses which are fed upon by maggots
Maggots concentrate toxin
Toxic maggots are ingested by waterfowl
Death leads to additional carcasses for toxin production
Toxin affects peripheral nerves
Affected animals can sometimes recover with supportive treatment, e.g. aggressive oral fluid therapy. Antitoxin available through the National Wildlife Health Center http://www.nwhc.usgs.gov/
ELISA test for type C toxin now available for diagnosis from the National Wildlife Health Center http://www.nwhc.usgs.gov/
Management actions include carcass pickup and disposal, monitor and modifying environmental conditions
2.9.4. Avian tuberculosis - Mycobacterium avium

Seen in turkeys, raptors more often than in waterfowl
Seen in species living near sparrows, starlings (reservoir species), and in scavenger species
Transmitted by direct contact with infected birds, ingestion of contaminated feed and water, or contact with contaminated environment
Chronic disease leads to general clinical signs of emaciation and weakness and specific signs related to the affected organ system
Zoonotic potential in immunocompromised humans
2.10. Fungal diseases
2.10.1. Aspergillosis - Aspergillus fumigatus

Opportunistic organism found in the environment
Sensitive species: swans, eider ducks, snow geese, seabirds, etc.
Acquired through inhalation of spores from environment, especially in stressful captive situations
Brooder pneumonia in chicks
Clinical signs include emaciation, dyspnea, voice change, chronic anemia
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Difficult to diagnose in early stages
Antigen and antibody titers may be helpful, high WBC counts often present
Changes in protein electrophoresis patterns, galactomannan levels
Radiology, laparoscopy
Cultures of infected tissues, e.g. trachea, lungs, air sacs
Combination antifungal therapy needs to be given over a long period of time

2.10.2. Other - mycotoxins (aflatoxins), algal toxins
2.10.2.1. Aflatoxins
Aspergillus flavus or parasiticus
Has affected domestic ducklings and other species in the SE and Gulf coast states
Clinical signs include depression, blindness, tremors
Chronic exposure can lead to long term health problems
2.10.2.2. Fusariotoxins
Fusarium sp
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2 classes of toxins
Metabolites that mimic estrogen
Trichothecenes
Has affected sandhill cranes feeding in contaminated fields
Clinical signs include anorexia, vomiting, GI bleeding
2.11. Parasitic diseases
2.11.1. Hematozoans



The most commonly seen species are:
Plasmodium spp.
Hemoproteus spp.
Leukocytozoon spp.
In low numbers, these may not be pathogenic, but numbers may increase with a primary stressor, leading to clinical disease.
2.11.2. Other protozoans
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Coccidia
Infection of kidneys is common
Seen in young birds
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Cryptosporidium
Replicate in GI and respiratory tracts
Found in domestic and wild ducks and geese
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Sarcocystis
Rice grainlike macroscopic cysts in muscle
Does not cause obvious morbidity or mortality

2.11.3. Ectoparasites

Airsac mites (from fowl)
Leeches - external, nasal and oropharynx
"Wet feather" from feather shaft mites (Cytodites) or feather lice (Holomen spp.)
Myiasis
2.11.4. Trematodes

Mollusk intermediate hosts
Limited host specificity
Can cause hemorrhagic enteritis or hepatic damage/fibrosis
Can occur in pancreatic and bile ducts of waterfowl
2.11.5. Cestodes

Little known pathology unless coupled with other debilitating conditions
2.11.6. Nematodes
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Gapeworm
Cyathostoma bronchialis
Found primarily in young geese
Adult worms are located in the trachea
Cause inflammatory response leading to dyspnea
Proventricular worms

Echinuris (Acuaria daphnia intermediate host), Tetrameres, Eustrongylides, Porrocaecum
Burrow into mucosa and submucosa
Can cause obstructions of the proventriculus
Gizzard worm – Ventricular worms

Amidostomum anseris and Epimidiostomum
Found primarily in geese
Can result in erosion of the ventricular lining
2.11.7. Acanthocephalans

Thorny headed worms
Attach deeply or can penetrate through intestinal wall
Invertebrate intermediate host ingested by bird
Causes severe granulomatous hemorrhagic enteritis
Seen in Eider ducks and scoters that feed on bivalves
2.12. Miscellaneous diseases
2.12.1. Gout
Articular or visceral forms
Uric acid crystals precipitate in the kidneys
Can lead to postrenal obstruction
Rapid and severe rise in uric acid levels
Precipitation on visceral surfaces, joints
Hyperkalemia can lead to cardiac arrest

2.12.2. Capture myopathy
Caused by improper handling or stress that causes overexertion
Striated muscle damage
Warm temps are a risk factor
Light colored muscles on necropsy exam
2.12.3. Frostbite
Dry gangrene of extremities
Tropical and neotropical species are more susceptible
Can develop secondary septicemia or bacterial endocarditis

2.12.4. Amyloidosis
Commonly seen in Anseriformes, gulls and shorebirds
Deposition of amyloid A in various organs
Degradation product of acute phase, reactive protein
Seen with chronic infections
Can lead to severe hypoalbuminemia
2.12.5. Environmental contaminants

Petroleum
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Heavy metals
Lead , mercury
Arsenic, cadmium, selenium
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Pesticides
Organophosphates, organochlorines etc.
PCBs, dioxins
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External effects of oil on waterfowl
Skin, ocular burns
Feather contamination leading to loss of waterproofing, loss of buoyancy and the inability to fly
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Internal effects of oil on waterfowl
Gastrointestinal
Respiratory
Neurologic
Hematologic
Reproductive
Immune system


2.12.6. Foreign body ingestion and entanglement
Fishing gear : lead sinkers, jigs, fish hooks, fishing line
Plastic trash: six pack rings, cigarette lighters, balloons



2.12.7. Trauma
Predation
Fishing line and hooks
Male aggression
Hit by vehicles
Gunshot
2.12.8. Bumblefoot
Seen in captive situations with improper flooring surfaces or perches
Lesions become infected, usually with Staphylococcus sp.
Correct predisposing factors, use proper antibiotics, debridement of lesions and topical meds

3. Raptors
3.1. Raptor Taxonomy Order Falconiformes
Order Falconiformes | |
Cathartidae |
New World Vultures incl. Condors |
Accipitridae |
Accipiters: Goshawk, Cooper's, Sharp-shinned |
Buteos: Red-tail, Red-shouldered, Broad-wing | |
Harriers: Marsh Hawk | |
Kites | |
Eagles: Bald eagle, Golden eagle | |
Old World Vultures | |
Buzzards | |
Pandionidae |
Osprey |
Falconidae |
Falcons Kestrel, Merlin, Peregrine Caracaras |
Generally diurnal
Spend most of their time on land
Carnivorous
Molt annually (gradual molt)
Some sexual dimorphism (females generally larger than males)
Young are altricial
Hooked beak and talons
Crop present
Generally no grit in thin walled ventriculus
Small cecum, no distinct phallus
Anisodactyl- three digits forward, one in back
3.1.1. Family Cathartidae (New World vultures)
Do not have a grasping foot
Small unfeathered head and hooked bill
Weak talons because only eating dead prey
Regurgitate as a defensive action
Acute sense of smell used to find carcasses
3.1.2. Family Accipitridae (Kites, Hawks, Eagles) Accipiters
Goshawks, Coopers and sharp shinned hawks
Woodland birds
Prey on smaller birds
Short rounded wings with long tails
Highly stressed in captivity
3.1.3. Family Accipitridae - Buteos
Red tail, red shouldered, broadwing hawks
Soaring hawks with broad tails and rounded wings
Feed on small mammal species
3.1.4. Family Accipitridae - Harriers
Marsh hawk (aka Northern harrier)
Long pointed wings, fly close to ground with wings upraised
Long legs
Eat small mammals, frogs
Hover over wetlands and open fields
3.1.5. Family Accipitridae - Kites
Mississippi, swallow tailed, black shouldered, others
Eat insects, mice, lizards, frogs
Eat and drink while in flight
Found in open woodlands and swamps, rangelands
3.1.6. Family Accipitridae - Eagles
Bald, Golden eagles
Large birds
Goldens feed on medium sized mammals, snakes, birds, carrion
Balds feed on fish, carcasses
Large broad wings
Powerful feet, beaks
3.1.7. Family Pandionidae - Osprey
Fish eaters
Platform nesters near fresh or salt water
Hover over water, dive
Highly stressed in captivity
Subject to fishing line and hook injuries, mercury toxicity
3.1.8. Family Falconidae - Falcons, Caracaras
Kestrel, merlin, peregrine, gyrfalcon
Long wings, bent back at wrist
Catch prey by climbing high and stooping down at high speeds
Prone to bumblefoot in captivity
3.2. Raptor Taxonomy Order Strigiformes
Order Strigifiormes | |
Tytonidae |
Barn owls |
Strigidae |
Great horned owl, Barred owl, Screech owl, Saw-whet owl, Snowy owl |
Mainly nocturnal
Spend much of time on land
Carnivorous
Molt annually
Primary feathers have serrated edges for silent flight
Slight sexual dimorphism
Young are altricial
Hooked beak and claws
Triangulate sound to locate prey
Crop absent
Semi zygodactyl (two toes in front, two in back)
3.2.1. Order Strigiformes Tytonidae
Barn owls
Roost and nest in dark cavities in old buildings, cliffs, trees
Common in west, uncommon in eastern US
3.2.2. Order Strigiformes Strigidae
Great horned, barred, screech, saw whet, snowy, great grey, boreal owls
3.3. Handling and restraint

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The weapons - talons and beak
Always have these weapons under control at all times
Be aware of different species' behavior, e.g. falcons like to bite!
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Use hood to decrease visual and auditory stress
Transport
Sturdy boxes or crates
Sufficient ventilation, avoid placing boxes so that air circulation is impaired
Keep darkened
Do not use perch, use tail wraps to protect tips of feathers
Cover floor with carpeting


3.4. Noninfectious diseases

Competition pressure among young in the nest or adults in groups in captivity can lead to starvation
Trauma - interaction with man-made objects (hit by vehicles, flying into windows or buildings, electrocution, barbed wire entanglement, leg hold traps), ocular trauma in owls
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Predisposing factors include high dietary levels of protein and calcium, hypervitaminosis D, poor renal function, dehydration, stress
Correct diet, decrease Ca, P, Mg, and Vit D3, ensure adequate levels of Vitamins A and B
Rickets and Metabolic bone disease are a commonly seen in young raptors that are kept in captivity and fed only skeletal meat. This occurs when bids are not fed whole prey, which includes bone as a source of calcium and phosphorus. Clinical signs of metabolic bone disease involve similar signs seen in poultry including rickets, pathologic fractures, and a soft bills.

3.4.1. Toxicity
3.4.1.1. Lead

Most frequently seen in eagles
From ingesting lead in prey
Clinical signs include weakness, inability to fly, neurologic signs, emaciation
3.4.1.2. Mercury
Exposure occurs through accumulation of mercury in the food chain, agricultural use, point source industrial and mining discharge into the environment
Most commonly a problem in piscivores, e.g., osprey, eagles
Toxic form is methylmercury
Neurologic signs, emaciation
3.4.1.3. Pesticides

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Cholinesterase inhibitors
Raptors are victims of secondary poisoning through their prey
Convulsions, paralysis, miosis, dyspn
Birds that die rapidly may be found with vegetation clenched in talons
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Rodenticides
Secondary poisoning in raptors
Anticoagulant hydroxycoumarins and indanediones, most commonly brodifacoum
Inhibit vitamin K1 activation
Clinical signs include pallor and excessive external hemorrhage from superficial wounds
Can lead to sublethal effects
Treat with vitamin K1 supplementation for 4-6 weeks
3.4.1.4. Asian vulture die-off
Precipitous population decline in the 1990 s in Gyps sp. in India >95% of vultures have died
Necropsy findings showed birds with severe visceral gout and acute renal failure
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Diclofenac identified as the toxic agent
Human NSAID recently used in Pakistan for pain relief in domestic livestock
Vulture feeding on carcasses ingested diclofenac in lethal quantities
All vultures with visceral gout had diclofenac in their kidneys
Experimental exposure trials conducted
3.5. Infectious diseases
3.5.1. Viral diseases
Poxvirus - especially eagles
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Herpesvirus - Owl herpes, falcon herpes, eagle herpes
Transmitted through feeding on infected prey
May develop carrier status
Depression, sudden mortality
Diagnosed through virus isolation, intranuclear IB in liver, spleen, bone marrow
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Adenovirus - from avian derived food
Melena, anemia
High mortality in kestrels with hemorrhagic enteritis
Two types of intranuclear IB
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Paramyxovirus
Low to moderate susceptibility
Have seen anorexia, torticollis, and sudden death in owls
May show long term fecal viral shedding
Nonpurulent encephalitis
West Nile Virus - Raptors moderately susceptible
3.5.2. Bacterial diseases

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Bumblefoot/pododermititis
Falcons especially susceptible
Initial injury, inappropriate perching surfaces
Plantar surface of metatarsal pad
Staph aureus, others
Antibiotics, bandaging, surgery, correct predisposing conditions
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Avian Tuberculosis
Widespread problem in raptors
GI form predominant
Chlamydiosis - chronic form seen in raptors
3.5.3. Fungal diseases

Candida - oropharyngeal mucous membranes and esophagus are often affected
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Aspergillus
Common, often fatal
Acute and chronic forms
Seen as a secondary problem with primary stressor
Northern species of raptors more susceptible
3.5.4. Parasitic diseases
3.5.4.1. Protozoa

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Trichomonas - frounce
Flagellated organism in mucosa of oropharynx, esophagus and crop, can be generalized
Common in pigeons and doves which are then consumed by raptors
Falcons most susceptible
Plasmodium
Haemoproteus
Leukocytozoon
3.5.4.2. Liver/intestinal trematodes

Found in small intestine, liver
Diarrhea, weakness
Eggs shed intermittently
Treat with praziquantel
3.5.4.3. Cestodes

Only rarely cause clinical disease
Treat with praziquantel
3.5.4.4. Nematodes
Ascarids
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Capillaria
Very common in raptors
Found in oropharynx, esophagus, intestinal tract
Earthworms play a role in transmission
Can become infected by ingestion of infected prey
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Syngamus
Adult worms live in trachea
Ingestion of transport hosts (earthworms, snails)
Eggs are coughed up and excreted in feces
Clinical signs include upper airway obstruction, sneezing, headshaking
Seratospiculum
Mites, lice, Hippoboscid flies


3.6. Avian Vacuolar Myelinopathy "Coot and Eagle Brain Disease"
First described in bald eagles in 1994. Also seen in American coots and ducks.
Restricted to the Southeastern US so far.
Clinical signs of ataxia, wobbly or uncoordinated flight, swimming in circles
Birds often found dead
NO gross lesions; histologic examination shows vacuolization and diffuse spongy degeneration of white matter in the central nervous system.
Etiology unknown. Toxic exposure is suspected.
4. References and Resources
4.1. Websites
National Wildlife Health Center . 6006 Schroeder Rd., Madison, WI 53711. (608) 271-4640.
4.2. Texts and Articles
4.2.1. Waterfowl references
Altman, Robert B., et al. Avian Medicine and Surgery. Philadelphia. W.B. Saunders Co., 1997. Chapter 55
Bellrose, FC. Ducks, Geese and Swans of North America. Stackpole Press. Harrisburg, PA, 1974.
Best practices for migratory bird care during oil spill response. U.S. Fish and Wildlife Service, November, 2003.
Beynon, Peter H. Manual of Raptors, Pigeons and Waterfowl. BSAVA, 1996.
Cottam, C. Food habits of North American diving Ducks. USDA Technical Bulletin #643, 1939.
Ducks, Geese and Swans of the World. University of Nebraska Press. Lincoln, NE, 1978.
Feierabend, JS and Russell, AB. Lead poisoning in wild waterfowl. National Wildlife Federation, Washington, DC, 1986.
Friend, M. Ed. Field Manual of Wildlife Diseases: General Field Procedures and Diseases of Birds . United States Department of the Interior, United States Geological Survey,1999.
Harrison, Gregg J. and Teresa L. Lightfoot. Clinical Avian Medicine. Palm Beach, FL: Spix Pub., c2006. Chapter 36.
Hyde, DO (ed). Raising wild ducks in captivity. EP Dutton and Company, NY.1974.
Johnsgard, PA. Waterfowl: their biology and natural history. University of Nebraska Press. Lincoln, NE, 1968.
LaBonde, Jerry. Private collections of waterfowl. Proceedings of the Association of Avian Veterinarians, 1996, pp. 215-223.
Larsen, R. Scott, et al. Clinical features of avian vacuolar myelinopathy in American coots. JAVMA, v.221 (1), 2002: 80-85.
Martin, RM. Wildfowl in Captivity. John Gifford Co., London,1973.
Ritchie, Branson W., et al. Avian Medicine: Principles and Application. Lake Worth, Fla., c1994: Chapter 46.
Russell, WC, Choules, DL and Gauthier, DA. Detergents and waterfowl. Journal of Zoo Animal Medicine, 12:10-13, 1981.
Souza, MJ, and LA Degernes. Mortality Due to Aspergillosis in Wild Swans in Northwest Washington State, 2000-02. Journal of Avian Medicine and Surgery, 19 (2), 2005: 98-106.
Wild Waterfowl and its Captive Management, Vols. 1 & 2. American Gabe Breeder's Cooperative Federation. Salt Lake City, Utah, 1974.
Wobeser, GA. Diseases of Wild Waterfowl. 2nd ed. Plenum Press. NY. 1997.
4.2.2. Raptor references
Altman, Robert B., et al. Avian Medicine and Surgery. Philadelphia. W.B. Saunders Co., 1997. Chapter 52
Beynon, Peter H. Manual of Raptors, Pigeons and Waterfowl. BSAVA, 1996.
Harrison, Gregg J. and Teresa L. Lightfoot. Clinical Avian Medicine. Palm Beach, FL: Spix Pub., c2006. Chapter 40.
Heidenreich, Manfred. Birds of prey. Blackwell Science, 1997.
Redig, P.T. et al. 1994. Raptor biomedicine. Univ. of Minnesota Press, c1993.
Rodriguez R, et al. The Normal Electrocardiogram of the Unanesthetized Peregrine Falcon (Falco peregrinus brookei). Avian Diseases, 48 (2), 2004: 405-409.
Wobeser, G, et al. Secondary poisoning of eagles following intentional poisoning of coyotes with anticholinesterase pesticides in Western Canada. Journal of Wildlife Diseases, 40, 2004: 162-172.
Wünschmann, Arno, et al. Pathologic Findings in Red-Tailed Hawks (Buteo jamaicensis) and Cooper's Hawks (Accipiter cooperi) Naturally Infected with West Nile Virus. Avian Diseases: Vol. 48 (3): 570-580.




