Accipitriformes/Falconiformes Flashcards

1
Q

What are the five main groups of accipitriformes and falconiformes birds?

A
  • Taxonomy:
    • 5 families:
      • Cathartidae – New World vultures
      • Accipitridae – hawks, eagles, kites, harriers, buzzards, Old World vultures
      • Falconidae – falcons, falconets, kestrels, merlins, hobbies, caracaras
      • Pandionidae – ospreys
      • Sagittariidae – secretary birds
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2
Q

Describe the special senses of falconiform and accipitriform birds.

A
  • Special Senses
    • Generally diurnal, rely heavily on sight for hunting.
    • Perceive UV light.
    • Each eye has two foveae – temporal for binocular vision, central for monocular vision.
      • Exceptions – Andean condors (Vultur gryphus), black vultures (Coragyps atratus) only have a nasal fovea.
      • Pectin is plicated in most raptors.
      • Raptors lack consensual pupillary light reflexes.
    • Sense of smell is poorly developed, except in vultures.
    • Most falconiformes have less developed sense of hearing vs owls, except harriers (similar facial disc).
    • Taste buds at base of tongue.
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3
Q

What is the name and function of the notch in falcon beaks?

Clinically, why does it matter?

A
  • Beak
    • Sharply hooked, notch behind tip of the upper beak forms tomial tooth for severing neck of prey.
      • Preserve tomial tooth when trimming beak.
      • Overgrowth of upper beak seen with day-old chick only diets.
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4
Q

Describe the feathers of falconiform birds.

What species are sexually dimorphic?

How long does molt take? How is molt induced?

What are stress marks? What causes them?

A
  • In general, plumage is not sexually dimorphic except – northern harrier (Circus cyaneus), American kestrel (Falco sparverius), and merlin (Falco columbarus).
    • Integrity of primary remiges and tail retrices important for flight performance.
      • Tail guards to protect feathers in rehab.
      • Imping may be very beneficial in hastening the return of flight after feather damage.
    • Molting typically in symmetrical pairs, one feather from right and one from left once per year in early summer after breeding.
      • Takes about 6 months.
      • Steppe buzzard (Buteo buteo vulpinis) has a chaotic molt pattern.
      • Old World vultures molting may take 2-3 years.
      • Goshawks and eagles molt only partially each year.
      • Induction of molting via manipulation of photoperiod or oral exogenous thyroid hormone.
        • 18-20 hours light per day after 4-6 weeks of 10 hours light per day.
          • Molt will start within few weeks.
          • Onset and rate of molt with thyroxine tends to be rapid.
          • Increased ambient temp may speed molt, corticosteroids may slow progression.
    • Stress marks appear as lines across feathers because of interruption in normal flow of nutrients during growth.
      • i.e. cysteine deficiency.
      • Pinching off syndrome – normal growth of feather for most of normal growth, then blood supply withdraws and feather pinches off in hour-glass presentation.
        • Related to viral dz, genetics, quill mites.
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5
Q

Describe the anatomy and physiology of falcon skin.

Do they sweat?

What is a common neoplasm?

Any unique glands?

Is feather plucking an issue?

A
  • Skin
    • Sweat glands absent.
    • Adenocarcinoma and blockage of uropygial gland reported.
    • Savanna hawk (Buteogallus meridionalis) – supraorbital aka salt gland.
      • Water and electrolyte homeostasis, paired glandular structure with ducts opening in the nasal cavity.
    • Harris hawk (Parabuteo unicinctus) – only species showing psychological feather plucking.
      • Temporary beak modification technique to prevent self-mutilation in this spp described.
    • Seborrhea sicca in eagles, especially feet of captive birds.
      • SQ abscesses caused by staph commonly seen.
      • Papillomatosis on feet/eyelids sometimes.
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6
Q

Describe the talons of various falconiform species.

What is unique about the tendon anatomy?

What is unique about vulture talons? What about osprey talons?

What is the foot arrangement of typical falconiform species?

How is tendon avulsion controlled?

A
  • Feet
    • Vultures – talons are blunt, do not capture live prey.
    • Digital flexor tendons have unidirectional, interlocking ratcheting mechanisms.
    • Ospreys (Pandion haliaetus) – highly curved talons, spicules on ventral surface of feet.
      • Ability to swivel their fourth digit to rear (semi-zygodactylous).
      • All other falconiformes are anisodactyl and perch with three digits forward and one backward.
    • Talon of digit 3 has a specialized sharp edge on the medial side, used for feather grooming.
    • Talon avulsion – tx by controlling bleeding and covering with protective material i.e. nail polish, and covering with protection and antibiotic powder or talc powder.
    • Regrowth of a talon will take up to 6 months.
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7
Q

What is the function of the operculum in the falconiform naris?

A
  • Nares
    • Buteo spp (falcons) and eagles have a bony baffle or operculum to facilitate air flow in the nostrils during high-speed flight.
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8
Q

Describe the GI Anatomy of Falconiform Birds?

Is there a crop?

What is the pH of the stomach?

Are there ceca?

Is there a gallbladder?

A
  • Gastrointestinal tract
    • All falconiformes except the bearded vulture have an esophageal expansions (different from a true diverticular crop).
      • Simple stomach, pH 1 in diurnal raptors, capable of digesting bones.
      • Ceca is absent or vestigial lymphoid type.
      • GB usually present.
      • Ventriculus less muscular and koilin layer is more mucoid vs granuvorous birds.
      • Ventriculus has a thick lamina densa.
      • Liver is bilobed, does not typically extend past keel.
    • E. coli, Proteus, Staph, Micrococcus, Corynebacteriu, Bacillus, Strep, Salmonella isolated from lower intestines, cloaca, and fecal samples of healthy raptors.
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9
Q

Describe the urogenital system anatomy of falconiform birds.

How many ovaries and oviducts?

A
  • Urogenital system
    • Cathartidae, Accipitridae, and Falconidae have two ovaries and two oviducts.
      • Unlikely both ovaries are functional.
      • No phallus.
      • Some falcons and hawks have two ovaries that may be functional but only one oviduct (left).
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10
Q

What are some unique musculoskeletal adaptations of the genera Falco, Buteo, & Accipiter?

A
  • MS anatomy
    • Femur and humerus usually pneumatized.
    • Genus Falco – two sesamoids in metacarpophalangeal joint, one sesamoid in interphalangeal joint of major digit.
      • Two intratendinous ossifications are present in region of carpometacarpus and major digit.
      • Os prominens at cranial margin of carpus in Buteo and Accipiter, articulates with distal radius.
      • Falcons – tarsometatarsus has a medullary cavity running entire length of bone.
        • Hawks and eagles, medullary cavity absent from proximal third of the tarsometatarsus.
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11
Q

Describe the appropriate husbandry for falconiform birds.

A
  • Housing
    • Indoor (mews) and outdoor facilities should be provided.
    • Highly migratory species, small Accipiters, southern temperate zone species (Harris’ hawk) cannot tolerate cold.
      • Supplemental heat when ambient temp below 0 deg C.
      • Eagles, RTHA, goshawks, and most falcons may tolerate extreme cold if protected from wing.
    • Accipiters cannot be housed with other species.
      • Sexes of merlins and N goshawks should be housed separately, since larger female may kill mate.
        • Table of compatible species published.
    • Perches
      • Falcons – broad, flat perches with artificial turf.
      • Buteos and goshawks – elliptical perch, wrapped with rope.
      • Multiple perches may be detrimental if hopping with hard landing instead of flying, feet can become bruised.
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12
Q

Describe the proper nutrition of falconiform birds.

How much do they typically eat (% BW)?

What is the typical stomach capacity?

Are there seasonal changes in appetite?

When do they cast?

Are there any food species that should be avoided?

What about feeding chicks?

A
  • All raptors are carnivores.
  • Smaller raptors eat approx. 20% body weight daily, medium 10-15%, large 6-8%.
  • Stomach capacity is 40 ml/kg.
  • Reduction in food intake observed in warm weather.
    • Breeding females should receive calcium and vit D3.
    • Probiotics for raptor chicks will reduce enteritis and bacterial overgrowth in first 14 days of life.
  • Casts typically 12-18 hours after ingestion.
    • Hawks may eat more than one meal before casting.
  • Whole prey required.
    • Pigeons are a special risk for feeding raptors because of high prevalence of trichomonas and columbid herpesvirus.
      • Should be frozen and thawed if feeding.
  • Buzzards – nonspecialized diet, scavengers.
    • May encounter long periods of food deprivation between feedings.
    • Most are calcium-deficient because they usually ingest meat and viscera.
  • Osprey require fish.
    • Supplement thiamine.
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13
Q

What are the most common nutritional diseases of falconiform birds?

How do those diseases present?

Are there any age- or species-specific concerns?

A
  • Secondary nutritional hyperparathyroidism.
    • CS similar to other birds.
    • Raptors need vit D3, cannot utilize vit D2.
    • C:P should be 2:1.
    • Seen in free-flying vultures fed china or plastic by parents instead of bone fragments.
  • Thiamine deficiency.
    • CS – loss of appetite, star gazing, muscle weakness, tremors, opisthotonus, seizures, death.
      • Most common in juveniles consuming all-meat diets or piscivorous birds fed thawed fish.
      • Tx – IM thiamine, diet supplementation.
      • CS may be permanent.
  • Vitamin A deficiency.
    • Pustules in mouth, esophagus, crop, nasal passages.
      • Caseous nodules may block salivary glands, syrinx, or area under eyelids.
      • Xerophthalmia.
      • Pu/Pd, gout, reduced egg and sperm production.
      • Hyperkeratosis of plantar surface of feet, predisposes bumblefoot.
      • Reduced immune response leads to diseases i.e. asper.
  • Vitamin E deficiency.
    • CS – poor muscle function, muscular dystrophy, spastic leg paralysis, degeneration of pipping muscle in neonates, poor hatchability, spraddle legs, muscle twitching, encephalomalacia, incoordination, torticollis, testicular degeneration, infertility and steatitis.
  • Fatty liver-kidney syndrome of merlins from feeding of day-old chicks and inbreeding has been reported.
  • Accipiters prone to neuro signs and collapse from hypoglycemia.
    • Birds with neuro signs fed all-meat diets should be given glucose, B vit (thiamine), vit A, and Ca.
  • Young secretary birds (Sagittarius serpentarius) fed on standard raptor diets may suffer Ca:P imbalance because principal food in wild is snakes (high in calcium phosphate).
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14
Q

Describe the signs of capture myopathy in secretary birds.

A
  • CS – depression, limb paresia or paralysis, hock-sitting, lateral or sternal recumbency and death.
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15
Q

Describe the use of injectable anesthetics in raptorial birds.

Are there any drug combinations or routes of administration that should be avoided?

A
  • Injectable anesthetics unreliable.
    • Ketamine/xylazine has caused deaths, severe bradycardia.
    • IV ketamine may cause convulsions, prolonged apnea, cardiac arrest.
    • Xylazine alone results in hypersensitivity.
    • Tiletamine zolazepam is suitable for anesthesia via parenteral injection.
    • Alphaxalone – death in RTHA, high prevalence of sinus arrest and tachycardia.
    • Propofol CRI in RTHA – minimal effects of BP, reduced ventilation.
      • Prolonged recovery, excitation observed.
    • Ketamine or tiletamine zolazepam have been used orally in bait.
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16
Q

How long should falconiform birds be fasted prior to anesthesia?

Have any advserse events associated with inhalant anesthesia?

A
  • Fast 6-8 hours prior.
  • Arrhythmias with isoflurane have been reported in bald eagles.
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17
Q

Surgery in wild falconiforms can deem them irreleasable.

What procedures may deem them nonreleasable or provide the potential for complications that may make them that way?

A
  • Limb amputation usually results in bumblefoot on remaining foot.
  • Scale established as a guide for digit amputation.
    • If missing both second digits, one or both halluxes, or all of these, considered not releasable.
  • In males, loss of wing may be problematic as wings are used for positioning on the female during mating.
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18
Q

What is the most common cause of clinical herpesvirus infections in raptors?

How is it acquired?

What clinical signs are present?

What lesions are present at necropsy?

Describe the inclusion bodies.

How is diagnosis confirmed?

A
  • Alphaherpesvirus.
    • Columbid herpesvirus- (CoHV-1) most common cause of clinical herpesvirus infections in raptors.
      • Results from ingestion of infected pigeons.
    • CS – frequently absent, lethargy and anorexia may occur.
    • Gross lesions – pinpoint and variably sized tan foci in liver, spleen, BM, miliary areas of lytic necrosis.
    • Cells at junction of necrotic foci may contain eosinophilic, IN viral inclusions with distinct halo and hyperchromasia of the nuclear membrane.
    • Viral particles detected in droppings of by electron microscopy.
    • Viral isolation frequently unsuccessful.
    • PCR can confirm.

Terio

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19
Q

What species is most susceptible to faconid adenovirus 1? Are other species affected?

Are there any age groups that are particularly susceptible?

How do these birds present?

What lesions are present on necropsy?

Describe the inclusion bodies.

A
  • Adenovirus.
    • Fatal infections most commonly reported in falcons, also hawks, kites, and owls.
    • Falconid adenovirus-1 associated with mortality.
      • Widespread in healthy peregrines based on serology.
      • Juveniles particularly susceptible.
      • Interspecies infection may occur.
      • Epitheliotropic and lymphotropic.
      • CS – lethargy, anorexia, or death.
      • Lesions – hepatomegaly, splenomegaly with discrete white foci.
      • Acute hemorrhage in GIT, lungs, repro tract, renal swelling.
      • Histo – widespread hepatic necrosis, intranuclear inclusion bodies. Inclusions may be large and fill entire nucleus or be surrounded by a clear halo.
        • Classically basophilic but may be amphophilic or eosinophilic.
        • Ventricular epithelial cell inclusions may be present in absence of other lesions in falcons.
        • Virus isolation, PCR confirm diagnosis.

Terio

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20
Q

Describe avian poxviral infection in birds of prey?

Are wild or captive birds more commonly affected?

Are there any unique presentations? If so, what species?

A
  • Avian pox virus.
    • More common in captive birds.
    • Direct and fly or mosquito-mediated transmission suspected.
    • Dry form – unfeathered skin and face.
      • Considered self-limiting but may result in secondary infection.
      • Exudation and crusting frequent.
      • Histo – epidermal hyperplasia with edema and pathognomonic large eosinophilic granular cytoplasmic inclusions (Bollinger bodies).
        • Poxviral particles can be seen in BB via EM.
        • Inclusions more common in superficial layers of epidermis.
    • Wet form – extension of cutaneous lesions to mucosa.
    • Systemic pox has also been described in a juvenile TUVU.
      • Wet and dry lesions.
      • Cytoplasmic inclusions.
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21
Q

Describe the typical presentaitons of West Nile infections in accipiter birds of prey.

What are the common clinical signs?

Are there any species specific presentations?

What lesions are present at necropsy?

What is the triad of histologic lesions?

A
  • Accipitridae:
    • Hatch year birds most likely fatal.
    • CS – vision impairment, neuro signs.
    • Pinched feathers if acute infection is survived for several molts.
    • Other gross lesions – patchy beige discoloration of myocardium, white discoloration (fibrin) in fundus of eye, unilateral or bilateral collapse of cerebral hemispheres.
    • BAEA – may present with splenomegaly or cardiac dilation with a rounded, beige discolored apex.
    • Triad of histo lesions – myocarditis, endophthalmitis, meningoencephalomyelitis hallmark of WNV dz.
    • Lymphoplasmacytic inflammation in all sites.
    • Extensive cerebellar necrosis with hydrocephalus ex vacuo and parenchymal collapse most commonly occurs in bald eagles and red tailed hawks.
      • Usually bilateral, symmetrical.
      • Characterized by rarefaction of the brain parenchyma with infiltration by gitter cell and perivascular lymphoplasmacytic infiltrates.
      • Multifocal necrosis of exocrine pancreatic cells may be seen.
      • Detecting WNV antibodies in CSF supports diagnosis, even in absence of detectable antigen in tissue or negative PCR.

Terio

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22
Q

How does West Nile affect falcons and vultures?

A
  • Falconidae:
    • Similar lesions and antigen distribution as hawks.
    • More common in falcons (kestrels, merlins) – fibrinoid necrosis of medium caliber arteries and arteritis in spleen and heart.
      • May result in myocardial necrosis and necrosis of brain parenchyma.
  • Cathartidae:
    • Although many CA condors seropositive, cause of death in only a single juvenile with nonsuppurative encephalitis and concurrent asper.
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23
Q

What is the most sensitive tissue for West Nile Virus surveillance?

A
  • Determining raptor spp and tissue sensitivity for improved WNV surveillance.
    • Feather pulp most sensitive tissue for WNV RNA, kidney second.
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24
Q

What is the most prominent finding at necropsy in falcons affected with high pathogenic avian influenza?

What other lesions are present?

What is a common route of transmission?

Has vaccination been shown to be protective?

A
  • Avian Influenza Virus. OIE.
    • Hemorrhagic pancreatic necrosis most prominent finding in HPAI infected falcons.
    • Pulmonary congestion, focal hemorrhage, catarrhal tracheitis has also been induced. Mild multifocal gliosis.
    • Virus found most consistently and at highest conc in brain in H5N1 outbreak in Germany 2006.
      • Marked nonsuppurative encephalitis primary lesion and cause of death.
    • Vaccination of gyrfalcon x saker hybrid falcons with inactivated H5N2 vx has been shown to prevent clinical dz following experimental infection with HPAI H5N1.
    • Transmission – wild birds used as prey for hunting falcons, poultry,

Terio

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25
Q

What is the etiologic agent that causes Newcastle Disease?

What strain type most commonly present in raptors? What signs does this result in?

What tissues can the virus be isolated from?

A
  • Newcastle Disease Virus. OIE.
    • Avulavirus genus; Paramyxoviridae family.
    • Avian paramyxovirus serotype 1 (PMV1).
      • Lentogenic, mesogenic, velogenic strains based on pathogenicity.
        • Velogenic most.
        • Raptors usually infected via prey.
        • Neurotropic and viscerotropic dz.
          • Anorexia, vomiting, paralytic ileus.
          • Bloody diarrhea.
          • CNS signs – ataxia, head tilt, tremors, wing and leg paralysis.
          • Torcicollis develops late in the disease.
          • Hemorrhage and congestion in proventriculus and resp tract typical in poultry, rare in birds of prey.
          • No gross lesions besides swelling of pancreas detected in raptors with neuro signs.
          • Lymphoplasmacytic and histiocytic pancreatitis is the microscopic lesion in falcons with viscerotropic form.
          • Neurotropic form – nonsuppurative encephalomyelitis.
    • Virus can be isolated from spleen, brain, or lungs.

Terio

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26
Q

Vultures appear to be resistant to the pathogens they encounter in carcasses.

Why is this?

A
  • Vultures appear resistant to pathogens encountered in carcasses.
    • May be result of bald head and neck in carcass feeders, low gastric pH, gut microflora inhospitable to certain pathogens, hypothesized differences in specific molecule patterns in pathogens (toll-like receptors).
      • African vultures shown to have Ab to anthrax.
      • Intoxication and trauma more significant causes of mortality vs infectious disease in these spp.
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27
Q

How does Avian cholera present in raptorial birds?

How is it transmitted?

A
  • Pasteurella multocida – Avian cholera.
    • Serotype 1, 3, 4 most common isolates from eagles, hawks, falcons, owls.
    • Transmitted orally or by inhalation or cat bite.
    • Pathogenesis – endotoxemia, hyperemia and fibrinous polyserositis.
    • Systemic inflammation with intralesional bacteria in acute form.
    • Chronic form – oropharyngeal and esophageal granulomas in Buteo hawks.
      • Multinucleated giant cells, intralesional bacteria.
    • Cytology – bipolar bacteria, confirm with isolation and serotyping.
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28
Q

Aspergillosis is one of the most important causes of death in captive raptors.

What risk factors may predispose birds to disease?

What species are particularly susceptible?

What are the etiologic agents?

What lesions are present at necropsy?

Can additional diseases develop as a sequelae?

A
  • Aspergillosis – one of most important causes of death in captive raptors.
    • Predisposing factors – ambient and husbandry conditions, esp high humidity and temp or dry air with high amounts of dust, or stress from excessive fasting in falconry.
      • Trauma and other chronic debilitating conditions (i.e. lead tox) may predispose.
    • Gyrfalcons, Accipiter spp, eagles, merlins, and some owls (barn) appear most susceptible.
      • Goshawks, gyrfalcons, immature RTHA, golden eagles more likely.
      • Raptors from arctic or subarctic climates and ospreys and rough-legged buzzards also of particular risk.
    • Caused by inhalation of spores of A. fumigatus, but A. niger and A. flavus may also result in disease.
    • Lesions throughout resp tract and other organs.
      • Primary asper lesion often in caudal thoracic air sac – where spores first settle.
      • Acute asper – miliary lesions in lungs and air sacs, may be related to aspiration of high number of spores.
      • Chronic asper – may be restricted to resp tract or affect other organs.
      • Granulomas may be in trachea, nasopharynx, air sacs, lung parenchyma, serosa of other organs.
      • May lead to obstruction of resp tract and death from asphyxia.
      • Air sac thickening, severe fibrinous air sacculitis with abundant fungal growth on air sacs and in pneumatized bones may be seen.­
    • Granulomas contain numerous septae, dichotomously branching fungal hyphae, positive with PAS reaction and with the Grocott methenamine silver (GMS) stain.
      • Fungal culture, PCR, or IHC recommended for dx.
    • Chronic asper may lead to pulmonary parenchymal fibrosis and produce secondary right ventricular dilatation and cor pulmonale.
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29
Q

What is the difference between acute and chronic aspergillus infections in raptors?

Besides air sacs, are other sights colonized?

What diagnostics may indicate active aspergillosis?

What treatment is recommended?

What prevention can be done?

A
  • Infection by inhalation of spores.
    • Acute infection following inhalation of overwhelming numbers of spores from the environment.
    • Chronic infection usually develops following low-level exposure coupled with compromised immune function caused by recent capture, change of ownership, poor ventilation, neonatal and geriatric conditions, corticosteroids, respiratory irritants, or lead poisoning.
      • Localized forms involve granulomas in syrinx oe sinuses.
  • Resp tract most often affected, but spores may migrate.
  • Ocular and skin infections reported.
  • Interclavicular air sac most commonly affected in gyrfalcons.
  • By time resp signs or weight loss is apparent, usually extensive disease.
    • Alteration or loss of voice pathognomonic for syringeal form of asper.
  • Dx – heterophilia, monocytosis, rads, deep tracheal or air sac culture.
    • ELISA for Buteo spp available.
    • Specific conjugates must be made for use in falcons and Accipiters.
    • PCR available.
    • Protein electrophoresis may show increase in beta and gamma globulins.
    • Endoscopy of trachea and air sacs confirms diagnosis and establishes prognosis.
  • Tx – oral itraconazole BID for 5 days then once daily for 1-3 months; nebulization with clotrimazole, two 1 hour sessions per day for 4-8 weeks; amphotericin B intratracheally or injected into posterior thoracic air sacs or applied directly to lesions via endoscope.
    • Ampho B may also be administered IV.
    • Voriconazole may be given orally.
      • Liquid form may also be nebulized.
    • Fluconazole is not effective.
    • A 1:250 dilution of F10 has been used to nebulize raptors alone or in combo with oral itra.
    • Birds with severe resp signs have a poor prognosis, surgical removal of localized lesions is needed.
  • Prophylaxis – itra for 3-4 weeks recommended during stressful periods.
    • Young gyrfalcons, daily administration of itra or terbinafine is initiated and continued until the onset of cooler weather.
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30
Q

Describe the presentation of candidiasis in raptorial birds.

Are there any predisposing factors?

Is it more common in wild or captive birds?

What lesions are present?

A
  • Candidiasis – Candida albicans.
    • Normal in upper Gi healthy individuals.
    • Vit A deficiency, prolonged abx treatment, or concomitant infections that disrupt mucosal barriers predispose.
    • More common in captive individuals.
    • Lesions in oral mucosa, soft palate, upper esophagus, crop.
      • May form pseudomembranes (severe thickening and necrosis of the crop epithelium).
      • Histo – hyperplasia of epithelium, lymphoplasmacytic inflammation, intralesional yeast and pseudohyphae.
        • Highly elongated filamental structures with parallel walls and septal constrictions.
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31
Q

What is the microsporidian parasite of falcons?

What lesions are present with this disease?

Are any coninfections suspected?

How is this disease thought to be transmitted?

A
  • Enterocytozoon bieneusi genotype D.
    • Obligate, intracellular, microsporidian parasite recently classified as fungal.
    • Fatal infection in falcons in the Middle East.
    • Yellowish, well demarcated, raised nodules in liver, kidneys, spleen, intestine.
    • May be coinfected with caryospora spp.
    • Pyogranulomatous inflammation.
    • Diphtheritic membrane formation in intestines.
    • Organism – oblong, up to 2 microns, intracytoplasmic.
      • Rarely observed on histo.
      • IHC with cross-reacting polyvalent rabbit antiserum vs E. cuniculi aids in detection.
      • PCR can be used for confirmation.
      • Detection of microsporidia in fecals difficult due to small size.
    • Infected feces from ducks, cranes, and pigeons may be source for falcons.
32
Q

What are the common ectoparasites of raptors?

Lice - what species, how to treat

Fleas - what species

Ticks - what species

Flies - what species and treatment

Myiasis - what presentation, which age group

Mites - species adn treatment

A
  • Ectoparasites.
    • Lice – Crasperdorrhynchus, Laemobothrion, Colpocephalum, Degeeriella, Falcopipeurus.
      • Pyrethrin and fipronil sprays effective.
    • Fleas – Echidnophaga gallinacean (stickfast flea).
    • Ticks – Ixodes ricinus.
    • Myasis – Blow-fly larvae infestation in external auditory canals of hawks, esp nestlings.
    • Mites – Knemidokoptes – scales of feet. Tx liquid paraffin and ivermectin.
      • Dermanyssus gallinae – red mites, birds housed in wooden mews, may cause feather breakage in juveniles.
        • Tx ivermectin, spray premises with insecticide.
    • Hippoboscidae – flat flies (Ornithomyia avicularia).
      • Remove manually or dust with pyrethrin, malathion, or carbaryl.
33
Q

What is the etiologic agent of serratospiculosis in falcons?

Where do these worms colonize?

Describe the life cycle.

What clinical signs occur?

A
  • Spiurid nematodes – genus Serratospiculum, Serratospiculoides.
    • Infect air sacs of falcons and hawks.
    • Serratospiculosis.
    • Common in prairie falcons, may cause death.
    • S. seurati – Middle East.
    • Adult worms colonize air sacs, lodge in mesenchymal layer.
    • Adult females are large, lay eggs in air sacs.
      • Eggs travel to lungs, are coughed and swallowed, pass in feces.
      • Beetles ingest eggs and in infect raptors via ingestion.
      • L3 larvae penetrate proventricular and ventricular wall and lodge in air sacs, completing life cycle.
    • Large numbers can be found in healthy individuals or can cause clinical signs.
    • CS – poor stamina, labored breathing, poor doers.
    • Air sac membranes grossly thickened.
    • Secondary bacterial infections, asper.
    • May result in hemorrhage, edema, mild necrosis, histiocytic inflammation.
34
Q

What are the liver flukes of eagles?

What is the proposed life cycle?

A
  • Opisthorchiid liver flukes – Opisthorchis spp, Metorchis bilis, Amphimerus elongatus.
    • Common in bald eagles and white-tailed sea eagles, also seen in harriers.
    • Severe in hatch year bald eagles, clinical significant uncertain.
    • Mortality attrinbuted to massive infection with M. bilis.
      • Two IM hosts, may include aquatic snail as primary IM host and amphibian or fish as secondary IM host.
      • Adults in biliary system, lay eggs.
        • Granulomatous cholangitis, pericholangitis, necrosis of hepatocytes.
    • Amphimerus in NA bald eagles reside in bile ducts, extensively migrate within liver parenchyma.
      • Serpentine migration tracts, granulomatous hepatitis.
35
Q

What is the life cycle of caryospora spp?

How is it diagnosed?

What lesions are present in raptorial birds?

A
  • Caryospora.
    • Monoxenous (one host) life cycle, some spp facultative heteroxenous.
    • Life cycle occurs in epithelial cells of small intestine of raptors or snakes.
    • Oocysts ID on fecal float or direct smears.
    • Oocysts are large, sporulated, one sporocyst with eight sporozoites.
    • Infection typically clinically insignificant but disease can occur.
      • C. neofalconis – catarrhal enteritis with petechial hemorrhage.
      • Concurrent infection with C. perfringens type A/B can result in hemorrhagic enteritis.
      • Histo – protozoa within cytoplasm of enterocytes beneath the nucleus.
36
Q

What is the etiologic agent of frounce?

What is the source of infection?

What lesions are present?

Any species resistant?

How is it diagnosis?

Are there any risk factors?

A
  • Trichomoniasis aka frounce.
    • Trichomonas gallinae.
      • Rock pigeons primary host, mourning doves and song birds can also be infected.
      • Disease common in raptors fed pigeons.
      • Lesions – yellowish mucosal plaques in oropharynx and upper esophagus.
        • May extend deeper into soft tissues and underlying bone.
      • Uncommon in vultures.
        • A unique trichomonad T. gypaetinii isolated from Egyptian and Cinereous vultures in Spain.
      • Characteristic motile, flagellated protozoa on wet mount.
      • Fibrinoheterophilic and necrotizing diphtheritic inflammation characteristic.
      • Concurrent fungal and bacterial infections common.
      • Test for culture and PCR more sensitive than smears or histo.
      • Ddx – avian pox, herpesvirus, candidiasis, salmonellosis, capillariasis.
      • Paper: Oral pH may be a risk factor.
        • Oral pH in some risk factors becomes more acidic with age.
        • Adults less susceptible to infection.
        • Not found to be a risk factor in Golden Eagles.
        • GOEA nestling diets with > 10% rock doves, nestlings had a high probability of T. gallinae infection.
        • Compared to historical data, seems to be more pigeons in the diet potentially due to change in habitat.
37
Q

How does cryptosporidium present in raptorial birds?

A
  • Cryptosporidium baileyi.
    • Upper resp tract disease, may extend into lungs or middle ears, conjunctiva.
    • Mucoid exudate in trachea, epicardium, middle ear.
    • Fibrinous airsacculitis.
    • Round, intracellular, extracytoplasmic cryptosporidial organisms.
    • PAS reaction and acid fast stains help visualize the organisms.
    • PCR.
38
Q

What is the etiologic agent of malaria in raptorial birds?

How is this transmitted?

Are any species particularly susceptible?

What gross adn histologic lesions are present?

What distinguishes plasmodium from other hemosporidians?

A
  • Plasmodium
    • Examination on blood films or impression smears of lungs, liver, spleen.
      • Hepatomegaly, splenomegaly.
    • Avian malaria.
      • Transmitted by culicine and anopheline mosquitoes.
      • Gyrfalcons, gyrfalcon hybrids and snowy owls particularly susceptible to fulminant disease.
      • In raptors – P. relictum.
      • Clinical Signs: Anemia, liver and spleen swollen and discolored red to black.
        • Lungs markedly edematous.
        • Some cases cerebellar petechiae.
      • Histo – intraerythrocytic parasites, especially in pulmonary and brain capillaries.
        • BM hypercellular due to marked erythroid hyperplasia.
        • Black pigment hemozoin.
        • Extraerythrocytic meronts in endothelial cells and tissue MP.
        • Plasmodium spp undergo asexual reproduction in erythrocytes.
          • Distinguishes them from other hemosporidians.
          • Plasmodium and Hemoproteus spp digest and convert hemoglobin to hemozoin (malarial pigment).
            • Golden brown or black granules that are refractile with polarized light.
            • Pigment in cytoplasm of the parasite and can be seen in blood or MP in the BM, spleen, and liver.
        • Asexual reproduction of Hemoproteus occurs exclusively in dneothelial cells, not in circulating erythrocytes.
        • PCR followed by DNA sequencing commonly
39
Q

Pododermatitis is a common problem of captive raptos.

What causes it?

What secondary infection is common? Have other bacteria been isolated?

How is it treated?

What are five key components of prevention?

A
  • Bumblefoot.
    • Initiated by abnormal pressures on feet.
    • Inactivity, lack of exercise, hypovitaminosis A may play a role.
    • Infection usually secondary, commonly staph aureus.
      • Strep, e. coli, proteus, pasteurella, pseudomonas, klebsiella, clostridium, Corynebacterium, nocardia, actinomycces, candida, asper also isolated.
      • Classified by different authors into 3-5 stagges.
      • If swollen, take rads.
    • Tx – removal of underlying causes, wound management.
    • Early – skin tougheners (camphor, tincture of benzoin), alteration of perch.
    • Ulceration, swelling, inflammation – surgical debridement, irrigation with saline or chlorhexidine, ball bandaging, foam shoes.
      • Culture and determination of antibiotics essential.
      • Cephalosporins, fluoroquinolones, lincomycin, clindamycin.
      • Topical cocktails – dimethylsulfoxide, dexamethasone, enro.
      • Slow-release antibiotic-impregnated beads with surgical debridement.
        • Piperacillin, rifampicin, amoxicillin, clinda, endo, pefloxacin, gentamicin.
        • Beads can be left indefinitely.
      • Meloxicam and carprofen for analgesia.
      • May administer vit A.
    • 5 key elements for the prevention of bumblefoot:
      • Nutritious, balanced diet and preventing obesity.
      • Providing perches of appropriate size, shape, cover.
      • Providing adequate maneuvering space for free-lofted birds so they can land normally.
      • Keeping the talons at appropriate lengths and blunting the talon tips of captive birds not used for hunting.
      • Providing exercise and observing the feet regularly to recognize the condition early.
40
Q

Pansteatitis affects what species of raptorial birds most commonly?

What is an underlying nutritional deficiency?

What lesions are present on necropsy?

A
  • Pansteatitis
    • RTHA, BAEA during winter in northern latitudes.
    • Vit E deficiency.
    • Increased CK, lipemia.
    • Internal and SQ adipose discolored yellowish beige with chalky consistency.
    • Adipocyte necrosis and associated granulomatous inflammation.granular pigment stains with hematoxylin phloxine saffron and Ziehl Neelsen, periodic acid-Schiff positive.

Terio

41
Q

Describe hepatic lipidosis in raptorial birds.

When is it normal?

What is found on necrosy?

What are the risk factors?

A
  • Hepatic lipidosis
    • Considered normal up to 1 week age, associated with resorption of yolk.
    • Pathologic hepatic lipidosis, usually obese, rounded liver margins, hepatomegaly.
    • Sedentary life style in captivity, high caloric intake primary risk factors.

Terio

42
Q

Describe atherosclerosis in raptorial birds.

Are wild or captive raptors more affected?

What arteries are affected?

Are there any species predispositions?

What lesions are found on necropsy?

What is the unique lesion in falcons and kites?

A
  • Atherosclerosis
    • Reported in free-ranging birds of prey, more common in captive raptors.
    • Primarily affects large arteries – brachiocephalic trunk, pulmonary artery, aorta.
    • Brahminy kites suspected to have a genetic predisposition.
      • Individuals as young as 55 days have been dx with moderate to marked atherosclerosis and lipidosis of major organs.
    • Vessels thickened due to presence of raised yellow atheromatous plaques that cause narrowing or occlusion of the vascular lumina.
    • Lipid within intima and media assoc with foamy MP, cholesterol clefts.
    • Ischemic cardiomyopathy may be associated.
    • Dissecting aneurisms with or without rupture resulting from advanced cases in falcons and kite

Terio

43
Q

What was associated with lead levels in nestling bald eagles in PEI?

A

Vaasjo, E., Beauchamp, G., & Desmarchelier, M. (2022). Health status including lead levels of nestling bald eagles (haliaeetus leucocephalus) on prince edward island, canada in 2012 and 2013. Journal of Zoo and Wildlife Medicine, 53(1), 204-208.

Prevalence of lead decreased with increasing wt, age, and BCS. Young eaglets can have detectable levels of lead, and may be negatively impacting their BCS and weight.

Lead prevalence NOT impacted by location or measurements of the eaglet.

44
Q

General PK CCFA in bald eagles?

A

Sadar, M. J., Cox, S. K., Duvall, A., & Jones, M. P. (2021). Pharmacokinetics of a Single Intramuscular Injection of Ceftiofur Crystalline Free Acid in Bald Eagles (Haliaeetus leucocephalus). Journal of Avian Medicine and Surgery, 35(3), 290-294.

CCFA may be dosed at 10 mg/kg IM every 60 hrs (3-5d) or 20 mg/kg IM every 80-160 hrs (3-7d) in BAEA. One bird had bruising at the injection site.

CCFA in RTHA lasts 5 days.

45
Q

What was observed following administration of high oral doses of meloxicam to American kestrels?

A

Summa, N. M., Guzman, D. S. M., Larrat, S., Troncy, E., Bird, D. M., Lair, S., & Fitzgerald, G. (2017). Evaluation of high dosages of oral meloxicam in American kestrels (Falco sparverius). Journal of avian medicine and surgery, 31(2), 108-116.

Administered meloxicam orally via feeding tube into the proventriculus at 2, 10, and 20 mg/kg q12h x 7 days.

No clinical signs or mortality.

No evidence of renal toxicity.

Significant correlation between hepatic lipidosis and meloxicam dose.

46
Q

What risk factors were associated with atherosclerosis in raptors in Northern California?

A

Lujan-Vega, C., Keel, M. K., Barker, C. M., & Hawkins, M. G. (2021). Evaluation of Atherosclerotic Lesions and Risk Factors of Atherosclerosis in Raptors in Northern California. Journal of avian medicine and surgery, 35(3), 295-304.

Greater severity of lesions in aorta vs pulmonary artery.

Hepatic and pulmonary arteries NOT commonly affected.

Peripheral vessels - Commonly kidney, heart (myocardial and coronary arteries), gonads, spleen.

Falconidae highest prevalence.

Risk in Accipitridae significantly less vs Falconidae.

Adult raptors, females, captive birds at higher risk.

47
Q

What was observed in a PK study of single dose voriconazole PO with and without food in RTHA?

A

Parsley, R. A., Tell, L. A., & Gehring, R. (2017). Pharmacokinetics of a single dose of voriconazole administered orally with and without food to red-tailed hawks (Buteo jamaicensus). American Journal of Veterinary Research, 78(4), 433-439.

Voriconazole 15 mg/kg PO in a dead mouse or without food.

Overall voriconazole well absorbed, food delayed absorption and resulted in significant delay in time to maximum plasma concentration.

Mean plasma concentration reached target for 8 hrs in unfed birds and 12 hrs in fed birds (time above MIC increased in fed birds).

Cmax was decreased and tmax was delayed in fed birds.

48
Q

General PK concentrated buprenorphine in RTHA?

How did fentanyl affect iso MAC in RTHA?

What was observed with buprenorphine, hydromorphone, tramadol, butorphanol in kestrels?

A

Gleeson, M. D., Guzman, D. S. M., Knych, H. K., Kass, P. H., Drazenovich, T. L., & Hawkins, M. G. (2018). Pharmacokinetics of a concentrated buprenorphine formulation in red-tailed hawks (Buteo jamaicensis). American journal of veterinary research, 79(1), 13-20.

Buprenorphine in RTHA - Mild to moderate sedation at high dose SC. Rapid absorption. Plasma concentration maintained 24-48h. A previous study showed minimal effects regarding behavior change and sedation.

Fentanyl CRI in RTHA dose-dependent decreased in iso MAC.

Butorphanol no change in thermal withdrawal kestrels.

Hydro caused substantial sedation in kestrels.

Buprenorphine rapidly absorbed and high bioavailability in kestrels, analgesia for > 9 hrs, SR formulation maintained up to 48h!

49
Q

What ratio had a strong correlation with cardiac silhouette width in bald eagles? Which species has the smallest ratio?

A

Locke, S., Johnson, D., Shimp, J., & Pridgen, T. J. (2020). Radiographic Reference Intervals of the Cardiac Silhouette Width in the Bald Eagle (Haliaeetus leucocephalus). Journal of Avian Medicine and Surgery, 34(3), 260-267.

Cardiac width vs thorax width and sternum width both strongly correlated with cardiac silhouette width.

Cardiac width vs hepatic and coracoid widths moderate to weak correlation, respectively. Not recommended for evaluation of cardiac size.

BAEA have the smallest ratio, supporting hypothesis that larger birds have smaller hearts in relation to body size.

Cardiac to thoracic width ratio:

Osprey > Budgie > Kestrel > AF Grey > Spix > Bonelli’s Eagle > BAEA

In peregrine falcons, sternal width most accurate predictor of cardiac width.

Sternal and thoracic width most useful in general. Ratio of cardiac to thoracic can be impacted by respiratory motion.

Woo, K. M., Barron, G. H., Daugherty, A. L., Woo, J. M., Kehoe, S. P., Aguilar, L. A., & Cavanaugh, S. M. (2019). Measurements of the radiographic cardiac silhouette of ospreys (Pandion haliaetus). American journal of veterinary research, 80(9), 840-845.

Osprey have strong correlation for sternal width, moderate correlation for thoracic width vs cardiac width.

50
Q

What spp of raptor has had significantly higher concentrations of serum lipids vs other raptor spp, predisposing to atherosclerosis?

Cardiac arrhythmias with isoflurane have been reported in what raptor spp? What arrythmia most common?

What infectious disease of raptors is frequently associated with myocarditis?

What heavy metal has been associated with cardiomyopathy in raptors?

A

Oster, S. C., & Pariaut, R. (2022). Cardiac Disease of Raptors. Journal of Avian Medicine and Surgery, 35(4), 382-389.

Atherosclerosis - Suggested decreased activity, high fat diets, increased age predisposing factors. Brahminy kite (Haliastur indus) - significantly higher levels of serum lipids, may predispose to atherosclerosis.

Arrythmias - Eagles have been reported to developed with iso anesthesia (2nd deg AV block).

Myocarditis has been associated with WNV.

Endocarditis has been assoc with septicemia caused by pododermatitis.

Cardiomyopathy assoc with lead toxicity.

PEFA - Sternal width most accurate predictor of cardiac width.

Harris hawks have a narrow heart width on VD rads.

Bonelli’s eagles - Sternal width and thoracic width preferred method to evaluate cardiac width.

51
Q

What are some risk factors for pododermatitis in raptors?

What shoe material has been shown to have the lowest measured forces on the MT pad in a limb model?

A

Barboza, T., Beaufrére, H., & Moens, N. (2020). Effects of Perching Surfaces and Foot Bandaging on Central Metatarsal Foot Pad Weight Loading of the Peregrine Falcon (Falco peregrinus). Journal of avian medicine and surgery, 34(1), 9-16.

Risk factors - obesity, poor perch design, nutritional deficiencies, lack of exercise, abrupt decrease in exercise, disrupted blood supply to foot, dz contralateral limb, talon overgrowth, repeated trauma.

Silicone shoe or neoprene decreased measured forces on the MT pad the most. When bandage is not an option, neoprene surface is best followed by turf, but harder to sanitize.

52
Q

What sample for WNV testing is most sensitive for PCR detection (nonvascular feather quill, vascular immature feather pulp, oropharyngeal swab, cloacal swab, kidney sample)?

A

Kritzik, K. L., Kratz, G., Panella, N. A., Burkhalter, K., Clark, R. J., Biggerstaff, B. J., & Komar, N. (2018). Determining raptor species and tissue sensitivity for improved West Nile Virus surveillance. Journal of wildlife diseases, 54(3), 528-533.

Feather pulp most sensitive PCR sample, consistent with a previous study in corvids.

Detected most frequently in vascular feather pulp of Cooper’s hawks.

Coopers, RTHA, and Swainson’s hawks can serve as sentinels for other avian spp, targeting feather pulp as substrate for viral detection by PCR.

Highest rate of infection mid-late summer, after human cases typically, so raptors are NOT a good early warning system for human WNV.

53
Q

What were the most common causes of mortality found in a retrospective of raptor mortality in Ontario, Canada?

A

Smith, K. A., Campbell, G. D., Pearl, D. L., Jardine, C. M., Salgado-Bierman, F., & Nemeth, N. M. (2018). A retrospective summary of raptor mortality in Ontario, Canada (1991–2014), including the effects of West Nile Virus. Journal of Wildlife Diseases, 54(2), 261-271.

Trauma majority of deaths across all spp. Followed by emaciation, significantly higher in males.

Of infectious dz, WNV most common. Immature RTHA significantly greater odds of WNV infection. Deaths greater in summer and fall vs spring. RTHA and GHOs most common spp.

Toxicosis most commonly dx in BAEA (lead).

54
Q

What was observed with fluoroscopic evaluation of GI transit times in RTHA with and without a hood?

A

Doss, G. A., Williams, J. M., & Mans, C. (2017). Contrast fluoroscopic evaluation of gastrointestinal transit times with and without the use of falconry hoods in red-tailed hawks (Buteo jamaicensis). Journal of the American Veterinary Medical Association, 251(9), 1064-1069.

Overall GI transit faster in RTHA vs psittacines. Ventricular contraction rate lower vs Amazon parrots.

Hood delayed crop emptying but otherwise no change in total transit time vs no hood.

55
Q

Cardiac width in Bonelli’s eagles strongly correlated with what other measurements on rads?

A

Lopes, F., Jesus, S., Med, V., Márquez, I. L., Fernández, V. M., Nunes, T., … & González, F. G. (2019). Radiographic reference values for the cardiac silhouette in Bonelli’s eagle (Aquila fasciata). Journal of Avian Medicine and Surgery, 33(1), 53-58.

Cardiac width in Bonelli’s eagles strongly correlated with sternal and thoracic widths.

In general, larger birds have proportionally smaller hearts.

56
Q

What was observed in a retrospective study of femoral fx in birds of prey?

A

Vigneault, A., Fitzgerald, G., & Desmarchelier, M. (2021). A retrospective study of femoral fractures in wild birds of prey: 119 cases. Journal of Zoo and Wildlife Medicine, 52(2), 564-572.

Femoral fx in birds < 1 kg mostly treated with single IM pin.

Femoral fx in larger birds treated with IM pin or EST IM pin tie in fixator.

Birds with a fibrous callous forming before surgery could be attempted, high surgical risk cases, and proximal fractures or nestlings all healed with conservative tx (cage rest).

Femur fracture is overall low prevalence vs antebrachial fx.

Birds with multiple fx bones or a comminuted femoral fx do not necessarily carry a poor prognosis.

IM pin - Stabilizes vs bending but not rotation or shearing.

ESF - More time consuming, can create iatrogenic fissures, premature loosening of pins may occur. Remove ASAP and allow bird to bear wt, but keep in place long enough for stabilization.

57
Q

Among raptors with ulnar fractures, what factors were associated with better prognosis for release?

A

Vergneau-Grosset, C., Kapatkin, A. S., Paul-Murphy, J., Guzman, D. S. M., & Hawkins, M. G. (2019). Release rates and complications for birds of prey with antebrachial fractures at a veterinary teaching hospital. Journal of avian medicine and surgery, 33(4), 388-397.

Among birds with only ulnar fracture, closed fracture and fracture of middle third of the ulna significantly more likely to be released.

Of birds treated with external coaptation, decreased ROM main complication.

No difference in prognosis for birds tx surgically or conservatively. External coaptation and/or cage rest can be considered an appropriate therapeutic option for single radius or single ulnar fractures.

PT recommended starting 7-10 days after trauma - joint ankylosis occurred in both surgical and nonsurgical groups.

58
Q

What was observed regarding prevalence of Caryospora oocysts in fomites and fecal samples from gyrfalcon chicks?

A

Juárez, A., García, Y. M., Sauza, R. P., Luna, J. C. M., & Samour, J. (2020). Prevalence of Caryospora (Apicomplexa: Eimeriidae) Oocysts in the Environment of a Gyrfalcon (Falco rusticolus) Breeding Center in the United Arab Emirates. Journal of Avian Medicine and Surgery, 34(2), 152-157.

Zero prevalence in chicks until after 60 days old, then prevalence increased with age.

Transmission direct via oocyst ingestion or indirect via ingestion of sporozoites in prey tissues.

Multiplication in SI epithelium of DH, excreted in feces.

CS - Coelomic pain, mucoid hemorrhagic diarrhea (adults), sudden death in juveniles. Neuro signs assoc with thiamine deficiency from protozoal depletion of vit B within body.

Oocysts persist in environment, more found per meter squared within environment sand of breeding pair chambers. Not found in gravel, nest, feeding platform, or water.

Presence of caryospora oocysts in feces are a risk factor, especially in small areas like breeding chambers. Hygiene important for controlling spread.

Sporulation inhibited with hot water > 140F for 30-60 sec.

59
Q

What is the causative agent of inclusion body herpesvirus hepatitis in raptors?

Clinical signs?

Lesions?

A

Raghav, R., & Samour, J. (2019). Inclusion Body Herpesvirus Hepatitis in Captive Falcons in the Middle East: A Review of Clinical and Pathologic Findings. Journal of Avian Medicine and Surgery, 33(1), 1-6.

Inclusion body herpesvirus hepatitis in raptors caused by columbid herpes-1 (CoHV-1).

Avian herpes are all alphaherpesvirinae.

Persistent asymptomatic latent infections with intermittent recrudescence and shedding.

Gyr falcons and prairie falcons highly susceptible.

CS - Acute/nonspecific clinical signs; acute death; occasionally neuro signs. Biliverdinuria, regurg.

Endoscopy - Small yellow amorphous caseous necrotic foci, liver and spleen.

Severe leukopenia (BM destroyed).

Dx by liver biopsy.

Mortality rate almost 100% in falcons. Avoid feeding pigeons to raptors. Also infects owls.

60
Q

What spp of soft tick has been associated with rickettsia hoogstraali and relapsing fever borrelia in raptors? Treatment?

A

Latas, P., Auckland, L. D., Teel, P. D., & Hamer, S. A. (2020). Argas (persicargas) giganteus soft tick infection with Rickettsia hoogstraali and relapsing fever Borrelia on wild avian species of the desert southwest, USA. Journal of wildlife diseases, 56(1), 113-125.

Argas (persicargas) giganteus soft tick. Birds presented moribund, paralyzed, obtunded. Infected with Rickettsia hoogstraalii > relapsing fever Borrelia. All birds with borrelia also positive for rickettsia.

Tickborne relapsing fever Borrelia spp = zoonotic risk, causes fever, headache, joint aches, nausea in people.

Treated with oral ivermectin, topical pyrethrin, oral doxycycline. Most birds recovered.

Ticks mobile and moved between cages in a wildlife center.

61
Q

What was observed in an evaluation of blood lead and mercury in Chesapeake, Delaware, and Barnegat bay BAEA?

A

Eleftheriou, A., Murphy, L., & Welte, S. (2017). Evaluation of lead and mercury prevalence in bald eagles (haliaeetus leucocephalus) from the mid-atlantic United States. Journal of Zoo and Wildlife Medicine, 48(3), 910-914.

Eagles with clinically significant lead found near Chesapeake, Delaware bays.

Most birds with clinically significant mercury levels were near Delaware and Barnegat bays.

Mercury exposure bioaccumulates in fish as methylmercury (most toxic form).

62
Q

How does snowfall influence blood lead levels in BAEA in the MS river valley?

A

Lindblom, R. A., Reichart, L. M., Mandernack, B. A., Solensky, M., Schoenebeck, C. W., & Redig, P. T. (2017). Influence of snowfall on blood lead levels of free-flying bald eagles (Haliaeetus leucocephalus) in the Upper Mississippi River Valley. Journal of wildlife diseases, 53(4), 816-823.

Levels highest immediately following hunting season (Dec to mid Jan; early winter) and lower when the previous month’s snowfall was greater than 11 cm.

Snowfall can cover lead-tainted carcasses and decrease exposure in scavenging birds.

63
Q

What are risk factors for Trichomonas gallinae in Golden eagle nestlings?

A

Dudek, B. M., Kochert, M. N., Barnes, J. G., Bloom, P. H., Papp, J. M., Gerhold, R. W., … & Heath, J. A. (2018). Prevalence and risk factors of Trichomonas gallinae and Trichomonosis in Golden Eagle (Aquila chrysaetos) nestlings in Western North America. Journal of wildlife diseases, 54(4), 755-764.

Probability of trichomonas gallinae infection increased as the proportion of rock pigeons in the nestling diet increased.

Proportion of rock pigeon in eagle diets higher in recent study period.

Trichomonas gallinae - Flagellated protozoan parasite, primarily upper GI caseous lesions, can lead to suffocation or starvation.

Bird-eating raptors that feed on infected prey are susceptible. Common in columbiformes.

Major cause of death in nestlings in Bonelli’s eagles in Spain.

Oral pH may also affect risk of infection - pH decreases with hawk age, adults are less susceptible to infection.

Treatment with carnidazole appeared successful in golden eagle nestlings (not detected on visit following tx). Oral pH of golden eagle juveniles (even fledglings) high enough to promote infection.

64
Q

What is the most consistent sign of Horner syndrome in birds of prey?

A

LaChance, M. K., Fitzgerald, G., Lair, S., & Desmarchelier, M. R. (2019). Horner syndrome in birds of prey. Journal of avian medicine and surgery, 33(4), 381-387.

Ptosis of upper eyelid most consistent sign of Horner syndrome in birds of prey. Feather asymmetry and unilateral miosis also observed (less likely).

Ptosis of upper eyelid only compatible sign in many birds.

65
Q

What is the most common cause of ocular morbidity in raptors?

Name 3 tests for tear production in birds and differentials for decreased and increased tear production.

Name 2 ways to measure IOP in birds and list factors contributing to variations in IOP.

What are the 2 primary muscle groups involved in function of nictitans in birds?

A

Carter, R. T., & Lewin, A. C. (2021). Ophthalmic Evaluation of Raptors Suffering From Ocular Trauma. Journal of Avian Medicine and Surgery, 35(1), 2-27.

Trauma most common cause of ocular morbidity in raptors - gunshot/window strike in diurnal spp; HBC in nocturnal spp. Juveniles most likely to be released.

Nocturnal spp increased risk of blunt ocular trauma (lack protective supraorbital ridge present in diurnal raptors).

Tests for tear production - STT, modified STT (strips cut in half for small birds), phenol red thread test (PRT).

STT measured both basal and reflex tear production.

PRT only measures basal and residual tear volume (not reflex). Best for small eyes, low tear production.

Decreased tear production ddx neuroloxic injury, keratitis, hypovitaminosis A. Nocturnal spp generally lower vs diurnal spp tear production.

Increased tear production ddx ocular pain, obstruction of lacrimal drainage system. Hatchlings generally higher tear production.

Tonopen - Requires topical ax, limited in small patients.

Tonovet (rebound tonometry) - Topical ax not required, can be used with small corneal diameter.

Factors contributing to variations in IOP:

Type of instrument for measuring, diurnal (Tonovet overestimates) vs nocturnal, time of day, age of patient, body position.

2 primary muscles nictitans = pyramidalis and quadratus muscles, innervated by abducens nerve.

66
Q

What difference was found in ocular histomorphometry of free-living common kestrels?

A

Werther, K., Candioto, C. G., & Korbel, R. (2017). Ocular histomorphometry of free-living common kestrels (Falco tinnunculus). Journal of avian medicine and surgery, 31(4), 319-326.

Retinas of females were significantly thicker than males near the insertion of the pectin.

No other significant differences.

In general:

Diurnal raptors - 2 fovea

Nocturnal raptors - 1 fovea

Avian retina is not vascularized

67
Q

What is the primary cause of death in wild populations of California condors?

A

Nguyen, N., Saggese, M. D., & Eng, C. (2018). Analysis of historical medical records of california condors (Gymnogyps californianus) admitted for lead exposure to the los angeles zoo and botanical gardens between 1997 and 2012: A case series study. Journal of Zoo and Wildlife Medicine, 49(4), 902-911.

Lead toxicosis remains primary cause of death in wild populations of CA condors.

Clinical signs not observed in majority. 65% no evidence of GI metallic FB.

91% released following chelation (good px with tx).

Subadult condors appear most at risk.

68
Q

General PK sustained release buprenorphine IM and SC in kestrels? PD?

A

Guzman, D. S. M., Knych, H. K., Olsen, G. H., & Paul-Murphy, J. R. (2017). Pharmacokinetics of a sustained release formulation of buprenorphine after intramuscular and subcutaneous administration to American kestrels (Falco sparverius). Journal of avian medicine and surgery, 31(2), 102-107.

Buprenorphine SR 1.8 mg/kg IM or SC in kestrels, adminsitration every 12-72 hours. No sig difference between IM vs SC. Maximum plasma concentrations lower for SR formulation vs standard formulation, no sedation noted.

Guzman, D. S. M., Ceulemans, S. M., Beaufrère, H., Olsen, G. H., & Paul-Murphy, J. R. (2018). Evaluation of the thermal antinociceptive effects of a sustained-release buprenorphine formulation after intramuscular administration to American kestrels (Falco sparverius). Journal of avian medicine and surgery, 32(1), 1-7.

Original PD study with regular buprenorphine - Buprenorphine increased the thermal withdrawal threshold for up to 6 hrs, caused mild sedation in kestrels.

Buprenorphine SR study increased thermal threshold up to 24h, had a slower onset. Sedative effects were mild.

Results of these studies support use of buprenorphine and hydro for kestrels.

69
Q

Describe clinical signs, life cycle, treatment for serratospiculosis in falcons.

A

Veiga, I. B., Schediwy, M., Hentrich, B., Frey, C. F., Marreros, N., & Stokar-Regenscheit, N. (2017). Serratospiculosis in captive peregrine falcons (Falco peregrinus) in Switzerland. Journal of avian medicine and surgery, 31(3), 250-255.

Serratospiculum, family Diplotrianidae. Most cases in Falconidae.

Nematodes within coelomic cavity/thoracic and abdominal air sacs.

Serratospiculum seurati most common in falcons in middle east.

Serratospiculum tendo most common in raptors in europe.

LC: Bird ingests IM insect host infected with L3, penetrate through PV/ventricular wall into air sacs and lungs, eggs are regurgitated and swallowed/passed in feces or pellets.

Prophylaxis - Regular deworming, ivermectin/insect proof enclosure.

70
Q

A recent chapter discussed the status of vultures and NSAID regulations.

What NSAID was primarily responsible for vulture declines in Southeast Asia?

What was responsible for vulture declines in Africa?

What NSAIDs have been implicated with vulture mortality?

A

Vulture Declines in South Asia
* 1990s: White-rumped vulture (WRV), long-billed vultures(LBV) had population declines of 92%, along with slender-billed vulture (SBV)
* Inadvertent NSAID toxicity (diclofenac)

Vulture Declines in Southeast Asia
* Substantial declines in WRV, SBV, and red-headed vultures (RHV)
* Isolated populations due to poisonings – ingesting baits intended to kill prey species/problem animals
* Vultures food limited due to declines in ungulate populations
* Diclofenac, nor other NSAIDs, not widely used

Vulture Declines in Africa
* 62% decline over 30 years due to poisonings and trade of body parts
* Inadvertent poisoning – poisoning crop-raiding animals, consuming livestock
* Deliberate poisonings reduce circling vultures that may alert authorities to poaching

Status of Vultures in Europe
* Increase in griffon and cinereous vulture populations in 20 years
* Bearded vulture successfully reintroduced

Research
* Early modelling: diclofenac caused decline in South Asia
* Multizoo metaanalysis: diclofenac, carprofen, flunixin, ibuprofen, phenylbutazone all associated with mortality
* Meloxicam not associated with mortality – nontoxic at all doses of inadvertent exposure in nature
* Recent research suggest tolfenamic acid is an NSAID safe for vultures

Advocacy
* Ban on diclofenac in India, Nepal, Pakistan in 2006, Bangladesh in 2010
* Multidose vials (human use) banned in India and Pakistan
* Ketoprofen banned in VSZs in Bangladesh, to be banned nationally by 2022
* Ketoprofen, aceclofenac banned in Tamil Nadu, India
* Nepal, Pakistan not licensing or limiting availability of aceclofenac
* Saving Asia’s Vultures from Extinction (SAVE) lobbies for bans on ketoprofen, aceclofenac, nimesulide, carprofen, flunixin

71
Q

A recent study investigated the pharmacokinetics of grapiprant in red-tailed hawks.

What is the scientific name of the red-tailed hawk?

What is the mechanism of grapiprant?

How did the pharmacokinetics of grapiprant change when administered with food?

What dosing interval is potentially suggested based on this study?

A

AJVR 2022 83(6):ajvr.21.10.0170
Absorption of grapiprant in red-tailed hawks (Buteo jamaicensis) is decreased when administered with food
Rodriguez P, Paul-Murphy JR, Knych HK, Drazenovich TL, Hawkins MG

Key Points:
- Grapiprant = specific antagonist for prostaglandin EP4 receptor
- 30 mg/kg grapiprant PO q 24h in fasted RTHAs achieved plasma concentrations > canine minimum effective concentration (MEC) of 164 ng/mL
- RTHAs achieved mean plasma grapiprant concentrations > 164 ng/mL at 16 hours post-administration and maintained up to 24 hours
– RTHA plasma grapiprant concentrations were decreased when administered with food
– Plasma concentrations were reduced by 88% when RTHAs were fed
- Increasing to q 12 h with food may achieve plasma concentrations similar to the canine MEC
- Unclear if dose can be considered therapeutic in RTHAs without pharmacodynamic data

TLDR: RTHA plasma grapiprant concentrations were decreased when administered with food

72
Q

A recent study measured the effects of detomidine and medetomidine and ketamine on tear production and intraocular pressure in common buzzards.

What was the effect of alpha-2 adrenoreceptor agonists on IOP?

How did the addition of ketamine affect that?

A

JAMS 2022 36(3) 242-249
Measuring the Effects of Detomidine and Medetomidine Alone and in Combination with Ketamine on Tear Production and Intraocular Pressure in Common Buzzards (Buteo buteo)

Key Points:
- Baseline IOP was higher than has previously been published in this species
- a-2 adrenoreceptor agonists can affect IOP, but the mechanism(s) by which this occurs is unknown.
- In this study, both detomidine and medetomidine were found to decrease IOP In some
- IOP decreased significantly after anesthesia with ketamine compared with sedation with detomidine
- When ketamine was given after sedation with medetomidine, IOP was reduced in both eyes; however, only the reduction in IOP measured in the left eye was statistically significant
- When a-2 adrenoreceptor agonists were considered as a single group, IOP was found to decrease significantly after ketamine administration compared with a-2 adrenoreceptor agonists alone.
- Both detomidine and medetomidine significantly decreased STT
- However, after ketamine administration, the STT values differed between groups, with no further change in the detomidine group, but a significant decrease in tear production in left eye and an insignificant increase in right eye after medetomidine
- When evaluated with alpha 2’s as a single group, STT did not change significantly after ketamine

73
Q

A recent study evaluated the agreement between point-of-care glucometers and lab analyzers in North American raptors.

How do POC glucometers estimate BG in birds?
- Pigeons? Auklets?

What analyzer seemed to be best?
- Which sample was needed to be the most reliable?

A

JAMS 2022;36(3):278-286
Evaluation of the Agreement Between 2 Point-Of-Care Glucometers and a Laboratory Automated Analyzer in North American Raptors
Hiebert K, Reich S, Allender MC

Key Points:
- In Hispaniolan Amazon parrots, human POC glucometers underestimated BG
– Human POC glucometers underestimated BG in pigeons & rhinoceros auklets
– POC glucometers do not seem to be accurate or reliable in other avian species
- Veterinary POC glucometer (AlphaTrak 2) overestimated BG in plasma & whole blood for raptors
– Degree of overestimation was variable and actual BG couldn’t be reliably extrapolated
- Human POC glucometer (Contour Next EZ) underestimated BG in whole blood for raptors
– Degree of underestimation was variable and actual BG couldn’t be reliably extrapolated
– However, glucometer showed promise for accurate & reliable WITH PLASMA in raptors
– Didn’t meet FDA guidelines for human POC glucometers intended for healthcare
– But did meet lenient FDA guidelines for OTC human POC glucometers

74
Q

A recent study explored the relationship between anticoagulant exposure and wind turbine mortalities.

What toxin has been shown to predispose birds to collision trauma?
- Is that a factor in wind turbine mortalities?

What are the mechanisms for anticoagulant toxicity?
- Give examples of first and second generation anticoagulants

Did anticoagulant exposure differ in turbine mortalities?

A

JWD 2022 58(2):348-355
Anticoagulant exposure in golden eagle (Aquila chrysaetos) power line electrocution and wind turbine mortalities
Viner TC, Kagan RA, Lehner A, Buchweitz JP

Key Points:
- Toxicants may affect eagle behavior and flight capability
– Studies have suggested that exposure to lead predisposes birds to collision trauma
– However, recently shown to NOT be a predisposing factor in wind turbine mortalities
– Subclinical lead toxicosis may inhibit soaring and hunting behavior
- Anticoagulant rodenticides classified as 1st or 2nd generation
– 1st generation: developed earlier, require multiple feedings for rodenticide effectiveness
– Ex: warfarin, chlorphacinone, and diphacinone
– 2nd generation: may kill rodents after a single feeding
– Ex: difenacoum, brodifacoum, bromadiolone, and difenthialone
– MOA for both generations: vitamin K antagonist
– In 2008, US EPA restricted 2nd generation use to agriculture and professionals
- Anticoagulant exposure didn’t differ between power line and wind turbine mortalities
– Only two anticoagulants were detected in the eagles (brodifacoum and bromadiolone)
- Similar anticoagulant exposure across life stages indicates opportunity for exposure is constant
– Anticoagulants may have similar effects, or lack thereof, on soaring/perching behaviors

TLDR: Anticoagulant or lead exposure does not predispose golden eagles to wind turbine mortalities

75
Q

A recent study described the digestive and feeding behavior differences between lappet-faced vultures and griffon vultures.

Which species is a ripper?

Which species is a gulper?

How does their anatomy and diet differ?

Which species appeared to have more efficient digestion?

A

JZWM 2023 53(4):769-776
DIGESTIVE AND FEEDING BEHAVIOR DIFFERENCES BETWEEN LAPPET-FACED VULTURES (TORGOS TRACHELIOTOS) AND GRIFFON VULTURES (GYPS FULVUS) EX SITU
Daneel A, Whitehouse-Tedd K, Whitehouse-Tedd G, Dierenfeld ES, Janssens GPJ

Background:
- Vultures are threatened with extinction across most of their range
– Feeding strategies vary among vulture species
- “Rippers” = lappet-faced vultures prefer tougher carcass components
– Wide skulls and strong beaks
– Diet lower in digestible energy, need to consume more
- “Gulpers” = African vultures of the Gyps genus prefer internal organs & muscle
– Intermediate beak strength and narrow skulls
– Diet higher in digestible energy, don’t need to consume as much
– Reliant on the “rippers” to open carcasses
- Ex situ vultures are likely to be fed small mammalian/avian prey as whole carcasses
– If/when offered larger mammalian prey, likely butchered
– Small enough that bones, cartilage, and other fibrous components can be consumed
– May provide divergent nutrient profiles compared with their natural diet
- Green-colored biliverdin is the main bile pigment in birds

Key Points:
- Lappet-faced vultures consumed larger quantities, less selective
- Griffon vultures ate soft tissues selectively and consumed less
- No difference in passage rate between species
- Striking species differences in excreta color despite similar diet
- Green excreta in griffon vultures suggests high amount of bile secretion and digestibility
- Lappet-faced vultures excreta shifted from light brown to dark brown throughout the day
- Lower N and C in lappet-faced vulture excreta suggests more efficiently digestion
– May also reflect higher intake of skeletal minerals
– N and C in excreta negatively correlated w/ food intake & green excreta
– Excreta color may be an easy marker of digestive performance

76
Q

A recent case series described treatment snake and scorpion envenomation of various birds of prey.

What treatments were used in this case series? What is recommended?

What considerations should be made when giving antivenom?

What diagnostics may be sueful in envenomation cases?

A

Journal of Zoo and Wildlife Medicine, 53(4) : 870-881 2023
OUTCOMES OF TREATMENT OF SNAKE AND SCORPION ENVENOMATION IN BIRDS OF PREY, WITH AND WITHOUT ANTIVENOM
Siegrist, Audrey A., Boyer, Leslie, Balchan, Neil R., Vázquez, Hilda, Alagón, Alejandro, et al

Key Points:
- Some raptor species are specialized snake predators and may be exposed to envenomation from
– Crotalids (pit viper sub-family) – venom generally causes local tissue injury, neurotoxicity, and/or complex coagulopathy
– Coral snakes (elapid family) – venom generally causes pre- and postsynaptic neurotoxicity
– Bark scorpions (Centruroides sculpturatus) – venom causes neurotoxicity
- Treatments
– NSAIDS – considered contraindicated in human med due to added bleeding risk from effects on platelet aggregation
– Corticosteroids – likely little effect on acute edema because crotalid venom injury is related to endothelial and intracellular toxic damage rather than inflammation
– Diphenhydramine – likely little effect as venom action is via ion channel not histamine
– IV fluids – necessary for hypovolemic shock, but consider antivenom volume prior to administering to avoid fluid overload
– Antivenom – only horse and sheep products currently available so proteins and immunoglobulin product type carry risk of anaphylactic reactions (and delayed reactions like serum sickness) in nondomestic species
– Have epinephrine on hand
– IV admin is preferable due to rapid uptake and greater bioavailability but can be given IM (in multiple locations due to large volume, ex. 3-10 mLs)
- Diagnostics
– Whole blood clotting test – may be useful for rapid clotting analysis
– Venom antigen ELISA – may be useful for scorpion venom diagnosis if it becomes commercially available
- Snake bites caused death in 6/16 raptors identified in other cases

Take-Home Message:
- Avian envenomation can be fatal but treatable
- Early intervention with supportive care (fluids, pain relief (consider opioids), antimicrobials, and anti-venom product if appropriate and available) can be tried
- Whole blood clotting test of putting fresh blood in red-top to observe clotting may be useful for coagulation monitoring

77
Q

A recent study established reference intervals for B-hydroxybutyrate, amino acids, and chemistry values in red-tailed hawks.

What is BHB?
- What is it an indicator of?

A

JZWM 2023 54(1) 152-158
EVALUATION OF β-HYDROXYBUTYRATE, AMINO ACIDS, AND SELECTED CHEMISTRY VALUES IN THE PLASMA OF FREE-RANGING RED-TAILED HAWKS (BUTEO JAMAICENSIS)

Key Points:
- BHB is a ketone produced by metabolism of non-esterified fatty acids (NEFA) in the liver during periods of negative energy balance. As BHB leaves the liver and enters teh blood, it is taken up by other tissues and utilized as an alternate energy source.
- BHB is often measured in cattle to diagnose negative energy balance, or diagnose diabetic ketoacidosis in companion animals
- BHB levels have been measured in other birds and they appear to have reliance on nondetrimental levels of ketosis to increase reliance on lipid metabolism and conserve glucose during catabolic states