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Birds of PreyBirds of PreyMedicine and ManagementMedicine and Management
Birds of PreyBirds of PreyMedicine and ManagementMedicine and Management
Michael P. Jones, DVMDiplomate, ABVP (Avian Specialty)
Birds of PreyBirds of PreyMedicine and ManagementMedicine and Management
Birds of PreyBirds of PreyMedicine and ManagementMedicine and Management
First and foremost are the Raptors.Everything else is JUST prey
Handling and Restraint
Care should be taken to minimize the amount of stress and discomfort the patient feels while allowing essential procedures to be completed
Handling and Restraint
Observe for signs of stress– Drooping posture– Weakness– Open-mouth respirations– Exaggerated respiratory effort– Excessive struggling
Equipment Goal:Neutralize weapons; mainly beak
and talons Equipment:
– Gloves-thick enough to provide protection from talons/beak
– Towels/blankets– Stockinettes/body wrap– Jesses– Hoods
Capture of Raptor Using a towel/blanket and gloves slowly yet
deliberately move towards raptor Quickly throw towel/blanket over raptor Press bird to the ground or cage floor Positon hands in order to grasp the legs near the
base of the body Then lift raptor to chest with feet directed away
from yourself and others Nets may also be used, but be careful not to injure
raptor with hoop or mesh
Handling and Restraint The person holding the raptor must have
complete control of bird to neutralize the weapons
Once completely restrained the bird may be positioned such that both legs are in one hand with an index finger between the limbs
Gloves may be removed if desired Further restraint (e.g. hoods, body wraps, etc.)
Handling and Restraint Many species, particularly owls,
eagles, and falcons like to bite which makes control of the head almost as important as control of the feet
Usually legs are controlled then the head is secured
Handling and Restraint Communication
Communication between the handler(s) and persons performing the procedures is vital to the well being of everyone involved
Always make sure the other person has complete control of the raptor before letting go. Ask questions!
Clinical Management
Complete historyPhysical examinationDiagnostic/therapeutic
proceduresHospitalizationDietary management
History
Often the history is vague when presented with wild birds of prey
Much more thorough history obtained from birds used in falconry or rehabilitation projects
Physical ExaminationSystematic
Assess all systems in order to determine releasability of patient
Release vs. Euthanasia
• Major objectives of rehabilitation: is to - restore animal to its formerly healthy state
- prepare and condition it physically and mentally
- release it in a suitable place and time to allow it to function normally
Release
Four assumptions for release:– Fully functional appendages– Good visual capability– Good athletic ability– Appropriate social conditioning
Release
Any raptor that is unable to mentally and physically meet the demands placed upon it in order to survive should not be considered for release
Violations
Violations of the four assumptions for release occur due to the following:– Pressure– Attachment– Time invested
Hospitalization
Factors to consider when housing raptors– Minimize stress– Patient cage size– Perch sizes and shapes– Dietary considerations– Flight cages for rehabilitation– Protection from other species/birds of prey– Isolation if necessary
Dietary Considerations In general, try to offer diets which are
similar to the prey species normally caught in the wild
– Osprey - fish
– Bald Eagles - fish as well as other prey
– Most diurnal/nocturnal raptors - small rodents and rabbits
– Falcons (other than Kestrels) - small birds, quail
– Accipiters (especially Sharp-Shinned and Cooper's hawks) - small birds© Michael McDermott
Dietary Considersations
Other sources of nutrition include venison, beef, day-old chicks and others.
Supplementation with vitamin supplements are also beneficial
Birds of PreyBirds of PreySelected Infectious DiseasesSelected Infectious Diseases
Birds of PreyBirds of PreySelected Infectious DiseasesSelected Infectious Diseases
BumblefootDestructive process which may involve skin, underlying soft
tissues or bone:
Staphylococcus aureus
Escherichia coli
Proteus spp.
Bumblefoot Classification
Type 1:Diffuse cellulitis often at the metatarsal pad(s) of one or more digits
Bumblefoot Classification
Type 2:Similar to Type 1: localized lesions of the digital or metatarsal pads
Bumblefoot Classification
Type 3: Discrete lesion(s) with hyperkeratinization, localized swelling and redness
Bumblefoot Classification
Type 4: Enlargement of the distal digital pads; the result of flexor tendon ruptures
Bumblefoot Classification
Type 5: Elements of Type 3 or 4; presence of osteomyelitis
Bumblefoot Therapy
Reduction of swelling and inflammation
Debridement of any necrotic tissuesEstablish drainage if abscesses are present
Elimination of pathogens
Bumblefoot Therapy
Protecting wound from further infectionsPromotion of granulation and healing with bandaging and dressings
Identification and removal of underlying cause(s)
Bacterial Diseases
Clostridium botulinum (Type C exotoxin) Clinical Signs:
– flaccid paralysis involving the neck and limbs
– paralysis of pharyngeal muscles
– respiratory paralysis
– death in a few hours to several days
Clostridium botulinum
Transmission:– consumption of contaminated meat or
maggots which have fed from it
– vultures seem to be resistant
Clostridium botulinum Diagnosis:
– clinical signs
– mouse inoculation
– other diagnostic samples
(should be frozen at -20o C) Treatment:
– supportive care
– administration of antitoxin (Type A or C)
Mycobacterium avium Clinical Signs:
– chronic wasting disease
– often associated with a good appetite Forms:
– respiratory form - respiratory system (lungs)
– skin and muscle form - localized infections resulting from talon puncture
– generalized - gastrointestinal tract and viscera
Mycobacterium avium Transmission:
– ingestion and inhalation
– M. avium is very persistent in the environment and resistant to many disinfecting agents
– Raptors may become infected consuming infected prey
Mycobacterium avium Diagnosis:
– presumptive diagnosis based upon history
– cytology - acid fast stain
– radiography
– biopsy
– endoscopy
– TB testing (0.1 ml avian tuberculin)
Mycobacterium avium
Treatment:– controversial due to zoonotic potential
– Combination therapy :
ethambutol, Isoniazid, Rifampin often rapid
Viral Diseases
Pox virus
Herpesvirus
Paramyxovirus
Pox virusDNA virus
Produce intracytoplasmic, lipophilic inclusion bodies (Bollinger bodies)
Pox Virus
Transmission
Arthropod vectors
Pox VirusClinical Forms
– Cutaneous form
– Diphtheritic form
– Septicemic/Atypical (Tumorous) form
– Neurologic Form
Pox VirusClinical Forms
– Cutaneous form: nodular proliferations of unfeathered skin around the eyes, beak, nares and legs• 4-9 day incubation period leading to small papules that
gradually enlarge
• Papules may develop into deep lesions of the dermis and underlying structures
• Pain and infection may lead to lethargy and depression
• May lead to septicemia
• Birds that survive may be left with permanent scars
Pox VirusClinical Forms
– Diphtheritic form: lesions on mucosa, tongue, pharynx, and larynx• Rarely seen in raptors
• Some suggest that it may not occur at all in raptors
• Caseous lesions in oropharynx
• Pseudomembranous deposits may slough and occlude airway
Pox VirusClinical Forms
– Septicemic/Atypical form: ruffled appearance, depression, cyanosis, anorexia, wart-like tumors of the skin
Pox VirusClinical Forms
– Neurologic form:• Group of falcons in Arab Gulf
• Inability to fly, vestibular disease
• May have been suffering from PMV-1
Pox VirusDiagnosis:– history – physical examination– clinical signs– Histopathology—characteristic Bollinger
Bodies– electron microscopy– virus isolation—from new, uninfected
papules/lesions– serum neutralization
Pox VirusTherapy:– usually non-specific treatment of secondary
bacterial or fungal infections
– preventative medicine (vaccination):
• pigeon pox
• fowl pox
• turkey pox
• falcon pox vaccine
Herpesvirus Herpesviridae family is divided into three
subfamilies: Herpesvirinae (hemorrhagic lesions)\
• Infectious Laryngotracheitis Herpesvirinae (necrotic lesions)
• Pacheco’s disease Herpesvirinae (lytic/neoplastic lesions)
• Marek’s disease
Herpesviruses Serologic relationship of avian herpesviruses:
– 12 Serotypes:• serotype 7 Columbid HV 1 (pigeon herpesvirus
encephalomyelitis)
• falconid HV 1 (falcon herpesvirus)
• strigid HV 1 (owl herpesvirus)
• eagle herpesvirus
Herpesvirus
Inclusion Body Hepatitis of Falcons (FHV-Falcon Herpesvirus)
Hepatosplenitis Infectosa Strigorum (OHV-Owl Herpesvirus)
Eagle Herpesvirus
Herpesvirus
Clinical Signs:– respiratory distress
– ocular lesions
– enteritis
– hepatic disease
– non-specific signs
Herpesvirus FHV—Peregrine falcon, Common kestrel,
Merlin, Red-necked falcon, Prairie falcon, American kestrel– affinity for reticuloendothelial cells and
hepatocytes– results in severe depression, weakness,
anorexia and mortality nearing 100%– focal/disseminated degeneration and necrosis
of the liver, pancreas, lung, kidney and brain
Herpesvirus OHV—Eagle owl, Great Horned owl, Striped owl,
Long-eared owl, Snowy owl, Little owl, Tengmalm’s owl and the Forest owl– affects epithelial and mesenchymal cells
– clinical signs and histologic lesions similar in many ways to FHV; Necrotic foci in the liver, spleen, intestines and jugular veins
Herpesvirus
Diagnosis:– clinical signs
– histopathologic lesions
– serologic identification
– virus isolation
– electron microscopy
Herpesvirus
Histopathological Lesions Hemorrhage in the respiratory and intestinal
epithelium multifocal necrosis of the liver, spleen and bone
marrow
Herpesvirus
Therapy– Supportive care– Acyclovir(Zorivax)
333 mg/kg PO q 12hrs x 7-14 days
Paramyxovirus in Birds of Prey(Newcastle Disease Virus - NDV)
Etiology: Paramyxovirus-1 Host susceptibility: All species
of birds are susceptible Distribution: Global Clinical Signs: Vary with
species, age, condition and virulence
PMV-1 in Raptors
Transmission:– ingestion or inhalation of
virus
– owls and vultures appear to be resistant, but may shed the virus in their feces
Paramyxovirus in Birds of Prey(Newcastle Disease Virus - NDV)
Lentogenic strains—mild or inapparent disease. Mesogenic strains—mild to severe disease Velogenic Neurotropic strains (VNND)—severe disease with
high mortality Velogenic viscerotropic strains (VVND)—severe disease and
mortality; however, hemorrhage within the intestinal tract differentiates this group from the others
Exotic Newcastle Disease is synonymous with VVND as well as VNND
California, Nevada, Arizona, Texas and New Mexico
PMV-1 in Raptors Neurologic Signs:
– torticollis, incoordination, tremors of head, convulsions Mortality is very high - affected birds may:
– remain asymptomatic– recover with supportive care– exhibit brief period of lethargy– exhibit 1 - 2 weeks of anorexia
and diarrhea followed by death– acute/peracute death
PMV-1 in Raptors Prior to 1972, cases of Newcastle Disease were most
likely the result of unregulated importation of psittacine birds.
After 1972 the importation of exotic birds into the US closely regulated thereby greatly reducing the incidence of NDV in the US
Illegally imported psittacines poultry, and migratory wild bird species play a role in the transmission of NDV
West Nile Virus Flavivirus (Family Flaviviridae)—first isolated
from woman in West Nile region of Uganda in 1937 Related to:
- St. Louis Encephalitis Virus (North/South America)
- Japanese Encephalitis Virus (East Asia)
First human case reported in New York City in August of 1999
New York strain virtually identical to Israeli strain Substantial die-off of birds in and around the Bronx Zoo
mid-August 1999 American Crows (Corvus brachyrhynchos)
West Nile Virus
Substantial die-off of birds in and around the Bronx Zoo mid-August 1999
American Crows (Corvus brachyrhynchos) and other corvids are particulary susceptible
138 species affected Vector—ornithophilic mosquito (Culex pipiens) Birds (pet, zoo, domestic or wild) may serve as
source of infection and may have been responsible for introduction of virus into the New World
West Nile Virus
Transmission
- Ornithophilic mosquitoes are priniciple vectors
- Culex univittatus in the Middle East
- C. pipiens in Europe and North America
- WNV has been isolated from avian species that maintain viremia sufficient to infect vector mosquitoes
- Pigeons
- House sparrow
West Nile Virus
Clinical Signs:- Primarily affects juvenile birds of susceptible species
where endemic; adult had high circulating antibodies- University of Minnesota Raptor Center - Phase 1: Depression, anorexia, weight loss, sleeping,
pinching off blood feathers, elevated white cell count.- Phase 2: In addition to the above, head tremors, green
urates, mental dullness/central blindness and general lack of awareness of surroundings, ataxia, weakness in legs.
- Phase 3: More severe tremors, seizures
West Nile Virus
Diagnosis:
- Antemortem- Clinical signs consistent with WNV
- Serology—Serum neutralization
- Postmortem- Necropsy—kidney and brain
West Nile Virus
Treatment and Prevention- No WNV specific treatment is available- Vaccination
- Equine WNV Vaccine—Fort Dodge- CDC killed vaccine- Raptor Center—production of killed vaccine- Recommendations for Equine Vaccine
- Birds > 300grams receive 1.0 ml IM- Birds < 300grams recive 0.3-0.5 ml IM- Third vaccine during periods of high mosquito
activity
West Nile Virus
Treatment and Prevention- Moving bird(s) indoors
- covering the facility with mosquito netting, and/or using a USDA-approved carbon dioxide mosquito trap
- Isolate infected birds in mosquito-proof areas away from other birds that may be at risk
- incinerate carcasses of dead birds
Fungal Diseases
Aspergillosis
Candidiasis
Aspergillosis Aspergillus fumigatus most common Ubiquitous in the environment Susceptibility related to stress and immune
function Local or systemic infection Clinical signs:
– open mouth breathing– depression– emaciation
Aspergillosis
Most frequently encountered non-traumatic disease in raptors– Goshawk (Accipiter gentilis)– Gyrfalcon (Falco rusticolus)– Red-tailed hawks (Buteo jamaicensis)– others
Aspergillosis
Acute form: exposure to high number of spores
Tracheal form: single or series of granulomatous lesions
Systemic form
Aspergillosis Clinical Signs:
– dyspnea– change/loss of voice– depression– anorexia– exaggerated respiratory effort– weight loss and emaciation
Aspergillosis Diagnosis:
– thorough history if dealing with birds used in falconry
– physical examination
– laboratory diagnostics (CBC and chemistry panel, cytology)
– radiography
– endoscopy
– serological testing
– fungal culture
AspergillosisItraconazole (10 mg/kg q 24 hrs)Amphotericin B– 1.5mg/kg IV q 8hrs x 3 days– 1.0 mg/kg IT q 8-12hrs– o.5 mg/ml sterile water-nasal flushClotrimazole– 0.2 ml (2mg)/kg IT q 24hrs x 5 days– 10 mg/ml-flush– nebulize 1% solution x 30-60 min.Fluconazole-5-15 mg/kg PO q 12hrs x 14-60 days
CandidiasisCandida sp.
Most commonly affects the GI tractClinical signs include:
–regurgitation/vomiting
–delayed crop emptying
–anorexia
–diarrhea
Candidiasis
Clinical Signs:– reluctance to swallow
– anorexia
– regurgitation/vomiting
– depression
Candidiasis
Cytology of lesions (oropharynx, esophagus, cloaca)
Cytology of feces Culture
Candidiasis
Therapy:– Nystatin (100,000 U/kg q 8 - 12 hrs)
– Fluconazole and Itraconazole for resistant strains of Candida sp. or with tissue invasion
5-15 mg/kg PO q 12 hrs x 24-60 days
– Itraconazole 10 mg/kg PO q 24 hrs
Parasitic and Protozoal Diseases
TrichomoniasisHelminths
HemoparasitesCoccidia
Trichomoniasis
History Clinical signs Cytology
Trichomoniasis
Therapy:– Metronidazole -
30 - 50 mg/kg q 12 hrs x 5 - 7 days– Carnidazole -
30 mg/kg PO q 12 hrs x 5 - 7 days20-30 mg/kg PO once20 mg/kg q 24h x 2 days
Coccidian Parasites
Significance as pathogens is yet to be determined with most species of coccidian parasites in raptors
Coccidian Parasites
Caryospora spp.
Cryptosporidium spp.
Eimeria spp.
Frenkelia spp.
Sarcocystis spp.
Toxoplasma gondii
Coccidian Parasites
Transmission:– ingestion of oocysts from prey species
– intermediate hosts: small rodents and birds (passeriformes)
– raptors serve as definitive hosts
Coccidian Parasites
Diagnosis:– most coccidia are not pathogenic
in raptors– clinical signs are usually vague– in captive birds of prey may
indicate the presence of another disease process which has compromised the immune system
Coccidian Parasites
Diagnosis:– diagnosis generally made by demonstration
of oocysts in samples from the intestinal tract
– “stress” may worsen clinical signs
Coccidian Parasites Clinical signs when present are usually the result of
an enteritis– Asymptomatic – Lethargy– Depression– Diarrhea (+ melena)– Poor body condition– Decreased reproductive success– Death
Coccidian Parasites
Therapy
– Sulfadimethoxine (Albon®)
25 - 55 mg/kg PO q 24h x 3 - 7 days
– Pyrimethamine(Fansidar)
0.5mg/kg PO q 12hrs x 14-28 days
(Toxoplasmosis, Atoxoplasmosis, Sarcocyctis sp.)
– Toltrazuril (Baycox)
7 mg/kg PO q 24hrs x 2-3 days
Common Helminths of North American Birds of Prey
Nematodes - are the most common parasites affecting captive and wild birds of prey
Capillaria spp. (thread worms) - oropharynx, esophagus, crop, small intestine and cecum
Common Helminths of North American Birds of Prey
Ascarids - large roundworms found in the small intestine, proventriculus, ventriculus and large intestine– Ascaridia spp.– Porrocaecum sp.– Contracaecum sp.
Helminths of Birds of Prey Spirurids (stomach worms) - found in the
lumen and submucosa of the proventriculus and ventriculus and eyes– Habronema sp.– Microtetrameres sp.– Tetrameres sp.– Thelazia sp.
Helminths of Birds of Prey
Syngamus trachea (gapeworms) and Cyathostoma sp.– may cause tracheobroncial
inflammation
– partial or complete obstruction in severe cases
Helminths of Birds of Prey Clinical Signs:
– dyspnea
– hemorrhage
– head shaking Younger and smaller raptors more
commonly affected
Helminths of Birds of PreyFilariid nematodes:
Serratospiculum amaculata
Prairie falcons (Falco mexicanus)
Peregrine falcon (Falco peregriunus)
Bald eagle (Haliaeetus leucocephalus)
Cooper’s hawk (Accipiter cooperii)
Serratospiculum amaculata
Helminths in Birds of Prey Trematodes (Flukes)
– Strigea falconis– Diplostomum spathaceum
Most require the snail and/or arthropods as intermediate host
Treatment:– Praziquantel (Droncit®) - 10 mg/kg
once; repeat in 7 days
Helminths in Birds of Prey Cestodes (Tapeworms)
– uncommon in birds of prey
– Clinical signs vary from asymptomatic to mild diarrhea and weakness
– generally located in the small intestine
– may see proglottids in feces or around vent
Helminths in Birds of Prey
Treatment of Cestodes (Tapeworms):– Praziquantel (Droncit®) 10 mg/kg once
Reinfection in captivity is unlikely
Treatment of Helminths in Birds of Prey
Nematodes:– Thiabendazole - 100 mg/kg PO; repeat in 10 - 14 days
– Levamisole - 20 mg/kg PO once or for 2 consecutive days; immunostimulant
– Ivermectin - 0.2 - 0.4 mg/kg IM, PO, SC; repeat in 2 weeks
– Fenbendazole - 10 - 50 mg/kg PO; repeat in 2 weeks; 25 mg/kg PO for 3 consecutive days; may be toxic to vultures
Treatment of Helminths in Birds of Prey
Trematodes:
– Praziquantel - 10 - 50 mg/kg PO once Cestodes:
– Praziquantel - 10 - 50 mg/kg PO once
External Parasites of Birds of Prey
Arthropods:– Ticks: Argas sp., Ixodes sp.
– Fowl mites: Ornithonyssus spp. (northern fowl mite), Dermanyssus spp. (red mite)
– Quill mites: Harpyrhynchus spp.
– Epidermoptid mites: Knemidocoptes spp.
External Parasites of Birds of Prey
Insects:– Feather lice: Mallophaga spp.
– Louse flies: Hippoboscidae sp. (louse flies)
– Feather flies: Carnus spp.
– Blow flies: Calliphoridae
External Parasites of Birds of Prey
Therapy:– most respond to Pyrethrin-based topicals or
manual removal
Hemoparasites
Plasmodium sp. Hemoproteus sp. Leukocytozoon sp. All are transmitted by arthropod vectors
Plasmodium sp.
Causes avian malaria Transmitted by mosquitoes P. circumflexum - sharp-
shinned hawks P. relictum - large falcons
(especially Gyrfalcons) Clinical Signs:
– dyspnea, weakness, vomiting, depression and convulsions
Plasmodium sp.
Diagnosis:– demonstration of parasites on stained
blood smears
– intraerythrocytic gametocytes, trophozoites or schizonts
– often displace the nucleus
– appear pigmented
– occupy less than 25% of cytoplasm
Hemoproteus sp. Normally considered nonpathogenic May cause problems if bird is
immunosuppressed Clinical Signs:
– anemia, splenomegaly, hepatomegaly and pulmonary edema
Transmission:
– Culicoides sp.
Hemoproteus sp. Diagnosis:
– presence of gametocytes in erythrocytes which partially encircle the nucleus; appear pigmented and occupy more than 50% of cytoplasm
Treatment:– Primaquine - 0.75 - 1.0 mg/kg PO once and– Chloroquine - .15 mg/kg PO at 12h intervals x 3
doses
Leukocytozoon sp.Leukocytozoon sp. Generally low pathogenicity except in young
raptors Clinical Signs:
– anemia, dyspnea, death Transmission:
– black flies, Culicoides sp., seasonal incidence
Leukocytozoon sp. Diagnosis:
– elongated gametocytes in leukocytes or erythrocytes that grossly deform the host cell
Treatment:– sulfonamides-Albon: 25-50 mg/kg PO q 24hrs x
3 days– pyremethamine-0.5 mg/kg PO q 12 hrs x 14-28
days; may use with Trimethoprim/sulfadiazine 30 mg/kg PO q 12 hrs
Hemoparasites
Therapy - Plasmodium sp.:- Supportive care—fluid therapy
- Blood transfusion if PCV < 18 %
- Benedryl or steroids if transfusion is needed
– Mefloquine HCl (Larium) -
30 mg at 0, 12, 24, 48 and 72 hrs, then weekly for 6 months
Hemoparasites Cloroquine/Primaquine regimen:
- Chloroquine: 20 mg/kg (PO, IV) initially; IV in acute cases
- Chloroquine: 10 mg/kg (PO) at 6, 18 and 24 hrs
- Primaquine: 1 mg/kg (PO) q 24hrs for 2 days
- repeat weekly for 3-5 weeks to prevent relapse
Preventative regimen:
Chloroquine:10 mg/kg (PO) weekly
Primaquine: 1 mg/kg (PO) weekly
Birds of PreyBirds of PreyMedicine and ManagementMedicine and Management
Birds of PreyBirds of PreyMedicine and ManagementMedicine and Management
First and foremost are the Raptors.Everything else is JUST prey