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Birds of Prey
Medicine and Management
First and foremost are the Raptors. Everything else is JUST prey
Care should be taken to minimize the amount of stress and discomfort the patient feels while allowing essential procedures to be completed
Equipment
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
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.)
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
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 history Physical examination Diagnostic/therapeutic procedures Hospitalization Dietary 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
- 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
Dietary Considerations
Michael McDermott
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 SharpShinned and Cooper's hawks) small birds
Dietary Considersations
Other sources of nutrition include venison, beef, day-old chicks and others. Supplementation with vitamin supplements are also beneficial
Birds of Prey
Selected Infectious Diseases
Bumblefoot
Destructive process which may involve skin, underlying soft tissues or bone:
Bumblefoot Classification
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 tissues Establish drainage if abscesses are present Elimination of pathogens
Bumblefoot Therapy
Protecting wound from further infections Promotion 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 virus
DNA virus
Produce intracytoplasmic, lipophilic inclusion bodies (Bollinger bodies)
Pox Virus
Transmission Arthropod vectors
Pox Virus
Clinical Forms
Cutaneous form Diphtheritic form Septicemic/Atypical (Tumorous) form Neurologic Form
Pox Virus
Clinical 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 Virus
Clinical 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 Virus
Clinical Forms
Septicemic/Atypical form: ruffled appearance, depression, cyanosis, anorexia, wart-like tumors of the skin
Pox Virus
Clinical Forms
Neurologic form:
Group of falcons in Arab Gulf Inability to fly, vestibular disease May have been suffering from PMV-1
Pox Virus
Diagnosis:
history physical examination clinical signs Histopathologycharacteristic Bollinger Bodies electron microscopy virus isolationfrom new, uninfected papules/lesions serum neutralization
Pox Virus
Therapy:
usually non-specific treatment of secondary bacterial or fungal infections preventative medicine (vaccination): pigeon pox fowl pox turkey pox falcon pox vaccine
Herpesvirus
Herpesviruses
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
FHVPeregrine 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
OHVEagle owl, Great Horned owl, Striped owl, Long-eared owl, Snowy owl, Little owl, Tengmalms 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
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
Lentogenic strainsmild or inapparent disease. Mesogenic strainsmild 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
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
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)
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 Vectorornithophilic 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
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
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
Diagnosis: - Antemortem
- Clinical signs consistent with WNV - SerologySerum neutralization
- Postmortem
- Necropsykidney and brain
Treatment and Prevention - No WNV specific treatment is available - Vaccination - Equine WNV VaccineFort Dodge - CDC killed vaccine - Raptor Centerproduction 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
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
Aspergillosis
Itraconazole (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 flush Clotrimazole 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
Candidiasis
Candida sp.
commonly affects the GI tract Clinical signs include:
regurgitation/vomiting delayed crop emptying anorexia diarrhea
Most
Candidiasis
Clinical Signs:
reluctance to swallow anorexia regurgitation/vomiting depression
Candidiasis
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
Trichomoniasis
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 days 20-30 mg/kg PO once 20 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
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
Nematodes - are the most common parasites affecting captive and wild birds of prey Capillaria spp. (thread worms) - oropharynx, esophagus, crop, small intestine and cecum
Ascarids - large roundworms found in the small intestine, proventriculus, ventriculus and large intestine
Ascaridia spp. Porrocaecum sp. Contracaecum sp.
Spirurids (stomach worms) - found in the lumen and submucosa of the proventriculus and ventriculus and eyes
Habronema sp. Microtetrameres sp. Tetrameres sp. Thelazia sp.
Clinical Signs:
dyspnea hemorrhage head shaking
Serratospiculum amaculata
Trematodes (Flukes)
Strigea falconis Diplostomum spathaceum
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
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
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.
Insects:
Feather lice: Mallophaga spp. Louse flies: Hippoboscidae sp. (louse flies) Feather flies: Carnus spp. Blow flies: Calliphoridae
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 - sharpshinned 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
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 Prey
Medicine and Management
First and foremost are the Raptors. Everything else is JUST prey