Birds of Prey

Medicine and Management

Michael P. Jones, DVM Diplomate, ABVP (Avian Specialty)

Birds of Prey
Medicine 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
 

Neutralize weapons; mainly beak and talons Equipment: Goal:

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 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

Physical Examination Systematic

 

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


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:

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 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


Herpesviridae family is divided into three subfamilies:

E Herpesvirinae (hemorrhagic lesions)\
Infectious Laryngotracheitis

F Herpesvirinae (necrotic lesions)

Pachecos disease

K Herpesvirinae (lytic/neoplastic lesions)

Mareks 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


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

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 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

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 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

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 - SerologySerum neutralization

- Postmortem
- Necropsykidney and brain

West Nile Virus



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

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

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


 

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

Trichomoniasis Helminths Hemoparasites Coccidia

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 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


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 Prey

Filariid nematodes:
Serratospiculum amaculata
Prairie falcons (Falco mexicanus) Peregrine falcon (Falco peregriunus) Bald eagle (Haliaeetus leucocephalus) Coopers 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 - 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


Therapy - Plasmodium sp.:

- Supportive carefluid 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 Prey
Medicine and Management

First and foremost are the Raptors. Everything else is JUST prey