Birds of Prey Medicine and Mgmt

Birds of PreyBirds of PreyMedicine and ManagementMedicine and Management


Michael P. Jones, DVMDiplomate, ABVP (Avian Specialty)



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


Type 2:Similar to Type 1: localized lesions of the digital or metatarsal pads


Type 3: Discrete lesion(s) with hyperkeratinization, localized swelling and redness


Type 4: Enlargement of the distal digital pads; the result of flexor tendon ruptures


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


– 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


– 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


– Septicemic/Atypical form: ruffled appearance, depression, cyanosis, anorexia, wart-like tumors of the skin


– 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

http://www.cdc.gov/ncidod/dvbid/westnile/flaviviruses_1.htm

http://www.cdc.gov/ncidod/dvbid/westnile/flaviviruses_1.htm

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.


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 - 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



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

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Birds of Prey Medicine and Mgmt