Sonia M. Hernandez-Divers, DVM, PhD, DACZM
Warnell School of Forestry and Natural Resources & the Southeastern Cooperative Wildlife Disease Study at the College of Veterinary Medicine, University of Georgia, Athens, GA
Probably because of their size and likelihood of being found injured, raptors continue to be one of the most commonly received groups of birds in wildlife rehabilitation facilities. Although they are susceptible to most of the same diseases as other birds, raptors possess some unique anatomical and life history traits that translate to clinical syndromes unique to this group. In addition, their size and visibility, their long-term associated with humans (i.e.: through falconry), their position in the trophic chain, and their role as indicators of their environment, make birds of prey important wildlife patients.
The word raptor is derived from the Latin rapere (to grip or grasp).
Birds of prey all have: hooked beaks, talons, are either predators or scavengers. Raptors belong to 2 major groups: the owls and the diurnal birds of prey. The Order Strigiformes (owls) has two families: Fa. Tytonidae (barn and grass owls) and Fa. Strigidae (all other owls). The Order Falconiformes (diurnal raptors) contains: Fa. Cathartidae (New World vultures), Fa. Pandionidae (osprey), Fa. Accipitridae (kites, hawks, Old World vultures), Fa. Sagittaridae (secretary bird), and Fa. Falconidae (falcons and caracaras).
Anatomy and Physiology
Gastrointestinal system: Vultures have well developed crops, whereas red tailed hawks have poorly developed crops and owls do not have crops. Their stomach is simple and muscular. The ceca are vestigial in falcons and hawks, but present in vultures and great horned owls. Owls perform egestion (casting) or the formation of pellets. This is a combination of activity of the stomach and esophageal peristalsis. Pellets are formed of bones, feathers and fur from digested prey. Owl pellets usually contain bones, whereas hawk pellets do not. Owls produce one pellet per meal but hawks eat more than one meal before producing a cast, and cast production is more associated with circadian rhythm.
Respiratory system: Raptors are fine-tuned athletes. They have extremely efficient respiratory systems for hunting during flight. Successful rehabilitation efforts depend on returning raptors to their full athletic ability.
Cardiovascular system: As with other animals, the heart rates increase with metabolic rates, such that smaller raptors have higher heart rates. Several publications illustrate normal ECG's and echocardiography of the raptor.
Skeletal system: Their feet are covered in thick scales to protect them from injury (i.e.: bites from squirrels). They have extremely strong toes, ending in triangular talons. The first digit is opposable toe for grasping prey. The digital flexor tendons and their sheath have unidirectional, interlocking ratcheting mechanisms that resist digital extension when the toes are flexed to enhance prey prehension.
Raptors require flight cages that allow for proper flight mechanics to occur in the process of rehabilitation. Supplemental heat is important for southern and migratory species and those that are debilitated or have high metabolic rates. At the very least, protection from wind and inclement weather is needed. Hospital cages are ok for short-term care, but must have visual barriers and be padded heavily, as well as contain appropriate sized perches that allow the foot to be held in an anatomical position and the tail to remain off the floor surface. Access to UV light is paramount for synthesis of Vit D3 if maintained in captivity long-term.
Diet/H20 requirements: Raptors are carnivorous birds, and nutritional requires vary with species. Captive diets should mimic free-ranging diets; however, most can be maintained on readily available rodents at least for short term periods of time. It is important to feed whole prey. Pre-prepared diets are commonly used in zoos. Small raptors eat 30% of their body wt daily, whereas larger raptors should be fed 8-10% of body wt daily. Diets composed of heart, muscle, liver or kidney are deficient in calcium and can lead to nutritional secondary hyperparathyroidism. High fat diets are also low in calcium and may prevent absorption of Vit D3. Raptors normally receive their water requirements from ingested prey; nonetheless, fresh water should be offered, both for drinking and bathing. Their estimated daily requirement is 50 ml/kg/24 hrs.
The female raptor is usually much bigger in size. The larger species become sexually mature later in life than smaller sp. Most raptors exhibit strong imprinting, thus care should be taken when orphans are reared.
Handling and Restraint
Safety of the handler is of utmost importance. Depending on the expertise of the handler, the size and type of bird being restrained, specialized equipment may be needed (i.e.: nets, leather gloves, hoods, Velcro strips, face shields, etc). The danger in handling most raptors is restraining the feet/legs and preventing the bird from "taloning" the handler. Additionally, some raptors are more prone to biting than others (i.e.: eagles, owls). The goal is to gain control of the legs and head as quickly as possible. Approach the bird with a towel or net quietly. Cover head, locate legs, restraint legs while pushing the body of the animal towards the ground and immobilizing wings with towel. After wrapping the bird's wings in the towel, lift the bird with head covered facing away from handler.
Premedication is useful and recommended for longer procedures. It can provide pre-op analgesia, keeps stress down during induction, may decrease the amount of isoflurane needed to induce/maintain bird. Combinations of midazolam/butorphanol, midazolam alone are most commonly used. (ADD)
Isoflurane or sevoflurane: are the safest volatile anesthetics that can be used in birds. Induction is relatively rapid and easy, and the recovery is short. Bird should be intubated during procedures to combat hypoventilation.
Common Medical Problems
Electrocution: Raptors are often found with severe soft tissue burns from electrocution. Several states have programs to avoid raptors from nesting on power line towers.
Vehicular trauma: This is the most common clinical presentation; however, consider that most raptors that are hit by cars may have been previously debilitated by some other disease process which requires further diagnostic investigation and treatment. Fractures are common and can be treated following fracture repair techniques applicable to other avian species.
Head trauma: Is a common presentation of raptors that have been struck by vehicles. Neurologic signs of varying degrees are common in these cases.
Ophthalmologic problems: The eyes of raptors are large and sensitive. The ciliary bodies contain striated muscle. The eyes are tightly encased, with anterior scleral ossicles which makeup a complete bony ring within the sclera. Lesions in both anterior and posterior chambers are common. Anterior segment luxations are more easily diagnosed. Posterior segment injuries are due to countercoup forces, thus fundic examination is very important. Ophthalmologic conditions in birds of prey are considered emergencies that need to be dealt with immediately.
Gunshot: Unfortunately many raptors are still shot either to prevent predation of farm animals or accidentally. All raptor species are legally protected under the Migratory Bird Act of 1918, The Bald Eagle Protection Act of 1940 and the Endangered Species Act of 1973.
Malnutrition/vitamin deficiencies: Raptors need UV light for synthesis of Vit D3. Vit A deficiency is also common in birds fed all meat diets. Raptors need to ingest pre-formed Vit A from the livers of prey. Vit A deficiency causes a hyperkeratosis of epithelial surfaces and metaplasia of other tissues like oral, pharyngeal and esophageal mucosa. Vit A deficiency can be a contributing factor in the formation of pododermatitis. Vitamin B deficiency is also reported in raptors that feed primarily on fish and are maintained on frozen fish. Clinical signs: opisthotonos, leg and wing paresis, paralysis. Thiamine (1-3 mg/kg/week) needs to be administered to raptors maintained on a diet of frozen fish.
Starvation/emaciation: This is common in traumatized raptors, orphans, geriatric animals or birds with underlying disease.
Re-feeding syndrome: This is a condition reported in starved mammals given excess calories which can result in a life-threatening hypophosphatemia, as well as inability to digest food. The emaciated raptor should be first rehydrated, then fed a low-calorie meal, then offered meat juice followed by "clean meat", followed by whole prey items.
Gout: This is a metabolic disorder characterized by deposition of uric acid in body tissues due to renal insufficiency. There are two presentations: uric acid deposition in joints (synovial), and internal organs (visceral). Synovial gout is easier to diagnose, as joints become swollen. Visceral gout involves white/tan granules on visceral surface of organs, chalky streaks beneath peritoneum, or plaques of urates on pericardium and/or mineralization of large vessels. Gout is caused by an initial event of hyperuricemia, which leads to a renal insult, which leads to increased amounts of uric acid and metabolic dysfunction.
Botulism results from intoxication due to ingestion of food containing Clostridium botulinum (large, G+, anerobic bacillus) toxins. Types A, C and E reported in raptors. Turkey vultures are 100,000 times resistant to type C toxin when compared to pigeons. Clinical signs: flaccid paralysis beginning with feet and legs, extending to wings and neck. Signs are due to effect of the toxin on the peripheral nerves at the motor end plate-interfering with release of acetylcholine. Disease in raptors follows outbreaks in waterfowl. Avian botulism is highly seasonal (late summer) and outbreaks occur in certain wetlands predictably on an annual basis.
Lead: Continues to be common in birds of prey. It is most commonly acquired by ingesting prey that have been shot with lead or have ingested lead (waterfowl). Lead toxicity causes pan-systemic effects to the gastrointestinal, CNS, renal, immunologic and hematopoietic systems. Clinical signs: lethargy, diarrhea, anorexia, vomiting, wing droop, poor mentation, muscle weakness, seizures, paresis, paralysis, emaciation, anemia, seizures and blindness.
Diagnosis: radiographs and blood lead levels. Toxicity is considered when blood lead levels are above 0.4 ppm (40 µg/dl). Treatment: supportive care, chelation therapy (CaEDTA 30-50 to 100 mg/kg BID). Treatment may also require removing remaining lead particles from the gastrointestinal tract.
Organophosphates and carbamates are ingested by eating prey (either insects, small vertebrates or livestock) that has been contaminated. Both types of drugs inactivate acetylcholinesterase, causing acetylcholine builds up and continued stimulation of motor end plates. Death is due to respiratory failure. Typical clinical signs: ataxia, inability to stand, opisthotonos, rigid paralysis, rapid respiration, muscle twitching, miosis/mydriasis, bradycardia. Diagnosis is based on serum cholinesterase levels, or brain levels. Treatment: supportive care, atropine (0.5 mg/kg), 2-pam (contraindicated in carbamate toxicity), and encouraging the emptying of the gastrointestinal tract.
Aspergillosis: This is a common disease of captive raptors. The development of aspergillosis is either related to a high load of the Aspergillus fungus, or to immune compromise of the host. Two presentations are typical: acute or chronic. Acute requires high number of Aspergillosis spores. Clinical signs: Acute-anorexia, PU/PD, dyspnea, death within 1 week due to miliary granulomas in lungs. Chronic-fungal colonization sites at the caudal thoracic and abdominal air sacs. Four types have been described: acute, tracheal, localized granuloma in air sacs/lungs, and systemic. Diagnosis and treatment depends highly on the presentation and type. Clinical signs can be quite subtle (change in behavior/voice, weight loss, and various degrees of exercise intolerance) and may then progress to respiratory signs, cachexia, dyspnea, vomiting. Diagnosis: radiography, upper airway endoscopy, celioscopy, ELISA (detecting antibodies), coupled with leukocytosis, Heterophilia, and monocytosis in chronic form. Treatment: supportive care, surgery to remove airway granulomas, intralesional antifungals, systemic antifungals +/- nebulization. Prevention might be more important in captive animals during the rehabilitation process and include maintaining a dust-free, hay free environment, minimizing stress, prophylactic treatment for high risk species and situations (careful judgment should be used to determine candidates for prophylaxis treatment) and serologically monitor.
Also called "bumblefoot", this condition is literally, inflammation of feet. This disease is multifactorial, with many contributing factors that lead to loss of integrity of integument of the feet and excoriation, ulceration, cellulitis, and abscessation, as well as bacterial infection, most often Staphylococcus aureus, but also E. coli and others. Common predisposing factors are puncture wounds from prey, talons, burns, trap injuries, inappropriately shaped perches, vitamin deficiencies, obesity, lack of exercise, excessive weight on one leg, or bruising from hopping from perch to perch. Clinical signs: swelling and inflammation to plantar surface of the foot.
Candidiasis: This condition is caused by Candida albicans. Causes white plaques on oral mucosa. Candidiasis must be differentiated from trichomoniasis, or primary Vit A deficiency. Candida is usually an opportunistic pathogen, indicative of immune system dysfunction. Clinical signs: anorexia, regurgitation or flinging food, diarrhea (if lower gastrointestinal tract is involved), milky mucus covering mucosal surface of the mouth and oropharynx. Diagnosis: cytology and culture. Treatment: nystatin topically (100,000-200,000 IU/kg BID for 7-10 days) or systemic antifungals such as fluconazole.
Trichomoniasis: This condition is caused by Trichomonas gallinae. Clinical signs: white plaques on oral mucosa, esophagus, crop, or proventriculus, anorexia, regurgitation. In some cases, lesions are not visible. Diagnosis: oral swab and examining a wet mount under the microscope. Prevention: do not feed fresh pigeons to raptors. Freezing does kill trichomonads.
Parasites have traditionally been considered part of the "normal flora" of wildlife patients. However, most recently, a variety of elegant wildlife disease ecology experiments have indicated that parasites can have a profound effect on both the individual and at the population level of a species. Infection with parasites presents a "trade-off" for any animal in which calories needed for injury repair are being utilized by the parasite. Any bird that presents for medical treatment due to injury or disease should be evaluated for parasitism. Adverse effects from parasitism may not be readily apparent, and are typically burden-dependent. Unless treatment for parasites is considered detrimental (i.e.: in cases of drugs for which the liver is needed to metabolize and concurrent septicemia), antiparasitic treatment should be considered.
Trematodes (flukes) are typically considered innocuous in low numbers.
Cestodes (tapeworms) are typically considered innocuous in low numbers.
Nematodes-(ascarids) have been reported to cause illness and death.
Capillaria (Capillaria contorta or C. tenuis-simus) can cause major mortality in free-ranging and captive raptors. Clinical signs: anorexia, bloody diarrhea, vomiting, weight loss. Treatment: Fenbendazole (20-25 mg/kg SID, for 5 days, repeat in 10 days), ivermectin (0.2 mg/kg).
Coccidia (Caryospora sp.) can cause intestinal clinical signs.
Hemo-parasites: Hemoproteus, Leucocytozoon, Plasmodium and Babesia reported frequently. Usually hemoparasites do not cause overt disease unless the animal is under a period of stress, in birds that are moved to geographic locations outside their range (i.e.: Plasmodium); however, they can cause severe anemia, exercise intolerance and death.
Arthropods: myasis, Hippoboscid flies, Mallophaga louse.
Avian pox: Pox is caused by a DNA virus. This disease is seasonal (associated with mosquito activity) and considered endemic. It is frequently reported, but rarely fatal. The virus causes wart-like lesions on face, feet, oral cavity (nodular proliferation of epithelium). Recovery can be spontaneous or may require surgical treatment of nodular masses if they are interfering with vision or feeding.
Newcastle Disease: This disease is caused by paramyxovirus-1. Depending on strain, clinical signs can vary from gastrointestinal, respiratory, or CNS, the latter of which is most common in raptors, such as: opisthotonos, head tremors, torticollis, seizures. Differential diagnoses should include: Vit B deficiencies, toxicities, botulism, listeriosis, or hypoglycemia. Diagnosis: hemagglutination inhibition, serum neutralization assay, ELISA.
Raptor Herpesvirus is also termed hepatosplenitis. "Falcon herpesvirus" affects prairie, peregrine, redheaded and gyrfalcons. Owl herpesvirus affects GHO, eagle, long-eared and snowy owls. These viruses cause acute and fatal diseases. Pigeons and passerines may be reservoir. Incubation is 6-12 days. Clinical signs not usually observed because acute death is most common. Leukocytopenia is evident. Pale tan puncta on oral mucosa can be found. Lesions include widespread necrosis of the liver and hematopoietic tissues (spleen, bone marrow, lymphoid cells in GI tract, thymic remnants, bursa, lung and kidney).
Marek's Disease is a highly contagious, lymphoproliferative disease caused by herpesvirus reported in American kestrels and great horned owls. It is a disease of young, growing birds. Pathogenesis: neoplastic proliferation of heterogenous population of cells of lymphocyte series which infiltrate the peripheral/autonomic nerves and also viscera, iris, muscle, brain and skin. This virus causes nodular to diffuse lymphoid proliferation in liver, spleen, kidneys, pancreas and mesentery and a 2-3 diameter increase in peripheral nerves. Clinical signs: progressive peripheral nerve dysfunction.
Rabies has been reported in raptors. Titers have reported in many raptors. A great horned owl was fed a skunk which tested positive for rabies shed the virus in its pharyngeal secretions for 97 days until euthanized!
Tuberculosis is caused by Mycobacterium avium. Clinical signs vary depending on which organs are affected. This disease is chronic and insidious with weight loss, muscle atrophy, malaise, diarrhea, lameness, pathologic fractures and lesions (yellow/tan granulomas) most commonly in liver, spleen, intestines, lung, air sacs, bone marrow, heart, gonad, skin and joints. It is likely acquired through ingestion of infected prey.
Salmonellosis: Caused by S. typhimurium, a G-, aerobic rod. Treatment with tetracyclines and other G- spectrum antibiotics.
Avian cholera is caused by Pasteurella multocida, a G-, aerobic rod. It causes acute septicemia or chronic disease (watery diarrhea, weight loss). Infections are associated with ingestion of affected waterfowl. Lesions include petechial hemorrhages of lungs, air sacs, kidney, heart, liver, splenomegaly and necrotic foci of heart, liver and spleen. Treatment can be accomplished with appropriate antibiotics.
Other bacterial diseases include Listeriosis, Erysipelas, Yersiniosis, infections with E. Coli
Avian Vacuolar Myelinopathy was first observed in 1994-5 in bald eagles. It is a neurologic disease affecting primarily bald eagles and American coots in the SE USA. It is characterized by spongy degeneration of the white matter of the CNS, particularly around the optic tectum. Clinical signs: inability to fly, difficulty swimming/walking and other neurological signs; some birds recover. This disease is seasonal (late fall-early winter), is quick in onset (5 days post-exposure), and associated with specific geographic locations. Additional hosts: mallards, ring-necked duck, bufflehead, Canada goose, great horned owl, and killdeer. Etiology: it is suspected to be a natural toxin, produced by cyanobacteria associated with aquatic plants. Diagnosis: at this time no pre-mortem test is available; diagnosis is made by history of the location of the waterways associated with AVM, clinical signs and histopathology. At least regionally, AVM has impacted bald eagle populations significantly, particularly in areas where eagles are breeding near waterways associated with AVM, such as South Carolina. It is suspected, but not investigated, that coots are also on the decline due to AVM. Currently the only effort to manage AVM is to manage waterways to discourage the aquatic plants thought to be associated with this disease.