Diseases and medicine of birds of prey (Proceedings)
Historically, birds of prey have fascinated man, and are commonly held in captivity for conservation education, falconry, captive breeding, or rehabilitation purposes.
Historically, birds of prey have fascinated man, and are commonly held in captivity for conservation education, falconry, captive breeding, or rehabilitation purposes. Although the classification of birds of prey is somewhat controversial, in general these birds are divided into two major orders: Strigiformes (owls) and Falconiformes (hawks, eagles, kites, falcons, caracaras, condors, and vultures).
Metabolic Bone Disease
Raptors, like many other animals, require vitamin D3 for the normal absorption and utilization of calcium. Metabolic bone disease can result from the deficiency of vitamin D, an absolute calcium deficiency, or an inappropriate calcium:phosphorus ratio. The consequence of any of these dietary problems is nutritional secondary hyperparathyroidism.
There are several effects of prolonged hypocalcemia or calcium deficiency. The excessive production of PTH works to maintain serum calcium levels at the expense of the bone matrix. The skeletal effects are due to the improper mineralization of osteoid, which can lead to skeletal fragility, pathologic fractures, bone deformities, and fibrous osteodystrophy. Insufficient parathyroid response or prolonged hypoparathyroidism can result in serious declines of serum calcium levels leading to hypocalcemic tetany. Treatment of hypocalcemic tetany requires parenteral administration of calcium gluconate. Diazepam may be used if needed, although most birds generally respond to parenteral calcium gluconate. These birds should not be given corticosteroids as these drugs adversely affect calcium absorption and renal excretion. The bird should be placed in a quiet dark area during recovery. Correction of the underlying dietary deficiencies is paramount (i.e., whole carcasses of a variety of adult prey items closely resembling the birds natural diet should be fed).
Mycobacterium avium or avian tuberculosis is a relatively important bacterial disease of raptors. Clinical signs associated with avian mycobacteriosis are highly variable and depend on the organ systems affected. M. avium can affect almost any system but is most commonly seen in the gastrointestinal tract, liver, and spleen in raptor species. The disease is usually chronic, resulting in a very thin, depressed bird. Although clinical signs can be variable, other consistent clinical signs in raptors infected with M. avian include wasting despite an excellent appetite, recurrent diarrhea, polyuria, anemia, and dull plumage. Lesions may also appear within bone marrow, joints, or muscle (particularly the muscles of the legs) resulting in shifting lameness, decreased use of a limb, and arthritis of affected joints. The organism is ingested by the host, causing lesions in the intestinal wall. These lesions then disseminate organisms to other organs, resulting in tubercles or granulomas. The intestinal tubercles may continuously shed organisms into the feces. Visceral tubercles, especially on the liver, are a primary finding at necropsy. Definitive diagnosis of M. avium infection can be difficult antemortem, although a markedly elevated WBC count, elevated liver enzymes, and radiographic evidence of masses or enlarged organs in a thin and depressed bird is suggestive. Presumptive diagnosis of avian tuberculosis can also be based on cytological evaluation of tissues/feces, with acid-fast stain. However, the presence of acid-fast organisms in the feces is not necessarily diagnostic of a mycobacterial infection. Liver biopsy (i.e., via endoscopic examination) of suspected birds may reveal early changes associated with M. avium. Diagnosis is confirmed by culturing of feces or affected organs, a procedure that requires a special medium and takes 4-6 weeks to grow. The presence of acid-fast rods in tissues or feces is highly suggestive of avian tuberculosis.
Treatment of raptors with human antituberculosis drugs is rarely successful and is seldom recommended. Birds with mycobacteriosis are generally euthanized because of the zoonotic potential in immunosuppressed people and to reduce or eliminate exposure to M. avium in the environment. In cases where treatment is attempted, a combination of drugs including isoniazid (30 mg/kg PO q24h), ethambutol (30 mg/kg PO q24h), rifampin (45 mg/kg PO q24h) may be used long term. Although the progression of the disease may be stopped, the infection usually remains and may be reactivated at any time.
Pododermatitis or bumblefoot, a general term describing any inflammatory or degenerative condition of the foot, is perhaps the most discussed disease of raptors. This disease is primarily a problem of captive raptors but may occasionally be seen in wild raptors. Predisposing factors include improper size and shape of perches, poor sanitation, trauma, puncture wounds from prey or self-inflicted by talons, and nutritional deficiencies (i.e., hypovitaminosis A). A commonly used grading schedule includes 5 types of lesions, with Type 1 representing very early signs and Type 5 being the most serious stage (i.e., osteomyelitis). Regardless of the classification scheme, early changes associated with bumblefoot include loss or thinning of the plantar epithelium with a smooth or shiny appearance to the epithelium but without disruption of the epithelial barrier. These changes carry a good prognosis if changes in the predisposing factors are made. As the disease progresses the infections or inflammatory lesions begin involving the subdermal tissues including connective tissues, tendons, and bone. The presence of osteomyelitis carries a poor prognosis. Gross changes include severely swollen areas, especially on the metatarsal pad. Staphylococcus aureus is the most common pathogen in bumblefoot, with some studies having isolated S. aureus from over 90% of the cases. E. coli and Proteus are also commonly isolated. An inappropriate or insufficient immune response to the bacteria is thought to play a role in the pathogenesis of bumblefoot.
Treatment depends on the severity of the lesions, but all include management changes such as individually designed perches or shelves wrapped in hemp rope or astroturf. Mild lesions may be managed medically. Medical management includes systemic antibiotics, topical treatment (i.e., piperacillin-dexamethasone-DMSO mixture) or hemorrhoidal ointment and the application of some type of bandages to the foot. Improving the diet and supplemental vitamin A may be indicated. Surgical management is recommended for moderate to advanced cases of bumblefoot. Surgery consists of debridement of all necrotic and granulomatous tissue using curettage, sharp or blunt dissection, radiosurgery, and electrocautery.
There are at least 32 species of pox viruses that cause disease in a wide variety of avian species. Avian poxviruses are large DNA viruses that include intracytoplasmic, lipophilic inclusion bodies (Bollinger bodies) that infect epithelial cells of the integument, respiratory tract, and oral cavity, resulting in hypoplasia of the affected cells. Transmission of avian pox requires viral contamination of broken skin. Mosquitoes and other blood sucking arthropods may play a major role as vectors in the transmissions of avian pox. Clinically, poxvirus infections appear in several forms: (1) a cutaneous form, (2) a diphtheritic form characterized by lesions on the mucosa, tongue, pharynx, and larynx, and (3) a septicemic form characterized by a ruffled appearance, depression, cyanosis, and anorexia, and wart-like tumors of the skin. The cutaneous form or dry pox is the most common form of disease in raptors and has been reported in a variety of diurnal raptors. There have been no reports of avian pox in owls, even after inoculation with infective material. Clinical lesions appear as papules or discrete nodular proliferations of non-feathered areas on the feet, beak, nares, and cere. These develop into vesicles that rupture and form crusts. Lesions may be on feathered areas and be overlooked. In some cases, vesicles may form at the mucocutaneous junctions of the face. In many cases, lesions may be self-limiting and resolve by sloughing, leaving only a small discolored scar at the site. These birds are generally immune to further infection. A presumptive diagnosis of poxvirus infection is often made through history, physical examination, and clinical signs; diagnosis is confirmed by cytological/histological examination (including electron microscopy), which will show large, eosinophilic, intracytoplasmic inclusion bodies (Bollinger's bodies).
Treatment is usually nonspecific and depends on the severity of the lesion and the situation in which the bird is kept. Surgical excision (including laser surgery) or curetting the lesion followed by cauterizing the area has been used. Also, a variety of topical ointments, antibiotics (for secondary infections), and vitamin A have been administered. The efficacy of treatment may be difficult to ascertain as spontaneous recovery often occurs. Vaccination is the best method of controlling poxvirus infections in gallinaceous birds; however, further evaluation of vaccine efficacy in raptors is needed.
West Nile Virus
West Nile virus (WNV) infection is caused by a Flavivirus and was first isolated from a woman in the West Nile region of Uganda in 1937. The first human case reported in North America occurred in New York City in August of 1999. Although many species of birds can be infected and affected with WNV, the American crow and other corvids are the most commonly reported avian species to suffer high morbidity and mortality. Presently, approximately over 138 species of birds have been affected with WNV. Transmission of WNV occurs primarily through ornithophilic mosquitoes (Culex sp.) as the principle vectors.
Clinical signs of WNV infection include, but are not limited to depression, anorexia, weight loss, head tremors, seizures, blindness, ataxia, and sudden death. Juvenile avian species are most commonly affected in endemic areas. Adult species often have high circulating antibody levels in endemic areas.
Antemortem diagnosis of WNV infection can be difficult. A presumptive diagnosis may be made if clinical signs are consistent with WNV infection; however, many diseases may cause similar clinical signs. Serologic evidence via serum neutralization may indicate an antibody response to infection. Paired samples submitted 2 weeks apart may indicate a rise in antibody levels and offer a more definitive diagnosis of WNV infection. Many cases are diagnosed postmortem; the kidney and brain are the preferred tissues to submit for histopathologic examination.
Treatment of birds infected with WNV may be unrewarding as there is no specific treatment available for WNV. Although there is a vaccine available for equids (Fort Dodge), there is presently no definitive data describing the efficacy of this vaccine in birds. Until an avian vaccine is developed, the best ways to prevent WNV include: moving birds indoors, covering outdoor facilities with mosquito netting, using USDA-approved carbon dioxide mosquito traps, isolating infected birds in mosquito proof areas away from other birds that may be at risk, and incinerating carcasses of dead birds.
Aspergillosis is one of the most frequently encountered mycotic diseases in avian species and one of the most devastating diseases of raptors. A. fumigatus is the species most commonly isolated in acute and chronic respiratory disease in birds of prey. The organism is ubiquitous in the environment of free-ranging and often captive raptors. Transmission is through inhalation of infective spores. Disease is usually the result of an immuno-compromised state within the affected animal. Stress, poor hygiene, very young or old age, chronic antibiotic administration, corticosteroids, and concomitant disease are some of the factors that predispose birds to aspergillosis. The incubation period is extremely variable, depending on the immunocompetency of the host and exposure dose. Acute aspergillosis is the product of inhalation of overwhelming numbers of spores from the environment, while the chronic forms, in most instances, develop clinically over a period of 1 to 3 weeks. Avian aspergillosis generally results in two types of disease; a localized nodular form or a systemic invasive form. Nodular lesions may be found as abscesses on air sacs, lungs, or trachea. Tracheal lesions (including aspergillomas) are common at the bifurcation near the syrinx and may result in blockage of one or both of the bronchi. Systemic infections usually originate in the respiratory tract and spread locally and hematogenously to other organs.
Clinical signs depend on the severity and form of the disease. Acute onsets of dyspnea, stridor, and death have been associated with nodules within the trachea and lungs. Depression, anorexia, and weight loss may be the only signs in chronic cases. Hematologic changes include a markedly elevated WBC count with heterophilia, monocytosis, and toxic changes in chronic cases. Radiographs may reveal thickened air sacs and soft tissue opacities within the lungs or abdominal area. Diagnosis is generally based upon clinical signs, antibody detection (ELISA), tracheal culture, hematology (leukocytosis), and endoscopy. For clinically inapparent cases, administer itraconazole (7-10 mg/kg q12h) for 4-6 weeks. When clinical signs are present, administer oral itraconazole (given with food) at 7-10 mg/kg q12h for 5 days, then once daily for 1-3 months as necessary; nebulization with clotrimazole (clotrimazole 5-10% solution in polyethylene glycol with 5% dimethylsulfoxide from a compounding pharmacy); and amphotericin B given intratracheally or injected transcostally into left and right posterior thoracic air sacs or applied directly to air sac lesions in other locations via endoscope. Note, however, that itraconazole, when administered at higher dosages, often causes patients to become transiently anorexic. Voriconazole may provide another effective pharmacological tool for treating aspergillosis. Working doses are stated to be at 12.5 mg/kg. Frequency of administration and subsequent bioavailability appears to vary among species of birds. Prevention of aspergillosis involves minimizing predisposing factors. The prophylactic treatment of birds under unavoidable stressful conditions has been recommended.
Candidiasis is another significant mycotic infection of raptors and is caused by Candida sp. This organism commonly affects the gastrointestinal tract and results in either plaque-like lesions on the mucosa of the tongue, pharynx, and crop or a deep-seated infection of the gastrointestinal tract with or without oral lesions. When not systemically affected, clinical signs associated with candidiasis can include reluctance to swallow, decreased appetite, vomiting, regurgitation, and depression. Diagnosis is usually made by demonstrating Candida sp. in Gram stains of lesions in the oral cavity, esophagus, cloaca, and feces or by culture. Therapy usually consists of nystatin given orally at 100,000 U/kg q8-12h. Nystatin is not absorbed systemically, and, therefore, must come in contact with the affected areas of the gastrointestinal tract. Fluconazole (5-15 mg/kg PO q12h x 14-60 days) and itraconazole have also proven effective for the treatment of resistant strains of Candida sp.
Trichomoniasis, also called "frounce," is a protozoal disease caused by Trichomonas gallinae and is of major significance in captive and wild birds of prey. Healthy pigeons and doves often harbor the organism. Infections are seen in captive raptors fed a diet of freshly killed pigeons and wild raptors that feed on pigeons (goshawks, falcons, and some species of owls). Clinical signs of trichomoniasis are caseous plaques in and around the oropharynx. Raptors that are affected often have difficulty swallowing and may flick pieces of food. Diagnosis is based upon history, clinical signs, and demonstration of the organisms from swabs of the exudate. Treatment with metronidazole (30-50 mg/kg q24h x 5-7 days) or carnidazole (Spartrix®, Wildlife Pharmaceuticals, Fort Collins, CO) (30 mg/kg q12h x 3 days; 20-30 mg/kg PO once or 20 mg/kg PO q24h X 2 days) is often effective.
Plasmodium, Hemoproteus, and Leucocytozoon are vector-borne diseases that are frequently observed on blood smears of raptors. Leucocytozoon spp. is considered nonpathogenic in adult raptors, although it has been associated with mortality in nestlings. Infections with Hemoproteus sp. and Leucocytozoon sp. may be found in large numbers within the bloodstream with no apparent clinical signs. If the parasite is an incidental finding, treatment is not necessary. Birds with clinical signs associated with these parasites (especially Hemoproteus) can be administered chloroquine (generally effective against erythrocytic forms) and primaquine (generally effective against tissue forms) according to established protocols (see Exotic Animal Formulary, 2005). Pyrimethamine may also be effective; mefloquine has also been used, but efficacy has not been determined. Despite reasonable success in treating clinical cases, the parasites are generally not totally eliminated from the host.
Lead poisoning (plumbism) is an intoxication resulting from absorption of hazardous levels of lead (generally from lead pellets) into body tissues. Lead-poisoned birds are: reluctant to fly when approached or unable to sustain flight for any distance when they do fly; depressed; anorexic; have bile-stained feces; and may be emaciated. A definitive diagnosis of lead poisoning is based on toxicological findings. Treatment of lead intoxicosis includes stabilizing the patient, removing the source of the lead, and removal of the lead from the tissue with chelating agents. CaEDTA (35 mg/kg IV, IM q12h) is generally administered for 5 days, followed by 5 days with no treatment. The bird is resampled and treated again for 5 days until the blood lead is below 5 μmol/L and the bird is clinically improving. CaEDTA is best diluted with isotonic saline to a concentration of no greater than 1% (10 mg/ml) and administered SC. CaEDTA chelates lead from bone, but not from soft tissues. Oral chelating agents such as D-penicillamine (Cuprimine®, Merck) (30-55 mg/kg PO q12h x 7-14 days) or dimercaptosuccinic acid (DMSA, Chemet, Bock Pharmacal) (25-35 mg/kg PO q12h x 5 days/wk x 3-5 wk) may be used as follow-up therapy.