Symposium on Non-Domestic Pet Medicine
Diseases of Birds of Prey
William H. Halliwell, D.V.M., Ph.D.*
The practicing veterinarian is continually challenged by the diversity of his patients and the complexity of their ills. Captive raptorial birds are not prevalent, but the great value placed on them by falconers and the awareness of the declining populations of these birds in the wilds caused by pesticide contamination and decreased habitat have made their appearance as patients more common. Raptors are composed of two major groups of predatory birds: the order Strigiformes (owls), including the families Strigidae and Tytonidae; and the order Falconiformes (the diurnal birds of prey), including the families Cathartidae, Accipitridae, Falconidae, Pandionidae, and Sagittaridae. Discussion of the taxonomy of these birds is afforded by several standard texts such as Brown and Amadon 1 (Falconiformes) and Peters 5 (Strigiformes). An outstanding ornithology text, Birds of Prey of the World, 3 is recommended for those interested in furthering their general knowledge of these magnificent birds.
CLINICAL EXAMINATION AND PHYSICAL RESTRAINT Clinical examination begins with identification of the animal and recording of the clinical history. Such information as age, sex, species, diet, and environment as well as an explanation of previous medical problems may provide an insight into the etiology of the chief complaint. History taking allows the veterinary clinician to evaluate, amplify, or clarify the preconceived diagnostic conclusions suggested by the client. Trained raptors will sit quietly on the fist and permit visual inspection. The eyes of the bird are often hooded with a leather hood-like appliance in order to reduce the nervousness caused by strange sur*Director of Pathology-Toxicology, Elars Bioresearch Laboratories, Colorado
Fort Collins,
Veterinary Clinics of North America: Small Animal Practice- Vol. 9, No.3, August 1979
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roundings and people. Many of the hawks are not trained to accept a hood and the initial examination is often easier in a dimly lit room with the aid of a small flashlight. Observation should permit determinations of demeanor, body condition, temperament, stature, feather condition and bloom, depression, clearness of the eyes, pigmentation of the feet and legs, and other signs that may assist in reaching a diagnosis. For palpation and other methods of physical examination, "casting" of the bird is required. Casting is accomplished by approaching the bird from the rear with a piece of cloth and, when the wings are folded in a normal position, quickly grasping the bird and holding the wings firmly against the body. The cloth is then wrapped around the body and an edge is folded over the head; the feet are pulled backward by pressure on the leash or jesses. After complete control over the bird is gained, the cloth may be removed to expose different parts of the body for closer inspection. If a lengthy examination is anticipated, the feet and talons may be taped in a clenched position to minimize injury to the bird and to its handlers. Short-term restraint for such maneuvers as radiographic examination, palpation, and ocular examination, intravenous or intramuscular administration of ketamine hydrochloride, 15 to 30 mg per kg of body weight, is recommended. (See the section on anesthesia for further clarification.) Palpation, percussion, and auscultation of the body cavities and internal organs can be accomplished. The heart rate is usually too rapid to be evaluated, but the respiratory system and air passages are easily inspected with a pediatric stethoscope. Palpation of the crop, trachea, paranasal sinuses, abdominal cavity and its contents, cloaca, preening gland, and feathers is completed in a step-wise fashion. The most important objective of this portion of the examination is to conduct a thorough, complete examination of all systems of the body, similar to that conducted on mammalian patients. The recording of the body temperature may be done in the cloaca or in the axilla at the juncture of the wing and body. However, in our experience the temperature varies widely, depending on the degree of excitement of the patient. In cases of unilateral paralysis of the leg, digital monitoring of the femoral pulse is indicated. Examination of the head should include an assessment of: symmetry (indicative of the presence or absence of abscesses), cysts, traumatic injury, paranasal sinusitis, ocular discharge, nasal exudation, and obstruction of the external orifice of the ear. The iris of falcons is dark brown whereas that of accipiters changes with age from a yellow color during the first year to a red color at four to five years of age. The nictitating membrane may be observed as may the cornea and sclera. The small amount of nonfeathered skin around the eye should be gray in falcons less than a year of age, but yellow in all other
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raptors and in mature falcons. If this skin is pale, hypovitaminosis A should be suspected. Examination of the mouth and oropharynx is accomplished by placing one hand on top of the head of the bird and grasping the upper beak with the thumb and forefinger. The lower mandible may then be pulled ventrally by the forefinger of the opposite hand. Overgrowth of the upper beak is common in captive birds. When the mouth is opened, the tracheal orifice will be recognized as it opens and closes with respiration; the esophageal opening is seen posterior to the tracheal orifice. At this time oral swabs of saliva can be collected on a spatula or Q-tip to check for parasites of the respiratory system (Serratospiculum sp.) or of the oral cavity (Capillaria or Trichomonas spp.). Lesions of hypovitaminosis A, candidiasis, ulceration, or impacted bones of prey species may be discovered. When impaction, candidiasis, or other inflammatory or obstructive diseases of the crop are suspected, passage of a stomach tube constructed from surgical tubing and external manipulation often may be required. Palpation of the trachea and thoracic inlet may be completed at this time. Gentle abdominal palpation may provide evidence of an enlarged liver, a retained egg in the reproductive tract, cloacal impaction by urates, or intestinal obstruction. The assessment of the feathers, feather tracts, subcutaneous tissues, muscle mass, bones, joints, feet, and talons is completed in sequential order.
ANATOMY AND PHYSIOLOGY Only those anatomic characteristics of raptors which deviate markedly from those of more common domestic species of poultry will be mentioned in this discussion. The most unique difference is the formation and egestion of a pellet. Pellets of indigestible material consumed by the raptor, including bones, teeth, hair, and feathers are formed in the stomach. Egestion is accomplished by gastric contraction and esophageal antiperistalsis. Owls generally egest a pellet for each meal, but hawks may have more than one meal before egestion occurs. In the red-tailed hawk, a poorly developed diverticulum of the posterior esophagus (the crop), anterior to the stomach, exists as a temporary holding space for food. In owls there is no true crop, only an indistinct enlargement of the esophagus. The stomach of a raptor is a simple muscular structure consisting of smooth muscle fibers radiating from a central aponeurosis. Owls have well developed ceca, as do most gallinaceous birds. However, the red-tailed hawk has only rudimentary vestiges of these structures. Gastric acidity is low in rap-
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tors; hawks are reported to have a normal pH of 1.7 and owls a pH of 2.4. 4 The respiratory physiology and functional anatomy of raptors is similar to that of other birds. The respiratory rate varies inversely with body size and ranges from a high rate of 50 respirations per minute in a 100 gm kestrel to a rate of 18 respirations per minute in a 1.5 kg red-tailed hawk. The cardiovascular system is extremely responsive as evidenced by reports in American kestrels of a heart rate at rest of 350 beats per minute and a heart rate of up to 660 beats per minute during fiight. 4 The metabolic rate of raptors increases with physical activity and is higher in the smaller birds. Evidence exists that in these birds there is a diurnal variation in body temperature which corresponds with the increased temperatures present during that part of the day in which they are most active. Maintenance food requirements for captive raptors on a diet of mice under standard laboratory conditions have been presented by Duke. 4 He states that small American kestrels require 138 gm per kg per day whereas larger birds such as the red-tailed hawk may require only 55 gm per kg of body weight per day. Most raptors can be maintained in captivity and can even reproduce without access to water. Their water requirements are adequately supplied by oxidative metabolism and the moisture in their prey, which is balanced by evaporative loss of moisture. Under conditions of stress, elevated environmental temperatures, or fever, water requirements are increased and the provision of supplemental sources of water is recommended.
NUTRITIONAL DISEASES Well-defined nutritional requirements of raptors have not been established; however, birds have been maintained for long periods of time on a duplication of their natural diet with laboratory rodents, coturnix quail, or cockrels raised to four to six weeks of age.
Impaction of the Crop Raptorial birds ingest all parts of their prey species. Smaller prey species such as voles or mice may be swallowed whole whereas larger prey species are torn apart by the bird and only selected portions are eaten. The indigestible portion of the diet is regurgitated as a pellet at various times after ingestion. The role attributed to roughage (castings) in the diet is debatable, and numerous birds have been maintained for years on a diet of only raw meat with supplemental vitamins and minerals. The only difficulty encountered has been an overgrowth of the beak that has required trimming and filing to
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shape it into a more normal configuration. A change in diet from one with no roughage to one with average to above average amounts of roughage may induce impaction of the crop. The clinical manifestations of crop impaction include repeated attempts to regurgitate a bolus, restlessness, and an interest in food but failure to eat adequate amounts. Treatment may require irrigation of the crop, digital manipulation of the retained bolus, or, in extreme cases, surgical removal of the impacted bolus. Malnutrition Malnutrition has been implicated as a primary or secondary factor in the death of almost 25 per cent of raptorial birds that have been necropsied. The food intake requirement is increased during cold weather and the food consumption is inversely proportional to the size of the bird. For example, small birds weighing 100 to 200 gm require amounts of food equivalent to 18 to 25 per cent of body weight each day, whereas larger raptors weighing 800 to 1200 gm require only 7 to 11 per cent of body weight in food each day for maintenance. A reduced caloric intake causes a loss of depot fat, first from subcutaneous fat depots, then from the abdominal fat deposits, and lastly from the fat depots around the coronary band of the heart. Large birds such as eagles may withstand a couple weeks of food deprivation before it becomes hazardous to their health. Small raptors, however, have a higher metabolic rate and may be in jeopardy after only 48 to 72 hours of starvation. Another manifestation of caloric deprivation is hypoglycemia. Normal blood glucose in most birds of prey is 350 to 400 mg per ml, and hypoglycemic tetany or increased nervousness are commonly observed at levels of approximately 100 mg per ml. Most often, hypoglycemic tetany is associated with reduced food intake, vigorous exercise, and cold temperatures that require an increased intake of food. Chemical Contamination Residues of DDT, DDE, polychlorinated biphenyls, dieldrin, and other toxic products are stored in fat depots. Loss of these depots allows redistribution of these toxic products into the fat-rich nervous system, causing clinical signs of intoxication. Hypocalcemia The role of calcium, phosphorus, and vitamin D3 in the health of raptors is often painfully evident when a patient is presented with hypocalcemia, tetany, rickets, osteoporosis, spontaneous fractures, or nutritional hyperparathyroidism. All of these clinical manifestations result from reduced absorption of calcium. Common causes of hypocalcemia include all-meat diets, lack of exposure to sunlight to induce
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sufficient production of vitamin D in the secretions of the uropygial gland, diets high in fat which reduce the absorption of calcium from the intestine, and the formation of calcium soaps that reduce the availability of calcium for absorption. Birds presented in a state of hypocalcemic tetany (Fig. 1) may be treated with subcutaneous or slow intravenous administration of dilute calcium gluconate solutions. If intravenous administration is selected, careful monitoring of the heart rate during infusion is recommended. Birds recovering from tetanic spasms should be kept quiet in a darkened room and fed food liberally sprinkled with calcium lactate or another readily absorbed form of calcium. The darkened room will reduce movement of the bird and may prevent the increased incidence of spontaneous fractures.
Vitamin A Deficiency Raptors require preformed vitamin A in their diets because they are unable to convert carotenoid precursors to the active form of the vitamin. Conditions resulting from deficiencies of vitamin A include hyperkeratosis of the squamous epithelium, particularly around the eyes, and lesions of the oropharynx which may vary from tiny focal pustules secondary to distention of hyperkeratotic glands (Fig. 2), to large yellow-brown hyperkeratotic plaques. These large plaques need to be distinguished from trichomoniasis, oral capillariasis, candidiasis, and oral fowl pox lesions. Other clinical signs associated with vitamin A deficiency are enlargement of the suborbital sinuses and conjunctival sacs with accumulated keratin, voice changes caused by hyperkeratosis of the syrinx, and a pale yellow color of the legs, feet, and cere rather than the healthy, bright yellow color that is normally seen.
Figure l. Body posture of a bird in hypocalcemic tetany. Note the extended wings. open mouth , and loss of postural control.
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Fig ure 2. Lesions seconda r y to vitamin A d e ficien cy, such as this pustular esophagitis, are caused by retention of desquamated keratin in the glands.
Vitamin A deficiency has also been implicated in the development of visceral and articular gout secondary to squamous metaplasia of the collecting tubules of the kidney. The development of foot infections with the formation of corns on the weight-bearing surface of the foot has also been attributed to vitamin A deficiencies. The diagnosis of vitamin A deficiency is based on clinical findings or on the postmortem analysis of the liver for vitamin A content. A normal raptor liver may contain 9000 to 13,500 p,g of vitamin A. Treatment consists of the administration of 5000 USP units of vitamin A per day for several weeks, eventually tapering the dosage so that vitamin A intoxication does not occur. 4
Vitamin B Deficiency Deficiencies of the water soluble vitamins thiamine (B 1) and riboflavin (B 2 ) have been implicated in a condition best described as "stargazing" (Fig. 3). Affected birds show opisthotonos with the head drawn backward, loss of balance, or generalized paralysis similar to the curly toed paralysis of poultry. Treatment of some of these patients with an injectable multiple B-vitamin preparation has resulted in clinical improvement. Other raptors with similar signs have been refractory to treatment with B-vitamins, however, and may have had encephalitis, other infections, or other conditions of nutritional origin.
Vitamin E-Selenium Deficiency Microscopic evidence of h yalin degeneration and necrosis of skel-
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Figure 3. A "star-gazing" posture is seen in a prairie falcon with vitamin B de ficiency.
eta] muscles suggestive of nutritional myopathy secondary to vitamin E-selenium deficiency has been reported in a barred owl and a turkey vulture, both of which wer e maintained on all-meat diets for more than a year. 4
INFECTIOUS DISEASES Infectious diseases include those caused by viruses, bacteria, mycotic agents and, to a lesser d egree, m ycoplasma and chlamydia. A brief summary of the common diseases will be included here . For an in-depth discussion the reader is referred to an authoritative text. 4
Avian Pox Avian pox (fowl pox) has been observed in most species of hawks, falcons, and eagles. The species of the strain that infects these birds has not bee n conclusively identified. The diagnosis of avian pox is based on gross lesions, and their distribution on the no nfeathered portions of the body - the feet, legs, and face, and around the eyes. The diagnosis may be confirmed by histologic examina tion of a biopsy specimen for the classic Bollinger bodies. The early lesions are 3 to 8 mm nodules, covered by an intact epithelium, which undergo superficial erosion 10 to 14 days later and may become even larger and more proliferative with a secondary bacterial infection (Fig. 4).
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Figure 4. Proliferative lesions of avian pox in the ep ithelium of the foot of a r edtailed hawk are exacerbated by a secon d ary bacterial infection .
Most cases of avian pox regress in three weeks without treatment. However, some benefit seems to be derived from the topical application of antiseptics and ether-based solutions, which may reduce shedding of virus or reduce secondary bacterial invasion. The transmission of avian pox depends on the presence of broken skin and has been attributed to mosquitoes or blood-sucking arthropods since most outbreaks are seen in the summer months. Inclusion Body Disease Inclusion body disease (herpes virus) of falcons and owls has been r ecorded in many species of falcons and qwls but not in hawks. The disease in falcons and owls is acute and fatal. The experimental inoculation of susceptible birds has provided evidence that the incubation period is six to 12 days, and that the route of infection may be oral or nasal, or from aerosol or intramuscular inoculation. The source of the virus h as not been elucidated but a h armless virus of pigeons or passerine birds has been implicated . Clinical signs are minimal; birds are found dead or may show signs of gastric upset such as regurgitation, diarrhea, and lethargy for 18 to 48 hours prior to death. The illness is accompanied by a severe to moderate leukopenia. At necropsy, the lesions provide widespread evidence of focal necrosis in the liver , spleen , bone marrow, gut-associated lymphoid tissue, lung, and kidney (Fig. 5). Histologic examination reveals numerous intranuclear inclusion bodies in hepatocytes, as well as epithelial cells.
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Figure 5. Inclusion body disease in a prairie falcon . Note the necrotic foci in the liver and the spleen.
Marek's Disease Marek's disease is a lymphoproliferative disease that has been described in owls and European kestrels. The disease affects immature birds less than one year of age. Clinical signs include paralysis, anorexia, and emaciation. Lesions found on necropsy examination include lymphoproliferative nodules in the liver, spleen, pancreas, and kidney. Microscopically there is invasion of the peripheral and autonomic nerves by heterogeneous populations of lymphocytes. The method of transmission is unknown but oral or nasal routes of feces, body secretions, and feather dander are suspected. Marek's disease should be differentiated from lymphoid leucosis, an infiltrative disease characterized by sparing of the nervous system, and a h omogeneous population of lymphocytes. Treatment has not been attempted. Newcastle Disease 1\' ewcastle disease is a highly contagious m yxovirus infection of birds. Several cases have been reported in raptors. The severity of the disease and the clinical signs observed have been variable as a result of variations in the susceptibility of the host and the virule nce of the virus. Clinical signs associated with Newcastle disease include opisthotonos, increased nervousness, and abnormal positioning of the head. At necropsy, observa tions from birds with Newcastle disease h ave included gastroenteritis, air sacculitis, and degenerative hepatitis, but the findings are sufficiently variable to be of little assistance in making an accurate diagnosis. Isolation of the virus from the brain, spleen ,
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lung, or liver, or serologic identification remain the best methods of diagnosis. Treatment for Newcastle disease has not been successful; however, vaccination has been reported to be effective in protection against challenge with a virulent virus strain. 8
Rabies Serologic evidence of rabies in raptors has been reported, but evidence of clinical infection has not been observed unless there has been intracerebral inoculation of the virus. 4
Avian Tuberculosis Avian tuberculosis is an insidious infection in raptorial birds and rarely is diagnosed prior to necropsy. The organ systems involved will determine the clinical signs. A chronic wasting syndrome accompanied by diarrhea, ascites, and vague gastrointestinal symptoms are most commonly encountered. Yellow-tan granulomas in the parenchymal organs and bone marrow are most commonly observed at necropsy. Treatment is not recommended since the causative organism, Mycobacterium avium, is highly resistant to antibiotics.
Coliform Septicemia Coliform septicemia (Escherichia coli infection) may cause hepatic abscesses (coligranulomas), air sacculitis, purulent pericarditis, and gastroenteritis (Fig. 6). The clinical signs are dependent on the organ system(s) affected. Cultures from feces and the regurgitated contents of the stomach as well as tracheal swabs have been helpful in making a diagnosis. Isolation and identification of the etiologic agent can be made with inoculation of eosin-methylene blue agar, MacConkey agar, or other selective media. Treatment of colibacillosis infections with tetracycline or chloramphenicol has been successful in selected cases.
Salmonellosis Salmonellosis (avian typhoid) may be caused by any of 1500 serotypes of the Salmonella species and may cause a gastroenteritis characterized by green fecal specimens, diarrhea, dehydration, and sudden death. Some cases of more chronic septicemia or peritonitis have been attributed to the Salmonella typhimurium serotype.
Staphylococcal Pododermatitis Staphylococcal pododermatitis (bumblefoot) is one of the most common and most debilitating diseases of birds of prey. The condition is most commonly caused by S. aureus. The disease is seen in wild birds but is more prevalent in captive raptors. The etiology is multifactorial and involves trauma to the bearing surface of the foot. This trauma may occur as the bird flies from perch to perch, or it may be caused by the surface texture of the perching surface. During periods
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Figure 6.
WILLIAM H. HALLIWELL
Escherichia coli and Proteus air saccu liris in a mature Peregrine falcon.
of inactivity, overweight birds may traumatize the sensitive epithelial and subepithelial tissues of the foot. The debilitation of the epithelium on the bearing surface of the metatarsal pad and the introduction of a pathogenic organism into this compromised tissue is the basic cause of the disease. Other factors may contribute to the development of bumblefoot. Hypovitaminosis A reduces epithelial integrity and thus may contribute to the development of corns on the bearing surface of the foot (Fig. 7), or to a poor moult. Raptors replace their feathers with new feathers once a year and simultaneously they exfoliate a layer of epidermis from the feet. Any nutritional deprivation that interfer es with this epithelial replacement will also contribute to the development of foot problems. A traumatized or otherwise debilitated foot is then susceptible to the introduction of bacteria from the environment by puncture from the hind talon (phalynx 1), other trauma, or simply by exposure to contaminated perching surfaces and surroundings. The bacteria introduced into these d ebilitated tissues then proliferate and cr eate a small abscess. If the immune system of the bird is adequate, the infection is usually eliminated. Occasionally, the bacterial invaders are not totally d estroyed and the infection is "walled off' by a connective tissue capsule. The bacteria within the capsule become quiescent and yet are isolated from most antibiotics applied to the foot or given parenterally. At some time in the progression of the disease, repeated trauma or similar circumstances may create a fissure in the capsule, causing the release of small numbers of bacteria into the surrounding tissue . A capsule then forms around these n ewly released organisms
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Figure 7.
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Epithelial "corns" arc located on the ventral surface of the metatarsal pad.
(Fig. 8). Eventually, a serpentine meshwork of fibrous connective tissue, necrotic material, and bacteria is formed , infiltrating around tendons, ligaments, vessels, and n erves of the foot. A common sequela of bumblefoot is the d evelopment of osteomyelitis in the bones of the foot. The most common organism cultured from bumblefoot infections is S. aureus, but others such as Proteus sp., Pseudomonas sp., and Streptococcus sp. have also been isolated. T he treatment for bumblefoot is multifaceted and includes the evaluation and correction of the environme n t and the behavior of the bird to prevent further trauma to the foot, an evaluation of the diet to correct contributory nutritional deficiencies, and the culture and antibiotic sensitivity testing of the infecting microorganism. In the early stages of the disease, the administration of systemic a ntibiotics and local application of indicated antibiotics suspended in dimethyl sulfoxide have been helpful adjunctive therapeutic m easures. Surgery has been considered as a treatment only as a last resort because of the previously mentioned infiltration around the anatomic structures of the foot and because of the poor h ealing properties of the epithelium of the foot. Avian Cholera Avian choler a (pasteurellosis), cau sed by Pasteurella multocida, has caused severe epornitics in water fowl with deaths estima ted to be in excess of 20,000 per year. Raptor populations associated with affected
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Fig ure 8. Bumblefoot may be characterized by large , e nca psulated areas of necrotic tissue throu ghout the me tata rsal pad.
water fowl populations have developed septicemia, which has often progressed to death. Postmortem lesions have included petechiae of the heart, lung, and air sac membranes, and pinpoint necrotic foci within the heart, liver, and spleen. The diagnosis is made by culture of the small, gram-negative, rod-shaped organism or by direct smears of infected organs stained with Wright's stain to demonstrate dipolar rods. The treatment of poultry with tetracycline and chloramphenicol has been successful. Mycotic Infections
Mycotic infections, particularly those caused by the Aspergillus sp., are common and usually fatal in raptorial birds (Fig. 9). The goshawk and gyrfalcon seem to be most susceptible to the disease , but it has been recognized in all birds of prey. The clinical signs include anorexia, slow weight loss, intolerance to exercise, and occasionally, when the syrinx is affected, the development of a hoarse croak instead of the normal scream. Mycotic infections appear to be most commonly associated with stress situations such as recent capture, surgery, or other d ebilitating conditions. Occasionally, radiography may d emonstrate an increased density of the air sacs of infected birds. Other methods of diagnosis include the culture of deep tracheal swabs or of saline irrigations from the air sacs. Currently, serologic techniques for diagnosis are being investigated . Diseases having similar clinical signs include tuberculosis, chronic air sacculitis, and chronic salmonellosis.
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Figure 9.
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Aspergillus sp. are growing in the air sacs of this red-tailed hawk.
Amphotericin B (Fungizone) in combination with broad spectrum antibiotics such as tetracycline or chloramphenicol is recommended for treatment of this fungus and any secondary bacterial infection. Amphotericin B is given by nebulization, intratracheal injection, or intravenous injection. Aerosol treatment with 25 mg of amphotericin B in 15 ml of Alevaire for four hours daily has been recommended until remission of clinical signs occurs. 4 Others have recommended intratracheal injection of amphotericin B combined with chloramphenicol, at a dose of 1 mg per kg and 50 mg per kg, respectively. The total volume should not exceed 3 ml for a bird weighing 0.5 kg. The diluents most commonly used are saline or 5 per cent dextrose solution. 4 Candidiasis Candidiasis, caused by Candida albicans, may result in small, truncated lesions with umbilicated tips of the oral cavity and the tongue (Fig. 10). Candidiasis of the esophagus and crop is characterized by pseudomembranous patches of necrotic epithelium which emit a foul odor, and cause impairment of ingestion. A differential diagnosis should include trichomoniasis, capillariasis, and hypovitaminosis A. Treatment with nystatin (Mycostatin), 10,000 units per kg three times daily for l 0 to 14 days, has been successful. During treatment good nursing care is necessary to prevent dehydration and loss of condition. Other Bacterial Diseases Other bacterial diseases affecting raptorial birds include anthrax,
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Figure 10. Truncated lesion s with umbilicated centers are typical of ora l can didiasis. Seen here on the ventral surface of the tongu e.
listeriosis, erysipelas, botulism, yersinosis, tularemia, mycoplasmosis, and chlamydiosis. Each of these diseases has been reported in bir ds of prey; however, the incidence is not high. T he reader is referred to other texts for a complete review of the clinical signs, necropsy findings, and recommended therapy for these diseases.2 ' 4
PARASITIC DISEASES Ectoparasites
Ectoparasites rarely threaten the life of the host, but they are vectors for various blood-borne diseases and may invade the epidermis causing proliferative lesions. Arthropods. Ticks in the adult, nymph, or larval stages, as well as mites, have been r eported in raptors. The species of mites that affect birds of prey include Dermanyssus gallinae and Ornithonyssus sylviarum, which feed from the external surface of the bird, and Cnemidocoptes, which burrow into the skin and cause proliferative lesions of the nonfeather ed por tions of the body. L ice commonly infest the feathers of r aptors. They are easily recognized by their large size (0.5 em or greater), their broad h ead, and their dorsoventrally flattened body. Hippoboscid flies frequently may be found cr awling through the feathers of raptors. These biting flies may transmit blood parasites or viral diseases from one bird to another.
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Maggots of tachinid flies inhabit the nests of many raptors and attack the emerging feather shafts of the nestlings and often invade the external ear of these birds. They cause varying degrees of mortality among nestlings . In all cases of external parasites , the treatment is physical removal of the p a rasite by use of a commercial insecticide powder such as 2 per cent Sevin. The powder is sprinkled along the dorsal midline of the bird from the head to the lumbar region. Additionally, preexisting lesions caused by the parasite should be treated appropriately. Protozoa. Protozoan parasites include Trichomonas gallinae and Trypanosoma spp. The most serious disease caused by these organisms is trichomoniasis, known to falconers as frounce. This infection is a stomatitis characterized by the development in the mouth and oropharynx of yellow-tan caseous plaques that may spread to the sinuses, liver, and respiratory system. Early in the course of the disease, the bird may be noted to ta ke smaller than normal bites of food; later, the bird may take small bits of food, eventually flicking them away because of the mechanical obstruction of the oropharynx (Fig. 11). The diagnosis of trichomoniasis is made by examining the saliva of the affected bird under a microscope at a magnification of 40 to 96x after the saliva has been diluted 50 per cent with saline solution. If numerous, small, sperm-like organisms in continual motion are observed, the diagnosis is confirmed. If treatment has been attempted prior to microscopic examination, visualization of the parasites may be difficult.
Figure 11. pharynx.
Cheesy, proliferative lesions of trichomoniasis in the mouth and oro-
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The treatment of choice for trichomoniasis is dimetridazole (Emtry!), 125 mg per kg. Dimetridazole is presently available only in powder form and must be weighed and placed in a capsule for administration. Metronidazole (Flagyl), administered orally at a dosage of 50 mg per kg two to three times daily for five to seven days, is also effective but requires a longer period of treatment. Trichomoniasis is most often transmitted to raptors by consumption of their prey- pigeons, quails, and small feral birds. Many different strains of the parasite exist with varying degrees of pathogenicity. Freezing of food for 24 to 48 hours has been found to kill most strains ofTrichomonads. Endoparasites
The endoparasites that affect raptors include trematodes (flukes), nematodes (roundworms), cestodes (tapeworms), and sporozoa (coccidia) (Fig. 12). Trematodes. Strigeid trematodes and several species of Dicrocoeliidae have been reported in raptors but little pathogenic significance has been attributed to their presence. Cestodes. Cestodes parasitize most species of raptors and may cause intestinal obstruction when present in large numbers. Diagnosis is made upon recognition of the small, mobile, pink-tan proglottids in the feces or around the vent. Treatment with 2, 5-dichloro-4nitrosalicylanilide (Yomesan), 156 mg per kg, has been found to beeffective.
Capillaria
~
Porrocaecum
~
Figure 12. Examples of the ova of common endoparasites of raptorial birds.
Trematode (fluke)
Serratospiculum
~
Coccidial Oocyst
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Nematodes. Nematodes, predominantly of the Ascaridia or Porrocaecum species, often have been reported in raptors. Their effect on the health of the bird is dependent upon the numbers present in the intestinal tract. Treatment with piperazine at the standard dose rate for small animals, or with thiabendazole, 100 mg per kg, administered in two doses 10 days apart, has been successful in eradicating the parasites. Levamisole and mebendazole are also effective. Serratospiculum amaculata, the air sac parasite of the genus Falco, does not appear to alter the health of prairie falcons when present in small numbers. However, in larger numbers, it may result in respiratory dyspnea. Migration of the parasites into the abdominal organs has been considered to be the cause of death in several birds. At necropsy, the parasites are found entangled in the walls of the air sacs. The embryonated eggs are found in the mouth and feces. Clinical improvement has been reported following treatment with thiabendazole, 100 mg per kg of body weight. 4 Tracheal infections with Syngamus species are manifested by open-mouthed breathing and gaping, hence the term "gapeworm." The large ova with bipolar plugs are found in the saliva and feces. Thiabendazole is the drug of choice because of its availability and therapeutic efficacy. 2 Mebendazole and levamisole are also effective agents of treatment. Several species of Capillaria infect raptors, affecting the mouth and oropharynx or the small intestine. The ova, found in the feces, have bipolar plugs. Treatment with thiabendazole, 100 mg per kg of body weight, is curative but several administrations at seven to 10 day intervals may be necessary for total effectiveness. Mebendazole and levamisole also show promise as effective therapeutic medications for this type of infection. Other parasites, including Physaloptera and Thelazia spp., have been observed in raptors, but their clinical significance has not yet been established. Sporozoa. Intestinal coccidiosis is not an uncommon condition in raptors. It is associated with bloody, mucoid droppings. Treatment with sulfadimethoxine for five to seven days at the standard dosage for small animals has resulted in clinical improvement in most cases. Renal coccidiosis has been observed in the collecting tubules of the kidneys of several raptors, but no systemic effect has been attributed to the presence of the parasite. The presence of such species of blood parasites as Haemoproteus, Leucocytozoon, and Plasmodium has been noted in many raptorial birds in which the disease was not clinically evident. However, isolated cases have shown that these parasites may become pathogenic. A recent report indicated that a large number of birds at a captive breeding site exhibited signs of lethargy and a depressed hematocrit. In some affected birds, up to 16 per cent of the erythrocytes were found
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to be parasitized. Treatment consisted of the administration of 25 mg per kg of chloroquine phosphate (Aralen phosphate) in divided doses10 mg per kg for the initial dose, followed six hours later by 5 mg per kg, followed by a 5 mg per kg dose 12 hours later, and completed with a final dose of 5 mg per kg 24 hours after administration of the third dose. Clinical improvement was noted 24 hours after completion of the treatment regimen. 4
TOXIC AND METABOLIC CONDITIONS Toxic Disorders Pesticide contamination of ecosystems has resulted in a biologic magnification of the persistent toxic products in animals at the top of the food chain. The pesticides having the greatest effect on raptors are the organochlorine compounds - DDT and its analogs - aldrin, dieldrin, heptachlor, and heptachlor epoxide. The industrial polychlorinated biphenyls have been incriminated also. Elevated levels of DDT or metabolites in raptors have been incriminated as causative factors in the following disorders: late breeding cycles, failure to ovulate, reduced clutch size, failure to recycle after loss of eggs, thinner than normal egg shells, increased mortality of embryos, and a reduced maternal instinct. DDT and its metabolites are reported to have a half-life of approximately 15 years. These pollutants are particularly toxic because of their affinity for the fat depots of the body. During periods of stress and food deprivation the fat depots are resorbed and the toxic material is released into the fluids of the body where it relocates to the organs of high fat content such as the brain, causing irritability, disorientation, coma, and death at levels of 30 parts per million. Lead poisoning, a result of feeding raptors prey containing lead pellets, has been reported. Poisoning from alkyl mercury, a seed dressing that passes through the food chain to the raptors, has been experimentally established as a cause of various disorders. Furthermore, excessive exposure to nicotine sulfate (Blackleaf-40), an agent used in birds to treat external parasites, has resulted in toxicity.
Metabolic Disorders Metabolic disorders recognized in raptors include visceral and articular gout and problems associated with molting and feather growth. Gout is a metabolic disorder characterized by the deposition of urates and uric acid crystals in the tissues of the body. Birds are uricotelic, and their nitrogenous wastes are excreted by the kidney as uric acid, which is produced by the catabolism of purines. Uric acid is synthesized in the liver and kidney. Gout in raptors is a metabolic dis-
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order of unknown etiology; however, renal lesions associated with hypovitaminosis A, pyelonephritis, excessive protein in the diet, and an unbalanced metabolism of amino acids have been suggested as causative factors. Visceral gout is rarely recognized before death. At postmortem examination there is a light dusting of urate deposits on visceral surfaces, predominantly on the pericardium and liver. It has been most commonly observed after periods of stress. Signs of articular gout in a raptor include feet that are swollen the entire length of the phalynx and an inability to adequately grasp the perch (Fig. 13). If the disease has been a persistent problem, urate deposits may be demonstrated radiographically around the joints. Feather growth problems are usually associated with a delayed or incomplete molt. The molt in raptors is dependent on many factors including nutritional status, thyroid function , adrenal-pituitary axis, behavioral problems, gonadal physiology, phototropic periods, and the interactions between these parameters. Individual feathers that have been pulled intact from the feather follicle are usually replaced with a new feather in five to six weeks. Adjacent feathers provide protection and direction for the replacement feathers; if several adjacent feathers are absent, a cardboard splint taped over the area will provide the necessary protection and guidance for proper orientation of the new feathers. A therapeutic regimen that stimulates new feather growth consists of oral thyroid therapy, 1 grain per kg per day, or progesterone, 2 mg per kg per week, administered intramuscularly. Two to three
Figure 13. Ar ticular gout in a Cooper's hawk. :"
Diseases of Birds of Prey
William H. Halliwell, D.V.M., Ph.D.*
The practicing veterinarian is continually challenged by the diversity of his patients and the complexity of their ills. Captive raptorial birds are not prevalent, but the great value placed on them by falconers and the awareness of the declining populations of these birds in the wilds caused by pesticide contamination and decreased habitat have made their appearance as patients more common. Raptors are composed of two major groups of predatory birds: the order Strigiformes (owls), including the families Strigidae and Tytonidae; and the order Falconiformes (the diurnal birds of prey), including the families Cathartidae, Accipitridae, Falconidae, Pandionidae, and Sagittaridae. Discussion of the taxonomy of these birds is afforded by several standard texts such as Brown and Amadon 1 (Falconiformes) and Peters 5 (Strigiformes). An outstanding ornithology text, Birds of Prey of the World, 3 is recommended for those interested in furthering their general knowledge of these magnificent birds.
CLINICAL EXAMINATION AND PHYSICAL RESTRAINT Clinical examination begins with identification of the animal and recording of the clinical history. Such information as age, sex, species, diet, and environment as well as an explanation of previous medical problems may provide an insight into the etiology of the chief complaint. History taking allows the veterinary clinician to evaluate, amplify, or clarify the preconceived diagnostic conclusions suggested by the client. Trained raptors will sit quietly on the fist and permit visual inspection. The eyes of the bird are often hooded with a leather hood-like appliance in order to reduce the nervousness caused by strange sur*Director of Pathology-Toxicology, Elars Bioresearch Laboratories, Colorado
Fort Collins,
Veterinary Clinics of North America: Small Animal Practice- Vol. 9, No.3, August 1979
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roundings and people. Many of the hawks are not trained to accept a hood and the initial examination is often easier in a dimly lit room with the aid of a small flashlight. Observation should permit determinations of demeanor, body condition, temperament, stature, feather condition and bloom, depression, clearness of the eyes, pigmentation of the feet and legs, and other signs that may assist in reaching a diagnosis. For palpation and other methods of physical examination, "casting" of the bird is required. Casting is accomplished by approaching the bird from the rear with a piece of cloth and, when the wings are folded in a normal position, quickly grasping the bird and holding the wings firmly against the body. The cloth is then wrapped around the body and an edge is folded over the head; the feet are pulled backward by pressure on the leash or jesses. After complete control over the bird is gained, the cloth may be removed to expose different parts of the body for closer inspection. If a lengthy examination is anticipated, the feet and talons may be taped in a clenched position to minimize injury to the bird and to its handlers. Short-term restraint for such maneuvers as radiographic examination, palpation, and ocular examination, intravenous or intramuscular administration of ketamine hydrochloride, 15 to 30 mg per kg of body weight, is recommended. (See the section on anesthesia for further clarification.) Palpation, percussion, and auscultation of the body cavities and internal organs can be accomplished. The heart rate is usually too rapid to be evaluated, but the respiratory system and air passages are easily inspected with a pediatric stethoscope. Palpation of the crop, trachea, paranasal sinuses, abdominal cavity and its contents, cloaca, preening gland, and feathers is completed in a step-wise fashion. The most important objective of this portion of the examination is to conduct a thorough, complete examination of all systems of the body, similar to that conducted on mammalian patients. The recording of the body temperature may be done in the cloaca or in the axilla at the juncture of the wing and body. However, in our experience the temperature varies widely, depending on the degree of excitement of the patient. In cases of unilateral paralysis of the leg, digital monitoring of the femoral pulse is indicated. Examination of the head should include an assessment of: symmetry (indicative of the presence or absence of abscesses), cysts, traumatic injury, paranasal sinusitis, ocular discharge, nasal exudation, and obstruction of the external orifice of the ear. The iris of falcons is dark brown whereas that of accipiters changes with age from a yellow color during the first year to a red color at four to five years of age. The nictitating membrane may be observed as may the cornea and sclera. The small amount of nonfeathered skin around the eye should be gray in falcons less than a year of age, but yellow in all other
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raptors and in mature falcons. If this skin is pale, hypovitaminosis A should be suspected. Examination of the mouth and oropharynx is accomplished by placing one hand on top of the head of the bird and grasping the upper beak with the thumb and forefinger. The lower mandible may then be pulled ventrally by the forefinger of the opposite hand. Overgrowth of the upper beak is common in captive birds. When the mouth is opened, the tracheal orifice will be recognized as it opens and closes with respiration; the esophageal opening is seen posterior to the tracheal orifice. At this time oral swabs of saliva can be collected on a spatula or Q-tip to check for parasites of the respiratory system (Serratospiculum sp.) or of the oral cavity (Capillaria or Trichomonas spp.). Lesions of hypovitaminosis A, candidiasis, ulceration, or impacted bones of prey species may be discovered. When impaction, candidiasis, or other inflammatory or obstructive diseases of the crop are suspected, passage of a stomach tube constructed from surgical tubing and external manipulation often may be required. Palpation of the trachea and thoracic inlet may be completed at this time. Gentle abdominal palpation may provide evidence of an enlarged liver, a retained egg in the reproductive tract, cloacal impaction by urates, or intestinal obstruction. The assessment of the feathers, feather tracts, subcutaneous tissues, muscle mass, bones, joints, feet, and talons is completed in sequential order.
ANATOMY AND PHYSIOLOGY Only those anatomic characteristics of raptors which deviate markedly from those of more common domestic species of poultry will be mentioned in this discussion. The most unique difference is the formation and egestion of a pellet. Pellets of indigestible material consumed by the raptor, including bones, teeth, hair, and feathers are formed in the stomach. Egestion is accomplished by gastric contraction and esophageal antiperistalsis. Owls generally egest a pellet for each meal, but hawks may have more than one meal before egestion occurs. In the red-tailed hawk, a poorly developed diverticulum of the posterior esophagus (the crop), anterior to the stomach, exists as a temporary holding space for food. In owls there is no true crop, only an indistinct enlargement of the esophagus. The stomach of a raptor is a simple muscular structure consisting of smooth muscle fibers radiating from a central aponeurosis. Owls have well developed ceca, as do most gallinaceous birds. However, the red-tailed hawk has only rudimentary vestiges of these structures. Gastric acidity is low in rap-
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tors; hawks are reported to have a normal pH of 1.7 and owls a pH of 2.4. 4 The respiratory physiology and functional anatomy of raptors is similar to that of other birds. The respiratory rate varies inversely with body size and ranges from a high rate of 50 respirations per minute in a 100 gm kestrel to a rate of 18 respirations per minute in a 1.5 kg red-tailed hawk. The cardiovascular system is extremely responsive as evidenced by reports in American kestrels of a heart rate at rest of 350 beats per minute and a heart rate of up to 660 beats per minute during fiight. 4 The metabolic rate of raptors increases with physical activity and is higher in the smaller birds. Evidence exists that in these birds there is a diurnal variation in body temperature which corresponds with the increased temperatures present during that part of the day in which they are most active. Maintenance food requirements for captive raptors on a diet of mice under standard laboratory conditions have been presented by Duke. 4 He states that small American kestrels require 138 gm per kg per day whereas larger birds such as the red-tailed hawk may require only 55 gm per kg of body weight per day. Most raptors can be maintained in captivity and can even reproduce without access to water. Their water requirements are adequately supplied by oxidative metabolism and the moisture in their prey, which is balanced by evaporative loss of moisture. Under conditions of stress, elevated environmental temperatures, or fever, water requirements are increased and the provision of supplemental sources of water is recommended.
NUTRITIONAL DISEASES Well-defined nutritional requirements of raptors have not been established; however, birds have been maintained for long periods of time on a duplication of their natural diet with laboratory rodents, coturnix quail, or cockrels raised to four to six weeks of age.
Impaction of the Crop Raptorial birds ingest all parts of their prey species. Smaller prey species such as voles or mice may be swallowed whole whereas larger prey species are torn apart by the bird and only selected portions are eaten. The indigestible portion of the diet is regurgitated as a pellet at various times after ingestion. The role attributed to roughage (castings) in the diet is debatable, and numerous birds have been maintained for years on a diet of only raw meat with supplemental vitamins and minerals. The only difficulty encountered has been an overgrowth of the beak that has required trimming and filing to
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shape it into a more normal configuration. A change in diet from one with no roughage to one with average to above average amounts of roughage may induce impaction of the crop. The clinical manifestations of crop impaction include repeated attempts to regurgitate a bolus, restlessness, and an interest in food but failure to eat adequate amounts. Treatment may require irrigation of the crop, digital manipulation of the retained bolus, or, in extreme cases, surgical removal of the impacted bolus. Malnutrition Malnutrition has been implicated as a primary or secondary factor in the death of almost 25 per cent of raptorial birds that have been necropsied. The food intake requirement is increased during cold weather and the food consumption is inversely proportional to the size of the bird. For example, small birds weighing 100 to 200 gm require amounts of food equivalent to 18 to 25 per cent of body weight each day, whereas larger raptors weighing 800 to 1200 gm require only 7 to 11 per cent of body weight in food each day for maintenance. A reduced caloric intake causes a loss of depot fat, first from subcutaneous fat depots, then from the abdominal fat deposits, and lastly from the fat depots around the coronary band of the heart. Large birds such as eagles may withstand a couple weeks of food deprivation before it becomes hazardous to their health. Small raptors, however, have a higher metabolic rate and may be in jeopardy after only 48 to 72 hours of starvation. Another manifestation of caloric deprivation is hypoglycemia. Normal blood glucose in most birds of prey is 350 to 400 mg per ml, and hypoglycemic tetany or increased nervousness are commonly observed at levels of approximately 100 mg per ml. Most often, hypoglycemic tetany is associated with reduced food intake, vigorous exercise, and cold temperatures that require an increased intake of food. Chemical Contamination Residues of DDT, DDE, polychlorinated biphenyls, dieldrin, and other toxic products are stored in fat depots. Loss of these depots allows redistribution of these toxic products into the fat-rich nervous system, causing clinical signs of intoxication. Hypocalcemia The role of calcium, phosphorus, and vitamin D3 in the health of raptors is often painfully evident when a patient is presented with hypocalcemia, tetany, rickets, osteoporosis, spontaneous fractures, or nutritional hyperparathyroidism. All of these clinical manifestations result from reduced absorption of calcium. Common causes of hypocalcemia include all-meat diets, lack of exposure to sunlight to induce
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sufficient production of vitamin D in the secretions of the uropygial gland, diets high in fat which reduce the absorption of calcium from the intestine, and the formation of calcium soaps that reduce the availability of calcium for absorption. Birds presented in a state of hypocalcemic tetany (Fig. 1) may be treated with subcutaneous or slow intravenous administration of dilute calcium gluconate solutions. If intravenous administration is selected, careful monitoring of the heart rate during infusion is recommended. Birds recovering from tetanic spasms should be kept quiet in a darkened room and fed food liberally sprinkled with calcium lactate or another readily absorbed form of calcium. The darkened room will reduce movement of the bird and may prevent the increased incidence of spontaneous fractures.
Vitamin A Deficiency Raptors require preformed vitamin A in their diets because they are unable to convert carotenoid precursors to the active form of the vitamin. Conditions resulting from deficiencies of vitamin A include hyperkeratosis of the squamous epithelium, particularly around the eyes, and lesions of the oropharynx which may vary from tiny focal pustules secondary to distention of hyperkeratotic glands (Fig. 2), to large yellow-brown hyperkeratotic plaques. These large plaques need to be distinguished from trichomoniasis, oral capillariasis, candidiasis, and oral fowl pox lesions. Other clinical signs associated with vitamin A deficiency are enlargement of the suborbital sinuses and conjunctival sacs with accumulated keratin, voice changes caused by hyperkeratosis of the syrinx, and a pale yellow color of the legs, feet, and cere rather than the healthy, bright yellow color that is normally seen.
Figure l. Body posture of a bird in hypocalcemic tetany. Note the extended wings. open mouth , and loss of postural control.
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Fig ure 2. Lesions seconda r y to vitamin A d e ficien cy, such as this pustular esophagitis, are caused by retention of desquamated keratin in the glands.
Vitamin A deficiency has also been implicated in the development of visceral and articular gout secondary to squamous metaplasia of the collecting tubules of the kidney. The development of foot infections with the formation of corns on the weight-bearing surface of the foot has also been attributed to vitamin A deficiencies. The diagnosis of vitamin A deficiency is based on clinical findings or on the postmortem analysis of the liver for vitamin A content. A normal raptor liver may contain 9000 to 13,500 p,g of vitamin A. Treatment consists of the administration of 5000 USP units of vitamin A per day for several weeks, eventually tapering the dosage so that vitamin A intoxication does not occur. 4
Vitamin B Deficiency Deficiencies of the water soluble vitamins thiamine (B 1) and riboflavin (B 2 ) have been implicated in a condition best described as "stargazing" (Fig. 3). Affected birds show opisthotonos with the head drawn backward, loss of balance, or generalized paralysis similar to the curly toed paralysis of poultry. Treatment of some of these patients with an injectable multiple B-vitamin preparation has resulted in clinical improvement. Other raptors with similar signs have been refractory to treatment with B-vitamins, however, and may have had encephalitis, other infections, or other conditions of nutritional origin.
Vitamin E-Selenium Deficiency Microscopic evidence of h yalin degeneration and necrosis of skel-
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Figure 3. A "star-gazing" posture is seen in a prairie falcon with vitamin B de ficiency.
eta] muscles suggestive of nutritional myopathy secondary to vitamin E-selenium deficiency has been reported in a barred owl and a turkey vulture, both of which wer e maintained on all-meat diets for more than a year. 4
INFECTIOUS DISEASES Infectious diseases include those caused by viruses, bacteria, mycotic agents and, to a lesser d egree, m ycoplasma and chlamydia. A brief summary of the common diseases will be included here . For an in-depth discussion the reader is referred to an authoritative text. 4
Avian Pox Avian pox (fowl pox) has been observed in most species of hawks, falcons, and eagles. The species of the strain that infects these birds has not bee n conclusively identified. The diagnosis of avian pox is based on gross lesions, and their distribution on the no nfeathered portions of the body - the feet, legs, and face, and around the eyes. The diagnosis may be confirmed by histologic examina tion of a biopsy specimen for the classic Bollinger bodies. The early lesions are 3 to 8 mm nodules, covered by an intact epithelium, which undergo superficial erosion 10 to 14 days later and may become even larger and more proliferative with a secondary bacterial infection (Fig. 4).
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Figure 4. Proliferative lesions of avian pox in the ep ithelium of the foot of a r edtailed hawk are exacerbated by a secon d ary bacterial infection .
Most cases of avian pox regress in three weeks without treatment. However, some benefit seems to be derived from the topical application of antiseptics and ether-based solutions, which may reduce shedding of virus or reduce secondary bacterial invasion. The transmission of avian pox depends on the presence of broken skin and has been attributed to mosquitoes or blood-sucking arthropods since most outbreaks are seen in the summer months. Inclusion Body Disease Inclusion body disease (herpes virus) of falcons and owls has been r ecorded in many species of falcons and qwls but not in hawks. The disease in falcons and owls is acute and fatal. The experimental inoculation of susceptible birds has provided evidence that the incubation period is six to 12 days, and that the route of infection may be oral or nasal, or from aerosol or intramuscular inoculation. The source of the virus h as not been elucidated but a h armless virus of pigeons or passerine birds has been implicated . Clinical signs are minimal; birds are found dead or may show signs of gastric upset such as regurgitation, diarrhea, and lethargy for 18 to 48 hours prior to death. The illness is accompanied by a severe to moderate leukopenia. At necropsy, the lesions provide widespread evidence of focal necrosis in the liver , spleen , bone marrow, gut-associated lymphoid tissue, lung, and kidney (Fig. 5). Histologic examination reveals numerous intranuclear inclusion bodies in hepatocytes, as well as epithelial cells.
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Figure 5. Inclusion body disease in a prairie falcon . Note the necrotic foci in the liver and the spleen.
Marek's Disease Marek's disease is a lymphoproliferative disease that has been described in owls and European kestrels. The disease affects immature birds less than one year of age. Clinical signs include paralysis, anorexia, and emaciation. Lesions found on necropsy examination include lymphoproliferative nodules in the liver, spleen, pancreas, and kidney. Microscopically there is invasion of the peripheral and autonomic nerves by heterogeneous populations of lymphocytes. The method of transmission is unknown but oral or nasal routes of feces, body secretions, and feather dander are suspected. Marek's disease should be differentiated from lymphoid leucosis, an infiltrative disease characterized by sparing of the nervous system, and a h omogeneous population of lymphocytes. Treatment has not been attempted. Newcastle Disease 1\' ewcastle disease is a highly contagious m yxovirus infection of birds. Several cases have been reported in raptors. The severity of the disease and the clinical signs observed have been variable as a result of variations in the susceptibility of the host and the virule nce of the virus. Clinical signs associated with Newcastle disease include opisthotonos, increased nervousness, and abnormal positioning of the head. At necropsy, observa tions from birds with Newcastle disease h ave included gastroenteritis, air sacculitis, and degenerative hepatitis, but the findings are sufficiently variable to be of little assistance in making an accurate diagnosis. Isolation of the virus from the brain, spleen ,
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lung, or liver, or serologic identification remain the best methods of diagnosis. Treatment for Newcastle disease has not been successful; however, vaccination has been reported to be effective in protection against challenge with a virulent virus strain. 8
Rabies Serologic evidence of rabies in raptors has been reported, but evidence of clinical infection has not been observed unless there has been intracerebral inoculation of the virus. 4
Avian Tuberculosis Avian tuberculosis is an insidious infection in raptorial birds and rarely is diagnosed prior to necropsy. The organ systems involved will determine the clinical signs. A chronic wasting syndrome accompanied by diarrhea, ascites, and vague gastrointestinal symptoms are most commonly encountered. Yellow-tan granulomas in the parenchymal organs and bone marrow are most commonly observed at necropsy. Treatment is not recommended since the causative organism, Mycobacterium avium, is highly resistant to antibiotics.
Coliform Septicemia Coliform septicemia (Escherichia coli infection) may cause hepatic abscesses (coligranulomas), air sacculitis, purulent pericarditis, and gastroenteritis (Fig. 6). The clinical signs are dependent on the organ system(s) affected. Cultures from feces and the regurgitated contents of the stomach as well as tracheal swabs have been helpful in making a diagnosis. Isolation and identification of the etiologic agent can be made with inoculation of eosin-methylene blue agar, MacConkey agar, or other selective media. Treatment of colibacillosis infections with tetracycline or chloramphenicol has been successful in selected cases.
Salmonellosis Salmonellosis (avian typhoid) may be caused by any of 1500 serotypes of the Salmonella species and may cause a gastroenteritis characterized by green fecal specimens, diarrhea, dehydration, and sudden death. Some cases of more chronic septicemia or peritonitis have been attributed to the Salmonella typhimurium serotype.
Staphylococcal Pododermatitis Staphylococcal pododermatitis (bumblefoot) is one of the most common and most debilitating diseases of birds of prey. The condition is most commonly caused by S. aureus. The disease is seen in wild birds but is more prevalent in captive raptors. The etiology is multifactorial and involves trauma to the bearing surface of the foot. This trauma may occur as the bird flies from perch to perch, or it may be caused by the surface texture of the perching surface. During periods
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Figure 6.
WILLIAM H. HALLIWELL
Escherichia coli and Proteus air saccu liris in a mature Peregrine falcon.
of inactivity, overweight birds may traumatize the sensitive epithelial and subepithelial tissues of the foot. The debilitation of the epithelium on the bearing surface of the metatarsal pad and the introduction of a pathogenic organism into this compromised tissue is the basic cause of the disease. Other factors may contribute to the development of bumblefoot. Hypovitaminosis A reduces epithelial integrity and thus may contribute to the development of corns on the bearing surface of the foot (Fig. 7), or to a poor moult. Raptors replace their feathers with new feathers once a year and simultaneously they exfoliate a layer of epidermis from the feet. Any nutritional deprivation that interfer es with this epithelial replacement will also contribute to the development of foot problems. A traumatized or otherwise debilitated foot is then susceptible to the introduction of bacteria from the environment by puncture from the hind talon (phalynx 1), other trauma, or simply by exposure to contaminated perching surfaces and surroundings. The bacteria introduced into these d ebilitated tissues then proliferate and cr eate a small abscess. If the immune system of the bird is adequate, the infection is usually eliminated. Occasionally, the bacterial invaders are not totally d estroyed and the infection is "walled off' by a connective tissue capsule. The bacteria within the capsule become quiescent and yet are isolated from most antibiotics applied to the foot or given parenterally. At some time in the progression of the disease, repeated trauma or similar circumstances may create a fissure in the capsule, causing the release of small numbers of bacteria into the surrounding tissue . A capsule then forms around these n ewly released organisms
DISEASES OF BIRDS OF PREY
Figure 7.
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Epithelial "corns" arc located on the ventral surface of the metatarsal pad.
(Fig. 8). Eventually, a serpentine meshwork of fibrous connective tissue, necrotic material, and bacteria is formed , infiltrating around tendons, ligaments, vessels, and n erves of the foot. A common sequela of bumblefoot is the d evelopment of osteomyelitis in the bones of the foot. The most common organism cultured from bumblefoot infections is S. aureus, but others such as Proteus sp., Pseudomonas sp., and Streptococcus sp. have also been isolated. T he treatment for bumblefoot is multifaceted and includes the evaluation and correction of the environme n t and the behavior of the bird to prevent further trauma to the foot, an evaluation of the diet to correct contributory nutritional deficiencies, and the culture and antibiotic sensitivity testing of the infecting microorganism. In the early stages of the disease, the administration of systemic a ntibiotics and local application of indicated antibiotics suspended in dimethyl sulfoxide have been helpful adjunctive therapeutic m easures. Surgery has been considered as a treatment only as a last resort because of the previously mentioned infiltration around the anatomic structures of the foot and because of the poor h ealing properties of the epithelium of the foot. Avian Cholera Avian choler a (pasteurellosis), cau sed by Pasteurella multocida, has caused severe epornitics in water fowl with deaths estima ted to be in excess of 20,000 per year. Raptor populations associated with affected
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HALLIWELL
Fig ure 8. Bumblefoot may be characterized by large , e nca psulated areas of necrotic tissue throu ghout the me tata rsal pad.
water fowl populations have developed septicemia, which has often progressed to death. Postmortem lesions have included petechiae of the heart, lung, and air sac membranes, and pinpoint necrotic foci within the heart, liver, and spleen. The diagnosis is made by culture of the small, gram-negative, rod-shaped organism or by direct smears of infected organs stained with Wright's stain to demonstrate dipolar rods. The treatment of poultry with tetracycline and chloramphenicol has been successful. Mycotic Infections
Mycotic infections, particularly those caused by the Aspergillus sp., are common and usually fatal in raptorial birds (Fig. 9). The goshawk and gyrfalcon seem to be most susceptible to the disease , but it has been recognized in all birds of prey. The clinical signs include anorexia, slow weight loss, intolerance to exercise, and occasionally, when the syrinx is affected, the development of a hoarse croak instead of the normal scream. Mycotic infections appear to be most commonly associated with stress situations such as recent capture, surgery, or other d ebilitating conditions. Occasionally, radiography may d emonstrate an increased density of the air sacs of infected birds. Other methods of diagnosis include the culture of deep tracheal swabs or of saline irrigations from the air sacs. Currently, serologic techniques for diagnosis are being investigated . Diseases having similar clinical signs include tuberculosis, chronic air sacculitis, and chronic salmonellosis.
DISEASES OF BIRDS OF PREY
Figure 9.
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Aspergillus sp. are growing in the air sacs of this red-tailed hawk.
Amphotericin B (Fungizone) in combination with broad spectrum antibiotics such as tetracycline or chloramphenicol is recommended for treatment of this fungus and any secondary bacterial infection. Amphotericin B is given by nebulization, intratracheal injection, or intravenous injection. Aerosol treatment with 25 mg of amphotericin B in 15 ml of Alevaire for four hours daily has been recommended until remission of clinical signs occurs. 4 Others have recommended intratracheal injection of amphotericin B combined with chloramphenicol, at a dose of 1 mg per kg and 50 mg per kg, respectively. The total volume should not exceed 3 ml for a bird weighing 0.5 kg. The diluents most commonly used are saline or 5 per cent dextrose solution. 4 Candidiasis Candidiasis, caused by Candida albicans, may result in small, truncated lesions with umbilicated tips of the oral cavity and the tongue (Fig. 10). Candidiasis of the esophagus and crop is characterized by pseudomembranous patches of necrotic epithelium which emit a foul odor, and cause impairment of ingestion. A differential diagnosis should include trichomoniasis, capillariasis, and hypovitaminosis A. Treatment with nystatin (Mycostatin), 10,000 units per kg three times daily for l 0 to 14 days, has been successful. During treatment good nursing care is necessary to prevent dehydration and loss of condition. Other Bacterial Diseases Other bacterial diseases affecting raptorial birds include anthrax,
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WILLIAM H. HALLIWELL
Figure 10. Truncated lesion s with umbilicated centers are typical of ora l can didiasis. Seen here on the ventral surface of the tongu e.
listeriosis, erysipelas, botulism, yersinosis, tularemia, mycoplasmosis, and chlamydiosis. Each of these diseases has been reported in bir ds of prey; however, the incidence is not high. T he reader is referred to other texts for a complete review of the clinical signs, necropsy findings, and recommended therapy for these diseases.2 ' 4
PARASITIC DISEASES Ectoparasites
Ectoparasites rarely threaten the life of the host, but they are vectors for various blood-borne diseases and may invade the epidermis causing proliferative lesions. Arthropods. Ticks in the adult, nymph, or larval stages, as well as mites, have been r eported in raptors. The species of mites that affect birds of prey include Dermanyssus gallinae and Ornithonyssus sylviarum, which feed from the external surface of the bird, and Cnemidocoptes, which burrow into the skin and cause proliferative lesions of the nonfeather ed por tions of the body. L ice commonly infest the feathers of r aptors. They are easily recognized by their large size (0.5 em or greater), their broad h ead, and their dorsoventrally flattened body. Hippoboscid flies frequently may be found cr awling through the feathers of raptors. These biting flies may transmit blood parasites or viral diseases from one bird to another.
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Maggots of tachinid flies inhabit the nests of many raptors and attack the emerging feather shafts of the nestlings and often invade the external ear of these birds. They cause varying degrees of mortality among nestlings . In all cases of external parasites , the treatment is physical removal of the p a rasite by use of a commercial insecticide powder such as 2 per cent Sevin. The powder is sprinkled along the dorsal midline of the bird from the head to the lumbar region. Additionally, preexisting lesions caused by the parasite should be treated appropriately. Protozoa. Protozoan parasites include Trichomonas gallinae and Trypanosoma spp. The most serious disease caused by these organisms is trichomoniasis, known to falconers as frounce. This infection is a stomatitis characterized by the development in the mouth and oropharynx of yellow-tan caseous plaques that may spread to the sinuses, liver, and respiratory system. Early in the course of the disease, the bird may be noted to ta ke smaller than normal bites of food; later, the bird may take small bits of food, eventually flicking them away because of the mechanical obstruction of the oropharynx (Fig. 11). The diagnosis of trichomoniasis is made by examining the saliva of the affected bird under a microscope at a magnification of 40 to 96x after the saliva has been diluted 50 per cent with saline solution. If numerous, small, sperm-like organisms in continual motion are observed, the diagnosis is confirmed. If treatment has been attempted prior to microscopic examination, visualization of the parasites may be difficult.
Figure 11. pharynx.
Cheesy, proliferative lesions of trichomoniasis in the mouth and oro-
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WILLIAM H. HALLIWELL
The treatment of choice for trichomoniasis is dimetridazole (Emtry!), 125 mg per kg. Dimetridazole is presently available only in powder form and must be weighed and placed in a capsule for administration. Metronidazole (Flagyl), administered orally at a dosage of 50 mg per kg two to three times daily for five to seven days, is also effective but requires a longer period of treatment. Trichomoniasis is most often transmitted to raptors by consumption of their prey- pigeons, quails, and small feral birds. Many different strains of the parasite exist with varying degrees of pathogenicity. Freezing of food for 24 to 48 hours has been found to kill most strains ofTrichomonads. Endoparasites
The endoparasites that affect raptors include trematodes (flukes), nematodes (roundworms), cestodes (tapeworms), and sporozoa (coccidia) (Fig. 12). Trematodes. Strigeid trematodes and several species of Dicrocoeliidae have been reported in raptors but little pathogenic significance has been attributed to their presence. Cestodes. Cestodes parasitize most species of raptors and may cause intestinal obstruction when present in large numbers. Diagnosis is made upon recognition of the small, mobile, pink-tan proglottids in the feces or around the vent. Treatment with 2, 5-dichloro-4nitrosalicylanilide (Yomesan), 156 mg per kg, has been found to beeffective.
Capillaria
~
Porrocaecum
~
Figure 12. Examples of the ova of common endoparasites of raptorial birds.
Trematode (fluke)
Serratospiculum
~
Coccidial Oocyst
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Nematodes. Nematodes, predominantly of the Ascaridia or Porrocaecum species, often have been reported in raptors. Their effect on the health of the bird is dependent upon the numbers present in the intestinal tract. Treatment with piperazine at the standard dose rate for small animals, or with thiabendazole, 100 mg per kg, administered in two doses 10 days apart, has been successful in eradicating the parasites. Levamisole and mebendazole are also effective. Serratospiculum amaculata, the air sac parasite of the genus Falco, does not appear to alter the health of prairie falcons when present in small numbers. However, in larger numbers, it may result in respiratory dyspnea. Migration of the parasites into the abdominal organs has been considered to be the cause of death in several birds. At necropsy, the parasites are found entangled in the walls of the air sacs. The embryonated eggs are found in the mouth and feces. Clinical improvement has been reported following treatment with thiabendazole, 100 mg per kg of body weight. 4 Tracheal infections with Syngamus species are manifested by open-mouthed breathing and gaping, hence the term "gapeworm." The large ova with bipolar plugs are found in the saliva and feces. Thiabendazole is the drug of choice because of its availability and therapeutic efficacy. 2 Mebendazole and levamisole are also effective agents of treatment. Several species of Capillaria infect raptors, affecting the mouth and oropharynx or the small intestine. The ova, found in the feces, have bipolar plugs. Treatment with thiabendazole, 100 mg per kg of body weight, is curative but several administrations at seven to 10 day intervals may be necessary for total effectiveness. Mebendazole and levamisole also show promise as effective therapeutic medications for this type of infection. Other parasites, including Physaloptera and Thelazia spp., have been observed in raptors, but their clinical significance has not yet been established. Sporozoa. Intestinal coccidiosis is not an uncommon condition in raptors. It is associated with bloody, mucoid droppings. Treatment with sulfadimethoxine for five to seven days at the standard dosage for small animals has resulted in clinical improvement in most cases. Renal coccidiosis has been observed in the collecting tubules of the kidneys of several raptors, but no systemic effect has been attributed to the presence of the parasite. The presence of such species of blood parasites as Haemoproteus, Leucocytozoon, and Plasmodium has been noted in many raptorial birds in which the disease was not clinically evident. However, isolated cases have shown that these parasites may become pathogenic. A recent report indicated that a large number of birds at a captive breeding site exhibited signs of lethargy and a depressed hematocrit. In some affected birds, up to 16 per cent of the erythrocytes were found
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to be parasitized. Treatment consisted of the administration of 25 mg per kg of chloroquine phosphate (Aralen phosphate) in divided doses10 mg per kg for the initial dose, followed six hours later by 5 mg per kg, followed by a 5 mg per kg dose 12 hours later, and completed with a final dose of 5 mg per kg 24 hours after administration of the third dose. Clinical improvement was noted 24 hours after completion of the treatment regimen. 4
TOXIC AND METABOLIC CONDITIONS Toxic Disorders Pesticide contamination of ecosystems has resulted in a biologic magnification of the persistent toxic products in animals at the top of the food chain. The pesticides having the greatest effect on raptors are the organochlorine compounds - DDT and its analogs - aldrin, dieldrin, heptachlor, and heptachlor epoxide. The industrial polychlorinated biphenyls have been incriminated also. Elevated levels of DDT or metabolites in raptors have been incriminated as causative factors in the following disorders: late breeding cycles, failure to ovulate, reduced clutch size, failure to recycle after loss of eggs, thinner than normal egg shells, increased mortality of embryos, and a reduced maternal instinct. DDT and its metabolites are reported to have a half-life of approximately 15 years. These pollutants are particularly toxic because of their affinity for the fat depots of the body. During periods of stress and food deprivation the fat depots are resorbed and the toxic material is released into the fluids of the body where it relocates to the organs of high fat content such as the brain, causing irritability, disorientation, coma, and death at levels of 30 parts per million. Lead poisoning, a result of feeding raptors prey containing lead pellets, has been reported. Poisoning from alkyl mercury, a seed dressing that passes through the food chain to the raptors, has been experimentally established as a cause of various disorders. Furthermore, excessive exposure to nicotine sulfate (Blackleaf-40), an agent used in birds to treat external parasites, has resulted in toxicity.
Metabolic Disorders Metabolic disorders recognized in raptors include visceral and articular gout and problems associated with molting and feather growth. Gout is a metabolic disorder characterized by the deposition of urates and uric acid crystals in the tissues of the body. Birds are uricotelic, and their nitrogenous wastes are excreted by the kidney as uric acid, which is produced by the catabolism of purines. Uric acid is synthesized in the liver and kidney. Gout in raptors is a metabolic dis-
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order of unknown etiology; however, renal lesions associated with hypovitaminosis A, pyelonephritis, excessive protein in the diet, and an unbalanced metabolism of amino acids have been suggested as causative factors. Visceral gout is rarely recognized before death. At postmortem examination there is a light dusting of urate deposits on visceral surfaces, predominantly on the pericardium and liver. It has been most commonly observed after periods of stress. Signs of articular gout in a raptor include feet that are swollen the entire length of the phalynx and an inability to adequately grasp the perch (Fig. 13). If the disease has been a persistent problem, urate deposits may be demonstrated radiographically around the joints. Feather growth problems are usually associated with a delayed or incomplete molt. The molt in raptors is dependent on many factors including nutritional status, thyroid function , adrenal-pituitary axis, behavioral problems, gonadal physiology, phototropic periods, and the interactions between these parameters. Individual feathers that have been pulled intact from the feather follicle are usually replaced with a new feather in five to six weeks. Adjacent feathers provide protection and direction for the replacement feathers; if several adjacent feathers are absent, a cardboard splint taped over the area will provide the necessary protection and guidance for proper orientation of the new feathers. A therapeutic regimen that stimulates new feather growth consists of oral thyroid therapy, 1 grain per kg per day, or progesterone, 2 mg per kg per week, administered intramuscularly. Two to three
Figure 13. Ar ticular gout in a Cooper's hawk. :"
