Golden Eagle Training Delays: Causes and Concerns

Committee for Eagle Rehabilitation Excellence

Training Delays: Causes and Concerns

Written for CERE by Vickie Joseph DVM, Lynn Tompkins and Bob Fox

Raptors are brought to wildlife rehabilitation centers for a variety of reasons, the majority of which are caused either directly or indirectly by human activity. In most cases, if the bird is non- releasable, euthanasia is the most humane option. The time needed to recondition a raptor for release back to the wild is highly variable and influenced by the age of the raptor, the type or severity of injuries and condition when injured. Eagles admitted as fledglings or post fledglings often lack the skills needed to survive after their medical issues have been resolved. The following document will look at a variety of injuries and illnesses that may cause delays in the eagle’s training and ultimate release.

The three most common forms of electrocution are a result of a flash burn, phase to phase, or phase to ground exposure (Lehman et al 2007, Eccleston et al 2018). A flash burn is the result of an electrical arc causing thermal burns but does not actually enter the body. An electrical arc is a short circuit between two points of contact. There must be a conductive portion (such as wet, dirty feathers). Dry feathers act as an insulator and are less conductive. A flash burn occurs as the electricity moves across the surface of the body and does not penetrate the body. Flash burns may cover large surfaces of the body, and often are only partial thickness. However, third degree burns are possible. Phase to phase is contact between two wires or conductors. This creates a short circuit at full line potential (wing to wing). This is the most dangerous type of electrocution, often traveling through vital organs, resulting in death. Phase to ground occurs because electricity is always looking for a path to ground. This occurs when a bird touches a wire and non-insulated pole or pole equipment. This type of electrocution is less severe than phase to phase and can be survivable.

Externally, visible signs of electrocution may involve burns to the feathers and skin, edema of the wings and legs, limb fractures secondary to muscular contractions initiated by the current or a fall from the pole, traumatic limb or digit amputations and lacerations at the contact sites (R A Kagan 2016). If a bird survives the electrocution, the damage both externally and internally can be progressive over a two-week period. As tissues die from thermal burns, rupture of damaged vessels and thrombosis (local coagulation or clotting of the blood) may occur. Treatment for electrocution involves the immediate concerns of identifying electrocution lesions and documenting any internal damage and broken bones from the electrocution, while progressive concerns realize that slow death of tissues may occur and may take one to two weeks to see the full effects of electrocution. Full recovery may take several weeks or months depending on the degree of injury.

Lead toxicity
Lead toxicity in raptors is a global problem. Research has suggested that 26-90% of raptors show some level of lead in their blood and that 25-30% show signs of lead toxicity (Hunt et al 2012, Frauke et al 2017). Whether the lead level is lethal or sub-lethal, both have undesirable consequences. Lead particles that are ingested are broken down by the stomach acids forming toxic lead salts. These salts enter the blood stream and are transported to the liver, kidney and eventually to the skeletal system, where they can reside for years. The first effect of lead in the circulatory system is the inhibition of the enzymes for heme synthesis, leading to a decrease in blood hemoglobin, increases in the rate of red blood cell destruction and anemia associated with iron deficiency. Lead can also be released from the skeletal repositories and enter back into the blood stream. Lead is eventually eliminated from the body by sloughing off renal tubular epithelial cells, bile and/or pancreatic secretions (Kolb 2018). Effects of lead on the body can be reflected as neurological disorders such as impaired motor function, cognitive disabilities, intellectual development, developmental abnormalities, and impaired gastrointestinal motility. Systemic disorders such as cardiovascular disease, thermoregulation, reproductive disorders, hematologic abnormalities, skeletal fragility, vision abnormalities, and organ dysfunction and failure of the liver and kidney are also possible scenarios. Large long-lived raptor scavengers are more prone to exposures, while nestlings and fledglings may be more prone to permanent deficiencies. Treatment for lead toxicity requires that all medical issues be identified and treated simultaneously as well as chelation therapy for lead. Initially fluid therapy is required to help flush the liver and kidneys of the lead toxins and maintain hydration. Chelation therapy specific for lead toxicity may last for days or weeks depending on the degree of toxicity and clinical signs. Full recovery may take months. Fledgling or young eagles must be evaluated once their free flight training starts for any residual neurologic deficiencies that may be present from lead toxicity.

West Nile Virus
West Nile Virus (WNV) is an arbovirus (a mosquito-borne virus) found worldwide. While most infections of WNV occur through mosquitoes taking a blood meal, some infections may occur from the ingestion of an infected prey. This is very significant in the raptor species. WNV transmission may occur year-round in tropical and subtropical climates, while temperate regions see WNV infections from June through October. The rate and severity of infections will vary considerably from year to year and region to region, influenced by the hosts, environmental factors such as rainfall and temperature, and of course the prevalence of mosquito vectors (Nemeth 2006). It is a known fact that WNV will infiltrate many organ systems (brain, liver, spleen, kidney, heart, eye, and skin). The development of disease will be influenced by the species of raptor affected, genetic factors influencing their susceptibility, age of the raptor and the maturity of their immune system, concurrent disease, and stress factors. Many of the

pathological changes are a result of the direct effect of the virus or secondary to the marked inflammatory response caused by the virus resulting in tissue necrosis and degeneration. Raptors that survive the infection may suffer from relapses of the neurologic signs and have feather pulp abnormalities affecting the molt for up to 4 years (Gamino 2013).

Clinical signs can progress rapidly over 7 days. Not so obvious are the effects of this virus on the eyes, heart, and kidney. Anterior uveitis and fundic changes of the eyes such as fibrin adhesions, chorioretinal lesions and retinal atrophy are possible. These changes will need the evaluation by a veterinarian or veterinary ophthalmologist. Some of these changes will be permanent and affect the raptor’s vision for the rest of its life. Heart or myocardial lesions are varied and may include myocardial necrosis, degeneration, mineralization, fibrosis and hemorrhage. Certainly, this will affect the raptor’s stamina and ability to fly. Most raptors affected with WNV will have kidney tubular epithelial and glomerular cell degeneration and necrosis. Although recovery from this viral infection is possible, it takes time (weeks – months), and requires persistent evaluations to determine if some of the changes are permanent.

Impact Injury
Impact injuries can happen for a variety of reasons. Free flying raptors may hit a window, fencing, moving vehicles and even prey species. Nestling raptors may fall from great heights if the nest gives way. Certainly, our first instinct is to look at the bird and decide if it appears normal. However, it is always important to remember that impact injury = internal trauma (Joseph 2006). Impact injuries can involve multiple organs such as the heart, liver, eyes, brain, kidney, and lungs to name a few. The bird may present with a fractured wing or leg, but what we cannot see could be more devastating than the fracture itself. How we approach, stabilize, and treat the bird with impact injury will ultimately affect the outcome for this individual. Here are some examples of what to be aware of:

Head trauma may lead to long term neurologic deficiencies. The degree of neurologic deficits may not become evident immediately but may progress with the stress of training. With any head or eye trauma, even if the eye appears normal, traumatic cataracts can form later affecting the bird’s vision. Heart, liver, and lungs are certainly affected with impact injuries. The liver and heart lie directly under the keel and can be affected by any impact injury. The injuries to these organs can be progressive and have long term consequences. Contusions to the lungs may leave the lungs scarred and affect the bird’s reparatory system, especially with activity and exercise. Significant impact injuries may result in the slow death of cardiac muscle causing muscle necrosis and myocardial infarct up to 2-3 weeks post trauma (Joseph 2006, Graham et al 2007). In either case, as the training begins or the eagle is asked to perform at a higher level, clinical signs of respiratory or exercise intolerance may become evident. These eagles may require diagnostics such as cardiac ultrasounds, detailed radiographs, or endoscopy of the lungs to determine the degree of impairment.

It is imperative to have a full understanding of the molting process in the Golden Eagle. For any species of bird, molting is an energy demanding process, drawing on energy reserves and protein, which involves the replacement of 20-40% of the bird’s mass. Research has suggested that altogether, the bird’s plumage weighs more than any other part of its body (Welty 1975). Sequential molting is most widespread in avian species, including the Golden Eagle. The difference between the power required for sustained flight and maximum power available is small, in large birds of prey like the eagles. For eagles and large raptors flying efficiently with feather gaps in their wing feathers verses smaller birds is not sustainable. To maintain proper flight, the eagle does not molt and replace numerous wing feathers simultaneously. The molt is symmetrical in the wing and tail feathers, reducing the chance of asymmetry in flight feathers and reducing flight performance.

To understand how the molting process can be delayed or affect the eagle in training, feather growth must be understood ( Zuberogoitia et al 2018, Raptor Resource 2019). The nestling covered in natal down, is fed by the parents, resulting in a high increase of body mass growth (muscle and bones). As the flight feathers start to grow, the energy of growth is redirected to feather growth. This is at the expense of body growth. A term of pre-juvenile (first pre-basic ) molt may be used to describe the replacement of natal down with juvenile feathers. Complete growth of the juvenile wing and tail feathers may take 3-4 months in the eagle. These feathers are considered weaker and looser in texture verses adult feathers. Any medical condition or mechanical injury affecting the eagle at this stage can result in feathers that are damaged. Eagles with feather issues at this stage may not be ready for training and release until they have gone through their molt as a one-year-old. This molt, often referred to as the second pre-basic molt, starts during their second calendar year (1 year of age) and starts to replace the juvenile feathers. In most instances, this molt starts in the spring and finishes before winter. It is well documented that juvenile plumage may be molted in several molt cycles, (one per calendar year), leading to the recognition of subadult plumage until adult plumage is achieved.

Damaged feathers may result from a variety of factors. Any mechanical injury to the wing may result in damage to the feather follicles, resulting in the production of poor-quality feathers. Another possibility is the situation noted by raptor rehabilitators, that some raptors suffering blunt trauma to the wing (i.e., hit by car or gunshot) without fractures or broken feathers, may develop an asymmetrical molt of the affected wing several weeks after the trauma. Electrocutions can certainly result in damaged feathers, both from the electrocution itself or trauma from the fall. Also noted, nutritional deficiencies, feather parasites, bacterial or viral infections such as West Nile Virus, affecting the feather follicle or the young vascularized feather may result in a feather becoming constricted at the base, pinching off and falling out (Nemeth 2009). Eaglets fed a fatty squirrel diet by the parents, can suffer moderate feather damage in response to the greasy fat clogging the feather follicles and coating the feathers. This has been documented occasionally in fledgling eagles arriving at the raptor rehabilitation center. Identifying the etiology of the feather disorder and treating accordingly will give the eagle the best chance to recover and produce normal feathers. Although unlikely, exposure to defoliants such as sulfuric acid may cause irritation to the skin and subsequent feather damage, requiring several molts to correct the situation, as was the case in a short-eared owl (communications with Lynn Tompkins, Blue Mountain Wildlife ). Treatment to reverse damage to the feather follicle can take several months. In the case of grease laden feathers, mechanical removal of the

fat from the feathers is necessary, but often the quality of the feathers is poor, and the eagle must remain in captivity until it goes through the second pre-basic molt. Certainly, raptors suffering feather abnormalities related to West Nile Virus may need to go through 1 or 2 molts before the feathers are normal.

There is not a reliable safe way to stimulate the young eagle to molt bad feathers. The molt is stimulated by photoperiod which stimulates specific hormones, in addition to latitude, climate temperatures, protein in the diet and health. As previously mentioned, the eagle naturally starts the molt cycle in the spring and finishes up before winter. Some eagles in a captive situation may be under a moderate degree of stress and suffering from a nutritional imbalance. This may hinder the eagle to molt naturally. Once placed with a master falconer for training, as the eagle relaxes in their environment, is provided high quality food (protein) and starts creance and free flight sessions, the stress factors are reduced, paving the way for the eagle to go into a dramatic molt. Some will drop several primaries and secondaries at the same time, which is not a sequential molt and leads to asymmetry of the wing. It is also possible that a juvenile eagle, suffering from starvation, once in the raptor rehabilitation setting, fed a high-quality diet and medical issues addressed and treated, may start dropping damaged feathers, resulting in delays in training. It has been documented in Golden Eagles there exist a neurophysiological mechanism for selectively replacing damaged feathers by repeatedly pecking at the damaged feather, loosening it from the follicle and causing it to fall out (Zuberogoitia 2018). The suggestion to pull damaged feathers out to stimulate regrowth is not advised. The possibility of damaging the feather follicle is of concern and may lead to permanent abnormal feather growth at the site of removal. Any of these situations require that the eagle be given time to complete an abnormal molt before training is resumed.

Depending on the location of eagle training, seasonal weather may cause significant delays. In areas with heavy snow, the ability to get to the training fields and prey availability will be affected. Training during this period which can last weeks, may be inconsistent and daily training may not resume until spring with the snow melt. In some parts of the southwest, the heat can be intolerable and affect the ability to train the eagle during heat waves. Regardless of where the eagle training is taking place, the falconer must be aware of seasonal risks and effects on training.

180 Day Rule
In many states, there is the 180-day rule affecting raptors arriving at rehabilitation centers. Understandably, this rule has been put into place to prevent raptors destined for release from being held in a captive situation beyond 6 months. CERE understands the importance of such a rule; however, CERE strongly believes the 180-day rule should not apply to eagles entering the free flight program, or it should start when the free flight training begins. Injured or ill eagles may take anywhere from 2-6 months to fully recover from their medical issues. This leaves little time for preparing the eagle for release to the wild. Starting the 180-day rule once the eagle enters training with the ability of one extension is the best-case scenario for any eagle entering this program.

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