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Use of deslorelin acetate implants to mitigate aggression in two adult male domestic turkeys (Meleagris gallopavo) and correlating plasma testosterone concentrations.

Abstract: Two adult, male domestic turkeys were treated with implants of deslorelin acetate, a gonadotropin-releasing hormone agonist, to reduce intermale aggression and aggression directed toward the animal care team at a zoologic institution. The turkeys were manually restrained and either two 4.7-mg or two 9.4-mg implants were placed within the pectoral musculature on 3 occasions over the course of approximately 1.5 years. Plasma testosterone concentrations were measured by radioimmunoassay every 2 weeks for the first month after a new implant placement and then monthly thereafter. Testosterone concentrations remained low and aggressive behavior was decreased for a period of several months after implant placement. At necropsy of both birds, no adverse gross or histologic lesions were noted at the implantation sites in the pectoral musculature or within the gonadal tissue. Deslorelin acetate implants are a treatment modality to consider for mitigation of aggression in male domestic turkeys.

Key words: intermale aggression, testosterone, deslorelin acetate, avian, domestic turkey, Meleagris gallopavo

Clinical Report

Two male, domestic, broad-breasted white turkeys (Meleagris gallopavo) were acquired at approximately 1 month of age by a zoologic institution (Disney's Animal Kingdom, Bay Lake, FL, USA) for long-term care. Both birds had a history of a maxillary debeaking procedure, obesity, bilateral pododermatitis, and diffuse, poor feather quality. Both turkeys were housed together for management reasons, with no other birds, and were only separated when aggression became significant. They had access to an indoor 12.2-[m.sup.2] barn stall and an approximately 4000-[m.sup.2] grass paddock. The turkeys were offered water ad libitum and fed a balanced game bird pellet with enrichment food items offered intermittently throughout the day to encourage natural foraging behavior. Other environmental enrichment included water pools, puzzle feeders, and browse items, which did not affect aggression levels but did aid in weight and activity level maintenance. No psychotropic or behavior-modifying drugs or sedatives were administered to either bird at any time. Aggressive behavior between the birds and toward the animal care team was subjectively noted through daily observations from the animal care team and included pecking, charging, and booming vocalizations.

Case 1

Approximately 16 months after arrival at the institution, an initial trial of leuprolide acetate (100 pg/kg IM q 14 days X 3 treatments; Lupron Depot, Takeda Pharmaceutical Company Limited, Osaka, Japan), was administered to one turkey to decrease aggression. This bird was approximately 17 months old, weighed 18.6 kg, and was considered subordinate to the cohoused, conspecific, male turkey (case 2). No consistent reduction of aggressive behavior was observed after treatment. Four months later, a second trial of leuprolide acetate (50 [micro]g/kg IM once) was administered, and the turkey was observed to have minimally decreased aggressive behavior. One month after this, the bird was manually restrained for placement of two 4.7-mg deslorelin acetate implants (Suprelorin, Peptech Animal Health Pty Ltd, Macauarie Park, NSW, Australia) into the pectoral musculature. Aggression decreased within 2 weeks and lasted for approximately 3.5 months. At 3.5 months after the implant, aggression increased. At 4 months after the first implant, two 4.7-mg deslorelin implants were similarly placed into the pectoral musculature. This resulted in decreased aggression within 2 weeks and lasted for approximately 5 months. At 5 months after the second implant, aggression increased, and two 9.4-mg deslorelin implants were similarly placed in the pectoral musculature. This resulted in decreased aggression within 2 weeks and lasted for approximately 7 months.

Throughout the time when deslorelin acetate implants were present, plasma testosterone concentrations were measured by radioimmunoassay (University of Tennessee Veterinary Medical College, Diagnostic Laboratories, Knoxville, TN, USA), with the exception of 3 individual samples that were measured by radioimmunoassay at a second laboratory (IDEXX Laboratories, Westbrook, ME, USA). Blood samples were obtained by manually restraining the turkey for venipuncture of the right jugular vein approximately every 2 weeks for the first month after a new deslorelin implant was placed and then monthly thereafter. Blood samples were collected into heparinized containers, centrifuged, and stored frozen at -80[degrees]C until processing. Banked plasma samples, collected before gonadotropin-releasing hormone (GnRH) agonist therapy, were analyzed opportunistically (Fig 1).

Seven months after placement of the last implants, the bird presented in acute respiratory distress and died following cardiac arrest. Necropsy results showed intracoelomic bleeding and exsanguination from fractures in both the hepatic and splenic capsules. Histopathologic examination did not support any underlying infectious or neoplastic cause. A traumatic cause of the hemorrhage was considered the most likely, although no inciting traumatic incident was observed. Normal spermatogenesis was noted in the testicles microscopically. No gross abnormalities were noted in the pectoral skeletal musculature, and the implants were not seen at the time of necropsy.

Case 2

The second turkey, 17 months old (17.7 kg) and 16 months after arrival at the institution, had a similar presentation to the conspecific bird in case 1. However, this bird was considered the dominant turkey of the pair. This turkey was treated with the same regimen of leuprolide acetate and deslorelin acetate implants at the same time intervals as the turkey in case 1. Testosterone plasma concentration was similarly measured (Fig 1). Aggressive behavior was reduced after the deslorelin acetate implants, similar to the first turkey in onset and duration, although this may have been due to synergistic effects of both birds being treated simultaneously. After the death of the conspecific turkey, no further treatments to mitigate aggression were needed, and no plasma testosterone concentrations were measured in this solitary bird. Eighteen months after the final deslorelin acetate implant, the turkey was euthanized because of chronic, progressive decreased mobility.

At necropsy, severe osteoarthritis was evident in the coxofemoral joints bilaterally, but no other abnormalities were observed in the gonadal tissue or pectoral skeletal musculature and the deslorelin implants were not found. Histopathologic examination was not performed on either the gonadal tissue or pectoral skeletal musculature.


Wild turkeys maintain a competitive social structure that encourages behaviors leading to the establishment of a social hierarchy. Similar aggressive behaviors are also observed in domestic turkey breeds and are frequently directed between unfamiliar males. In commercial turkey operations, aggression is thought to amplify in smaller groups and in smaller enclosures. (1)

In the cases we describe, aggression was not observed initially, likely because the birds were immature at 1 month of age. In commercial operations, onset of sexual maturity is expected at approximately 7.5-8 months of age. (2) Although development of aggression may have correlated with onset of sexual maturation in these cases, no significant notation during this period was made, and mitigation through medical therapy was not deemed necessary until 17 months of age.

Testosterone is correlated with intermale aggression in animals, (3) with castration decreasing aggression and replacement of testosterone restoring aggressive behavior. (4) Testosterone is the main androgen produced by sexually mature, male birds (5) and is secreted in a pulsatile pattern in sexually mature, male turkeys. (6) It is an end product of the hypothalamic-pituitary-gonadal axis, which, in birds, is similar to that in mammals, where GnRH is primarily responsible for release of gonadotropin from the hypothalamus. (7-9) Avian GnRH-1, (10) -2, (11) and -3 (12) are the unique forms of GnRH that are recognized in birds. Avian GnRH1 is thought to control release of both follicle-stimulating hormone and luteinizing hormone from the anterior pituitary gland and avian GnRH-2 is thought to control sexual behaviors. (7) All types of avian GnRH can bind and activate each of the 2 recognized avian GnRH receptors, but there are differences in receptor affinity and specificity. (7,9,13)

Both leuprolide and deslorelin acetate are GnRH superagonists that function to downregulate the hypothalamic-pituitary-gonadal axis by negative feedback, after an initial surge to suppress reproduction and associated hormones, including follicle-stimulating hormone and luteinizing hormone. Differences in avian GnRH types, GnRH receptor subtypes, and inherent species specificities may all contribute to differences in efficacy or duration of effect of synthetic mammalian GnRH agonists, such as leuprolide and deslorelin acetate. Moreover, both are considered superagonists because of their higher affinity for GnRH receptors and longer half-life than endogenous GnRH. (14)

Leuprolide acetate, in a sustained-release depot formulation, was administered to both turkeys in this case series. The depot formulation suppresses the reproductive system by a constant, nonpulsatile release of leuprolide acetate from biodegradable microspheres. (8) This drug has been evaluated previously in several avian species, including cockatiels (Nymphicus hollandicus) and Hispaniolan Amazon parrots (Amazona ventralis). (15-17) Although testosterone levels were not actively monitored during the period in which leuprolide acetate was administered to these turkeys, aggressive behavior was only minimally decreased after the second trial. Aside from inherent differences in avian GnRH types and receptor subtypes, contributing factors for the minimal change in behavior after leuprolide acetate administration could have been seasonality and use of doses (50-100 [micro]g/kg) below or at the low end of the wide dose range published (100-1200 [micro]g/kg). (18) The low dose administered was conservative because of limited published information on the use of leuprolide acetate to reduce aggression and was an attempt at allometrically scaling the dose to the large size of these birds. Repeated administration of leuprolide acetate is recommended to be effective; however, this was less desirable for these turkeys because of the need for repeated handling and was considered a nonviable long-term management option. (18) In addition, leuprolide acetate injections for these large birds were costly, which contributed to the choice of the low dose and the preference for the more cost-effective deslorelin acetate implants.

Deslorelin acetate implants have been recommended as a contraceptive because of the prolonged antigonadotropic effects in many species, particularly in carnivores. (19) Deslorelin acetate implants are frequently used as a contraceptive in female animals, and control of male reproduction and associated behaviors with deslorelin has been reported in several species, including domestic dogs, (20,21) domestic cats, (22) domestic boar, (23) cheetah (Acinonyx jubatus), an African wild dog (Lycaon pictus), (25) sea otters (Enhydra lutris), (25) red wolves (Canis lupus rufus), (25) grey wolves (Cams lupus), (25) a black-footed cat (Fells nigripes), (25) black flying foxes (Pteropus alecto), (26) ferrets (Musteki putorius furo), (27) lion-tailed macaques (Macaco silenus), (28) a bearded dragon (Pogona vitticeps),29 and common brushtail possums (Trichosurus vulpecula), (30) with variable results and duration of efficacy that appear to be species specific. A single 4.7-mg implant is labeled by the manufacturer for a minimum of 6 months of effective contraception in domestic dogs outside of the United States, whereas a single 9.4-mg implant is labeled for a minimum of 12 months of effective contraception. (20) In the United States, a single 4.7-mg implant is labeled by the manufacturer for the management of adrenal cortical disease in domestic ferrets (Suprelorin F, Virbac Animal Health, Fort Worth, TX, USA) but is not approved by the US Food and Drug Administration (FDA) and is marketed as an FDA Indexed Product under MIF 900-013. (31) The use of deslorelin acetate implants in any avian species is not approved by the FDA and is not approved for use in any animal intended to enter the human or animal food supply. However, deslorelin acetate implants are commonly used extralabel in multiple species. (19)

Use of deslorelin acetate implants have been documented in retrospective studies and case reports in mostly psittacine birds for management of various conditions. (32-37) However, prospective studies are limited to those involving domestic chickens, (38) Japanese quail (Coturnix japonica), (39-41) and domestic pigeons (Columba livia). (42) Although most research has focused on female reproduction suppression, one report in male Japanese quail implanted with a single 4.7-mg deslorelin acetate implant evaluated circulating testosterone concentrations, which were reduced in all birds 3 days after implantation. (39) In male domestic pigeons implanted with a single 4.7-mg deslorelin acetate implant, plasma luteinizing hormone concentrations were decreased at 7, 28, and 56 days after administration. Body weight did not change, and effect on fertility was unclear. (42) Similarly, circulating testosterone concentrations in the turkeys in this case series were considered to be lower when the deslorelin acetate implants were present than what would be expected without GnRH agonist therapy. In both turkeys in this case, deslorelin acetate implants of both 9.4 mg and 18.8 mg resulted in decreased aggression between the turkeys and toward the animal care staff for similar periods to onset and duration. A synergistic effect between the birds was likely, where decreased aggression in one bird resulted in decreased aggression in the second bird. Moreover, the onset of effect was measured as the time when the animal care team could cohouse the turkeys consistently without observed aggression.

A previous study evaluating plasma testosterone concentrations in captive subadult male eastern wild turkeys in the United States (n = 3) found circulating levels of testosterone measured by radioimmunoassay were 32-63 ng/100 mL at 6 weeks and increased to 87-108 ng/100 mL at 34 weeks of age. In January and February, plasma testosterone concentrations rose to 146.0 [+ or -] 62.3 ng/100 mL and plateaued in mid-March and April to 254.4 [+ or -] 140.5 ng/100 mL. In the single dominant captive male, testosterone level peaked in mid-March at 560 ng/100 mL, which was markedly higher than levels in the 2 subordinate captive male turkeys. In the same study, testosterone concentrations in wild trapped subadult and adult male turkeys (n = 11) ranged from 202.2 [+ or -] 61.9 ng/100 mL in January and February. In March and April, mean testosterone concentration in killed subadult and adult male turkeys (n = 30) was 344.9 [+ or -] 110.8 ng/100 mL. (43) Despite a small sample size in this study, patterns of testosterone were similar to the 2 turkeys in this case report with relatively elevated testosterone concentrations between January and May. Likewise, the turkey considered the dominant male of the pair (case 2) generally had increased testosterone concentrations compared with the subordinate male, although this is not always consistent.

Before receiving any GnRH agonist, the turkeys maintained low levels of testosterone, aside from single elevated values in January and February 2008, although baseline data are limited. The elevated plasma concentrations could have been spurious or caused by the onset of breeding season. After initially receiving leuprolide acetate treatment, few plasma samples were available for testosterone concentration analysis; however, after a second dose of leuprolide acetate in October 2009, consistently low concentrations of plasma testosterone were measured in both birds. The first two 4.7-mg deslorelin implants, placed in November 2009, resulted in consistently low testosterone plasma concentrations for approximately 3.5 months until February and March, just before the second implant placement. This increased concentration could be because of the end of the deslorelin implant lifespan or natural testosterone concentration elevations associated with breeding season. The second two 4.7-mg deslorelin implants were placed in March 2010, which resulted in low testosterone concentrations until the 9.4-mg deslorelin implants were placed in September 2010. Testosterone concentrations did not increase until March 2011, which could have been caused by the end of the deslorelin implant lifespan or natural increases in testosterone concentrations associated with breeding season. After the death of the subordinate bird (case 1) in April 2011, the conspecific bird (case 2) received no other GnRH agonist therapy, and no further measurements of plasma testosterone concentrations were done; thus, the duration of low levels of circulating testosterone could not be evaluated. If the turkeys had not had any GnRH agonist therapy, testosterone profiles may have been more similar to wild turkeys with consistently higher levels achieved in January through May.

No adverse effects were associated with the deslorelin implants in the turkeys clinically or found at necropsy, which is consistent with other studies. (34,40) Although deslorelin implants are recommended to be implanted subcutaneously under sedation or anesthesia, the IM administration of the implant under manual restraint was well tolerated by the turkeys. Administration is presumably more painful by the IM route than by the SC route, but no analgesics were provided because the birds had minimal reaction and normal behavior immediately after the implantation. This was likely because of the exaggerated pectoral musculature, ease of access to the muscles under manual restraint, and large size of the birds, with an average weight of 17.9 kg at the time of necropsy. Moreover, the turkeys were considered obese and high-risk anesthetic candidates; thus, sedation and anesthesia were avoided, and subcutaneous access was more difficult to obtain under manual restraint. Implantation sites that contain a high degree of adipose, bone, or cartilage should be avoided in favor of sites with more musculature and vascularity. (19) The pectoral musculature in these cases was thought to be adequately vascular for absorption of drug from the implant.

At necropsy, the implants were not found. This may be because of implant migration, expulsion from the body, or breakdown of the product. Although the implant does not dissolve completely, it may break down over time as it becomes more porous and more challenging to retrieve. It is possible to surgically remove deslorelin acetate implants; however, this was not done for either turkey because it is unnecessary for product function, the product does not typically result in adverse effects, and removal requires general anesthesia and potentially invasive surgery to investigate the pectoral musculature. (19)

Castration may be considered as an alternative to repeated deslorelin acetate implants in birds. However, despite having castration techniques described for avian species, castration was not considered a viable management option for either turkey because of their large size, increased anesthetic risk during a prolonged procedure, and potential for testicular regrowth with incomplete castration. (44)

In conclusion, this case report documents the use of deslorelin acetate implants to decrease aggression between 2 adult, male domestic turkeys and the corresponding plasma testosterone concentrations that were lowered relative to levels in nondeslorelin-treated birds. However, further controlled prospective studies are needed to assess the deslorelin acetate dose, associated testosterone concentrations, and objective ethogram-based behavioral scoring evaluation.

Acknowledgments: We gratefully acknowledge the animal husbandry and health staff at Disney's Animal Kingdom who cared for these birds.

Christine M. Molter, DVM, Deidre K. Fontenot, DVM, and Scott P. Terrell, DVM, Dipl ACVP

From the William R. Pritchard Veterinary Medical Teaching Hospital, University of California-Davis, 1 Shields Ave. Davis, CA 95616, USA (Molter); and the Department of Animal Health, Disney's Animal Kingdom, 1200 N. Savannah Circle E, Bay Lake, FL 32830, USA (Fontenot, Terrell).


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Author:Molter, Christine M.; Fontenot, Deidre K.; Terrell, Scott P.
Publication:Journal of Avian Medicine and Surgery
Article Type:Report
Date:Sep 1, 2015
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