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A yearling female mallard duck (Anas platyrhynchos) presented to the Wildlife Center of Virginia (Waynesboro, VA, USA) after being rescued from an artificial pond at a city park in Stanton, VA, USA. The bird was observed being aggressively pursued and attacked by multiple male ducks. In addition to mallards, multiple species of domestic ducks and geese were present in the pond.
On presentation, the duck had widespread abrasions over the dorsum, lacerations over the skull, and moderate bilateral periorbital swelling. The bird weighed 1.19 kg, was in poor to fair body condition (body condition score, 2/5), had decreased mentation, and was severely lethargic, mildly dehydrated, and unable to stand. Physical examination did not reveal any palpable instability of the long bones or the vertebral column; however, marked deviation of the vertebral column and asymmetry of the pelvic limbs was observed. Because of the bird's debilitated state, further diagnostic tests were not performed. Initial treatment consisted of topical wound care for superficial lesions on the back, head, and neck with chlorhexidine gluconate 2% scrub and topical vitamin A/D ointment. Antimicrobial therapy with sulfamethoxazole trimethoprim oral suspension (100 mg/kg PO q12h) (1) and subcutaneous fluid therapy with lactated Ringer's solution (60 mL) with added vitamin B were administered. The bird was placed in a warmed incubator to provide supplemental heat and oxygen. Several hours later the bird was removed from the enclosure for further examination and to obtain radiographs (Figs 1 and 2). The bird died during the second examination. A cardiac venipuncture was performed immediately after death to obtain a blood sample for a complete blood cell count and serum biochemical analysis. Abnormal results were eosinophilia (490 cells/[micro]L; reference interval, 140-240 cells/[micro]L), increased serum protein (6.9 g/dL; reference interval, 3.5-5.5 g/dL), and high concentrations of AST (86 IU/L; reference interval, 12-73 IU/L), calcium (13.5 mg/dL; reference interval, 8.7-12.7 mg/dL), creatinine kinase (CK, 22 945 IU/L; reference interval, 165-378 IU/L), and uric acid (162 mg/dL; reference interval, 2 12 mg/dL). (2)
The physical, radiographic, and microscopic findings were most consistent with chronic severe nutritional osteodystrophy, or rickets. Radiographs revealed poor corticomedullary definition of long bones and a decreased radiographic density of bones in the distal extremities (Figs 3 and 4). The cervical vertebrae and caudal synsacrum appeared well aligned: however, the midvertebral column showed prominent scoliosis (Fig 3) and marked coxofemoral malalignment.
At postmortem examination, the carcass was in poor to fair nutritional condition with scant subcutaneous or intracoelomic fat stores present. Gross examination of the vertebral column revealed severe lateral deviation in several locations beginning at the first thoracic vertebrae and extending caudally to involve the synsacrum (Fig 5). The spinal anomaly contributed to malalignment of the pelvis and subsequent asymmetry of the pelvic limbs. The pectoral musculature was in an advanced state of atrophy. The keel was very soft and malleable when dissected from the body. Several nematodes were present in the trachea, morphologically consistent with Syngamus species.
Histopathologic examination of longitudinal sections of the femur and tibiotarsal bones and articular joints demonstrated expanded physeal cartilage with a marked and irregular increase in the hypertrophic cartilage zone (Fig 6). The metaphyses contained sparse, thin, bony trabeculae with retention of cartilage cores and few intertrabecular connections. The cortical bone was irregularly thin with scalloped areas and a focal microscopic fracture. The periosteum along the metaphysis was mildly thickened. The epiphyses and metaphyses of long bones of the antebrachium and pelvic limbs all had similar microscopic changes. A longitudinal section of the stifle joint showed a disrupted tibiotarsal physis with variable expansion of the hypertrophic cartilage zone and focal replacement by proliferating mesenchymal spindle cells (fibroblasts) extending into the metaphysis. Multifocally, the metaphyseal trabeculae were thin and sparse, contained unmineralized cartilage cores, and occasionally were lined by osteoclasts. Histopathologic examination of skeletal muscle (pectoralis superficialis) revealed severe neurogenic atrophy, characterized by different diameters and angulation of the myofibers. The parathyroid glands were moderately hyperplastic. No significant gross or microscopic lesions were found in the lungs, heart, liver, kidneys, pancreas, intestines, or spleen.
Although information is limited about the function of the avian eosinophil, peripheral eosinophilia in birds can be loosely interpreted as a response to internal or external parasitism or exposure to foreign antigen (hypersensitivity response). (3) The high AST and CK values in this duck were consistent with muscle damage resulting from the attacks by other ducks in the pond. The mild hyperproteinemia and mild hypercalcemia were likely associated with hemoconcentration caused by dehydration. Hyperuricemia might have been caused by severe tissue damage, starvation, or severe dehydration.
Other differential diagnoses for this case are an anomalous genetic malformation or trauma-related injuries. Because genetic anomalies that result in a similar diagnosis have been reported, hereditary predisposition to nutritional osteodystrophy in this duck cannot definitively be dismissed. (4-6) In mammals, several heritable traits associated with rickets and osteomalacia have been identified and are commonly linked to a defect in either vitamin D metabolism or renal tubular function. (7) The possibility of an underlying genetic predisposition to nutritional osteodystrophy was not investigated in this case. Although the histologic findings alone cannot provide a definitive cause, the lesions observed in this bird along with the case history are suggestive of rickets.
Postmortem examination revealed no gross or microscopic evidence of previous traumatic injuries that could explain the bird's clinical presentation. The traumatic injuries to the skin and soft tissues observed during the initial physical examination were likely the result of inter- and intraspecific aggression brought on by the high waterfowl density and intensive and aggressive mating behavior at the city pond. This bird was obviously debilitated and could not adequately flee from aggression.
Rickets, one manifestation of metabolic bone disease, is a musculoskeletal disease syndromes characterized by abnormal endochondral ossification (7) and failure of mineralization of osteoid or of the maturing cartilaginous growth plate. (7,9) These bone malformations can lead to pathologic fractures and are most commonly observed in young, rapidly growing animals. (7-10) Lesions are typically most severe in the fastest growing bones, including the radius, the tibia, and the metacarpals and metatarsals. (7)
Rickets can be caused by a hereditable trait (7) or a variety of nutritional imbalances. (9) By definition, rickets is caused by a deficiency of vitamin D and, more specifically, vitamin [D.sub.3]. (8,9,11,12) Nutrient imbalances that might lead to rickets are excessive alkalinity of the intestinal tract; a high level of dietary fat; calcium complexing with oxalates or phytates in the intestine; dietary deficiency of calcium, vitamin D, or phosphorus; and high phosphorus-to-calcium ratio in the diet. (7,8) Vitamin D deficiency can be caused by low dietary levels, malabsorption, (7,9) or synthesis failure. The latter may occur in liver or kidney disease (4) or under conditions of inadequate exposure to ultraviolet (UV) light. (9,13)
Birds obtain vitamin D directly from the diet and by the action of UV-B on vitamin D precursors in the cutaneous tissues. (13) Vitamin D is intimately involved in calcium and phosphate homeostasis, and it plays a crucial role in bone formation and remodeling. (7) As in mammals, avian vitamin [D.sub.3] is synthesized in the skin from 7-dehydrocholesterol. Ultraviolet light in the range of 290-315 nm is required for the initial conversion from 7-dehydrocholesterol to previtamin [D.sub.3]. Birds metabolize vitamin [D.sub.3] to the circulating form [25-(OH)D3] and then to the active form [1,25-(OH)2D3; calcitriol] in the liver and kidneys, respectively, by using the same pathway as mammals. Calcitriol facilitates the intestinal absorption of Ca (14,15) by increasing the synthesis of Ca binding proteins. (15)
The etiology of this patient's osteodystrophy could not be confirmed, and a hereditary component cannot be ruled out; however, an inadequate diet likely played a significant role. Although a municipal coin-slot feeding station containing a commercial growth waterfowl chow is present on site, the public is frequently observed feeding inappropriate foods such as bread, popcorn, and other "junk food." Natural foodstuffs, such as aquatic invertebrates and aquatic vegetation are likely an underrepresented component of the diet because of the manmade nature of the pond and overforaging by the high concentration of waterfowl drawn by the supplemental feeding.
Metabolic bone disease is a common yet preventable condition in waterfowl living in public parks. Supplemental feeding of wild waterfowl by park visitors might be a well-intended attempt to promote healthy interactions with wildlife in heavily urbanized areas, but such actions could have negative consequences on the resident wildlife population, the regional environment, and public health.
Supplemental feeding could interfere with waterfowl population dynamics by promoting overcrowding and aggressive food competitive behavior and delaying or stopping migration patterns. Overcrowding often contributes to an immunocompromised state in individuals within that population and increases the potential for infectious disease outbreaks. (16-18) Artificially high waterfowl densities in urban and suburban parks could also pose public health concerns. Potentially zoonotic agents might be directly or indirectly spread to humans through increased physical contact with the waterfowl, their feces, or carcasses. (17-19) Additionally, supplemental feeding and associated increased waterfowl populations might attract scavenging and predatory species (eg, feral cats, rodents, raccoons, opossums, foxes, crows, gulls, pigeons), which could present additional public health challenges. (20)
Public education is necessary to inform park users of the consequences of supplemental feeding to waterfowl populations. Public outreach might be best achieved by posting educational signage in public parks where waterfowl are present. As shown in this case, medical management is often ineffective when treating chronic cases of metabolic bone disease; consequently, preventive measures are likely to have the greatest effect on individual animal and population health.
This case was submitted by Ana Carolina Ewbank, DVM, The Raptor Center, College of Veterinary Medicine, University of Minnesota, 1920 Fitch Ave, St Paul, MN 55108, USA; Mark G. Ruder, DVM, PhD, USDA, Agricultural Research Service, Arthropod-Borne Animal Diseases Research Unit, 1515 College Ave, room 101, Manhattan, KS 66502, USA; David L. MeRuer, MSc, DVM, Dipl ACVPM, Wildlife Center of Virginia, 1800 S Delphine Ave, PO Box 1557, Waynesboro, VA 22980, USA; and Anibal G. Armien, DVM, PhD, Dipl ACVP, Department of Veterinary Population Medicine, College of Veterinary Medicine, University of Minnesota Veterinary Diagnostic Laboratory, 1333 Gortner Ave, St Paul, MN 55108-1098, USA.
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|Title Annotation:||animal bone disease diagnosis|
|Publication:||Journal of Avian Medicine and Surgery|
|Article Type:||Clinical report|
|Date:||Jun 1, 2013|
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