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Bilateral Anterior Uveitis in a Northern Saw-whet Owl (Aegolius acadieus) With a Metastatic Pectoral Malignant Mesenchymoma.

Abstract: A captive, adult, male northern saw-whet owl (Aegolius acadicus) was examined for blepharospasm of the left eye. The owl was diagnosed with bilateral anterior uveitis and a corneal ulceration in the left eye. It was treated with oral and topical nonsteroidal anti-inflammatory medications and a topical antibiotic. Multiple recheck examinations and medication adjustments were performed over the next 4 months, at the end of which time the bilateral anterior uveitis was controlled with a topical nonsteroidal anti-inflammatory applied 3 times per week to both eyes. The owl was re-examined 2 months later after 2 suspected neurologic episodes. On physical examination, the owl was quiet and had difficulty standing and ambulating. Five firm multilobular and immobile masses were identified overlying the pectoral muscle and sternum. Fine-needle aspiration from 1 mass revealed neoplastic cells consistent with a sarcoma. The owl was euthanatized. On the basis of results of histopathologic examination, the mass was diagnosed as a pleomorphic spindle cell sarcoma with features of rhabdomyosarcoma, liposarcoma, and osteosarcoma. Numerous tumor cells were immunopositive for myoglobin and desmin, indicating striated muscle origin. Although a metastatic lesion was present in 1 adrenal gland, lesions of inflammation or neoplasia were absent in either eye on histopathologic examination. This report describes an apparent ocular manifestation of systemic disease in an avian species with clinically diagnosed recurrent anterior uveitis.

Key words: anterior uveitis, paraneoplastic syndrome, mesenchymoma, pleomorphic sarcoma, avian, northern saw-whet owl, Aegolius acadicus

Clinical Report

An adult, male northern saw-whet owl (Aegolius acadicus) was admitted to The Raptor Center at the University of Minnesota (UMN) in May 2016 for a painful left eye. The owl was originally presented to The Raptor Center as an adult in October 2008 with a left humeral fracture. The owl did not regain adequate flight for release and therefore was placed as an educational ambassador at a local nature center. The color of the irises had gradually changed from yellow to orange over the previous 4 years, but with no associated clinical signs until a few days before presentation.

Physical examination of the owl was unremarkable. On ophthalmic examination, the owl was visual bilaterally with a positive dazzle reflex and direct pupillary light reflex, as well as signs of positive functional vision. The left eye (OS) had blepharospasm and was diagnosed with blepharitis, a superficial but suspected infected corneal ulceration with cellular infiltration, positive fluorescein stain, and anterior uveitis (+1-2 flare; scale, trace to 44 flare). The right eye (OD) appeared nonpainful with no signs of blepharospasm, but anterior uveitis (+1-2 flare) was observed. The irises of both eyes (OU) were orange, with the left iris having a darker hue than the right (Fig 1). Bilateral fundic examination revealed healed chorioretinal scars with hypo- and hyperpigmented areas diffusely around the pecten. No signs of active inflammation with cellular infiltration were appreciated in the posterior segment. Cytologic examination of a corneal scraping and culture and sensitivity testing from the corneal ulceration OS were recommended but declined by the nature center for financial concerns. The owl was treated with a topical nonsteroidal anti-inflammatory ophthalmic solution (diclofenac 0.1% q12h OD), topical antibiotic (ciprofloxacin 0.3% ophthalmic solution q4-6h OS), and a topical hyaluronic acid ophthalmic lubrication q4-6h OS (I-drop Vet; IMed Pharma, Dollard-des-Ormeaux, QC, Canada). Treatment with an oral nonsteroidal anti-inflammatory (meloxicam, 0.5 mg/kg PO q12h) was initiated.

A recheck examination 1 week later revealed that the corneal ulceration OS had healed (no fluorescein stain uptake). The flare OD had resolved but persistent +1 flare OS was still present, indicating mild anterior uveitis. The intraocular pressure was within normal limits OU (14 mm Hg OD, 15 mm Hg OS). Treatment with topical diclofenac was initiated OS with 1 drop q12h and decreased OD to 1 drop q24h. Treatment with meloxicam was continued.

The owl experienced episodic recurrence of bilateral anterior uveitis over the next 4 months. Topical diclofenac and oral meloxicam were used to control the uveitis by modifying the frequency of diclofenac and the dosage of meloxicam, based on clinical response. A complete evaluation including blood tests, infectious disease titers, and diagnostic imaging was recommended because of a suspicion that the bilateral anterior uveitis was an ocular manifestation of a systemic disease (infectious or neoplastic), (1,2) but declined because of financial limitations. The nature center agreed to bring the owl for recheck examinations and to continue the topical and oral medication with diclofenac and meloxicam, respectively.

On final ophthalmologic recheck 4 months after the initial presentation, the owl was visual and appeared comfortable OU. No signs of active uveitis were appreciated OU, but the right cornea had developed diffuse moderate edema. Both irides were persistently orange, with the left iris slightly darker than the right. The intraocular pressure remained within normal reference intervals. Meloxicam was discontinued, and treatment with topical diclofenac was continued (1 drop 3 times/ wk OU). Ophthalmic recheck examination was recommended in months.

Six months after the initial presentation, the owl was presented for re-evaluation after 2 seizure-like episodes. The first episode occurred 5 days before and the second episode occurred on the day of presentation. The episodes were described as a loss of balance, falling off the handling glove, and inability to stand but with no loss of consciousness.

Each episode lasted for approximately 15 minutes. On physical examination, the owl was in fair body condition and weighed 87 g. Body temperature was 39.4[degrees]C (102.9[degrees]F) (normal body temperature for a bird with a body weight of 87 g: 39.8[degrees]C-40.2[degrees]C [100.4[degrees]F-103.6[degrees]F]), (3,4) heart rate was greater than 200 beats per minute (bpm) with a normal rhythm (normal resting heart rate for a bird with a body weight of 87 g: 110-336 bpm), (5) and the respiratory rate and effort was moderately increased at 60 breaths per minute (normal respiratory rate for a bird with a body weight of 87 g: 20-30 breaths per minutes). (6) Five firm, immobile masses ranging from 0.2 to 2 cm in diameter were palpable and appeared to be associated with pectoral muscle tissue (Fig 2). No signs of active uveitis were present, and the owl was currently being treated with topical diclofenac at the last prescribed dosage. No other behavior changes or clinical signs were reported.

Blood was collected for an in-house complete blood count and serum biochemical profile (VetScan, Abaxis, Union City, CA, USA). The total white blood cell count was at the upper limit of the reported normal reference interval for this species (17 800 cells/[micro]L [reference mean [+ or -] SD: 11 600 [+ or -] 3600 cells/[micro]L; range, 7.1-18.3 cells/[micro]L). (3) The white blood cell differential revealed a moderate heterophilia (76%; 29% [+ or -] 10%; range, 27%-56%), (3) and a mild lymphopenia (13%; 35% [+ or -] 15%; range, 11%-60%) (3) consistent with a stress leukogram. Approximately 80%) of the lymphocytes were reactive, characterized by a basophilic cytoplasm and amorphous cell margins. The bird had a mild regenerative anemia (packed cell volume [PCV] 34%; 48% [+ or -] 5%; range, 39%-55%), characterized by polychromasia and anisocytosis and a mild hypoproteinemia (3.2 g/dL; 6.3 [+ or -] 1.7 g/dL; range, 4.4-10.5 g/dL). (7) Plasma biochemical results (Table 1) indicated an increased uric acid concentration, attributed to a recent meal, and mild hypocalcemia, which was not considered clinically significant.

The owl was sedated with isoflurane via facemask for whole-body radiographs and fine-needle aspiration of the mass. Radiographs revealed multiple soft tissue masses in the right axillary region and overlying the pectoral muscles, a healed left humeral fracture, as well as changes consistent with mild osteoarthritis in the left shoulder joint, and moderate-severe osteoarthritis in the left stifle. The owl had temporary vertical nystagmus and ataxia after sedation. The bird was treated with supportive fluids (45 mL/kg SC lactated Ringer's solution) and meloxicam (1 mg/kg PO) and was hospitalized overnight.

Results of cytologic examination of the fine-needle aspirate revealed a moderately cellular sample composed of blood with scattered dense, cohesive, disorganized aggregates of stellate to spindloid mesenchymal cells. Cells were characterized by a moderate amount of granular basophilic cytoplasm sometimes containing scattered, fine, clear punctate vacuoles with indistinct cell margins. Most cells contained a single round to oval to elongate nucleus with coarsely stippled chromatin and 1-3 variably sized prominent nucleoli. Occasional multinucleated cells were observed. Anisocytosis and anisokaryosis were moderate; occasional fine pink extravascular material was associated with cell aggregates. The cytologic diagnosis was a soft tissue sarcoma (Fig 3).

The next morning, the owl was quiet, responsive, and standing. Its respiratory effort had worsened and was now severely increased, and it was appreciably lame on the left pelvic limb. Because of the progressive respiratory signs, severe arthritis, and poor long-term prognosis associated with a large sarcoma, the nature center elected euthanasia.

A postmortem examination was performed at the Minnesota Veterinary Diagnostic Laboratory. Results revealed the owl was underweight (body weight: 85 g) with only scant internal adipose tissue. A well-demarcated white, firm, homogeneous multilobular mass was found in the right pectoral muscle. The mass was approximately 4.5 x 3.5 x 2.5 cm, extending from the right shoulder joint region to the caudal aspect of the keel bone (Fig 4). The skin was firmly attached to the mass. The mass penetrated the keel bone and abutted against the pericardium without adhering to it. The remainder of the examination was unremarkable.

Histologic examination revealed the mass was multifocally necrotic and highly infiltrative, based on skin, adipose, bone, and muscle involvement (Fig 5). The bulk of the neoplasm consisted of haphazardly interwoven bundles of densely packed, spindle-shaped cells that were occasionally nestled within a scant amount of eosinophilic homogeneous extracellular matrix. The spindle-shaped tumor cells had indistinct cell borders and elongate euchromatic nuclei with marked anisokaryosis and 1 prominent nucleolus per nucleus. Up to 8 mitotic figures per high-power field were present. The cytoplasm of the tumor cells was eosinophilic and fibrillar. In some areas, a few tumor cells had multiple nuclei that tended to line up along the long axis of the cell so that these cells resembled "strap cells." Tumor cells were present within bone marrow cavities of the sternum. The skin was ulcerated in areas of tumor cell infiltration of the dermis. Small areas of the pectoral neoplasm were characterized by the deposition of small islets of homogeneous eosinophilic material interpreted to be osteoid distant from the sternum. The deposited material was directly associated with pleomorphic round to oval to spindle-shaped tumor cells. In other areas, clusters of markedly swollen tumor cells that contained clear, fine-vacuolar cytoplasm were interspersed within the mass. One adrenal gland was infiltrated and slightly enlarged by neoplastic spindle cells. One coronal section through both cerebral hemispheres and sagittal sections through brainstem and cerebellum were examined histologically with no evidence of lesions, including metastases. Lesions were absent in kidneys, liver, lungs, testes, pancreas, and heart.

A peroxidase-based polymer system was used for immunohistochemistry (IHC). Myoglobin (Dako, catalog no. A0324; rabbit polyclonal antiserum at a 1:2000 dilution; Dako/Agilent Technologies, Santa Clara, CA, USA), desmin (Dako, catalog no. M0760; mouse monoclonal antibody at a 1:100 dilution), and smooth muscle actin (SMA; Dako, catalog no. M0851; mouse monoclonal antibody at a 1:100 dilution) were used as primary antibodies. Although the SMA-specific IHC does not include a specific antigen retrieval procedure, the IHC protocol for SMA and myoglobin includes heating the slide with the deparaffinized section to a temperature of 125[degrees]C for 30 seconds in a pressure cooker at 19 pounds per square inch with a target retrieval solution (Dako catalog no. SI699) at pH 6. Many of the tumor cells were positive for myoglobin and desmin but negative for SMA. The specificity of these markers was verified according to the immunoreactivity pattern of smooth muscle fibers of the feather follicle erector muscle (immunopositive for SMA and desmin but immunonegative for myoglobin) and unaffected pectoral striated muscle fibers within the section (immunopositive for myoglobin and desmin and immunonegative for SMA).

On histopathologic examination, both eyes had similar focally extensive and well-delineated lesions that were largely limited to the central retina. The retina had marked outer retinal atrophy, vacuolization (retinoschisis), and M tiller cell hypertrophy characterized by numerous optically empty, variably sized vacuoles that expanded and completely distorted and partially effaced the outer retina (retinoschisis) (Fig 6). These vacuoles were bordered by homogeneous pale eosinophilic cellular processes whose nuclei were occasionally present at the outermost portion of the degenerated retina. Immunohistochemical stains for glial acid fibrillar protein (Dako, catalog no. M0349; rabbit polyclonal anti-human at a 1:1500 dilution--peroxidase based polymer system) revealed that these cells presented strong cytoplasmic positivity and thus were interpreted as hypertrophied Miiller cells. A complete absence of photoreceptor outer segments was also present in the affected retinal portion, whereas the inner nuclear, inner plexiform, ganglion, and nerve fiber layers were relatively spared. Other minor changes were a mild posterior cortical cataract OU and mild peripheral corneal vascularization OD. No histologic evidence of inflammatory infiltration was present in the ocular tissues.

Final diagnosis on the basis of histopathologic and immunohistochemical results was a malignant mesenchymoma with differentiation into striated muscle cells, osteoblasts, and adipocytes in the pectoral muscle with metastasis to the adrenal gland. The retinal lesions were consistent with focally extensive and severe outer retinal atrophy and retinoschisis.

Discussion

This report describes the diagnosis of a malignant mesenchymoma with metastasis to 1 adrenal gland in a northern saw-whet owl. Differentiation into striated muscle was confirmed by immunohistochemical findings. The malignant mesenchymoma may also be termed "composite sarcoma." (8,9) The differential diagnosis of an undifferentiated pleomorphic sarcoma was considered (10); these are tumors whose histogenesis is not clearly defined, whereas malignant mesenchymomas are defined by the presence of tumor cells that differentiate into 2 or more mesenchymal tissue types. The owl had been treated for recurrent bilateral anterior uveitis for 6 months before the diagnosis. The recurrent anterior uveitis may have been a paraneoplastic ocular manifestation related to the malignant mesenchymoma. No signs of intraocular metastasis or inflammation were found on histopathologic examination of the eyes despite the clinical signs of disease.

Neoplasia is an uncommon finding in most avian species. A study of 5957 captive wild bird postmortem examinations in 1977 revealed only 1.8% had a neoplastic lesion. The study also showed that 40% of these neoplastic lesions were benign and 60% were malignant, with lymphosarcoma as the most likely neoplastic diagnosis. (11) To our knowledge, malignant mesenchymomas have not been described in birds. Only 1 bird (an Indian red jungle fowl, Gallus gallus murghi) was diagnosed with rhabdomyosarcoma in connection with leukemic lymphosarcoma of visceral distribution. (11) Rhabdomyosarcoma has since been described in 5 case reports in avian species over the last 32 years. Rhabdomyosarcoma has been described in the extraocular muscles in a budgerigar (Melopsittacus undulatus) and peregrine falcon (Falco peregrinus cassini), (12,13) in the cutaneous muscles with metastasis to the brain in a white leghorn chicken, (14) and in the pectoral and proximal wing muscles of a European robin (Erithacus rubecula) and a yellow-headed caracara (Milvago chimachima). (15,16) None of these cases had signs of anterior uveitis associated with rhabdomyosarcoma. The white leghorn chicken showed neurologic signs secondary to a metastatic lesion in the brain. (14)

Potential causes of the uveitis in this bird are historical trauma, as well as underlying systemic disease. Ocular manifestations of systemic inflammatory or neoplastic diseases are well-known to human and veterinary ophthalmologists. (1,2) The eye is an immunologically privileged organ with a blood-ocular barrier that prevents potential blood-borne antigens/antibodies or infectious agents from entering the eye and causing destructive intraocular inflammation and infection with risk of blindness. (17,18) This barrier can deteriorate after trauma or with severe systemic disease. (2,19) Systemic diseases involving the central nervous system or vasculature are most likely to involve the eye secondarily. (2) The northern saw-whet owl in this report had no signs of metastasis of the mesenchymoma to the brain or ocular tissue despite being presented for bilateral anterior uveitis 6 months before the diagnosis of neoplasia. Reports in people describe paraneoplastic vasculitis associated with malignant neoplasia from the release of tumor angiogenic factors, cytokines, or both, causing endothelial damage and vasculitis with increased vascular permeability and inflammation as a result. (20) Paraneoplastic vasculitis could account for the development of bilateral anterior uveitis in this owl, with no evidence of ocular metastasis of the mesenchymoma. No reports have correlated mesenchymoma and anterior uveitis in the veterinary or human literature. This clinical report suggests that anterior uveitis could potentially represent an ocular manifestation of mesenchymoma in birds. Alternatively, uveitis could have been related to previous trauma, although the delay between trauma and the development of uveitis makes that less likely. Other underlying systemic diseases cannot be fully excluded but seem unlikely given the lack of gross or microscopic lesions supporting other systemic pathology.

Ocular histopathology did not reveal signs of chronic anterior uveitis or vasculitis. Clinical versus pathologic identification of intraocular inflammation may not always be concordant. Pigmentary uveitis in golden retrievers is a disease in which ophthalmologists observe significant signs of uveitis with flare and fibrin in the later stages of disease, ultimately causing secondary glaucoma. (21,22) Uveitis is rarely identified on the histologic and immunohistochemical evaluation of these globes. (22,24) This owl's anterior uveitis was controlled with topical anti-inflammatory medication at the last recheck examination 2 months before euthanasia, and no sign of active uveitis was noted on the physical examination 1 day before euthanasia. If the uveitis was controlled with topical medications, histopathology may not have revealed signs of active inflammation, just as is seen for pigmentary uveitis in golden retrievers.

On histopathologic examination, marked outer retinal atrophy and retinoschisis were identified as abnormal ophthalmic findings in both eyes. Retinoschisis is an extreme form of cystic degeneration of the retina in which parts of the retina have separated into 2 layers between the retinal pigment epithelium and the rest of the neuroretina. (25) The disorder leads to partial or total vision loss and can be a juvenile X-linked genetic disease or an age-related degenerative finding in people. (26) Retinoschisis has been reported as a rare finding in dogs, and the underlying cause is not known. (25,27) Raptors are prone to retinal detachments and vitreal hemorrhage secondary to head trauma. (28,29) We postulate that the owl's retinoschisis and outer retinal atrophy may have occurred secondary to a previously undiagnosed retinal detachment that occurred concurrently with the fractured left humerus in 2008 and hence was unrelated to the anterior uveitis or mesenchymoma that was later diagnosed. To our knowledge, this is the first report describing retinoschisis in a northern saw-whet owl with history of a traumatic event 8 years before.

The underlying cause of the suspected neurologic signs was not found. The owl demonstrated clinical signs that could have been consistent with a central nervous system lesion, including dull mentation, periodic loss of balance, and ataxia. The owl did not appear to have a seizure, because the bird did not lose consciousness during the 15-minute episodes of loss of balance and inability to right itself. There were no electrolyte abnormalities that could explain the neurologic signs, and there were no lesions in the brain postmortem. One possible cause of the loss of balance is syncope related to a cardiac arrhythmia. Although an arrhythmia was not auscultated, the mesenchymoma had penetrated the keel and was directly contacting the heart, which could have triggered an arrhythmia and secondary syncope. It is also possible that the bird was weak and depressed secondary to the advanced neoplasia, and the apparent loss of balance was a reflection of pain and decreased use of the left pelvic limb because of arthritis. The increased respiratory rate and effort may have been related to pain, stress, or the large-mass lesions compressing the air sacs and limiting mobility of the keel.

In this report we describe a geriatric, captive northern saw-whet owl with recurrent bilateral anterior uveitis suspected to be an ocular manifestation associated with a mesenchymoma. Anterior uveitis was diagnosed 6 months before discovering the neoplasia and was hypothesized to be an ocular manifestation of a systemic disease at the initial diagnosis. Mesenchymoma originating from the pectoral muscle with metastasis to the adrenal gland has not been previously diagnosed in this species, or in any member of the Strigiformes order. Retinoschisis and outer retinal atrophy were incidental findings on histopathologic examination and were suspected to have been caused by trauma 8 years before and therefore unrelated to the anterior uveitis, neurologic abnormalities, and mesenchymoma.

References

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(7.) Ammersbach M, Beaufrere H, Gionet Rollick A, Tully T. Laboratory blood analysis in Strigiformes--part 11: plasma biochemistry reference intervals and agreement between the Abaxis Vetscan V2 and the Roche Cobas c501. Vet Clin Pathol. 2015:44(1): 128-140.

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(10.) Paiva ACG. Morgado de Abreu MAM, Souza MP. Undifferentiated pleomorphic sarcoma. An Bras Dermatol. 2018:93(1): 154-155.

(11.) Effron M, Griner L. Benirschke K. Nature and rate of neoplasia found in captive wild mammals, birds, and reptiles at necropsy. J Natl Cancer Inst. 1977; 59(1):185-198.

(12.) Gulbahar MY, Ozak A, Guvenc T, Yarim M. Retrobulbar rhabdomyosarcoma in a budgerigar (Melopsittacus undulatus). Avian Pathol. 2005:34(6): 486-488.

(13.) Coello MJF, Schaeffer LS. Retrobulbar rhabdomyosarcoma in a neotropical peregrine falcon (Falco peregrinus cassini). Vet Ophthalmol. 2014; 17(l):73-75.

(14.) Grewal S, Patel HS. An unusual case of rhabdomyosarcoma in a fowl. Avian Pathol. 1985:14(1): 177-180.

(15.) Manarolla G, Radaelli E, Pisoni G, et al. Rhabdomyosarcoma of the pectoral muscles of a free-living European robin (Eritliacus rubecula). Avian Pathol. 2008;37(3):311-314.

(16.) Maluenda AC, Casagrande RA, Kanamura CT, et al. Rhabdomyosarcoma in a yellow-headed caracara (Milvago chimachima). Avian Dis. 2010:54(2): 951-954.

(17.) Taylor AW. Immunosuppressive and anti-inflammatory molecules that maintain immune privilege of the eye. In: Dart DA, Dana R, D'Amore P, Niederkom JY, eds. Immunology, Inflammation and Diseases of the Eye. San Diego, CA: Elsevier; 2011:44-49.

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Michala de Linde Henriksen, DVM, PhD, Dipl ACVO, Leslie Sharkey, DVM, PhD, Dipl ACVP, Dana Franzen-Klein, DVM, Arno Wiinschmann, Dr med vet, Dipl ACVP, Leandro B. C. Teixeira, DVM, MSc, Dipl ACVP, Richard Dubielzig, DVM, Dipl ACVP, and Michelle Willette, DVM, MPH, Dipl ACVPM

From Comparative Ophthalmology. Department of Veterinary Clinical Sciences (de Linde Henriksen), Clinical Pathology, Department of Veterinary Clinical Sciences (Sharkey), and Department of Veterinary Population Medicine (Wiinschmann), College of Veterinary Medicine, University of Minnesota, 1365 Gortner Avenue, St Paul, MN 55108. USA; The Raptor Center, College of Veterinary Medicine, University of Minnesota, 1920 Fitch Avenue, St Paul, MN 55108. USA (Franzen-Klein, Willette); and the Department of Pathobiology Sciences, School of Veterinary Medicine, University of Wisconsin, 2015 Linden Drive, Madison, WI 53706. USA (Teixeira, Dubielzig). Present address: Comparative Ophthalmology. Department of Clinical Sciences, College of Veterinary Medicine and Biosciences. Colorado State University, 300 West Drake, Fort Collins, CO 80523, USA (de Linde Henriksen).

Caption: Figure 1. Photographs of a northern saw-whet owl on the first day of presentation for a painful left eye (OS) with blepharospasm. (A) OS appears discolored compared with the right eye (OD). (B) The owl showed no sign of pain OD but had evidence of anterior uveitis with +1 flare present in the anterior chamber. (C) A complicated corneal ulceration (white arrow) was present OS with cellular infiltration and anterior uveitis with +2 flare.

Caption: Figure 2. The northern saw-whet owl described in Figure 1, showing the mass lesions overlying the keel. The owl's head is at the top of the image; 3 of the 5 mass lesions are visible (arrows).

Caption: Figure 3. (A) Classical spindloid mesenchymal cells within the mass (black arrows). (B) Cells that have a more round to oval shape with somewhat more defined cytoplasmic margins, fine cytoplasmic vacuolization (black arrow), and oval to angular nuclei (white arrow). (C) A large round cell (black arrow) characterized by abundant eosinophilic granular cytoplasm. (X500, Wright Giemsa stain).

Caption: Figure 4. Cross section through the right pectoral muscle (S indicates sternum; Sub, subcutis). The muscle is largely replaced and expanded by a white firm infiltrative mass. Remnants of the muscle (*) are compressed.

Caption: Figure 5. (A) The pectoral mass was largely composed of plump to elongated neoplastic cells with indistinct cell borders. Occasional multinucleated cells (arrows) are present. These cells resemble myoblasts. Mitotic figures (arrowhead) were scattered among the neoplastic cells (hematoxylin and eosin, X40). (B) The pectoral mass also had regions in which eosinophilic homogeneous material (arrows) (interpreted as osteoid) was closely associated with the tumor cells (hematoxylin and eosin, X40). (C) The mass had regions in which the tumor cells contained large vacuoles (arrows) containing scant fine lacy material (hematoxylin and eosin, X40).

Caption: Figure 6. The outer segment of the retina is markedly expanded and distorted by variably sized optically empty spaces. Cellular processes, presumably of Muller cells, traverse the spongy meshwork. Photoreceptor neurons are no longer present in the depicted retinal segment. The inner segment of the retina is relatively spared. OPL indicates outer plexiform layer; INL, inner nuclear layer; G, ganglion cell layer (hematoxylin and eosin, X40).
Table 1. Observed biochemical values along with
reported global reference intervals for the order
Strigiformes. (7)

                            Observed    Reference

Analyses (units)              value     interval

AST (U/L)                      371       117425
Bile acids ([micro]mol/L)      <35       <35-93
CK (U/L)                       925       0-2964
Uric acid (nmol/L)          >2200 (a)   193-1483
Glucose (mmol/L)              17.6      12.0-24.8
Total calcium (mmol/L)      0.54 (a)    1.36-2.90
Phosphorus (mmol/L)           0.38      0.36-2.81
Total protein (g/L)            38         29-54
Albumin (g/L)                  31         2047
Globulin (g/L)                  7         0-23
Potassium (mmol/L)             3.9       2.2-6.8
Sodium (mmol/L)                160       139-166

(a) Indicates values outside the published reference interval.
Abbreviations: AST, aspartate aminotransferase: CK. creatine
kinase.
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Title Annotation:Clinical Report
Author:Henriksen, Michala de Linde; Sharkey, Leslie; Franzen-Klein, Dana; Wunschmann, Arno; Teixeira, Leand
Publication:Journal of Avian Medicine and Surgery
Date:Jun 1, 2019
Words:4785
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