Vertebral osteomyelitis and septic arthritis associated with Staphylococcus hyicus in a juvenile peregrine falcon (Falco peregrinus).
Key words: acute hematogenous osteomyelitis, AHO, bone infection, paresis, Staphylococcus hyicus, spinal cord, raptor, avian, peregrine falcon, Falco peregrinus
A 6-week-old, parent-reared, male peregrine falcon (Falco peregrinus) was presented with a history of inability to stand properly. The owner first observed the condition 6 days earlier during a routine check-up of the breeding aviaries. Duration and origin of the clinical condition were unknown. The 2 siblings of the bird, and the parent's offspring from former years did not demonstrate any comparable clinical signs. Food intake and defecation were normal, and no obvious injuries were noted. At clinical examination, the falcon was bright, alert, and responsive. Partial loss and destruction of feathers was observed at the left flank and the lateral left thigh, and all tail feathers were broken. Body weight and developmental status were normal according to the falcon's age. Hypertonus of the hind limbs including the phalanges was present, resulting in a resting position on the pelvis with cranially extended legs and dorsal flexion of the tail. When placed on its feet in a physiologic position, the falcon was unable to stand and quickly became recumbent as described. When touched at the caudal thoracic vertebral column, spontaneous shaking tail movements were seen. Neurologic examination was performed, and examination of the cranial nerves (including menace response, pupillary light reflex, palpebral reflex, jaw and tongue tone, and oculocephalic reflex) revealed no alteration. Vent sphincter reflex and pedal flexor reflex were normal, and superficial and deep sensation was present in both legs. Wing function was unimpaired. Based on the clinical findings, a spinal lesion between the spinal cord intumescences was suspected. Radiographs in ventrodorsal and lateral planes demonstrated shortened vertebral bodies of thoracic vertebrae (T) 5-7, with irregular vertebral endplates, consecutive widening of the intervertebral disc spaces, and severe, relatively smooth, periosteal reactions ventrally (Fig 1). Estimated white blood cell count and differential blood count were within physiologic reference values (Table 1). Plasma biochemical analysis showed no significant alteration, including calcium at 8.7 mg/dL (Table 2). Fecal examination was negative for parasites. Differential diagnoses at this time included spinal trauma, infection or neoplasia, congenital central nervous system disorder, rickets, and hypovitaminosis (eg, [B.sub.1], E).
The falcon was hospitalized for further diagnostic tests and symptomatic therapy. Fluid therapy (Ringer's solution, 5% glucose, and amino acids [Volamin, Merial, Hallbergmoos, Germany]; [1:1:1] 20 mL,/kg SC q24h) was administered supplemented with vitamin [B.sub.1] complex (8.0 mg). Initially, vitamins A, [D.sub.3], E, and C (0.3 mL IM; Ursovit A[D.sub.3]EC, Serumwerk, Bernburg, Germany) were administered, and a supplementation of minerals and vitamins was added to the falcon's diet. The legs were loosely hobbled with a cotton-padded bandage to avoid excessive abduction. The next day, computed tomography (CT) examination was performed with a third-generation 16-slice CT scanner (Brilliance TM CT 16, Philips Medical Systems, Hamburg, Germany). For CT examination, the falcon was loosely wrapped in a towel that covered its eyes and placed in a pasteboard box between 2 rolled-up towels. Except for some air holes, the box was closed to all sides to reduce external influences and avoid motion of the bird. Because the bird remained motionless during the examination, general anesthesia was not necessary. Contrast medium injection was not performed, because plain CT was considered diagnostic due to the characteristic findings. The CT results demonstrated severe destruction of the caudal vertebral endplate of T5 and the cranial vertebral endplate of T7, with almost complete osteolysis of T6. Remaining parts of the vertebral bodies of T5-7 were sclerotic, and severe amorphous periosteal reactions were visible ventrally. The spine showed a kyphotic angulation at the level of T5-7, with narrowing of the spinal canal. Presumptive diagnosis was discospondylitis or vertebral osteomyelitis of T5-7 with a pathologic fracture of T6 (Fig 2A). Oral administration of marbofloxacin (20 mg/ kg q24h) and meloxicam (0.2 mg/kg q24h) were added to the therapy. In the daytime (12 h/d), the falcon was placed in a padded hanging construction with its feet tied to a perch in a physiologic posture. Physiotherapy was administered daily on the hind limbs. During these 5-minute sessions, stretch and hold exercises were alternated with range of motion movements. (3) Five days after admission, laser therapy (Diode Laser, scil Vet, MLT Ltd, Ingelheim, Germany) was commenced according to previous reports in reptiles. (4) Two bouts of 30 seconds were administered with a power of 2 watts and a distance of 10 cm with a defocusing hand piece on the skin in the area of T5-7. These sessions were continued once daily.
Ten days after admission, the falcon showed no improvement of its clinical condition. Additionally, a mild, fluctuating, yellow swelling of the left elbow was noted, which was considered primarily as decubital damage from increased pressure on the elbow caused by the sitting posture. A follow-up hematologic examination was performed that revealed leukocytosis (52 500 cells/[micro]L) and heterophilia (84% heterophils). Because of lack of improvement of the clinical symptoms and the development of further clinical signs, a second CT including a postcontrast scan (2 mL/kg; Xenetix 300, Guebet GmbH, Sulzbach, Germany) was done to evaluate the progression of the vertebral changes and assess the concurrent soft tissue changes, as well as the changes in the appendicular skeleton. Contrast injection was performed to gain maximum information, including associated soft tissue changes, for deciding the prognosis and possible further treatment. General anesthesia was again not necessary. Results of the follow-up contrast-enhanced CT showed that the areas of destruction in the vertebral region had increased, with further narrowing of the spinal canal. The perivertebral tissue showed an increased uptake of the contrast agent. Additionally, signs of septic arthritis with soft tissue swelling of the left elbow joint and severe osteolysis of the subchondral bone of the right shoulder (Fig 2B) and left elbow joint had appeared, which had not been present on the initial scan. The damage of the spinal cord was estimated to be irreversible. Because of the poor prognosis regarding the future ability to stand and the progressive course of the disease, it was decided to refrain from further therapeutic attempts and to euthanatize the falcon.
A complete pathologic examination was performed. In addition to a coarse enlargement of T57 (Fig 3), the right shoulder and left elbow joints were enlarged, fluctuating, with a yellow joint capsule and yellowish, cloudy synovial fluid. The spleen was markedly enlarged (1.4 x 0.7 x 0.7 cm) and pale. In the cloaca, a 1.6 x 1.2 x 0.8-cm solid accumulation was detected, which was microscopically identified as urates. Swab samples for bacteriologic culture were taken from both affected joints, aspirated material from the vertebral swelling, and heart blood, liver, and lung tissue. All samples were cultured on Columbia agar with sheep blood (Oxoid Ltd, Basingstoke, Hants, UK) and Gassner medium (Oxoid Ltd) at 37[degrees]C for 48 hours aerobically and microaerobically (5% C[O.sub.2]) and on Sabouraud medium (Oxoid Ltd) at 28[degrees]C. Cytologic smears of the synovial fluid from the swollen joints, stained with modified Wright-Giemsa stain, identified a purulent to pyogranulomatous arthritis. Marked degeneration of heterophils indicated a toxic microenvironment within the lesion, which is known to occur frequently with endotoxin-forming bacterial infections. (5) Sections from internal organs, the vertebral column, and the capsule of the right shoulder joint were fixed in 10% buffered formalin and embedded in paraffin wax. Sections of 4 [micro]m thickness were stained with hematoxylin and eosin. Histologic examination identified a chronic, active, lymphoplasmacytic and histiocytic, partly suppurative synovitis (Fig 4A). A chronic, active, partly necrotic, partly granulomatous osteitis, osteomyelitis, and myositis was detected in the area of T5-7 with intralesional coccoid bacteria and a focal pathologic fracture (Fig 4B). Ziehl-Neelsen staining of the lesions was negative for acid-fast bacteria. The vertebral lesions showed advanced processes of organization and osseous reorganization. From all locations except heart blood. Staphylococcus species was isolated, which was identified as Staphylococcus hyicus by sequencing of 16S rRNA (LGC Genomics GmbH, Berlin, Germany). Single colonies of gram-negative rods were also isolated from the shoulder joint, vertebrae, and liver, which were identified biochemically (API, bioMerieux, Marcy l'Etoile, France) as Escherichia coli. The antibiotic sensitivity test demonstrated the effectiveness of all tested antibiotics, including marbofloxacin against the S hyicus isolate in an inhibition zone assay according to Clinical and Laboratory Standards Institute Guidelines M31-A3 (Mast Diagnostica GmbH, Reinfeld, Germany, and Bayer AG, Leverkusen, Germany).
This clinical report describes a hematogenous osteomyelitis and polyarthritis in a juvenile peregrine falcon associated with S hyicus septicemia. Vertebral osteomyelitis caused by hematogenous spread of Staphylococcus species is a rare cause for paralysis, paresis, and inability to stand in birds. (6,7) At first clinical assessment and radiographic imaging, the enlargement of T5-7 was suspected to be the consequence of poorly healed vertebral fractures. Normal blood calcium levels and a normal radio-opacity of the bones did not support deficits in calcium metabolism. Other differential diagnoses for the neurologic signs included hypovitaminosis E and B, but these are not expected to cause lytic and proliferative osseous changes, and signs should have improved after vitamin supplementation. Bacterial infection is also a possible reason for the clinical signs, but initially this was not considered because the falcon was in good general condition (despite its neurologic deficits), and penetrating wounds were not discovered that could have served as port of entry for bacteria. At this time, spinal trauma was the tentative diagnosis. Neurologic examination revealed normal cranial and spinal reflexes, but muscle tone of the hind limb was spastic, resulting in hypertonus. A painful reaction was recognized at the caudal thoracic spine. Urate accumulation in the cloaca indicated difficulties with defecation. Compared with characteristics of neurologic signs in relation to the location of spinal cord damage in dogs, (8) these findings suggested an upper motor neuron disease, which seemed to correspond with the T5-7 location. However, studies in birds to confirm this hypothesis are still lacking. Radiographic results were able to identify shortened vertebrae with irregular endplates and ventral periosteal reactions but did not give evidence about the integrity of the spinal cord. Magnetic resonance imaging would have been superior in the diagnosis of acute spinal disorder, (9) but it was not performed because the risk associated with the necessity of prolonged general anesthesia was considered too high. Computed tomography, however, showed severe osteolysis with periosteal reactions of T5-7 and narrowing of the vertebral canal. As is known from dogs and cats, osteolysis of the vertebral endplates, fragmentation of the respective vertebrae, and paravertebral soft tissue swelling with contrast medium uptake accumulated in the inflamed region because of higher vascularization are considered indicative of discospondylitis or vertebral osteomyelitis. (10,11) Especially in chronic cases, discrimination between those 2 distinct pathologic conditions becomes rather difficult. (10) Few reports exist on discospondylitis in birds. (12,13) In dogs, discospondylitis is a common inflammatory condition of intervertebral disks that usually affects older animals. (14) In contrast, vertebral osteomyelitis originates from the active physis of the vertebral body in young animals and is more often associated with kyphosis. (10) Considering the falcon's young age and the kyphotic angulation of the spine, the present case was interpreted as vertebral osteomyelitis.
Vertebral osteomyelitis caused by hematogenous spread of Staphylococcus species seems to be rare in raptors, as corresponding references are lacking. Infections of the bone marrow with staphylococci are most commonly identified secondary to open fractures, pododermatitis, and penetrating wounds, (15) none of which could be identified in this case. Few reports exist on osteomyelitis of T5-7 in juvenile pet birds. (6) In domestic fowl, osteomyelitis and occasional concurrent synovitis are known, both as isolated cases and outbreaks within a flock. Infections are always limited to birds with active growth plates. Staphylococci and E coli are considered to be primary bacteria involved in this form of osteomyelitis, but other bacteria (eg, Enterococcus cecorum) have been reported. (7,16,17) The condition usually affects leg bones and contiguous joints. Few outbreaks have been reported affecting the T5-7 region. (7,16,17) The increased mobility of this region compared with other areas of the vertebral column seems to be a predisposing factor for the location of inflammation. The affected birds displayed paraplegia resulting from spinal cord damage, (7) which was not noted in the peregrine falcon. However, because of the corresponding clinical presentation, the same pathogenesis may be assumed for vertebral osteomyelitis in juvenile poultry as well as in the peregrine falcon in the present case.
In humans, hematogenous vertebral osteomyelitis usually affects older patients with underlying diseases (eg, urinary tract infections). Staphylococci and E coli are the most commonly isolated pathogens in these cases. (18-21) In contrast, acute hematogenous osteomyelitis (AHO) is a pediatric disease with a low incidence. In many aspects, the findings in the peregrine falcon resemble AHO. In neonates and infants, the femur and tibia are most commonly affected by AHO, with the metaphyseal portion being the site of initial lesions. (22) The predominant cause for AHO in neonates and infants is Staphylococcus aureus infection. (22,23) The passage of bacteria through transphyseal blood vessels crossing the growth plate connecting epiphyseal vessels with the metaphyseal sinusoids was suggested as cause for AHO in children. Destruction of variable areas of the growth plate and avascular necrosis of hyaline and physeal cartilage were suggested to be the reason for growth disturbances seen in those children. (24) It was postulated that the damage of germinal cells of the physis by either ischemia or direct chondrolysis causes retarded or accelerated growth of the affected bone segments. (22) Clinically, children with AHO may appear healthy apart from pain in the affected bone. Usually, a neutrophilic leukocytosis is present while other signs of inflammation are absent. (22) Similar to the syndrome in children, the peregrine falcon also showed a heterophilic leukocytosis, but despite severe neurologic deficits in the hind limbs, further signs of inflammation were not observed.
In avian species, acute hematogenous osteomyelitis was experimentally induced in 29-day-old broiler chickens by intravenous injection of S aureus, (25) This avian model closely mimicked human disease by affecting mainly the distal femur and proximal tibiotarsus. Temporary endothelial gaps in the extending tips of growing metaphyseal vessels were suggested as the location of bacterial passage from the blood stream into the metaphysis. Transphyseal vessels bridging the growth plate to the epiphysis were identified as well. The adjacent cartilaginous matrix seemed to prevent lateral movement of bacteria but also of inflammatory cells, and thus it provided a protective barrier for the bacteria. If bacteria were only deposited in the metaphyseal vessels, length growth was not affected, and unresorbed cartilage formed sequestrae containing bacteria. When bacteria passed through transphyseal vessels, the germinal part of the growth plate was damaged, resulting in inhibition of normal bone growth and leading to shortening or curvature of the affected limb. (25,26) A similar pathogenesis may be suggested for the development of vertebral osteomyelitis in juvenile raptors. In the peregrine falcon, epiphyseal fusion of the long bones was not completed at the time of first presentation, and an active physis was supposedly present in the vertebrae between endplates and the vertebral body. Vertebrae T5-7 showed an increased accumulation of osseous material, indicating a severe disturbance of physiologic bone growth. Involvement of the germinal part of the physis in the bacterial infection seems very likely. The chronic character of inflammation in vertebrae and joints suggests that, after initial AHO, staphylococcal septicemia persisted and led to a chronic form of the disease in the peregrine falcon.
Arthritis in the right shoulder and left elbow joints developed, most likely because of hematogenous spread of the staphylococci rather than as a sequela to osteomyelitis in adjacent bones, although alterations of the adjacent bones were already present. Acute septic arthritis is also known as a rare pediatric disease in humans and is considered part of the same clinical condition that induces AHO. (23,26) Because the arthritic lesions in the right shoulder and left elbow joint were not present on the first CT scan, the arthritis is believed to have developed secondary to the osteomyelitis. In this case, the final diagnosis of vertebral osteomyelitis and polyarthritis was made after euthanasia of the falcon and isolation of S hyicus from the vertebral lesion and the affected joints, liver, and lungs. Because of the chronic character of the histologic lesions and the intralesional evidence of bacteria, septicemia with S hyicus that spread into vertebrae and the right shoulder and left elbow joints is the most likely cause for osteomyelitis and arthritis in this falcon. Because S hyicus was not obtained from heart blood, septicemia was not active at the time of euthanasia. Single colonies of E coli were additionally isolated from liver, right shoulder, and vertebral lesions, but compared with the growth of S hyicus in nearly pure culture, the relevance of E coli remains questionable. Although E coli is also a known pathogen of vertebral osteomyelitis in avian species, (7) it may have been a contaminant or a secondary invader after chronic tissue destruction by S hyicus, although a partial participation in the pathogenesis of the osteomyelitis cannot be ruled out. Staphylococcus hyicus is regarded as a physiologic commensal of the avian skin which can act as secondary pathogen in bacterial dermatitis. (27) So far, S hyicus has not been described as a pathogen in raptors, but it has been associated with osteomyelitis in turkeys with an unknown route of infection. (28) In the peregrine falcon we describe, a primary site of entry was not identified. Staphylococcus hyicus may have entered the blood stream as an opportunistic pathogen through a small skin wound that had already healed at the time of clinical presentation. Another hypothetical route is entry via intestinal vessels during a transient dysbacteria. The isolate of S hyicus in this case was sensitive in vitro to marbofloxacin, although it was isolated from various organs after 7 days of treatment with this antibiotic. Possible explanations might be differences of resistance against marbofloxacin in vitro and in vivo, inaccuracy of the inhibition zone assay, or failure of the antibiotic to mount therapeutic levels within the affected tissue. Although bone penetration of marbofloxacin is described as sufficient, (29) the inflamed tissue might have served as a constant reservoir of ongoing spread of S hyicus.
In conclusion, hematogenous osteomyelitis should be considered a differential diagnosis in juvenile raptors with neurologic deficits in the hind limbs. Radiographs and hematologic testing are useful for diagnosis in suspected cases. In this falcon, local swelling and deformation of T5-7 vertebrae and leukocytosis strongly suggested hematogenous osteomyelitis. In suspect birds, joints should be examined for the presence of a coexisting septic arthritis. Imaging techniques can be used to estimate damage to bone structures and the level of compression of the spinal cord. In cases of vertebral osteomyelitis, conventional radiographs do not show abnormalities unless the disease is already advanced (sensitivity in humans, 48%). (30) Computed tomography allows identification of early bony alterations and is therefore more sensitive than radiography (sensitivity in humans, 65%). (30) When CT is used in combination with intravenous contrast agents, soft tissue extension can be evaluated. (9) Magnetic resonance imaging is the method of choice to evaluate acute hematogenous osteomyelitis (sensitivity in humans, 100%), (30) but its high risks, associated with the necessity of prolonged anesthesia and the limitation of most available magnetic resonance imaging systems to resolve small structures such as the spinal cord of a peregrine falcon, need to be considered. To select an effective antibiotic for treatment in suspect cases, samples for bacteriologic culture can be taken either from affected joints or, in early cases, from a blood culture. Definitive diagnosis of hematogenous osteomyelitis can only be made postmortem, therefore other differential diagnoses must be ruled out carefully.
Kristina Maier, DVM, Dominik Fischer, DVM, Antje Hartmann, Dr Med Vet, Dipl ECVD1, MRCVS, Olivia Kershaw, Dr Med Vet, Dipl ECVP, Ellen Prenger-Berninghoff, Dr Med Vet, Helene Pendl, Dr Med Vet, Martin J. Schmidt, PD Dr Med Vet (habil.), Dipl ECVN, and Michael Lierz, Prof Dr Med Vet, DZooMed, Dipl ECZM (WPH), Dipl ECPVS
From the Clinic for Birds, Reptiles, Amphibians, and Fish, Justus Liebig University Giessen, Frankfurter Str. 91-93, D35392 Giessen, Germany (Maier, Fischer, Lierz); the Department of Veterinary Clinical Sciences, Small Animal Clinic, Justus Liebig University Giessen, Frankfurter Str. 108, D-35392 Giessen, Germany (Flartmann, Schmidt); the Department of Veterinary Pathology, Freie Universitat Berlin, Robert-vonOstertag-Str. 15, D-14163 Berlin, Germany (Kershaw); the Institute for Hygiene and Infectious Diseases of Animals, Justus Liebig University Giessen, Frankfurter Str. 85-89, D-35392 Giessen, Germany (Prenger-Berninghoff); and PendlLab, Eschenweg 14, CH-6312 Steinhausen, Switzerland (Pendl).
(1.) Lanzarot MP, Montesinos A, San Andres MI, et al. Hematological, protein electrophoresis and cholinesterase values of free-living nestling peregrine falcons in Spain. J Wildl Dis. 2001;37(1): 172-177.
(2.) Hawkins MG, Barron HW, Speer BL, et al. Hematologic and serum biochemical values of selected raptors. In: Carpenter JW, ed. Exotic Animal Formulary. 4th ed. St Louis, MO: Elsevier Saunders; 2013:354-361.
(3.) Redig P, Cruz L. Fractures. In: Samour J, ed. Avian Medicine. 2nd ed. St Louis, MO: Mosby; 2008:215254.
(4.) Kraut S, Fischer D, Heuser W, Lierz M. Laser therapy in a soft shelled turtle (Pelodiscus sinensis) for the treatment of skin and shell ulceration. Tieraerztl Prax. 2013;41 (4):261-266.
(5.) Mischke R. Zytologisches Praktikum fur die Veterinarmedizin. Hannover, Germany: Schliitersche Verlagsgesellschaft mbH & Co KG; 2005.
(6.) Gerlach H. Gram-positive bacteria of clinical significance. In: Ritchie BW, Harrison GJ, Harrison LR, eds. Avian Medicine: Principles and Application. Lake Worth, FL: Wingers Publishing; 1994:965-968.
(7.) Wise DR. Skeletal abnormalities in table poultry--a review. Avian Pathol. 1975;4(1): 1-10.
(8.) Seim HB. Fundamentals of neurosurgery. In: Fossum TW, ed. Small Animal Surgery. 3rd ed. St Louis, MO: Mosby; 2007:1358-1367.
(9.) van Schuppen J, van Doom MMAC, van Rijn RR. Childhood osteomyelitis: imaging characteristics. Insights Imaging. 2012;3(5):519-533.
(10.) Jimenez MM, O'Callaghan MW. Vertebral physitis: a radiographic diagnosis to be separated from discospondylitis. Vet Radiol Ultrasound. 1995;36(3): 188-195.
(11.) Wunderlin N, Wigger A, Schmidt MJ, et al. Ubersicht iiber verschiedene bildgebende Verfahren zur Diagnose der Diskospondylitis beim Hund. Kleintierpraxis. 2008;53(9):539-546.
(12.) Bergen DJ, Gartrell BD. Discospondylitis in a yellow-eyed penguin (Megadyptes antipodes). J Avian Med Surg. 2010;24(l):58-63.
(13.) Field CL, Beaufrere H, Wakamatsu N, et al. Discospondylitis caused by Staphylococcus aureus in an African black-footed penguin (Spheniscus demersus). J Avian Med Surg. 2012;26(4):232-238.
(14.) Davis MJ, Dewey CW, Walker MA, et al. Contrast radiographic findings in canine bacterial discospondylitis: a multicenter, retrospective study of 27 cases. J Am Anim Hosp Assoc. 2000;36(1):81-85.
(15.) Naldo JL, Samour JH. Radiographic findings in captive falcons in Saudi Arabia. J Avian Med Surg. 2004; 18(4):242-256.
(16.) Stalker MJ, Brash ML, Weisz A, et al. Arthritis and osteomyelitis associated with Enterococcus cecorum infection in broiler and broiler breeder chickens in Ontario, Canada. J Vet Diagn Invest. 2010;22(4):643-645.
(17.) Glavits R, Fodor L, Dudas Z, et al. Association of Enterococcus cecorum with vertebral osteomyelitis and spondylolisthesis in broiler parent chicks. Acta Vet Hung. 2011 ;59(1): 11-21.
(18.) Mylona E, Samarkos M, Kakalou E, et al. Pyogenic vertebral osteomyelitis: a systematic review of clinical characteristics. Semin Arthritis Rheum. 2009;39(1): 10-17.
(19.) Park K-H, Chong YP, Kim S-H, et al. Clinical characteristics and therapeutic outcomes of hematogenous vertebral osteomyelitis caused by methicillin-resistant Staphylococcus aureus. J Infect. 2013;67(6):556-564.
(20.) Graham SM, Fishlock A, Millner P, Sandoe J. The management gram-negative bacterial haematogenous vertebral osteomyelitis: a case series of diagnosis, treatment and therapeutic outcomes. Eur Spine J. 2013;22(8): 1845 1853.
(21.) Nolla JM, Ariza J, Gomez-Vaquero C, et al. Spontaneous pyogenic vertebral osteomyelitis in nondrug users. Semin Arthritis Rheum. 2002; 31(4):271-278.
(22.) Nade S. Acute haematogenous osteomyelitis in infancy and childhood. J Bone Joint Surg Br. 1983;65(2): 109 119.
(23.) Nade S. Acute septic arthritis in infancy and childhood. J Bone Joint Surg Br. 1983;65(3):234-241.
(24.) Ogden JA. Pediatric osteomyelitis and septic arthritis: the pathology of neonatal disease. Yale J Biol Med. 1979;52(5):423-448.
(25.) Emslie KR, Nade S. Acute hematogenous staphylococcal osteomyelitis. A description of the natural history in an avian model. Am J Pathol. 1983;110(3):333-345.
(26.) Alderson M, Speers D, Emslie K, Nade S. Acute haematogenous osteomyelitis and septic arthritis--a single disease. An hypothesis based upon the presence of transphyseal blood vessels. J Bone Joint Surg Br. 1986;68(2):268 274.
(27.) Chenier S, Lallier L. Acantholytic folliculitis and epidermitis associated with Staphylococcus hyicus in a line of white Leghorn laying chickens. Vet Pathol. 2011 ;49(2):284-287.
(28.) Tate CR, Mitchell WC, Miller RG. Staphylococcus hyicus associated with turkey stifle joint osteomyelitis. Avian Dis. 1993;37(3):905-907.
(29.) Kroker R, Scherkl R, Ungemach FR. Chemotherapie bakterieller Infektionen; 4-Chinolone (Gyrasehemmer). In: Frey F1H, Loscher W, eds. Lehrbuch der Pharmakologie und Toxikologie fur die Veterindrmedizin. 3rd ed. Stuttgart, Germany: Enke Verlag; 2010:456-460.
(30.) Meyers SP, Wiener SN. Diagnosis of hematogenous pyogenic vertebral osteomyelitis by magnetic resonance imaging. Arch Intern Med. 1991; 151(4):683-687.
Table 1. Hematologic values of the peregrine falcon described in Figure 1 at first presentation and at day 10 after admission, with reference intervals for juvenile peregrine falcons. (1) Reference Parameter Presentation Day 10 interval Estimated WBC, 33 250 52 500 11 550-39 230 cells/pL Heterophils, % 78 84 38.8-82.7 Lymphocytes, % 18 16 12.9-58.7 Monocytes, % 4 0 0-4.55 Abbreviation: WBC indicates white blood cells. Table 2. Serum biochemistry values of the peregrine falcon described in Figure 1 at first clinical presentation (A) and reference intervals for peregrine falcons (B).2 Parameter A B AST, U/L 105 97-350 Bile acids, [micro]mol/L <35 20-118 CK, U/L 1641 357-850 Uric acid, mg/dL 21.2 4.4-22 Glucose, mg/dL 298 198-288 Phosphate, mg/dL 6.7 2.4-6.5 Calcium, mg/dL 8.7 8.4-10.3 Total protein, g/dL 2.3 2.5-4 Albumin, g/dL 0.8 0.8-1.3 Globulin, g/dL 1.5 1.6-2.83 Potassium, mmol/L 4.6 1.6-3.2 Sodium, mmol/L 149 152-168 Abbreviations: AST indicates aspartate aminotransferase; CK creatine kinase.
|Printer friendly Cite/link Email Feedback|
|Author:||Maier, Kristina; Fischer, Dominik; Hartmann, Antje; Kershaw, Olivia; Prenger-Berninghoff, Ellen; Pen|
|Publication:||Journal of Avian Medicine and Surgery|
|Article Type:||Clinical report|
|Date:||Sep 1, 2015|
|Previous Article:||Metronomic chemotherapy for myxosarcoma treatment in a kori bustard (Ardeotis kori).|
|Next Article:||Use of deslorelin acetate implants to mitigate aggression in two adult male domestic turkeys (Meleagris gallopavo) and correlating plasma...|