Printer Friendly

Avian pox infection with secondary Candida albicans encephalitis in a juvenile golden eagle (Aquila chrysaetos).

Abstract: A juvenile golden eagle (Aquila chrysaetos) was presented with proliferative epithelial lesions, consistent with avian poxvirus infection, around the eyes, on commissures of the beak, and on both feet. Despite treatment, the eagle declined clinically, and, 15 days after presentation, the eagle began seizuring and was euthanatized because of a poor prognosis. On postmortem examination, avian poxvirus infection was confirmed in the nodular skin lesions, and Candida albicans was cultured from the skin, lungs, and brain. Breaks in the skin barrier from poxvirus infection likely led to secondary infection with C albicans. Systemic vascular dissemination of C albicans to the brain resulted in thrombosis, hemorrhage, local hypoxia, and the clinically observed seizures. The combination of the breach in the primary immune system, immunosuppression, and a prolonged course of antibiotics were contributory factors to the opportunistic fungal infection in this eagle. Candida albicans should be considered as a differential diagnosis for encephalitis in an immunocompromised avian patient.

Key words. Candida albicans encephalitis, avian pox, avian, golden eagle, Aquila chrysaetos

Clinical Report

A juvenile male golden eagle (Aquila chrysaetos) was presented to the Veterinary Teaching Hospital at the Western College of Veterinary Medicine in August, 2006. Based on plumage, the eagle was younger than 12 months of age. One week before presentation, the eagle had been found in a river valley near Shaunavon, Saskatchewan, Canada (49[degrees] 39' 0" N/108[degrees] 25' 0" W). The eagle was unable to fly. The eagle had been fed 2 Richardson's ground squirrels (Spermophilus richardsonii) per day before admission.

On presentation, the eagle was standing upright in the transport cage. On physical examination, the eagle was depressed and lethargic, weighed 3.78 kg, was in thin body condition (2/5), and approximately 5% dehydrated. Multiple, nodular, proliferative epithelial lesions were present around the eyes, submandibular area, and commissures of the beak (Fig 1) and on both feet, with a mild swelling of the digits of the right foot. A moderate number of biting lice (unidentified) were present throughout the plumage. Maggots were present in the lesions of the cere and the right foot.

The eagle was anesthetized with isoflurane and was maintained on a mask at 2.5% isoflurane and 2 L/min oxygen flow rate. Fundic examination revealed no abnormalities. Wounds on the cere and feet were flushed with 0.9% saline and debrided, and the maggots were removed. A 1% silver sulfadiazine cream (Flamazine, Smith and Nephew, Saint Laurent, Quebec, Canada) was applied topically to the wounds, followed by an amorphous hydrogel (Curafil, Tyco Healthcare/ Kendall, Mansfield, MA, USA), and the feet were bandaged with a semipermeable, transparent, adhesive bandage (Tegaderm, 3M Animal Care Products, St Paul, MN, USA). When the bandages were changed, small white particles often aerosolized from the feet, which, in hindsight, may have been fungal spores.

[FIGURE 1 OMITTED]

Supportive care was initiated, which consisted of lactated Ringer's solution (30 mL/kg SC q12h) and assisted feeding every 12 hours with approximately 90 g at each feeding, for a daily total of 180 g (approximately 5% body weight) of killed, whole, 1-day-old chicks and killed whole laboratory mice of varying ages.

The eagle had been treated with amoxicillin and clavulanate potassium tablets (100 mg/kg PO q24h; Clavamox, Pfizer, Kirkland, Quebec, Canada) for 2 days before arrival; this was continued throughout hospitalization. Treatment with meloxicam (0.1 mg/kg PO q24h; Metacam, Boehringer Inglehein, Burlington, Ontario, Canada) was started, and carbaryl powder was dusted over the body and rubbed into the skin to treat the biting lice and maggots.

On the second day, blood was collected for a complete blood cell (CBC) count, and results demonstrated mild eosinophilia, marked monocytosis, and low hematocrit, with 2+ polychromasia and high total solids concentration (Table 1).' The results were consistent with mild anemia and dehydration. On day 6, the eagle remained depressed and anorectic but was perching and weight bearing on both feet. It was treated with an injection of vitamin B complex (0.5 mg/kg IM once) and a combination product of vitamin A (20 000 IU/kg) and vitamin D (3300 IU/kg) (Vitamin A and D, Professional Veterinary Laboratories, Winnipeg, Manitoba, Canada).

The swelling of the digits did not improve, and, on day 8, treatment with pentoxytilline, a peripheral vasodilator, was started (5 mg/kg PO ql2h Pentoxifylline, PCCA, London, Ontario, Canada). The meloxicam dose was increased to 0.2 mg/kg PO q24h. Results of a CBC count revealed marked leukocytosis characterized by marked heterophilia, marked eosinophilia, mild basophilia, and low hematocrit. The plasma total solid concentration was high (Table 1). The results indicated an established inflammatory response. The eagle was anesthetized with isoflurane for whole-body ventral dorsal and lateral radiographs. Results showed swollen tissues associated with the right foot and no evidence of osteomyelitis.

On day 10, anaerobic and aerobic bacterial culture and sensitivity testing was performed from swab samples from deep within the wound on the right foot. Standard culture and identification methods were used for isolation. (2) Proteus mirabilis (1+), Escherichia coli (few), and Acinetobacter species (1+) were grown on culture. The results of the sensitivity pattern did not arrive until day 14. All organisms were resistant to amoxicillin-clavulanic acid, which indicated resistance to the antibiotic that had been given systemically to the eagle for the past 14 days. On day 11, the eagle began regurgitating. The CBC count results from that day demonstrated a generalized improvement from 3 days earlier, however, there was still a marked leukocytosis characterized by a marked heterophilia and a marked eosinophilia (Table 1).

The CBC count was repeated on day 14 and results revealed leukocytosis, characterized by a marked heterophilia, a marked eosinophilia, and a monocytosis. The total solid concentration was still high (Table 1). The leukogram indicated a mild left shift and evidence of chronic inflammation. On day 15 after presentation the eagle had a seizure, with opisthotonus and leg and wing extension. Because of the deteriorating neurologic status, the general lack of improvement, and the poor prognosis, the eagle was euthanatized. The carcass was submitted for necropsy.

At necropsy, the eagle was in adequate body condition, with moderate amounts of mesenteric fat deposits. The bursa of Fabricius was evident, which confirmed this eagle to be a juvenile. Multifocal dermal proliferative nodules were present around the eyes, beak, and dorsal surface of the feet. The feet were swollen, with multifocal areas of dermal necrosis and ulceration, frequently covered with a gray exudate (Fig 2). The lungs, liver, and cerebrum were diffusely congested, and multifocal cerebellar hemorrhages were present. Representative tissue samples were collected in 10% neutral buffered formalin, processed routinely for histopathologic examination, and embedded in paraffin blocks. Sections 4- to 7-[micro]m thick were cut, mounted onto glass slides, and stained with hematoxylin and eosin. Additional staining with Oil Red O, Grocott methenamine silver, and Gram's stains were done when appropriate. Standard bacterial and fungal culture and identification methods were used to isolate pathogens from the cerebellum, lung, liver, and pooled tissues. (2)

On microscopic examination, multifocal areas of full-thickness epidermal proliferation with a parakeratotic hyperkeratosis were observed, interspersed with areas of intense epidermal necrosis in the skin of the feet and periocular region (Fig 3). Areas of necrosis were overlaid with a serocellular crust of necrotic epidermal cells and multifocal yeast and bacterial colonies. Many epidermal cells in the areas of hyperplasia contained large solid and ring-shaped intracytoplasmic, eosinophilic inclusion bodies that displaced the nucleus (Fig 3, inset). These inclusion bodies (Bollinger bodies) stained red with Oil Red O, which was consistent with avian pox infection. (3) Results of electron microscopy revealed abundant, enveloped, dumbbell-shaped virions within inclusion bodies, which confirmed avian pox virus infection.

Multifocal areas of hemorrhage surrounded vessels in the cerebellum. The lumen of some of these vessels was filled with eosinophilic amorphous material associated with erythrocytes and thrombocytes, interpreted as thrombi (Fig 4). Linear, septate fungal pseudohyphae were seen, within some thrombi, invading the surrounding neuropil (Fig 4, inset). A moderate inflammatory infiltrate of predominately heterophils was present in the leptomeninges.

[FIGURE 2 OMITTED]

Although mild, subacute, multifocal hepatitis and pulmonary congestion were present, fungal lesions were not seen histologically in the liver or lungs. No significant abnormalities were found on examination of heart, spleen, bursa, thyroid, kidneys, adrenal glands, proventriculus, esophagus, and small intestines.

Fungal culture of samples of the lungs and brain, and pooled samples from the skin grew Candida albicans. Bacterial culture yielded growth of E coli from the lungs, cerebellum, and kidneys, Staphylococcus aureus from the lungs and cerebellum, and Proteus species from the cerebellum. Sensitivity patterns from the E coli isolated from the skin did not match those sensitivity patterns of pooled E coli from the lungs, kidneys, and cerebellum. Sensitivity patterns of S aureus from brain did not match the sensitivity patterns of S aureus from the lungs. The eagle tested negative for West Nile virus after formalin-fixed tissue sections of the brain were submitted for immunohistochemistry (avidin-biotin-peroxidase complex).

Discussion

In this report, we described a case of cutaneous avian poxvirus infection, with subsequent secondary systemic dissemination of the opportunistic pathogens C albicans, E coli, S aureus, and Proteus species. Avian pox infection was confirmed in the skin examined from the cere and feet of this eagle, and C albicans was seen within numerous thrombosed vessels in the cerebellum. The eagle appeared to have sustained thromboembolic spread of C albicans from a primary focus (likely the ulcerated cutaneous poxvirus nodules) to the vessels in the brain, which resulted in local hypoxia, damage to the vessel wall, and hemorrhage. The chronicity of the proliferative pox lesions relative to the acute damage to cerebellar vessels and surrounding tissues supported the proposed pathogenesis. Immunosuppression from captivity and juvenile status, concurrent poxvirus infection, combined with the broad spectrum antibiotics all contributed to the opportunistic spread of C albicans.

Avipoxviruses (family Poxviridae) enter the body through a break in the mucous membrane or skin and cause disease that has 1 of 3 main presentations: dry (cutaneous), wet (dipththeretic), and systemic. (4) Dry pox often occurs on the featherless parts of the face and legs, and is the most common form seen in raptors. (5) The lesions are both proliferative and necrotizing and can progress to become ulcerative. Transmission can occur by fomites (shared perches, handling gloves), direct contact, or insect bites. (3) Natural pox infection has been reported in a golden eagle, (6) but the case outcome for that bird was not reported. It had the severe dry form of avian pox, much like that in the present case. Pox lesions likely have considerable functional significance for a wild avian predator, which leads to reduced ability to hunt and maintain body condition. Pox lesions have been documented to cause severe lesions on the feet of raptors, (7,8) which cause a decreased ability to capture prey. The extensive lesions around the beak may have prevented normal ingestion of prey. The lesions on the eyelids may have resulted in impaired vision and a subsequent decreased ability to visualize prey and reduced navigation in the environment, which resulted in the eagle first being observed in the river valley. Avian pox lesions in raptors have been reported to be infected by E coli, P mirabilis, and S aureus, (9) all of which are normal bacterial flora in raptors (10-12) that may opportunistically invade when there is a break in the skin.

[FIGURE 3 OMITTED]

Candida is part of the normal intestinal flora of healthy birds and is typically found in the upper gastrointestinal tract, primarily the oropharynx, crop, and esophagus. (13-16) Candida albicans is an opportunistic diploid fungus, with a worldwide distribution, and is the primary cause of candidiasis, which is often associated with immunosuppression. (17) Avian candidiasis is typically acquired from a secondary source when a bird is immunocompromised, young, stressed, or lacks proper nutrition, is exposed to contaminated feeding equipment, is on long-term antibiotic therapy, or has another primary disease. (5,18,19) Opportunistic infections develop when the skin barrier becomes broken or moistened and can lead to hematogenous transport to other organs. (20) The primary site of infection in this eagle was likely the cutaneous pox lesions. Poxvirus causes breaks in the skin barrier, which allows Candida species to enter and results in a deeper lesion and a more severe inflammatory response. (21,22) The maggots may have deepened the wounds and increased the probability of hematogenous spread.

[FIGURE 4 OMITTED]

Most reported candidal infections are localized; reports describe cloacal infections in geese (Anser species), (23) respiratory lesions in a blue and gold macaw (Ara ararauna), (24) lameness in a bluefronted Amazon (Amazona aestiva), (25) foot lesions in a mute swan (Cygnus olor), (26) ocular candidiasis in ornamental ducks (Anas species), (27) ocular ulcers in toco toucans (Ramphastos toco), (28) and skin lesions in a cockatiel (Nymphicus hollandicus). (29) There are only a few documented cases of systemic candidal infections, (30,31) and they are rarely associated with neurologic signs. Although fungal encephalitides have been reported in a few avian species, such as snowy owls (Nyctea scandiaca), (32) grey-winged trumpeters (Psophia crepitans), (33) and turkey poults (Meleagris gallopavo), (34) the causal fungal organism has been Dactylaria species, not Candida. Candida infections secondary to pox lesions are infrequent. (22,35)

Management of hospitalized raptors must be aimed at minimizing risk factors that can result in secondary opportunistic infections. The use of broad-spectrum antibiotics should be closely monitored for any sign of resistant bacteria or opportunistic fungal overgrowth that compromises the health of the patient. The age status of the bird should be considered, and all measures should be taken to decrease stress and handling as much as possible. Careful monitoring of the CBC count can aid in choosing appropriate medical treatment. Although causes of avian leucocytosis, heterophilia, eosinophilia, and monocytosis are numerous, (36) at the time of treatment, the hematologic values seen in this bird were attributed to the chronicity of the pox lesions, a suspected secondary bacterial infection, stress, and inflammation. When an animal is not responding to clinical treatments, bacterial and fungal cultures should be performed on samples of the affected lesions. Because of the low incidence of (superficial and systemic) fungal infections seen in raptors at our hospital, systemic antifungal agents were not administered in this case. In retrospect, the white cloud wafting from the foot each time the bandages were changed could have been candidal spores. If long-term antibiotics are used, prophylactic antifungal therapy should be considered, especially if the patient is nonresponsive to antibiotic therapy. When treating immunocompromised avian species, fungal encephalitis caused by C albicans should be considered as a differential diagnosis for neurologic disease.

Acknowledgments: We thank Dr Gary Wobeser for his guidance on this case, assistance with preparation of the manuscript, and unyielding support and advice.

References

(1.) ISIS. International Species Information System, Physiological Reference Values. CD-ROM. Apple Valley, MN: Minnesota Zoological Garden; 2002.

(2.) Quinn PJ, Carter ME, Markey BK, Carter GR. Clinical Veterinary Microbiology. London, UK: Mosby Year Book Europe Ltd; 1994.

(3.) Greenwood A. Pox disease in all taxa. In: Fowler ME, Miller RE, eds. Zoo and WiM Animal Medicine. 5th ed. St Louis, MO: Elsevier Science; 2003:739-740.

(4.) Phalen D. Viruses. In: Altman RB, Clubb SL, Dorrestein GM, Quesenberry K, eds. Avian Medicine and Surgery. Philadelphia, PA: WB Saunders; 1997:300-304.

(5.) Redig P. Falconiformes (vultures, hawks, falcons, secretary bird). In: Fowler ME, Miller RE, eds. Zoo and Wild Animal Medicine. 5th ed. St Louis, MO: Elsevier Science; 2003:152.

(6.) Moffatt RE. Natural pox infection in a golden eagle. J Wildl Dis. 1972;8:161-162.

(7.) Pearson GL, Pass DA, Beggs EC. Fatal pox infection in a rough-legged hawk. J Wildl Dis. 1975; 11:224-227.

(8.) Greenwood AG, Blakemore WF. Pox infections in falcons. Vet Rec. 1973;93:468-470.

(9.) Hernandez M, Sanchez C, Galka ME, et al. Avian pox infection in Spanish imperial eagles (Aquila adalberti). Avian Pathol. 2001;30:91-97.

(10.) Cooper JE, Needham JR. An investigation into the prevalence of Staphylococcus aureus on avian feet. Vet Rec. 1976;98:172-174.

(11.) Lamberski N, Hull AC, Fish AM, et al. A survey of the choanal and cloacal aerobic bacterial flora in free-living and captive red-tailed hawks (Buteo jamaicensis) and cooper's hawks (Accipiter cooperii). J Avian Med Surg. 2003;17:131-135.

(12.) Bangert RL, Ward ACS, Stauber EH, et al. A survey of the aerobic bacteria in the feces of captive raptors. Avian Dis. 1998;32:53-62.

(13.) Velasco MC. Candidiasis and cryptococcosis in birds. Semin Avian Exotic Pet Med. 2000;9:75-81.

(14.) Klaphake E, Clancy J. Raptor gastroenterology. Vet Clin North Am Exotic Anim Pract. 2005;8:307-327.

(15.) Reavill D. Fungal diseases. In: Rosskopf W, Woerpel R, eds. Diseases of Cage and Aviary Birds. 3rd ed. Baltimore, MD: Williams & Wilkins; 1996:586-595.

(16.) Samour JH, Naldo JL. Diagnosis and therapeutic management of candidiasis in falcons in Saudi Arabia. J Avian Med Surg. 2002; 16:129-132.

(17.) Duncan M. Fungal diseases in all taxa. In: Fowler ME, Miller RE, eds. Zoo and Wild Animal Medicine. 5th ed. St Louis, MO: Elsevier Science; 2003:728.

(18.) Oglesbee BL. Mycotic diseases. In: Altman RB, Clubb SL, Dorrestein GM, Quesenberry K, eds. Avian Medicine and Surgery. Philadelphia, PA: WB Saunders; 1997:327-330.

(19.) Deem SL. Fungal diseases of birds of prey. Vet Clin North Am Exotic Anim Pract. 2003;6:363-376.

(20.) Greene CE, Chandler FW, Itakura C. Candidiasis and rhodotorulosis. In: Greene CE, ed. Infectious Diseases of the Dog and Cat. 3rd ed. Philadelphia, PA: WB Saunders; 2006:627-633.

(21.) Tsai SS, Park JH, Hirai K, Itakura C. Aspergillosis and candidiasis in psittacine and passeriforme birds with particular reference to nasal lesions. Avian Pathol. 1992;21:699-709.

(22.) Tsai SS, Chang TC, Yang SF, et al. Unusual lesions associated with avian poxvirus infection in rosy-faced lovebirds (Agapornis roseicollis). Avian Pathol. 1997;26:75-82.

(23.) Beemer AM, Kuttin ES, Katz Z. Epidemic venereal disease due to Candida albicans in geese in Israel. Avian Dis. 1973;17:639-649.

(24.) Hines RS, Sharkey P, Friday RB. Itraconazole treatment of pulmonary, ocular, and uropygeal aspergillosis and candidiasis in birds--data from five clinical cases and controls. Proc Annu Conf Am Assoc Zoo Vet. 1990:322-327.

(25.) Goodman GJ, Widenmeyer JC. Systemic Candida parapsilosis in a 20-year-old blue fronted Amazon. Proc Annu Conf Assoc Avian Vet. 1986:105-118.

(26.) Degryse A-D, Van Cutsem J, Fransen J. Oral treatment with ketoconazole of plantar candidosis in a mute swan. J Small Anim Pract. 1985;26: 619-623.

(27.) Crispin SM, Barnett KC. Ocular candidiasis in ornamental ducks. Avian Pathol. 1978;7:49-59.

(28.) Karpinski LB, Clubb SL. Further investigations into the ocular problems of caged birds. Proc Annu Conf Assoc Avian Vet. 1985:101-108.

(29.) Reavill DR, Schmidt RE, Fudge AM. Avian skin and feather disorder: a retrospective study. Proc Annu Conf Assoc Avian Vet. 1990:248 255.

(30.) Wyatt RD, Simmons DG, Hamilton PB. Induced systemic candidiasis in young broiler chickens. Avian Dis. 1975;19:533-543.

(31.) Perez A. Canaries: systemic candidosis. Veterinaria Argentina. 1985;2:186-189.

(32.) Salkin IF, Dixon DM, Kemna ME, et al. Fatal encephalitis caused by Dactylaria constricta vat. gallopava in a snowy owl chick (Nyctea scandiaca). J Clin Microbiol. 1990;28:2845-2847.

(33.) Karesh WB, Russell R, Gribble D. Dactylaria gallopava encephalitis in two grey-winged trumpeters (Psophia crepitans). Avian Dis. 1987;31: 685-688.

(34.) Blalock HG, Georg LK, Derieux WT. Encephalitis in turkey poults due to Dactylaria (Diplorhinotrichum) gallopava: a case report and its experimental reproduction. Avian Dis. 1973; 17:197-204.

(35.) Bickford AA, Gallina AM, Winterfield RW, Bolte H. Studies of an unusual pox infection in turkeys. Avian Dis. 1971;15:614-625.

(36.) Fudge AM, Joseph V. Disorders of avian leukocytes. In: Fudge AM, ed. Laboratory Medicine: Avian and Exotic Pets. Philadelphia, PA: WB Saunders; 2000:19-27.

Alana N. Shrubsole-Cockwill, DVM, MVSc, Caroline Millins, BVSc, MSc, MVSc, Claire Jardine, MSc, DVM, PhD, Kelti Kachur, DVM, and Dennilyn L. Parker, DVM, MVSc, Dipl ABVP (Avian)

From the North Shore Veterinary Specialist Centre, 64 Atchison Drive, Crow's Nest, NSW, 2050, Australia (Shrubsole-Cockwill); Western College of Veterinary Medicine, 52 Campus Drive, Saskatoon, SK, S7N 5B4, Canada (Millins, Parker); Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, ON, N1G 2W1, Canada (Jardine); and General Veterinary Hospital, 11403 141 Street, Edmonton, AB, T5M 1V7, Canada (Kachur).
Table 1. Hematologic values and ISIS reference ranges of the juvenile
male golden eagle with avian poxvirus infection described in Figure 1
during a 2-week hospitalization period.

Parameter                          Day 2       Day 8        Day 11

WBC (x [10.sup.9]/L;
    x [10.sup.3] cells/dL)         17.6         60.8         33.8
  Heterophils (x [10.sup.9]/L;
    x [10.sup.3] cells/dL) (%)   8.10 (46)   44.99 (74)   25.69 (76)
  Bands (x [10.sup.9]/L;
    x [10.sup.3] cells/dL) (%)     0 (0)       0 (0)        0 (0)
  Eosinophils (x [10.sup.9]/L;
    x [10.sup.3] cells/dL) (%)   2.82 (16)   12.16 (20)   4.39 (13)
  Basophils (x [10.sup.9]/L;
    x [10.sup.3] cells/dL (%)      0 (0)      0.61 (1)     0.34(l)
  Lymphocytes (x [10.sup.9]/L;
    x [10.sup.3] cells/dL) (%)   2.29 (13)    0.61 (1)     2.03 (6)
  Monocytes (x [10.sup.9]/L;
    x [10.sup.3] cells/dL) (%)   4.40 (25)    2.43 (4)     1.35 (4)
PCV (%)                             32           32           46
Total solids (g/L)[g/dL]         48 [4.8]     60 [6.0]       N/A

                                               ISIS reference range
Parameter                          Day 14     (mean [+ or -] SD) (1)

WBC (x [10.sup.9]/L;
    x [10.sup.3] cells/dL)          39.0       14.18 [+ or -] 7.71
  Heterophils (x [10.sup.9]/L;
    x [10.sup.3] cells/dL) (%)   28.47 (73)     9.11 [+ or -] 6.04
  Bands (x [10.sup.9]/L;
    x [10.sup.3] cells/dL) (%)    0.39 (1)
  Eosinophils (x [10.sup.9]/L;
    x [10.sup.3] cells/dL) (%)   4.68 (12)      0.93 [+ or -] 0.01
  Basophils (x [10.sup.9]/L;
    x [10.sup.3] cells/dL (%)     0.39 (1)      0.30 [+ or -] 0.19
  Lymphocytes (x [10.sup.9]/L;
    x [10.sup.3] cells/dL) (%)    2.34(6)       3.82 [+ or -] 3.86
  Monocytes (x [10.sup.9]/L;
    x [10.sup.3] cells/dL) (%)    2.73 (7)      0.61 [+ or -] 0.85
PCV (%)                              42           42 [+ or -] 6
Total solids (g/L)[g/dL]          72 [7.2]        34 [+ or -] 6
                                                [3.4 [+ or -] 0.6]

Abbreviations: ISIS indicates International Species Information
System; WBC, white blood cell; PCV, packed cell volume.
COPYRIGHT 2010 Association of Avian Veterinarians
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2010 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Title Annotation:Clinical Reports
Author:Shrubsole-Cockwill, Alana N.; Millins, Caroline; Jardine, Claire; Kachur, Kelti; Parker, Dennilyn L.
Publication:Journal of Avian Medicine and Surgery
Article Type:Report
Geographic Code:1CANA
Date:Mar 1, 2010
Words:3758
Previous Article:Discospondylitis in a yellow-eyed penguin (Megadyptes antipodes).
Next Article:The ethics of exotic animal analgesia.
Topics:

Terms of use | Copyright © 2017 Farlex, Inc. | Feedback | For webmasters