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AVIAN- Diseases of the Avian Spleen

AVIAN- Diseases of the Avian Spleen

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Vol. 22, No.

10 October 2000


Refereed Peer Review

FOCAL POINT # The avian spleen is frequently
involved in systemic diseases; assessing the spleen can aid in the diagnosis of multisystemic illness.

Diseases of the Avian Spleen*
Timberlyne Animal Clinic, Chapel Hill, North Carolina

Lauren V. Powers, DVM

I Because the gross and histologic appearances of the avian spleen may be similar for several diseases, additional testing is typically needed to reach a definitive diagnosis. I The spleen has a limited number of responses to disease. I Chlamydiosis and mycobacteriosis are among the most common causes of splenomegaly in psittacines. I The spleen is a defensive organ that serves as a blood filter.

ABSTRACT: Because the spleen is often involved in systemic disease, splenic assessment can frequently help to diagnose systemic illness. However, the spleen’s response to disease is limited, and the gross and histologic appearances of the avian spleen are typically similar regardless of the underlying condition. Changes in the size of the spleen and splenic congestion, necrosis, infarction, and infiltration are common.


he avian spleen differs from the mammalian spleen in its response to disease. Splenomegaly is common and may be caused by a variety of infections and other disease processes. In fact, the gross and histologic appearances of the avian spleen are similar for many diseases; thus additional testing is usually indicated to accurately identify the underlying cause (Table I). This article discusses specific infectious and noninfectious diseases of the avian spleen, including steps that may be needed to reach a definitive diagnosis.

SPLENIC RESPONSE TO DISEASE The spleen has limited responses to disease. The most obvious changes are in its size, such as splenomegaly and splenic atrophy (or hypoplasia). Histologically, splenic congestion is a frequent finding in patients with bacterial or viral infections. Necrosis is a common pathologic change in the spleen and is often associated with viral infections. In chickens, splenic infarction can be associated with bacterial valvular endocarditis.1 The spleen is also frequently infiltrated with endogenous or foreign substances (e.g., amyloid), and intracellular bile and iron pigment may be observed. Splenomegaly Splenomegaly is a nonspecific response to numerous diseases. An enlarged spleen may look congested or appear pale. It may be diffusely enlarged or may contain multiple lesions. Acute viral infections, systemic bacterial diseases (e.g., chlamydiosis, mycobacteriosis), parasitemia, and immune-mediated hemolytic anemia can all cause splenomegaly. Noninfectious causes include amyloidosis and neoplasia.2
*A companion article entitled “The Avian Spleen: Anatomy, Physiology, and Diagnostics” appeared in the September 2000 (Vol. 22, No. 9) issue of Compendium.

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Chlamydiosis Infection with Chlamydia psittaci (currently under reclassificaDisease Category Differential Diagnosis tion to Chlamydiophila psittaci) is frequently diagnosed in psittaDegenerative Aging, glucocorticoids, acute viral infections, aflatoxicosis cines and columbiformes. Clinical Autoimmune Immune-mediated hemolytic anemia signs are highly variable and depend on the organ systems inMetabolic Lipidosis, hemosiderosis, hemochromatosis, amyloidosis, lysosomal storage disease, visceral gout volved. Depression, anorexia, and weight loss are common. Gross Neoplastic Lymphosarcoma, hemangiosarcoma, fibrosarcoma, necropsy findings include an enleiomyosarcoma, myeloid neoplasia, metastatic neoplasia larged, congested, and mottled Infectious liver and spleen (Figure 1). ThickBacterial Chlamydiosis, mycobacteriosis, colisepticemia, others ened air sacs with fibrin deposits may be present. Splenomegaly Viral Polyomavirus, adenovirus, herpesvirus, retrovirus, togavirus, with evidence of airsacculitis at paramyxovirus, reovirus, coronavirus, parvovirus, others necropsy is highly suggestive of Parasitic Sarcocystosis, toxoplasmosis, systemic coccidiosis, chlamydiosis.5 Chlamydiosis is atoxoplasmosis, Plasmodium, Leukocytozoon one of the most frequent causes of splenomegaly in psittacines. Fungal Disseminated aspergillosis, zygomycosis, candidiasis Splenic histiocytosis is typically Toxic Mycotoxins, polychlorinated biphenyls, selenium, others the predominant lesion. Intracytoplasmic chlamydial inclusions Hypoplasia and Atrophy can be identified on splenic impression smears stained A small spleen is typically either hypoplastic or atrophwith Gimenez or Macchiavellos stain or with immunofluic. Hypoplasia may result from bursal disease and deorescent antibody stains.5 creased lymphocyte “seeding” of the spleen in young Mycobacteriosis birds. In older birds, lymphocyte depletion and splenic Mycobacterium organisms are ubiquitous worldwide atrophy may be present in response to various physiologic and infect a large range of avian species. The Mycobacor pathologic stressors. Glucocorticoid release by the terium avium-intracellulare (MAI) complex is most often adrenal glands in chickens results in T- and B-cell death, involved, although Mycobacterium genavense, Mycobacleading to reduction in the size of splenic periarterial lymterium tuberculosis, and Mycobacterium bovis infections phoid sheaths and splenic atrophy.1 A certain degree of splenic atrophy may occur with aghave been diagnosed in psittacines. In a study of 48 pet ing. Splenic lymphocyte necrosis associated with viral inbirds in Switzerland, the majority of isolates were M. fections may eventually result in atrophy.2 Aflatoxins cause splenic atrophy through their inhibition of DNA, RNA, and protein synthesis.1 Apparent increases in the red pulp percentage can result from a relative white pulp lymphocyte loss in chickens.
TABLE I Diagnostic Differentials for Splenic Disease in Birds

BACTERIAL DISEASES Bacterial sepsis typically results in splenomegaly with multiple pale, necrotic foci and fibrin deposition. Heterophilic inflammation is frequently present.2 Culture and sensitivity and special stains (e.g., Gram’s stain) are useful to identify the causative organism. Thrombosis and infarction of the spleen can be caused by valvular endocarditis in turkeys and Erysipelas infection in poultry. Yersinia, Erysipelas,3 Salmonella, valvular endocarditis, and spirochetes in fowl can be associated with splenomegaly, and spirochetes can be observed on silver-stained sections of splenic tissue.4

Figure 1—Gross appearance of the spleen of a 3-week-old love-

bird (Agapornis species) that died of acute chlamydiosis. Note it is extremely enlarged and red (congested). (Courtesy of H. J. Barnes, DVM, PhD, North Carolina State University)


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genavense (34 of 48), followed by MAI complex (8 of 48), Mycobacterium fortuitum (2 of 48), M. tuberculosis (2 of 48), Mycobacterium gordonae (1 of 48), and Mycobacterium nonchromogenicum (1 of 48).6 Avian mycobacteriosis primarily involves the gastrointestinal tract and typically presents as a chronic wasting disease. Weight loss, lethargy, diarrhea, and polyuria are common clinical signs. Avian mycobacteriosis is frequently associated with marked splenomegaly with well-demarcated tan to yellow laminated caseous nodules. Mycobacteriosis in psittacines may cause a diffuse infiltration of the spleen with large macrophages laden with acidfast bacteria. In other avian species, multifocal granulomas containing macrophages, giant cells, and acid-fast bacilli are present. 1 Culture and acid-fast staining using ZiehlNeelsen stain are indicated for a definitive diagnosis (Figure 2). 2 Culture of MAI is difficult and often requires human laboratories experienced with Mycobacterium infections.

cluding reovirus, coronavirus, parvovirus, birnavirus, and paramyxovirus. Inclusion bodies can frequently be identified in the spleen on routine histopathology. The following viruses are of particular clinical importance in birds.

Polyomavirus Avian polyomavirus infection is associated with high morbidity and mortality in Figure 2—Histology of a chicken spleen demonstrating nonbudgerigar psittacines. acid-fast bacilli as red clusters (Ziehl-Neelsen acid-fast Peracute illness is common in stain; original magnification, ×200). (Courtesy of H. J. young parrots. Subcutaneous Barnes, DVM, PhD, North Carolina State University) hemorrhage and crop stasis are frequently seen before death. Gross lesions include a pale, enlarged spleen (Figure 3). Hemorrhage may be noted on the serosal surface of the spleen. Splenic karyomegaly is often present. Characteristic intranuclear inclusion bodies are most commonly found in the spleen and kidney and less frequently in the liver. Presence of these inclusions is suggestive of polyomavirus infection. Viral-specific DNA probes Figure 3—Gross appearance of the spleen of a 3-week-old and in situ hybridization techsun conure (Aratinga solstitialis) that died of acute poly- niques can be used to confirm omavirus. The spleen is mildly enlarged and very pale. infection.7 Polyomavirus has also been associated with acute mortality in passerines. Affected birds may die suddenly or have a 1- to 2-day history of Colibacillosis illness before death. An enlarged, congested spleen and Colibacillosis in chickens tends to cause fibrin deposerosal hemorrhage may be present. Intranuclear inclusition and autolysis of the spleen. In turkeys, hematogesions can be demonstrated in the spleen. Polyomavirus nous Escherichia coli organisms are taken up by elliphas also been reported in a green aracaris (Pteroglossus soid and red pulp macrophages.1 Colisepticemia is the viridis). At necropsy, there was splenic necrosis and most common cause of ellipsoid degeneration in broiler lightly basophilic to clear pannuclear inclusions and chickens. Experimental E. coli infections induce lymkaryomegaly in splenocytes, similar to lesions reported phocyte necrosis in the periarterial lymphoid sheath, in psittacines.8 inflammation, and bacterial colonization. Adenovirus VIRAL DISEASES Adenovirus infections have been associated with As a defensive organ and a “blood filter,” the spleen is lethargy, diarrhea, cloacal hemorrhage, and sudden death intimately involved in processing hematogenous viruses. in psittacines.7 Nucleic acid studies on a budgerigar adenovirus strain indicated that the virus was unique despite The spleen is frequently affected during a multisystemic sharing antigenic similarities with chicken strains. Focal viral infection. Numerous viruses can result in areas of grayish discoloration in an enlarged, congested splenomegaly and splenic necrosis or hemorrhage, inACID-FAST STAIN I INCLUSION BODIES I CROP STASIS I SPLENIC KARYOMEGALY

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spleen are common. Marked DNA probes, or viral-specific splenic reticuloendothelial cell antibodies may be used to hyperplasia and suggestive baconfirm infection. sophilic intranuclear inclusion Splenic necrosis and splenobodies may be identified in megaly can be associated with the spleen. Inclusions may also herpesvirus infection in other be seen in asymptomatic birds. avian species, including colA viral-specific DNA probe umbiformes (pigeon herpesthat can detect nucleic acid in virus-1), falconiforms, strigipsittacine tissue is available. formes, and anserines (duck Because polyomavirus and plague virus). Marek’s disease is adenovirus can produce simicaused by a highly contagious lar microscopic changes, the herpesvirus, and infection is Figure 4—Histologic appearance of Pacheco’s disease in the DNA probe is useful to dis- spleen of a cockatiel. Necrosis of the sheathed arteries is evi- most common in chickens; tinguish the two viruses. Ade- dent (H&E; original magnification, ×70). (Courtesy of H. however, similar lesions have noviral replication sites were J. Barnes, DVM, PhD, North Carolina State University) been reported in other avian found in lymphocytes and species. The classic form of the dendritic cells of the spleens of disease is neurologic accumulafour psittacines naturally infected with type 2 adention of lymphocytes. An acute form is characterized by ovirus. Affected birds showed marked splenomegaly, and the formation of lymphoid tumors in numerous organs, their spleens were pale and friable. Slight to moderate deincluding the spleen. The virus primarily infects chickens pletion of lymphocytes and scattered necrotic cells were 12 to 24 weeks of age. After experimental administration present. Lymphoid follicles and sinuses contained enof Marek’s disease virus in chickens, the ellipsoid cells belarged monocytes and macrophages with phagocytosed came disrupted and appeared to have migrated to the pecellular debris.7,9 riarterial lymphoid sheath. There was an early cytologic Adenoviruses affect a wide variety of avian species. infection of predominantly B cells and a few activated T Marble spleen disease is caused by a type 2 adenovirus cells in lymphoid tissue, including the spleen. The lymand affects pheasants between 2 and 8 months of age. phocyte necrosis stimulated an intense inflammatory reAt necropsy, the spleen is markedly enlarged and motsponse.1,7 tled. The type 2 adenoviruses that cause marble spleen Retrovirus disease in pheasants and hemorrhagic enteritis in turThe important avian type C retroviruses are the avian keys are serologically related to each other but not to other leukosis/sarcoma viruses, which cause neoplasia in avian adenoviruses. chickens, and reticuloendotheliosis virus, which causes Quail bronchitis virus is serologically related to an disease in turkeys and ducks. The most common inadenovirus that infects chickens, but the nucleic acid duced tumor in chickens is lymphoid leukosis. Lesions composition appears to be unique. Experimental quail are most common in chickens 4 to 9 months of age. bronchitis lesions include splenic mottling, splenoSimilar splenic lesions have been reported in other megaly, lymphocyte necrosis, hyperplastic ellipsoids, avian species, including psittacines, passerines, and and rare intranuclear inclusion bodies.1 columbiformes. Clinical signs depend on the location Herpesvirus of the tumors. Virulent strains of the herpesvirus responsible for Erythroblastosis and myeloblastosis, also induced by Pacheco’s disease are typically associated with sudden retroviruses, have been reported in psittacines. Macrodeath in psittacines. Premonitory signs may include descopic changes include an enlarged, friable spleen. pression, diarrhea, yellow or green urates, and regurgiCream-colored to grayish masses in the spleen may be tation. Most birds die within 1 to 2 days of showing seen. Microscopic changes are typified by sheets of lymclinical signs. Affected birds may have no gross lesions phoblasts with a high mitotic index arranged in diffuse at necropsy or may have splenomegaly with or without or nodular patterns. areas of hemorrhage. Histologic lesions include splenic Reticuloendotheliosis viruses affect the reticular and necrosis and hemorrhage (Figure 4). Intranuclear incluendothelial cells of the spleen. Chronic infection causes sion bodies (Cowdry type A) may be demonstrated in the development of solid tumors in the spleen and other the spleen.7 Histologic lesions are diagnostic in most organs. Macroscopic changes in young birds include a cases. Electron microscopy, cell culture, viral-specific decrease in the size of the spleen and other lymphoid orMARBLE SPLEEN DISEASE I QUAIL BRONCHITIS I PACHECO’S DISEASE I MAREK’S DISEASE

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pletion is followed by lymphoid hyperplasia.1 Plasmodium infection in raptors and passerines can lead to marked splenic enlargement with plasma cell, reactive lymphocyte, and macrophage accumulation. A gray–black pigment produced by the parasite may accumulate in the spleen of raptors.2 In fact, a large black spleen at necropsy is nearly pathognomic for Plasmodium ach of a canary affected with lymphosarcoma. The spleen infection in raptors.b Penguins is pale and enlarged (center). The spleen of normal passer- housed outdoors are highly Togavirus ines is elongated to comma-shaped. (Courtesy of H. J. susceptible to Plasmodium inThe family Togaviridae inBarnes, DVM, PhD, North Carolina State University). cludes three genera: Alphafection. virus, Rubivirus, and PestiOther Parasites virus. Eastern equine encephalitis virus, western equine A homogenous red, enlarged spleen in passerines is encephalitis virus, and Highlands J virus are currently consistent with atoxoplasmosis but may also be associatthe most commonly observed alphaviruses in North ed with leukemia or systemic bacterial disease. Psittacine America.7 Native avian species appear to be resistant to disease, perhaps because of natural selection. Nonnative sarcocystosis can cause splenomegaly with splenic infilbirds appear to be more susceptible to disease. Dependtration of plasma cells and macrophages. Acute toxoplasing on the species, birds infected with eastern equine mosis in canaries can be associated with splenomegaly as encephalitis virus may be asymptomatic or may die part of the systemic response to infection.10 Infection of black siskins (Carduelis atrata) with Isospora protozoa with no premonitory signs or after a short period of secauses hepatosplenomegaly and activation of splenic folvere enteritis or neurologic disease. Clinical signs are licles.11 Disseminated visceral coccidiosis from Eimeria most often seen in young birds. Affected species inspecies in captive cranes may result in splenitis with clude “exotic” galliforms, columbiformes, passerines, splenic formation of granulomatous nodules.12 anserines, and others. Changes at necropsy vary widely. A small, pale spleen or splenomegaly and splenic motNEOPLASTIC DISEASES tling may be seen. Splenic lesions in immunologically The neoplastic spleen is typically markedly enlarged and naive emus in the United States include severe, diffuse may be mottled red, purple, or grayish white. Foci of lymphocyte necrosis and severe necrosis of ellipsoid necrosis or hemorrhage can be seen histologically in larger cells.1,7 lesions (Figure 5).13 Avian leukosis virus can result in tuPARASITIC DISEASES mor formation in birds. Induced tumors include lymHemoparasites phoma and lymphosarcoma. Lymphoid neoplasia has Leucocytozoon smithi infection in turkeys results in been described in psittacines and frequently involves the splenic lesions, including transient congestion with nuspleen.14 Lymphosarcoma in a juvenile blue and gold macaw was associated with diffuse infiltration of the merous capillary-blocking protozoal organisms. Lymphospleen with pleomorphic lymphocytes.15 Both Marek’s discyte hyperplasia and germinal center formation then ocease virus and lymphoid leukosis virus can cause splenic cur, and hemosiderosis associated with erythrocyte tumors in chickens. Reticuloendotheliosis virus can also destruction may be present. In ducks infected with Leucocause splenic tumors in poultry and waterfowl. Myeloid cytozoon simondi, splenic lesions include congestion and neoplasia can also occur in the spleen. Fibrosarcoma and infiltration of macrophages, hemosiderosis, ellipsoid deleiomyosarcoma can occur as primary lesions. Metastasis generation, and the presence of megaloschizonts. of distant primary neoplasms to the spleen is occasionally Plasmodium infection in domestic fowl results in seen. Metastatic lesions typically occur as irregular enlargephagocytosis of infected erythrocytes around the ellipments or multiple firm, tan, gray, or white foci.16 soids and then in the red pulp. An initial lymphoid deaBarnes

gans. In older birds, the liver and spleen are typically enlarged and contain multiple, yellowish to grayish-white nodules. Induced tumors include lymphoma, lymphosarcoma, adenoma, and adenocarcinoma. 7 Reticuloendotheliosis results in large reticuloendothelial cells that tend to push normal tissue out of the way or follow normal Figure 5—Gross appearance of the liver, spleen, and stomtissue planes.a

HJ: Personal communication, North Carolina State University, 1999.

bPhalen D: Personal communication, Texas A&M University, 1999.


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METABOLIC DISEASES Pathologic changes associated with metabolic diseases of the avian spleen usually result from infiltration or deposition of a substance not normally found in the spleen. Such substances include amyloid, lipid, bile pigment, iron pigment, and urate tophi (seen with visceral gout).

Amyloidosis Amyloidosis is commonly that died of amyloidosis. Deposition of eosinophilic amyseen in anserines, gulls, and loid protein is visible around the vascular tree (H&E; OTHER DISEASES shorebirds.1,17 It is caused by original magnification, ×56). (Courtesy of H. J. Barnes, Toxicoses Experimental chronic selethe deposition of amyloid A DVM, PhD, North Carolina State University) nium toxicosis in mallard protein, a degradation prodducks (Anas platyrhynchos) resulted in lymphocytic uct of an acute phase reactant protein. Amyloidosis is necrosis and atrophy of the spleen and other lymphoid frequently associated with chronic inflammation, such organs.22 Such mycotoxins as citrinin, cyclopiazonic acid, as that associated with mycobacteriosis, aspergillosis, 17 fumonisin B, ochratoxin, and rubratoxin have been reand pododermatitis. Amyloidosis may be induced by ported to cause lymphoid necrosis or atrophy.1 Experivaccination in turkeys. Amyloidosis is uncommon in b mental exposure of nestling American kestrels (Falco pigeons and psittacines. In laying Japanese quail affectsparverius) to polychlorinated biphenyl (PCB) 126 ed with systemic amyloidosis, amyloid deposits were caused multifocal coagulative necrosis, reduced splenic predominantly seen in the spleen and liver.18 A pale, weight, and lymphocyte depletion of the spleen.23 homogenous, enlarged spleen is typical with amyloidosis. Variable deposition of amyloid protein is observed Mycoses histologically (Figure 6).2 Hematogenous spread of mycotic infections can result in granuloma formation in the spleen. An Amazon Lysosomal Storage Disease parrot (Amazona aestiva) was diagnosed with systemic Lysosomal storage disease involving the spleen, brain, candidiasis and necrotizing lesions in the lungs and gasspinal cord, and liver has been reported in a 6-monthtrointestinal tract and giant cell–containing granulomas old male emu (Dromaius novaehollandiae). The diagnoin the spleen.24 Hyphae typical of Zygomycetes were seen sis was made at necropsy using light and electron mi19 invading through the splenic blood vessel walls in an croscopy and histochemical staining. African grey parrot (Psittacus erithacus) that was also diagnosed with chlamydiosis. Rhizomucor pusillus was isoLipidosis lated as a pure culture from the lungs and liver of this Fatty infiltration of the liver—and often the spleen— bird.25 Splenomegaly as a response to chronic inflamcommonly occurs in psittacines, most notably budgerimatory disease is a common finding at necropsy and is gars, Amazon parrots, cockatiels, lovebirds, and Quaker seen in birds with systemic aspergillosis. parrots. Consumption of high-fat diets together with restricted exercise can lead to obesity and lipidosis of the liver and spleen.20 The spleen may be pale to white ACKNOWLEDGMENT with microscopic foci of splenocytes with vacuolated The author thanks David Phalen, DVM, PhD, Diplocytoplasm (fat). mate American Board of Veterinary Practitioners, Texas A&M University, College Station, for reviewing an earHEMOSIDEROSIS AND HEMOCHROMATOSIS ly draft of this manuscript. A mild-to-moderate degree of splenic hemosiderosis is found in most parrots with subacute to chronic disease. REFERENCES These birds generally have a mild, nonregenerative ane1. Pope CR: Lymphoid system, in Riddell C (ed): Avian mia. Hemosiderosis is frequently associated with erythHistopathology. Tallahassee, FL, American Association of Avian Pathologists, 1996, pp 18–44. rocyte destruction resulting from hemoparasite infecLEAD POISONING I MYCOTOXINS I HYPHAE

tions (e.g., Leucocytozoon, Plasmodium).1 Hemosiderosis of mononuclear phagocytic cells in the spleen was seen in white-fronted geese (Anser albifrons) with lead poisoning, presumably resulting from excess breakdown of erythrocytes.21 Iron deposits are frequently seen within the reticuloendothelial cells of the spleen in birds affected with Figure 6—Histologic appearance of the spleen of a goose hemochromatosis.

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2. Schmidt RE: Immune system, in Altman RB, Clubb SL, Dorrestein GM, et al (eds): Avian Medicine and Surgery. Philadelphia, WB Saunders Co, 1997, pp 645–652. 3. Mutalib A, Keirs R, Austin F: Erysipelas in quail and suspected erysipeloid in processing plant employees. Avian Dis 39(1):191–193, 1995. 4. Cooper GL, Bickford AA: Spirochetosis in California game chickens. Avian Dis 37(4):1167–1171, 1993. 5. Flammer K: Chlamydia, in Altman RB, Clubb SL, Dorrestein GM, et al (eds): Avian Medicine and Surgery. Philadelphia, WB Saunders Co, 1997, pp 366–367. 6. Hoop RK, Bottger EC, Pfyffer GE: Etiological agents of mycobacteriosis in pet birds between 1986 and 1995. J Clin Microbiol 34(4):991–992, 1996. 7. Ritchie BW: Avian Viruses: Function and Control. Lake Worth, FL, Wingers Publishing, 1995. 8. Lafferty SL, Fudge AM, Schmidt RE, et al: Avian polyomavirus infection and disease in a green aracaris (Pteroglossus viridis). Avian Dis 43(3):577–585, 1999. 9. Gomez-Villamandos JC, Bautista MJ, Carrasco L, et al: Electron microscopic evidence for infection of splenic dendritic cells by adenovirus in psittacine birds. Res Virol 146 (6):389–395, 1995. 10. Dorrestein GM: Passerines, in Altman RB, Clubb SL, Dorrestein GM, et al (eds): Avian Medicine and Surgery. Philadelphia, WB Saunders Co, 1997, pp 867–885. 11. Giacomo R, Stefania P, Ennio T, et al: Mortality in black siskins (Carduelis atrata) with systemic coccidiosis. J Wildl Dis 33(1):152–157, 1997. 12. Olsen GH, Carpenter JW: Cranes, in Altman RB, Clubb SL, Dorrestein GM, et al (eds): Avian Medicine and Surgery. Philadelphia, WB Saunders Co, 1997, pp 973–991. 13. Graham DL: Lymphoreticular and hematopoietic proliferative lesions in non-domestic avian species—A survey of diagnostic submissions. Proc Annu Conf Assoc Vet:461–464, 1995. 14. Coleman CW: Lymphoid neoplasia in pet birds: A review. J Avian Med Surg 9(1):3–7, 1995. 15. Coleman CW, Oliver R: Lymphosarcoma in a juvenile blue and gold macaw (Ara araruana) and a mature canary (Serinus canarius). J Assoc Avian Vet 8(2):64–68, 1994. 16. Schmidt RE, Quesenberry K: Neoplasia, in Altman RB, Clubb SL, Dorrestein GM, et al (eds): Avian Medicine and

Surgery. Philadelphia, WB Saunders Co, 1997, pp 590–603. 17. Lumeij JT: Hepatology, in Ritchie BW, Harrison GJ, Harrison LR (eds): Avian Medicine: Principles and Application. Lake Worth, FL, Wingers Publishing Co, 1994, p 536. 18. Nakamura K, Tanaka H, Kodama Y, et al: Systemic amyloidosis in laying Japanese quail. Avian Dis 42(1):209–214, 1998. 19. Kim DY, Cho DY, Taylor HW: Lysosomal storage disease in an emu (Dromaius novaehollandiae). Vet Pathol 33(3): 365–366, 1996. 20. Hoefer HL, Orosz S, Dorrestein GM: The gastrointestinal tract, in Altman RB, Clubb SL, Dorrestein GM, et al (eds): Avian Medicine and Surgery. Philadelphia, WB Saunders Co, 1997, p 447. 21. Ochiai K, Jin K, Goryo M, et al: Pathomorphologic findings of lead poisoning in white-fronted geese (Anser albifrons). Vet Pathol 30(6):522–528, 1993. 22. Green DE, Albers PH: Diagnostic criteria for selenium toxicosis in aquatic birds: Histologic lesions. J Wildl Dis 33(3): 385–404, 1997. 23. Hoffman DJ, Melancon MJ, Klein PN, et al: Developmental toxicity of PCB 126 (3,3',4,4',5–pentachlorobiphenyl) in nestling American kestrels (Falco sparverius). Fundam Appl Toxicol 34(2):188–200, 1996. 24. Carrasco L, Gomez-Villamandos JC, Jensen HE: Systemic candidosis and concomitant aspergillosis and zygomycosis in two Amazon parakeets (Amazona aestiva). Mycoses 41 (7–8):297–301, 1998. 25. Desmidt M, De Laender P, De Groote D, et al: Rhizomucor pusillus mucormycosis combined with chlamydiosis in an African grey parrot (Psittacus erithacus erithacus). Vet Rec 143(16):447–448, 1998.

Dr. Powers is an exotics and general veterinary practitioner at Timberlyne Animal Clinic in Chapel Hill, North Carolina. She is a Diplomate of the American Board of Veterinary Practitioners (Avian Practice).

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