Vol. 22, No.
10 October 2000
CE 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.
KEY FACTS
■ 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.
■ The spleen has a limited number
of responses to disease.
■ Chlamydiosis and
mycobacteriosis are among
the most common causes of
splenomegaly in psittacines.
■ The spleen is a defensive organ
that serves as a blood filter.
Diseases of the
Avian Spleen*
Timberlyne Animal Clinic, Chapel Hill, North Carolina
Lauren V. Powers, DVM
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 lim-
ited, and the gross and histologic appearances of the avian spleen are typically similar regard-
less of the underlying condition. Changes in the size of the spleen and splenic congestion,
necrosis, infarction, and infiltration are common.
T
he avian spleen differs from the mammalian spleen in its response to dis-
ease. Splenomegaly is common and may be caused by a variety of infec-
tions and other disease processes. In fact, the gross and histologic appear-
ances of the avian spleen are similar for many diseases; thus additional testing is
usually indicated to accurately identify the underlying cause (Table I). This arti-
cle 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 infec-
tions. Necrosis is a common pathologic change in the spleen and is often associ-
ated with viral infections. In chickens, splenic infarction can be associated with
bacterial valvular endocarditis.1 The spleen is also frequently infiltrated with en-
dogenous 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 Diagnos-
tics” appeared in the September 2000 (Vol. 22, No. 9) issue of Compendium.
Small Animal/Exotics Compendium October 2000

TABLE I Chlamydiosis
Diagnostic Differentials for Splenic Disease in Birds Infection with Chlamydia psit-
taci (currently under reclassifica-
Disease Category Differential Diagnosis tion to Chlamydiophila psittaci) is
Degenerative Aging, glucocorticoids, acute viral infections, aflatoxicosis frequently diagnosed in psitta-
cines and columbiformes. Clinical
Autoimmune Immune-mediated hemolytic anemia signs are highly variable and de-
Metabolic Lipidosis, hemosiderosis, hemochromatosis, amyloidosis, pend on the organ systems in-
lysosomal storage disease, visceral gout volved. Depression, anorexia, and
Neoplastic Lymphosarcoma, hemangiosarcoma, fibrosarcoma, weight loss are common. Gross
leiomyosarcoma, myeloid neoplasia, metastatic neoplasia necropsy findings include an en-
larged, congested, and mottled
Infectious liver and spleen (Figure 1). Thick-
Bacterial Chlamydiosis, mycobacteriosis, colisepticemia, others ened air sacs with fibrin deposits
Viral Polyomavirus, adenovirus, herpesvirus, retrovirus, togavirus, may be present. Splenomegaly
paramyxovirus, reovirus, coronavirus, parvovirus, others with evidence of airsacculitis at
necropsy is highly suggestive of
Parasitic Sarcocystosis, toxoplasmosis, systemic coccidiosis, chlamydiosis.5 Chlamydiosis is
atoxoplasmosis, Plasmodium, Leukocytozoon one of the most frequent causes of
Fungal Disseminated aspergillosis, zygomycosis, candidiasis splenomegaly in psittacines.
Splenic histiocytosis is typically
Toxic Mycotoxins, polychlorinated biphenyls, selenium, others the predominant lesion. Intracy-
toplasmic chlamydial inclusions
Hypoplasia and Atrophy can be identified on splenic impression smears stained
A small spleen is typically either hypoplastic or atroph- with Gimenez or Macchiavellos stain or with immunoflu-
ic. Hypoplasia may result from bursal disease and de- orescent antibody stains.5
creased lymphocyte “seeding” of the spleen in young
birds. In older birds, lymphocyte depletion and splenic Mycobacteriosis
atrophy may be present in response to various physiologic Mycobacterium organisms are ubiquitous worldwide
or pathologic stressors. Glucocorticoid release by the and infect a large range of avian species. The Mycobac-
adrenal glands in chickens results in T- and B-cell death, terium avium-intracellulare (MAI) complex is most often
leading to reduction in the size of splenic periarterial lym- involved, although Mycobacterium genavense, Mycobac-
phoid sheaths and splenic atrophy.1 terium tuberculosis, and Mycobacterium bovis infections
A certain degree of splenic atrophy may occur with ag- have been diagnosed in psittacines. In a study of 48 pet
ing. Splenic lymphocyte necrosis associated with viral in- birds 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.

BACTERIAL DISEASES
Bacterial sepsis typically results in splenomegaly with
multiple pale, necrotic foci and fibrin deposition. Het-
erophilic 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 en-
docarditis in turkeys and Erysipelas infection in poultry.
Yersinia, Erysipelas,3 Salmonella, valvular endocarditis, and Figure 1—Gross appearance of the spleen of a 3-week-old love-
spirochetes in fowl can be associated with splenomegaly, bird (Agapornis species) that died of acute chlamydiosis. Note
it is extremely enlarged and red (congested). (Courtesy of H. J.
and spirochetes can be observed on silver-stained sections
Barnes, DVM, PhD, North Carolina State University)
of splenic tissue.4

HETEROPHILIC INFLAMMATION ■ SPIROCHETES ■ AIRSACCULITIS

Compendium October 2000 Small Animal/Exotics

genavense (34 of 48), followed cluding reovirus, coronavirus,

by MAI complex (8 of 48), parvovirus, birnavirus, and
Mycobacterium fortuitum (2 of paramyxovirus. Inclusion bod-
48), M. tuberculosis (2 of 48), ies can frequently be identified
Mycobacterium gordonae (1 of in the spleen on routine
48), and Mycobacterium non- histopathology. The following
chromogenicum (1 of 48).6 viruses are of particular clinical
Avian mycobacteriosis pri- importance in birds.
marily involves the gastroin-
testinal tract and typically Polyomavirus
presents as a chronic wasting Avian polyomavirus infec-
disease. Weight loss, lethargy, tion is associated with high
diarrhea, and polyuria are morbidity and mortality in
common clinical signs. Avian Figure 2—Histology of a chicken spleen demonstrating nonbudgerigar psittacines.
mycobacteriosis is frequent- acid-fast bacilli as red clusters (Ziehl-Neelsen acid-fast Peracute illness is common in
ly associated with marked stain; original magnification, ×200). (Courtesy of H. J. young parrots. Subcutaneous
splenomegaly with well-de- Barnes, DVM, PhD, North Carolina State University) hemorrhage and crop stasis are
marcated tan to yellow lami- frequently seen before death.
nated caseous nodules. My- Gross lesions include a pale,
cobacteriosis in psittacines enlarged spleen (Figure 3). Hem-
may cause a diffuse infiltra- orrhage may be noted on the
tion of the spleen with large serosal surface of the spleen.
macrophages laden with acid- Splenic karyomegaly is often
fast bacteria. In other avian present. Characteristic intra-
species, multifocal granulo- nuclear inclusion bodies are
mas containing macrophages, most commonly found in the
giant cells, and acid-fast bacil- spleen and kidney and less fre-
li are present. 1 Culture and quently in the liver. Presence
acid-fast staining using Ziehl- of these inclusions is sugges-
Neelsen stain are indicated tive of polyomavirus infection.
for a definitive diagnosis (Fig- Viral-specific DNA probes
ure 2). 2 Culture of MAI is Figure 3—Gross appearance of the spleen of a 3-week-old and in situ hybridization tech-
difficult and often requires sun conure (Aratinga solstitialis) that died of acute poly- niques can be used to confirm
human laboratories experi- omavirus. The spleen is mildly enlarged and very pale. infection.7
enced with Mycobacterium in- Polyomavirus has also been
fections. 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 depo- serosal hemorrhage may be present. Intranuclear inclu-
sition and autolysis of the spleen. In turkeys, hematoge- sions can be demonstrated in the spleen. Polyomavirus
nous Escherichia coli organisms are taken up by ellip- has 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 lym- karyomegaly 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 ade-
The spleen is frequently affected during a multisystemic novirus strain indicated that the virus was unique despite
viral infection. Numerous viruses can result in sharing antigenic similarities with chicken strains. Focal
splenomegaly and splenic necrosis or hemorrhage, in- areas of grayish discoloration in an enlarged, congested

ACID-FAST STAIN ■ INCLUSION BODIES ■ CROP STASIS ■ SPLENIC KARYOMEGALY

Small Animal/Exotics
spleen are common. Marked
splenic reticuloendothelial cell
hyperplasia and suggestive ba-
sophilic intranuclear inclusion
bodies may be identified in
the spleen. Inclusions may also
be seen in asymptomatic birds.
A viral-specific DNA probe
that can detect nucleic acid in
psittacine tissue is available.
Because polyomavirus and
adenovirus can produce simi-
lar microscopic changes, the
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)
found in lymphocytes and
dendritic cells of the spleens of
four psittacines naturally infected with type 2 aden-
ovirus. Affected birds showed marked splenomegaly, and
their spleens were pale and friable. Slight to moderate de-
pletion of lymphocytes and scattered necrotic cells were
present. Lymphoid follicles and sinuses contained en-
larged monocytes and macrophages with phagocytosed
cellular debris.7,9
Adenoviruses affect a wide variety of avian species.
Marble spleen disease is caused by a type 2 adenovirus
and affects pheasants between 2 and 8 months of age.
At necropsy, the spleen is markedly enlarged and mot-
tled. The type 2 adenoviruses that cause marble spleen
disease in pheasants and hemorrhagic enteritis in tur-
keys are serologically related to each other but not to other
avian adenoviruses.
Quail bronchitis virus is serologically related to an
adenovirus that infects chickens, but the nucleic acid
composition appears to be unique. Experimental quail
bronchitis lesions include splenic mottling, spleno-
megaly, lymphocyte necrosis, hyperplastic ellipsoids,
and rare intranuclear inclusion bodies.1
Herpesvirus
Virulent strains of the herpesvirus responsible for
Pacheco’s disease are typically associated with sudden
death in psittacines. Premonitory signs may include de-
pression, diarrhea, yellow or green urates, and regurgi-
tation. Most birds die within 1 to 2 days of showing
clinical signs. Affected birds may have no gross lesions
at necropsy or may have splenomegaly with or without
areas of hemorrhage. Histologic lesions include splenic
necrosis and hemorrhage (Figure 4). Intranuclear inclu-
sion bodies (Cowdry type A) may be demonstrated in
the spleen.7 Histologic lesions are diagnostic in most
cases. Electron microscopy, cell culture, viral-specific
MARBLE SPLEEN DISEASE ■ QUAIL BRONCHITIS ■ PACHECO’S DISEASE ■ MAREK’S DISEASE
Compendium October 2000
DNA probes, or viral-specific
antibodies may be used to
confirm infection.
Splenic necrosis and spleno-
megaly can be associated with
herpesvirus infection in other
avian species, including col-
umbiformes (pigeon herpes-
virus-1), falconiforms, strigi-
formes, and anserines (duck
plague virus). Marek’s disease is
caused by a highly contagious
herpesvirus, and infection is
been reported in other avian
species. The classic form of the
disease is neurologic accumula-
tion of lymphocytes. An acute form is characterized by
the formation of lymphoid tumors in numerous organs,
including the spleen. The virus primarily infects chickens
12 to 24 weeks of age. After experimental administration
of Marek’s disease virus in chickens, the ellipsoid cells be-
came disrupted and appeared to have migrated to the pe-
riarterial lymphoid sheath. There was an early cytologic
infection of predominantly B cells and a few activated T
cells in lymphoid tissue, including the spleen. The lym-
phocyte necrosis stimulated an intense inflammatory re-
sponse.1,7
Retrovirus
The important avian type C retroviruses are the avian
leukosis/sarcoma viruses, which cause neoplasia in
chickens, and reticuloendotheliosis virus, which causes
disease in turkeys and ducks. The most common in-
duced tumor in chickens is lymphoid leukosis. Lesions
are most common in chickens 4 to 9 months of age.
Similar splenic lesions have been reported in other
avian species, including psittacines, passerines, and
columbiformes. Clinical signs depend on the location
of the tumors.
Erythroblastosis and myeloblastosis, also induced by
retroviruses, have been reported in psittacines. Macro-
scopic changes include an enlarged, friable spleen.
Cream-colored to grayish masses in the spleen may be
seen. Microscopic changes are typified by sheets of lym-
phoblasts with a high mitotic index arranged in diffuse
or nodular patterns.
Reticuloendotheliosis viruses affect the reticular and
endothelial cells of the spleen. Chronic infection causes
the development of solid tumors in the spleen and other
organs. Macroscopic changes in young birds include a
decrease in the size of the spleen and other lymphoid or-
Small Animal/Exotics Compendium October 2000

gans. In older birds, the liver pletion is followed by lym-

and spleen are typically en-
larged and contain multiple,
yellowish to grayish-white
nodules. Induced tumors
include lymphoma, lympho-
sarcoma, adenoma, and ade-
nocarcinoma. 7 Reticuloen-
dotheliosis results in large
reticuloendothelial cells that
tend to push normal tissue out
of the way or follow normal
tissue planes.a Figure 5—Gross appearance of the liver, spleen, and stom-
ach of a canary affected with lymphosarcoma. The spleen infection in raptors.b Penguins
Togavirus is pale and enlarged (center). The spleen of normal passer- housed outdoors are highly
The family Togaviridae in- ines is elongated to comma-shaped. (Courtesy of H. J. susceptible to Plasmodium in-
Barnes, DVM, PhD, North Carolina State University).
cludes three genera: Alpha-
virus, Rubivirus, and Pesti-
virus. Eastern equine encephalitis virus, western equine
encephalitis virus, and Highlands J virus are currently
the most commonly observed alphaviruses in North
America.7 Native avian species appear to be resistant to
disease, perhaps because of natural selection. Nonnative
birds appear to be more susceptible to disease. Depend-
ing on the species, birds infected with eastern equine
encephalitis virus may be asymptomatic or may die
with no premonitory signs or after a short period of se-
vere enteritis or neurologic disease. Clinical signs are
most often seen in young birds. Affected species in-
clude “exotic” galliforms, columbiformes, passerines,
anserines, and others. Changes at necropsy vary widely.
A small, pale spleen or splenomegaly and splenic mot-
tling may be seen. Splenic lesions in immunologically
naive emus in the United States include severe, diffuse
lymphocyte necrosis and severe necrosis of ellipsoid
cells.1,7
PARASITIC DISEASES
Hemoparasites
Leucocytozoon smithi infection in turkeys results in
splenic lesions, including transient congestion with nu-
merous capillary-blocking protozoal organisms. Lympho-
cyte hyperplasia and germinal center formation then oc-
cur, and hemosiderosis associated with erythrocyte
destruction may be present. In ducks infected with Leuco-
cytozoon simondi, splenic lesions include congestion and
infiltration of macrophages, hemosiderosis, ellipsoid de-
generation, and the presence of megaloschizonts.
Plasmodium infection in domestic fowl results in
phagocytosis of infected erythrocytes around the ellip-
soids and then in the red pulp. An initial lymphoid de-
aBarnes HJ: Personal communication, North Carolina State
phoid hyperplasia.1 Plasmodi-
um infection in raptors and
passerines can lead to marked
splenic enlargement with plas-
ma cell, reactive lymphocyte,
and macrophage accumula-
tion. 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
fection.
Other Parasites
A homogenous red, enlarged spleen in passerines is
consistent with atoxoplasmosis but may also be associat-
ed with leukemia or systemic bacterial disease. Psittacine
sarcocystosis can cause splenomegaly with splenic infil-
tration of plasma cells and macrophages. Acute toxoplas-
mosis in canaries can be associated with splenomegaly as
part of the systemic response to infection.10 Infection of
black siskins (Carduelis atrata) with Isospora protozoa
causes hepatosplenomegaly and activation of splenic fol-
licles.11 Disseminated visceral coccidiosis from Eimeria
species in captive cranes may result in splenitis with
splenic formation of granulomatous nodules.12
NEOPLASTIC DISEASES
The neoplastic spleen is typically markedly enlarged and
may be mottled red, purple, or grayish white. Foci of
necrosis or hemorrhage can be seen histologically in larger
lesions (Figure 5).13 Avian leukosis virus can result in tu-
mor formation in birds. Induced tumors include lym-
phoma and lymphosarcoma. Lymphoid neoplasia has
been described in psittacines and frequently involves the
spleen.14 Lymphosarcoma in a juvenile blue and gold
macaw was associated with diffuse infiltration of the
spleen with pleomorphic lymphocytes.15 Both Marek’s dis-
ease virus and lymphoid leukosis virus can cause splenic
tumors in chickens. Reticuloendotheliosis virus can also
cause splenic tumors in poultry and waterfowl. Myeloid
neoplasia can also occur in the spleen. Fibrosarcoma and
leiomyosarcoma can occur as primary lesions. Metastasis
of distant primary neoplasms to the spleen is occasionally
seen. Metastatic lesions typically occur as irregular enlarge-
ments or multiple firm, tan, gray, or white foci.16
bPhalen D: Personal communication, Texas A&M University,

University, 1999. 1999.

EQUINE ENCEPHALITIS VIRUS ■ Plasmodium INFECTION ■ LYMPHOSARCOMA

Small Animal/Exotics Compendium October 2000

METABOLIC DISEASES tions (e.g., Leucocytozoon,

Pathologic changes associat-
ed with metabolic diseases of
the avian spleen usually result
from infiltration or deposition
of a substance not normally
found in the spleen. Such sub-
stances include amyloid, lipid,
bile pigment, iron pigment,
and urate tophi (seen with vis-
ceral gout).
Amyloidosis Figure 6—Histologic appearance of the spleen of a goose hemochromatosis.
Amyloidosis is commonly that died of amyloidosis. Deposition of eosinophilic amy-
seen 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
the deposition of amyloid A DVM, PhD, North Carolina State University)
protein, a degradation prod-
uct of an acute phase reactant protein. Amyloidosis is
frequently associated with chronic inflammation, such
as that associated with mycobacteriosis, aspergillosis,
17
and pododermatitis. Amyloidosis may be induced by
vaccination in turkeys. Amyloidosis is uncommon in
b
pigeons and psittacines. In laying Japanese quail affect-
ed with systemic amyloidosis, amyloid deposits were
predominantly seen in the spleen and liver.18 A pale,
homogenous, enlarged spleen is typical with amyloido-
sis. Variable deposition of amyloid protein is observed
histologically (Figure 6).2
Lysosomal Storage Disease
Lysosomal storage disease involving the spleen, brain,
spinal cord, and liver has been reported in a 6-month-
old male emu (Dromaius novaehollandiae). The diagno-
sis was made at necropsy using light and electron mi-
croscopy and histochemical staining. 19
Lipidosis
Fatty infiltration of the liver—and often the spleen—
commonly occurs in psittacines, most notably budgeri-
gars, Amazon parrots, cockatiels, lovebirds, and Quaker
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
with microscopic foci of splenocytes with vacuolated
cytoplasm (fat).
HEMOSIDEROSIS AND HEMOCHROMATOSIS
A mild-to-moderate degree of splenic hemosiderosis is
found in most parrots with subacute to chronic disease.
These birds generally have a mild, nonregenerative ane-
mia. Hemosiderosis is frequently associated with eryth-
rocyte destruction resulting from hemoparasite infec-
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 erythro-
cytes.21 Iron deposits are fre-
quently seen within the retic-
uloendothelial cells of the
spleen in birds affected with
Experimental chronic sele-
nium toxicosis in mallard
ducks (Anas platyrhynchos) resulted in lymphocytic
necrosis and atrophy of the spleen and other lymphoid
organs.22 Such mycotoxins as citrinin, cyclopiazonic acid,
fumonisin B, ochratoxin, and rubratoxin have been re-
ported to cause lymphoid necrosis or atrophy.1 Experi-
mental exposure of nestling American kestrels (Falco
sparverius) to polychlorinated biphenyl (PCB) 126
caused multifocal coagulative necrosis, reduced splenic
weight, and lymphocyte depletion of the spleen.23
Mycoses
Hematogenous spread of mycotic infections can re-
sult in granuloma formation in the spleen. An Amazon
parrot (Amazona aestiva) was diagnosed with systemic
candidiasis and necrotizing lesions in the lungs and gas-
trointestinal tract and giant cell–containing granulomas
in the spleen.24 Hyphae typical of Zygomycetes were seen
invading through the splenic blood vessel walls in an
African grey parrot (Psittacus erithacus) that was also di-
agnosed with chlamydiosis. Rhizomucor pusillus was iso-
lated as a pure culture from the lungs and liver of this
bird.25 Splenomegaly as a response to chronic inflam-
matory disease is a common finding at necropsy and is
seen in birds with systemic aspergillosis.
ACKNOWLEDGMENT
The author thanks David Phalen, DVM, PhD, Diplo-
mate American Board of Veterinary Practitioners, Texas
A&M University, College Station, for reviewing an ear-
ly draft of this manuscript.
REFERENCES
1. Pope CR: Lymphoid system, in Riddell C (ed): Avian
Histopathology. Tallahassee, FL, American Association of
Avian Pathologists, 1996, pp 18–44.

LEAD POISONING ■ MYCOTOXINS ■ HYPHAE

Compendium October 2000
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 sus-
pected 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, Dor-
restein GM, et al (eds): Avian Medicine and Surgery. Phila-
delphia, WB Saunders Co, 1997, pp 366–367.
6. Hoop RK, Bottger EC, Pfyffer GE: Etiological agents of my-
cobacteriosis 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 poly-
omavirus infection and disease in a green aracaris (Pteroglos-
sus 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 den-
dritic cells by adenovirus in psittacine birds. Res Virol 146
(6):389–395, 1995.
10. Dorrestein GM: Passerines, in Altman RB, Clubb SL, Dor-
restein GM, et al (eds): Avian Medicine and Surgery. Phila-
delphia, 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 prolifera-
tive lesions in non-domestic avian species—A survey of diag-
nostic 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 (Seri-
nus 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
Small Animal/Exotics
Surgery. Philadelphia, WB Saunders Co, 1997, pp 590–603.
17. Lumeij JT: Hepatology, in Ritchie BW, Harrison GJ, Harri-
son 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 amyloi-
dosis 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 toxi-
cosis in aquatic birds: Histologic lesions. J Wildl Dis 33(3):
385–404, 1997.
23. Hoffman DJ, Melancon MJ, Klein PN, et al: Developmen-
tal 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.
ABOUT THE AUTHOR
Dr. Powers is an exotics and general veterinary practition-
er at Timberlyne Animal Clinic in Chapel Hill, North Caroli-
na. She is a Diplomate of the American Board of Veteri-
nary Practitioners (Avian Practice).