Pathology in Practice
In collaboration with the American College of Veterinary Pathologists
History
A 3-year-old 0.46-kg sexually intact male African
pygmy hedgehog (Atelerix albiventris) was evalu-
ated at the Veterinary Teaching Hospital at the Loui-
siana State University School of Veterinary Medicine
because of a 4-day history of lethargy, anorexia, and
decrease in water intake. The owners reported that
the hedgehog was less active, they had not seen it
defecate recently, and they thought it had possibly
urinated on itself.
Clinical and Gross Findings
At the first clinical evaluation, the hedgehog was
responsive, stable, and apparently clinically normal.
The hedgehog was admitted to the hospital for a full
diagnostic workup. During the second examination,
only 2 hours later, the hedgehog appeared lethargic
and SC fluid therapy was provided. Right after the
beginning of the fluid therapy, the hedgehog began
agonal breathing and was bradycardic (60 beats/min;
reference range, 180 to 280 beats/min) and hypother-
mic (rectal temperature, 33.0 °C; reference range, 35.4
to 37 °C). Clinicians noticed a mass on abdominal pal-
pation and suspected it to have been a splenic mass.
Supportive care was started with external warming and
administration of atropine (0.2 mg/kg, IM), but the ani-
mal had cardiac arrest and died.
On necropsy, the hedgehog was in good body
condition and had pale-pink mucous membranes
and a distended abdomen. The spleen was severely
enlarged (approx 7 X 3.5 X 2 cm). The splenic paren-
chyma was diffusely pale pink and friable, with multi-
focal to coalescent dark-red areas (hemorrhage) and
Bianca S. de Cecco, DVM, MSc1*; Emi Sasaki, DVM2; Javier G.
Nevarez, DVM, PhD3; Charles O. Cummings, DVM3; Ingeborg M.
Langohr, DVM, PhD2; Fabio Del Piero, DVM, PhD2
1Department of Veterinary Pathology, Faculty of Veterinary
Medicine, Federal University of Rio Grande do Sul, Porto
Alegre, RS, Brazil
2Louisiana Animal Diagnostic Disease Laboratory and Depart-
ment of Pathobiological Sciences, School of Veterinary Medi-
cine, Louisiana State University, Baton Rouge, LA
3Department of Veterinary Clinical Sciences, School of Veteri-
nary Medicine, Louisiana State University, Baton Rouge, LA
*Corresponding author: Dr. de Cecco (biasantanacecco@
gmail.com)
https://doi.org/10.2460/javma.20.09.0497
Figure 1—Postmortem photograph of the abdominal
cavity of a 3-year-old 0.46-kg sexually intact male Af-
rican pygmy hedgehog (Atelerix albiventris) that died
4 days after initial signs of lethargy, anorexia, and de-
crease in water intake. The splenic parenchyma is dif-
fusely pale pink (asterisk) and has multifocal to coalesc-
ing areas of hemorrhage (arrow) and multifocal yellow
to green areas of necrosis (arrowhead).
multifocal yellow to green areas (necrosis), which
replaced approximately 70% of the parenchyma
(Figure 1). The liver was also enlarged, comprised
5.65% (26/460 g) of the total body weight (reference
range,1 4.58% to 5.16% of the total body weight), and
had round borders, tan discoloration, and an accen-
tuated lobular pattern throughout. Sections of the
liver floated in neutral-buffered 10% formalin. The
kidneys exhibited multifocal, well-delimited, white to
yellow depressed areas (0.4 to 1.2 cm in diameter)
in the cortex. In the distal colon, a 2-mm-diameter
ulcer was in the mucosa, approximately 5 cm orad
of the rectum. No other clinically meaningful lesions
were observed.
Formulate differential diagnoses, then continue
reading.
Histopathologic Findings
Several samples of the main organs were collect-
ed and fixed in neutral-buffered 10% formalin. The
tissues were processed for routine histologic evalua-
tion, which revealed that the bone marrow had been
nearly completely replaced by neoplastic round cells
that had distinct cell borders and a moderate to
marked amount of cytoplasm with abundant eosino-
philic granules, consistent with eosinophils (Figure
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Figure 2—Photomicrograph of a tissue section of a kid-
ney from the hedgehog described in Figure 1. The nor-
mal renal parenchyma is partially replaced by neoplastic
round cells with distinct cell borders and a moderate to
marked amount of cytoplasm with bright eosinophilic
granules. H&E stain; bar = 200 µm.
2). These neoplastic cells had both immature and
mature morphology. The immature cells had round
to reniform nuclei, with coarsely stippled chromatin
and prominent nucleoli. The mature cells had multi-
lobulated and irregular nuclei, with dense chromatin
and inconspicuous nucleoli. Anisocytosis and aniso-
karyosis were mild, with 1 to 2 mitotic figures/10
hpf. The numbers of megakaryocytes and erythroid
blasts were markedly low.
Approximately 70% of the splenic parenchyma
was replaced by necrotic debris. The normal splenic
architecture was replaced by dense sheets of neo-
plastic cells like those described in the bone mar-
row. In the hepatic parenchyma, hepatocytes were
diffusely swollen with distinct clear cytoplasmic
vacuoles (lipid-type vacuolar degeneration). The si-
nusoids were often expanded by similar neoplastic
eosinophils as those described in the bone marrow.
Perivascular areas predominantly in the periportal
regions had aggregates of similar granulated im-
mature and fewer mature eosinophils. In the lungs,
similar neoplastic cells expanded the peribronchio-
lar and perivascular connective tissue and were ob-
served in the blood vessels and alveolar capillaries.
The renal interstitium (predominantly perivascular
areas) was expanded by multifocal to coalescent
sheets of immature eosinophils and fewer mature
eosinophils similar to those described previously for
other tissues in this animal. A few immature eosino-
phils were also entrapped in glomerular capillaries.
The renal tubules had occasionally attenuated epi-
thelium and intraluminal eosinophilic proteinaceous
casts. Multifocal mineral deposits were present in
the renal medullary tubules. An aggregate of im-
mature and mature granulated cells was also pres-
ent in the perirenal adipose tissue. In the colon, the
lamina propria and submucosa were severely infil-
trated by immature eosinophils and fewer mature
eosinophils similar to those described previously. In
the region of the grossly noted ulcer, the submu-
Figure 3—Photomicrograph of a tissue section of the
liver from the hedgehog described in Figure 1. The neo-
plastic eosinophils are highlighted by the strong, posi-
tive histochemical staining of the cytoplasmic granules.
Luna stain; bar = 200 µm.
cosa had a focus of variably sized and atypical pro-
liferating spindle cells. Eyes and periocular tissues,
nasal and oral cavities, salivary glands, pancreas,
trachea, esophagus, stomach, small intestine, and
cerebral choroid plexus were infiltrated by similar
neoplastic cells. Luna staining2 (Figure 3) high-
lighted the granules of both mature and immature
eosinophilic granulocytes.
Morphologic Diagnosis
and Case Summary
Multiple tissues: eosinophilic leukemia.
Liver: hepatic lipidosis.
Case summary: eosinophilic leukemia in an Afri-
can hedgehog.
Comments
Spontaneous neoplasia is common in adult Afri-
can pygmy hedgehogs. No gender preference is ob-
served. Increasing age is considered to be a risk fac-
tor; the median age of affected animals is 3.5 years,
with the normal life span of pet hedgehogs being
3 to 6 years.3 In retrospective studies, the preva-
lence of neoplasia ranged from 29% (4/14)4 to 53%
(35/66),3 and approximately 9% (3/35)3 of affected
animals had > 1 neoplasm present. The most com-
mon sites of neoplasia development in hedgehogs
are skin, mammary gland, lymphoid tissues, and the
gastrointestinal, endocrine, and reproductive sys-
tems. Approximately 85% (34/40)3 of these tumors
are malignant and tend to have a poor prognosis.
Hematopoietic tumors can account for up to 20%
(8/40) of tumors in hedgehogs.3 Lymphoma is the
most common of these, with the multicentric and ali-
mentary forms predominating, whereas leukemia in
hedgehogs is considered to be uncommon or even
rare.3,5,6 Descriptions of leukemias in hedgehogs in-
clude eosinophilic leukemia and acute lymphocytic
leukemia or lymphoma.2,6,7
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 Eosinophilic leukemia is an infrequent variant of
myeloid granulocytic leukemia, which has been de-
scribed in cats,8 a Syrian hamster,9 humans,10 and Af-
rican pygmy hedgehogs.3,6,7 This type of neoplasm is
considered to be chronic and has been designated
as chronic eosinophilic leukemia in humans.10 The
neoplastic cells can be observed in the peripheral
blood and consist of mostly immature granulocytes
with eosinophilic differentiation.6 High myeloid-to-
erythroid ratio has been observed in the bone mar-
row of affected animals.7 Some authors suggest that
hedgehogs may have a unique genetic susceptibility
to this specific type of leukemia.6
Animals with myelogenous leukemia can be
affected by concurrent cytopenias, like nonregen-
erative anemia and thrombocytopenia. Biochemi-
cal abnormalities depend on the organs affected by
neoplastic cells; the literature describes a predomi-
nance of liver injury, leading to hypoalbuminemia.6
Histologically, it is common to see a neoplastic cell
infiltrate in multiple organs including the bone mar-
row, liver, kidney, gastrointestinal tract, lungs, lymph
nodes, heart, and spleen.2,7 Even though eosinophils
can be easily recognized on cytologic or histologic
examination, immature cells can be a challenge to
identify. Histochemistry and immunohistochemistry
may help in the identification of the lineage of the
neoplastic cells. In the case of eosinophilic leukemia,
Luna stain is the most common method used for the
histochemical identification of granules of immature
and mature eosinophils.2 Cytochemical staining, in-
cluding myeloperoxidase, alkaline-phosphatase, and
Sudan black, can be performed to demonstrate the
eosinophil granules as well.6
Eosinophils can cause severe tissue damage be-
cause their granules contain toxic cationic proteins,
which act as primary mediators of cellular damage
when released into tissues. These toxins can cause
an increase in vascular permeability, smooth muscle
contraction, and secretion of mucus.2,11 This can lead
to tissue necrosis, which may have been the mech-
anism of the noted splenic necrosis in the African
pygmy hedgehog of the present report. The focal
ulceration in the colon could similarly have resulted
from eosinophil-associated injury, with secondary fi-
broblast proliferation, as was also described in cats
with hypereosinophilic syndrome.11 However, in our
case, it was not possible to differentiate between a
fibroblastic lesion associated with the eosinophilic
infiltrate and an incipient sarcoma. A previous un-
specified injury could have also led to this type of
fibroblastic proliferation.
Differential diagnoses for eosinophilic leukemia
include idiopathic hypereosinophilic syndrome and
paraneoplastic hypereosinophilia, both described as
increases of solely mature eosinophils in blood and
tissues.2,7 The diagnosis of idiopathic hypereosino-
philic syndrome is made by exclusion in the absence
of an eosinophilic neoplasm (eg, leukemia) or of pri-
mary causes for reactive increase of eosinophils (eg,
allergies, autoimmune disease, or parasitic infesta-
tion).7 Other neoplasms must be taken into account
when considering severe splenomegaly, especially
histiocytic sarcoma and lymphoma. Histopathology
is sufficient for differentiating eosinophilic leukemia
in these cases.12
Early detection of the neoplasm in hedgehogs
allows for a more accurate prognosis.5 Eosinophilic
leukemia has an aggressive behavior in hedgehogs,
and no treatment has been established for this con-
dition so far.6 Radiotherapy and chemotherapy can
be considered, with protocols extrapolated from
other mammals, but the efficacy of these modalities
in hedgehogs is unknown.5,7
Acknowledgments
This study was partially supported by the Louisiana
Animal Disease Diagnostic Laboratory. Dr. Bianca S. de Ce-
cco was supported by the Conselho Nacional de Pesquisa
and Coordenação de Aperfeiçoamento de Pessoal de Nível
Superior.
The authors declare that there were no conflicts of interest.
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