DIAGNOSTIC PATHOLOGY

Vet Pathol 46:63–70 (2009)

Feline Gastrointestinal Eosinophilic Sclerosing Fibroplasia

L. E. CRAIG, E. E. HARDAM, D. M. HERTZKE, B. FLATLAND, B. W. ROHRBACH, AND R. R. MOORE
Department of Pathobiology (LEC, BF) and Department of Comparative Medicine (BWR), University
of Tennessee, College of Veterinary Medicine, Knoxville, TN; IDEXX Laboratories, North Grafton,
MA (EEH); Marshfield Clinic Laboratories, Veterinary Diagnostic Services, Marshfield, WI (DMH);
and Experimental Pathology Laboratories, Inc., Research Triangle Park, NC (RRM)

Abstract. A retrospective study of cases of a unique intramural inflammatory mass within the feline
gastrointestinal tract was performed in order to describe and characterize the lesion. Twenty-five cases
were identified from archival surgical and postmortem tissues. The lesion most often occurred as an
ulcerated intramural mass at the pyloric sphincter (n 5 12) or the ileocecocolic junction or colon (n 5 9);
the remaining cases were in the small intestine. Seven cases also had lymph node involvement. The
lesions were characterized by eosinophilic inflammation, large reactive fibroblasts, and trabeculae of
dense collagen. Intralesional bacteria were identified in 56% of the cases overall and all of the
ileocecocolic junction and colon lesions. Fifty-eight percent of cats tested had peripheral eosinophilia.
Cats treated with prednisone had a significantly longer survival time than those receiving other
treatments. We propose that this is a unique fibroblastic response of the feline gastrointestinal tract to
eosinophilic inflammation that in some cases is associated with bacteria. The lesion is often grossly and
sometimes histologically mistaken for neoplasia.

Key words: Bacteria; cats; eosinophils; fibrosis; gastrointestinal tract; granulation tissue.

There are several conditions in cats in which Materials and Methods

eosinophilic inflammation is the predominant
feature, including feline indolent ulcer, eosinophilic
plaque, eosinophilic granuloma, and hypereosino-
philic syndrome.2,8 In this report we describe
another feline eosinophilic lesion that appears to
be limited to the gastrointestinal tract and associ-
ated lymph nodes. The typical presentation is an
ulcerated intramural mass at the pyloric sphincter
or ileocecocolic junction. A previous report of
similar lesions in the subcutis and abdomen of cats
in Japan proposed methicillin-resistant Staphylo-
coccus as the cause.14 In the cases reported here, the
lesions are restricted to the gastrointestinal tract
and associated lymph nodes, and all have a very
characteristic trabecular pattern of dense collagen
that resembles osteoid, sometimes leading to a
mistaken diagnosis of osteosarcoma. Many cases
also contain numerous mast cells, leading to the
diagnosis of sclerosing mast cell tumor. The goal of
this report is to further characterize this lesion,
suggest a pathogenesis, and propose the term
‘‘feline gastrointestinal eosinophilic sclerosing fi-
broplasia’’ for the lesion.
63
Case selection
Cases were selected during 2005–2008 based on
histologic appearance from the biopsy and necropsy
submissions to the Department of Pathobiology at the
University of Tennessee, College of Veterinary Medicine
(9 cases), IDEXX Laboratories (8 cases), Marshfield
Laboratories (7 cases), and Antech Diagnostics (1 case).
Referring veterinarians were contacted and medical
records were reviewed to collect signalment, history,
clinical laboratory findings, surgical findings, and
outcome information.
Cytopathology
Cytopathologic samples were obtained from 5 cats
(cats 9, 11, 12, 14, and 15) by ultrasound-guided fine-
needle aspirate or impression of tissue taken during
surgery. All slides were stained with modified Wright’s.
Histopathology
Tissue samples were fixed in 10% formalin, embedded
in paraffin, and stained with HE. Selected tissue sections
were also stained with Gram stain, Gomori’s methena-
mine silver, Fite-Faraco, Toluidine blue, and/or modi-
fied Steiner’s.
64 Craig, Hardam, Hertzke, Flatland, Rohrbach, and Moore
Immunohistochemistry
Selected slides were stained by immunohistochemis-
try. Antigen retrieval consisted of 25 minutes at 95uC in
a pH 9.0 ethylenediaminetetraacetic acid (EDTA) buff-
er. A 3% hydrogen peroxide block was applied for
5 minutes, and this was followed by a 5-minute
nonserum protein block. Monoclonal antibodies to
smooth muscle actin (Dako, Carpinteria, CA) at a
1 : 1,000 dilution and vimentin (Dako) at a 1 : 8,000
dilution were applied and incubated for 30 minutes. A
polymer-based detection kit (EnVision, Dako) and 3,3-
diaminobenzidine chromagen were applied. Slides were
counterstained with Mayer’s hematoxylin.
Data analysis
Survival time was measured from the date of
diagnosis. The Kaplan-Meier procedure (PROC
LIFETEST, SAS version 8.0, SAS Institute, Cary,
NC) was used to compute nonparametric estimates of
the survivor function and compare survival curves in
order to evaluate the association of survival time with
treatment and location of the lesion. Cats were right
censored if they were lost to follow-up or were alive
when the study was terminated.
Results
The signalment, presenting signs, sites affected,
and outcome are summarized in Table 1. The
breeds included 14 domestic shorthair, 4 domestic
longhair, and one each of the following: mixed
breed, Siamese, Siamese cross, Maine Coon cat,
Maine Coon cat cross, Himalayan, and exotic
shorthaired Persian. The ages ranged from 14
weeks to 16 years, with a mean of 8.8 years 6
4.4 SD. Eighteen were neutered males (72%) and 7
were spayed females (28%). The cases were
submitted by veterinarians in Tennessee, Florida,
Maryland, Pennsylvania, New Jersey, Massachu-
setts, Wisconsin, and Minnesota.
Vomiting was the most common presenting sign
(21/25, 84%), but there was wide variation in
duration, from days to years. Weight loss was the
second most common presenting sign (15/22, 68%).
Peripheral hypereosinophilia was detected in 7 of
the 12 cats (58%) on which bloodwork was
performed. Three cats had biliary obstruction with
hyperbilirubinemia and elevated serum enzymes
suggestive of hepatocellular damage. Of the 7 cats
tested for feline leukemia virus, all were negative. Of
the 7 cats tested for feline immunodeficiency virus, 5
were negative and cats 13 and 16 were positive.
All cases had a palpable abdominal mass.
Grossly, an intramural ulcerated mass at the
pyloric sphincter was the most common lesion (n
5 12, 48%), which was often considered surgically
nonresectable. Other intramural sites included
Vet Pathol 46:1, 2009
jejunum (n 5 2), small intestine (not otherwise
specified, n 5 1), ileum (n 5 1), ileocecocolic
junction (n 5 6), and colon (n 5 3). Seven cats also
had gross lymph node enlargement.
Cytology was performed in 5 cats (cats 9, 11, 12,
14, and 15). In cat 9, tissue imprints and fine-needle
aspirates (FNAs) were taken during surgery of the
pyloric sphincter mass. Large irregular to spindle-
shaped cells, pink extracellular matrix, numerous
eosinophils, and numerous neutrophils were pre-
sent (Fig. 1). Neutrophils occasionally contained
intracytoplasmic bacterial rods and cocci, and
extracellular bacteria were scattered throughout
the background. Also seen were occasional small to
intermediate-sized lymphocytes, occasional plasma
cells, and few degranulated mast cells. Ultrasound-
guided FNA of the pyloric mass in cat 11 had
similar findings. In cat 12, tissue imprints taken
during surgery were inconclusive because of low
cellularity, but the abdominal effusion in this cat
was characterized as an inflammatory exudate with
20% eosinophils. In cats 14 and 15, FNA of the
mass showed only increased numbers of eosino-
phils.
The histopathologic appearance of the typical
intestinal lesion was of an ulcerated mass expand-
ing the wall at the pyloric sphincter/proximal
duodenum (n 5 12, Fig. 2) or ileocecocolic
junction (n 5 9, Fig. 3). Lymph nodes were also
commonly affected (n 5 7), either by the same
sclerosing lesion as in the intestine (Fig. 4) or by
eosinophilic lymphadenitis with more typical fibro-
sis. The pancreas was extensively infiltrated by
eosinophils and fibroblasts in one cat (cat 12),
which also had extensive infiltration of the wall of
the common bile duct and a ruptured gall bladder.
All lesions consisted of branching and anasto-
mosing trabeculae of dense collagen separated by a
densely cellular population of large spindle-shaped
cells. The trabecular collagen merged gradually
into more typical granulation tissue at the periph-
ery of the lesions (Fig. 5). All lesions contained
variably dense infiltrates of eosinophils, mast cells,
and fewer neutrophils, lymphocytes, and plasma
cells within the fibroplasia (Fig. 6) as well as within
the surrounding tissues. Lesions were either trans-
mural (Fig. 3) or affected the inner layers of the
gastrointestinal wall (Fig. 1). The lesions did not
extend beyond the serosa, except to involve
pancreas or lymph nodes. Increased numbers of
eosinophils, lymphocytes, and plasma cells were
noted in unaffected portions of the intestines in 3
cats (cats 14, 17, and 19). Increased numbers of
globule leukocytes were noted in the adjacent
mucosa in 3 cats (cats 4, 11, and 12).
Vet Pathol 46:1, 2009 GI Eosinophilic Sclerosing Fibroplasia 65

Table 1. Summary of clinical presentation, pathologic findings, and outcomes in 25 cats.*

Weight Peripheral Lesion Intralesional

Case Signalment Vomiting Loss Eosinophilia Site(s) Bacteria Survival
1 Adult MN DSH Yes _ U Stomach Gram-negative Euthanatized at
rods surgery
2 16-year-old MN DSH Yes + _ Stomach No 4 months, then LTF
3 15-year-old MN DSH Yes, 5 years 2 U Pylorus Only on surface Diagnosed at
necropsy
4 9-year-old MN DLH Yes, 2 weeks + _ Pylorus Gram-negative 2 weeks
rods (euthanatized)
5 2-year-old FS Siamese Yes, 3 days + U Pylorus, LN Gram-positive 16 months
mix cocci (euthanatized)
6 4 year old MN DSH Yes, months + U Pylorus, LN No Alive (4 months)
7 5-year-old FS DSH Yes, 5 years + + Pylorus, LN Only on surface 4 months
(euthanatized)
8 13-year-old MN DSH Yes, months + + Pylorus/ Gram-positive 9 months
duodenum rods (euthanatized)
9 1-year-old MN mixed Yes, 6 + + Duodenum No Alive (1.5 years)
breed months
10 14-week-old MN Yes, days 2 U Duodenum Only on surface Diagnosed at
exotic SH Persian necropsy
11 8-year-old MN DSH Yes + + Duodenum Only on surface 3 days (euthanatized)
12 6-year-old MN DSH Yes, 1 week 2 _ Duodenum No 1 week (euthanatized)
13 8 year old MN Yes, 1 + U Jejunum, LN No 1 month
Maine coon mix month (euthanatized)
14 9-year-old MN DLH Yes + U Jejunum, LN Gram-negative Alive (6 months)
rods
15 13-year-old MN Yes, weeks U U Small No 1 month, then LTF
Siamese intestine,
LN
16 8-year-old MN DSH Yes U + Ileum No 1 week (died at home)
17 7-year-old MN DSH Yes, 1 year U U Ileocecocolic Gram-negative Alive (1 year)
junction and Gram-
positive rods
18 14-year-old FS DSH Yes, 1 year 2 U Ileocecocolic Gram-negative Alive (6 months)
junction rods
19 8-year-old FS DLH No + + Ileocecocolic Gram-negative Alive (2 years)
junction rods
20 10-year-old FS DLH Yes, 5 + U Ileocecocolic Gram-negative Alive (2 months)
months junction rods
21 10-year-old MN No + + Ileocecocolic Gram-negative 1 week (euthanatized)
Maine Coon cat junction rods
22 14-year-old FS DSH Yes, 2.5 + U Ileocecocolic Gram-positive 2 weeks
years junction, cocci (euthanatized)
LN
23 12-year-old MN DSH Yes _ _ Proximal Gram-negative Alive (1 year)
portion of rods
the colon
24 6-year-old MN No _ U Colon Gram-negative 1 week (died at home)
Himalayan rods
25 12-year-old MN DSH No + _ Colon Gram-negative Alive (1 month)
rods
* FS 5 female spayed; MN 5 male neutered; DSH 5 domestic shorthair; DLH 5 domestic longhair; U 5 unknown; LN 5
lymph node; LTF 5 lost to follow-up.
66 Craig, Hardam, Hertzke, Flatland, Rohrbach, and Moore Vet Pathol 46:1, 2009

Fig. 1. Cytology of duodenal mass; cat 9. An aspirate of the duodenal mass showing large spindle-shaped cells,
pink extracellular matrix (*), and eosinophils (arrow). Wright’s. Bar 5 20 mm.
Fig. 2. Duodenum and pancreas; cat 7. An ulcerated lesion (outlined by arrowheads) expands and replaces the
intestinal wall at the junction of the pylorus and duodenum. Dense collagen trabeculae are present throughout the
lesion. HE. Bar 5 5 mm.
Fig. 3. Ileocecocolic junction; cat 21. An ulcerated mass of fibroplasia with dense collagen trabeculae
(sclerosing fibroplasia) expands and replaces the intestinal wall. There are multiple necrotic foci and microabscesses
containing bacteria within the mass. HE. Bar 5 3 mm. Inset: Gram stain of short Gram-negative rods within a
microabscess. Bar 5 20 mm.
Vet Pathol 46:1, 2009 GI Eosinophilic Sclerosing Fibroplasia 67

In 14 cats (56%), bacterial colonies were present

within microabscesses and necrotic foci within the
lesion. The bacteria included Gram-negative rods,
Gram-positive rods, and Gram-positive cocci
(Table 1). In the cats with intralesional bacteria,
the dense collagen trabeculae formed irregular
radiating and concentric bands around central
microabscesses containing the bacteria (Figs. 2
and 3, insets). Some cases were also stained with
modified Steiner, Gomori’s methenamine silver,
and/or Fite-Faraco, but no spirochetes, fungi, or
acid-fast bacteria were detected. Culture taken at
necropsy of an affected mesenteric lymph node
from cat 22 was negative. The mural mass in cat 9
was cultured during surgery and 6 colonies of
Escherichia coli and 2 colonies of Clostridium
perfringens were grown. Both organisms were
sensitive to all antibiotics tested.
By immunohistochemistry (cat 9) the large spindle
cells were uniformly positive for vimentin and
smooth muscle actin (not shown) indicating myofi-
broblastic differentiation. The spindle-shaped cells
showed variable degrees of mitotic activity and
nuclear pleomorphism. Five cats were originally
diagnosed with sclerosing mast cell tumors (cats 6,
18, 21, 24, and 25), two cats were originally
diagnosed with osteosarcoma (cats 3 and 7), and
one cat was originally diagnosed with a hematopoi-
etic neoplasm (cat 16). The remaining 17 cats were
diagnosed with eosinophilic inflammatory lesions.
Three cats (cats 4, 20, and 21) were treated by
surgical biopsy only; cats with the more aborad
masses (cats 20 and 21) had complete excision and
longer survival than cat 4, at the pyloric sphincter.
Eight cats (cats 5, 7, 8, 11, 12, 16, 22, and 23) were
treated with surgical biopsy and antibiotics; 7 of
those died or were euthanatized for continued
clinical signs. Seven cats were treated with surgical
biopsy and prednisone (cats 2, 6, 9, 14, 17, 19, and
25). Cats 6, 14, and 17 were also treated with
antibiotics. Cat 9 was also treated with montelu-
kast sodium (Singulair, Merck, Rahway, NJ) and
famotidine (Pepcid, Rahway, NJ). Of the 7 cats
treated with prednisone, 5 were alive at the time of
this writing; 2 survived 6 weeks and 4 months after
Fig. 7. Comparison of survival between cats treated
with prednisone, cats treated with surgical biopsy alone,
and cats treated with antibiotics. The survival time was
significantly shorter for cats treated with antibiotics (P
5 .02). # 5 censored data point (cat still alive or lost
to followup).
surgery, and then were lost to follow-up. The
treatment was unknown in 7 cats (cats 1, 3, 10, 13,
15, 18, and 24).
Survival curves comparing treatment with surgi-
cal biopsy and prednisone (with or without
antibiotics), treatment with surgical biopsy and
antibiotics, and treatment with only surgical biopsy
are shown in Fig. 7. Mean survival time for cats
treated with antibiotics was significantly (P 5 .02)
shorter than for cats treated with prednisone;
however, the mean and standard error of the mean
for cats treated with prednisone or surgical biopsy
alone could not be calculated, as all but one of the
cats in these groups were censored (alive or lost to
follow-up).
Ten cats were euthanatized (40%); 6 of those
were euthanatized during surgery due to the
nonresectable or neoplastic appearance of the
mass. The other 4 were euthanatized due to
persistent vomiting and weight loss. Four cats died
spontaneously. Cat 3 died of hypertrophic cardio-
myopathy but had a 5-year history of vomiting.
Cat 10 died of peritonitis secondary to intestinal
perforation at the site of the lesion. Two cats (cats
16 and 24) died at home 1 week after surgery, but
no necropsy was performed. Eight cats were alive
at the termination of the study, 2 that had pyloric

Fig. 4. Lymph node; cat 5. Most of the lymph node is effaced by dense collagen trabeculae (sclerosing
fibroplasia) surrounding a central microabscess. HE. Bar 5 500 mm. Inset: Gram-positive cocci at the center of the
microabscess. Gram stain. Bar 5 20 mm.
Fig. 5. Duodenum; cat 12. Trabeculae of dense collagen separated by large spindle-shaped cells (sclerosing
fibroplasia) merges into more typical granulation tissue at the periphery of the lesion. HE. Bar 5 200 mm.
Fig. 6. Duodenum; cat 10. Eosinophils are numerous within the fibroblastic portion of the lesion. HE. Bar 5
100 mm.
68 Craig, Hardam, Hertzke, Flatland, Rohrbach, and Moore
Fig. 8. Comparison of survival between cats with
lesion in the distal intestines (ileocecocolic junction or
colon) with those with lesions at the pyloric sphincter.
# 5 censored data point (cat still alive or lost to follow-
up).
lesions and 6 with lesions at the ileocecocolic
junction or colon. The 2 surviving cats with pyloric
lesions were treated with prednisone.
Survival curves for cats with proximal (pyloric
sphincter) and distal (ileocecocolic junction and
colon) lesions are shown in Fig. 8. Mean survival
times were not statistically different when cats with
a lesion in the proximal gastrointestinal tract were
compared with those whose lesion was in the distal/
aborad portion.
Discussion
The described cases have a very characteristic
appearance consisting of dense collagen trabeculae,
fibroblasts, and eosinophils. In some instances,
cytology was representative of the histopathologic
findings in that eosinophilic matrix, fibroblasts,
and eosinophils were all present. In other cases,
cytology revealed only eosinophils. Histologically,
the collagen trabeculae can be very sclerotic,
leading to the mistaken diagnosis of osteosarcoma
in 2 cats included in this report. In addition, a
previously published case of a feline duodenal
osteosarcoma closely resembles this lesion.17 The
cat in the previous report was a 3-year-old neutered
male that presented with vomiting, icterus, and
peripheral eosinophilia. A proximal duodenal mass
had been biopsied 1.5 years earlier and diagnosed
as granulation tissue. At presentation there was a
mass within the proximal duodenum obstructing
the common bile duct. The histopathologic diag-
noses on the surgically excised tissues were
duodenal osteosarcoma and eosinophilic lymphad-
enitis. The photomicrographs more closely resem-
ble the lesion described in the current report than
osteosarcoma. That cat continued to have inter-
mittent vomiting and died 4 months after surgery.
Vet Pathol 46:1, 2009
Although the spindle cells in this lesion can be
quite large and feline myofibroblasts are known to
have a tendency to undergo malignant transforma-
tion in response to ocular trauma4 and vaccina-
tion,5,9 we do not believe this lesion is a neoplasm.
The inflammatory context and the gradual transi-
tion of this lesion to more typical granulation tissue
are not consistent with neoplasia. In addition, the
lesion can occur in very young animals (14 weeks in
one case). Large numbers of mast cells in some
lesions strongly suggest neoplasia and 5 cats were
diagnosed with sclerosing mast cell tumor. Al-
though numerous mast cells are present within
some of the lesions, these mast cells are widely
dispersed and/or perivascular and are not consis-
tent with a neoplasm. Four of the 5 cats diagnosed
with mast cell tumor had bacteria within the center
of the lesion. Of those 5 cats, 3 are still alive, 1 was
euthanatized at surgery, and 1 (that was also feline
immunodeficiency virus positive) died at home, 1
week after surgery.
In a previous study of 27 cats with similar
eosinophilic sclerosing lesions, 9 had lesions in the
cervical lymph nodes or subcutis.14 However, all of
the photographs were from an abdominal mass, so
it is unclear whether the cervical lesions also had
the distinctive collagen trabeculae described here.
In that study, Gram-positive cocci (specifically,
methicillin-resistant Staphylococcus aureus) were
present in most of the lesions, but rods were seen
in 6 of the cats, all of which were abdominal
masses.14 In our cats, bacteria were detected
histologically at the center of the lesion in 14 of
25 cats. Although this is only a slight majority of
the cases, the arrangement of the inflammation
around the bacteria and the presence of the same
bacteria and same lesion in draining lymph nodes,
suggests that bacteria may play a role in the lesion.
In this report the bacteria included Gram-negative
rods, Gram-positive cocci, and Gram-positive rods.
We hypothesize that these lesions were initiated by
bacterial organisms, which are difficult to find
histologically due to antibiotic therapy or the
exuberant inflammatory lesion. It is unknown
how the bacteria become embedded in the intestinal
wall, but the predisposition for lesions to occur at
the pyloric sphincter and ileocecocolic junction
suggest that physical forces, such as foreign-body
penetration, may play a role. Normal intestinal
luminal bacteria and bacterial products have been
shown to induce collagen synthesis and increase
transforming growth factor (TGF)-b and interleu-
kin (IL)-6 expression in intestinal myofibroblast
cultures.18 Although bacteria may incite the lesion,
antibiotics were not clinically effective in the
Vet Pathol 46:1, 2009 GI Eosinophilic Sclerosing Fibroplasia
treatment of most cases. This may be because the
bacteria are walled off by the lesion itself or
because the eosinophils continue to perpetuate the
lesion even after the bacteria are cleared.
The reason for the eosinophilic response is not
clear, but cats can have an eosinophilic dermato-
logic and oral response (eosinophilic granuloma
complex) to a variety of stimuli, including viruses,
bacteria, and fungi.2 Toxoplasma gondii was
recently reported to cause eosinophilic fibrosing
gastritis in a cat.12 Cats that develop eosinophilic
granuloma complex are thought to have an
inherited eosinophil dysregulation leading to an
inappropriate eosinophilic inflammatory response
to a variety of stimuli.2 Hypereosinophilia was
present in 7 of the 12 cats (58%) tested in this study.
We hypothesize that cats with a genetic predispo-
sition to this lesion develop eosinophilic inflamma-
tion in response to the introduction of bacteria (or
other antigens) into the intestinal wall, perhaps by
a foreign body or ulceration.
Other possible causes of intestinal eosinophilic
inflammation, such as fungi, oomycetes, and
parasites, were not detected. However, the possi-
bility of hypersensitivity to food or environmental
antigens contributing to this lesion cannot be ruled
out. Another possible association is herpesvirus
infection, which causes eosinophilic inflammation
in the skin of cats.2 Although identification of
herpesvirus was not attempted in this study, it
would be an interesting avenue of investigation for
future research on this lesion.
Eosinophils produce numerous mediators that
play a role in fibrosis.6 Eosinophil infiltration and
major basic protein (MBP) deposition were present
in lesions involving inflammatory fibrosis, and
were absent in cases of noninflammatory fibrosis
in a study of human patients.13 Another study
found elevated levels of MBP in the sera of some
human patients with diffuse cutaneous systemic
sclerosis.3 Previous studies have also shown that
activated eosinophils produce important fibrogenic
mediators, such as TGF-b and IL-1b, which lead to
fibroblast proliferation and extracellular matrix
deposition.1,7,11,16 An important mediator in the
initiation of TGF-b production by eosinophils is
leukotriene D4.10 Interestingly, cats with the
longest survival times in this study were treated
with prednisone, which inhibits the production of
leukotrienes via the arachidonic acid pathway.15
Lesions at the pyloric sphincter were more
difficult to surgically excise than those in the more
distal portion of the intestine. Cats with pyloric
sphincter lesions (n 5 12) were diagnosed by
incisional biopsy or larger samples submitted after
69
death. Two cats with lesions in this location were
diagnosed at necropsy and 2 were euthanatized
during surgery because of the location of the lesion.
Five were euthanatized for continued clinical signs
after incisional biopsy and antibiotic treatment. Of
the remaining 3 cats treated with prednisone, 2
were alive at the time of this writing (4 months and
1.5 years after diagnosis) and 1 was alive 4 months
after surgery when it was lost to follow-up. More of
the distal (aborad) intestinal lesions (ileocecocolic
junction or colon) were completely excised and 67%
(6/9) of those cats are still alive.
There was no breed predisposition noted in this
study; most of the cats were domestic shorthair, but
this is representative of the cat population. There
was a wide age distribution; range 5 14 weeks to 15
years, with an average of 8.8 years. Most of the
cases were male (72%), but the sex distribution of
the patient population of all contributing institu-
tions was not available, so the significance of this
apparent male predominance is unknown.
In conclusion, we have described a unique
inflammatory lesion of the feline gastrointestinal
tract, which often contains bacteria, but does not
respond to antibiotic treatment. The lesion is
characterized by dense collagen trabeculae, large
fibroblasts, and numerous eosinophils. The lesion
is often grossly and sometimes histologically
mistaken for neoplasia. Future studies will be
needed to determine the prevalence, optimal
therapeutic recommendations, prognosis, and
pathogenesis of this unique lesion.
Acknowledgements
We thank Dr. Timothy Becker for follow-up clinical
information on case No. 9 and Dr. Danielle Reel for
contributing case No. 8. We also thank Dee Stephenson
and Sharon Schlosshan for histology support, Ladonna
Mrkonjich for immunohistochemistry support, and the
staff of the UT Clinical Pathology Laboratory for
cytology support.
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