Feline Inflammatory
Bowel Disease
Inflammatory bowel disease (IBD) is a chronic gastrointestinal tract disorder involving the
proximal or distal portions of the gastrointestinal tract. Clinical signs may
vary depending upon the site of involvement. As the pancreatic and biliary
ducts are combined in cats, IBD may result in concurrent pancreatitis and cholangiohepatitis,
called "triaditis".
Etiology: The cause of IBD is not known, but
thought to be the result of an appropriate immune response to a persistent,
abnormal stimulus (luminal pathogen) or an abnormal, prolonged response to a
normal stimulus (dietary protein and enteric microflora). Improper immune
response against enteric bacteria is proposed to be an essential co-factor.
Signalment and clinical presentation: No gender, age, or breed predispositions
exist for feline IBD. Mostly middle to old-aged cats are affected, but IBD has
also been diagnosed with some frequency in cats less than one year old. Small
intestinal IBD typically results in vomiting and weight loss whereas large
intestinal IBD causes hematochezia. Other clinical signs include lethargy,
anorexia and ravenous appetite. In cats with triaditis, icterus and palpable
liver are seen. Severity of the signs does not correlate well with the
severity of the infiltrate and the site involved.
Diagnosis: Diagnosis of IBD is by histologic
exam and exclusion of other causes of gastrointestinal inflammation. Clinical
differential diagnoses include:
a) Endocrine disease (hyperthyroidism, exocrine pancreatic insufficiency)
b) Food intolerance
c) Infectious enteritis
d) Chronic parasitism
e) Neoplasia
Baseline tests: Baseline laboratory tests
should include complete blood count, serum biochemistry panel, urinalysis,
serum free T4 concentration, FeLV/FIV test, fecal analysis (zinc sulfate
flotation, direct smear, fecal wet mount, ELISA for antigen detection).
Changes in protein, liver enzymes, cholesterol, and potassium have been noted
in affected cats. Biochemical evidence for pancreatic and hepatic involvement
may be seen in cats with triaditis. Changes in the CBC are not specific, but
hemoconcentration, leukocytosis, neutro-penia, eosinophilia and basophilia have
been noted.
Imaging procedures: Survey and contrast
radiographs are not helpful in detecting IBD, but can be used to rule out other
conditions (e.g. obstruction, intra-abdominal masses). Ultrasound can be used
to choose appropriate procedures (endoscopy or exploratory laparotomy) for the
collection of a biopsy specimen.
Biopsy: Histologic examination of the
duodenum and colon is required for definitive diagnosis. Endoscopic or
full-thickness surgical biopsies may be used for histological evaluation. It
is important to obtain multiple tissue samples from each site and from
different areas (e.g. duodenum, jejunum, ileum, colon) of the alimentary
tract. The limitations of endoscopy are that only mucosal biopsy can be
performed (the disease could be deeper) and several areas of the digestive
tract cannot be reached by this method.
Full thickness biopsy may be warranted if endoscopic
biopsies are nondiagnostic and other causes of vomiting and diarrhea have been
ruled out. If laparotomy is performed, biopsies of stomach, duodenum, jejunum,
ileum, liver and pancreas should be obtained. Full thickness colonic biopsies
should be avoided (endoscopy is the preferred method for colon).
Histopathologic findings: Increased numbers of
inflammatory cells are present in the lamina propria. Typically, all cell
lines are present but the type of IBD is named for the predominant cell type.
-
Lymphoplasmacytic
IBD is the most common form. The lamina propria is infiltrated with
lymphocytes and plasma cells
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Eosinophilic
IBD is the second most common form. It is characterized as diffuse or focal
infiltration of mature eosinophils into one or more layers of the intestinal
tract. This form of IBD may be one component of feline hypereosinophilic
syndrome.
-
Suppurative
forms of IBD are uncommon; when present, an infectious etiology should be
investigated.
-
Regional
granulomatous gastro-enteritis is rare and typically manifests as a thickened,
partially stenotic segment of bowel. This form must be differentiated from
granulomatous inflammation caused by fungal disease, intestinal parasites,
feline infectious peritonitis, viral infection, foreign material,
toxoplasmosis, and neoplasia.
Other histologic findings include an increased number
of intraepithelial lymphocytes and altered mucosal architecture (villous fusion
or atrophy, edema, fibrosis, and dilation of lacteals). The submucosa is not
commonly affected, except in aggressive forms (e.g., eosinophilic and regional
granulomatous gastroenteritis).
Grading IBD: IBD is histologically graded into
mild, moderate and severe, based on the severity of the inflammation in the
biopsy sample (endoscopic and full thickness biopsy).
-
Mild:
Inflammation without archi-tectural distortion
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Moderate:
Inflammation with separ-ation and distortion of glands or crypts and mild
villous blunting
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Severe:
Inflammation with multifocal epithelial necrosis, marked separation of glands
or crypts, fibrosis, and marked villous blunting and fusion
Dilemma: A significant dilemma is to
distinguish between severe lymphoplasmacytic gastroenteritis and early
lymphosarcoma. In these cases, immunohistochemical staining of lymphocytes can
help to determine the phenotype of the infiltrating lymphocytes (monomorphic
populations of lymphocytes are suggestive of lymphosarcoma).
Treatment: Treatment is aimed at removing the
antigenic source of inflammation and/or suppress the cell mediated inflammatory
response in the gastrointestinal tract.
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Nutritional
therapy: The diet should contain a single, highly digestible, gluten-free,
novel protein (the one that animal has not been previously exposed to) and
reduced amounts of food additives. High fat diets should be avoided. If
colitis is present, consider high fiber diets containing either insoluble or
soluble fiber
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Pharmacologic
therapy: Nutritional therapy alone for moderate to severe IBD is seldom
successful and most animals require pharmacological therapy.
-by Kazuhisa Miyakawa, ECFVG Student
-edited by Dr. Vimala Vemireddi, ADDL Graduate Student
References:
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Weiss EJ, Gangne JM, Armstrong PJ: 1996.
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