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1 CE Credit
Inflammatory Bowel Disease in Cats
Kathleen Dunbar, BA, RVT
I
nflammatory bowel disease (IBD) is used to describe a group
of gastrointestinal (GI) diseases commonly diagnosed in adult
cats. The prevalence and cause of IBD are unknown. Idiopathic
by definition, IBD is characterized by inflammation of the stomach,
small intestine, and/or large intestine with associated GI signs,
including vomiting or diarrhea lasting more than 3 weeks. IBD is
not remedied by food trials or definitively ruled out using most
diagnostics. IBD can be confirmed only by biopsy.
Types of Inflammatory Bowel Disease
The types of IBD are classified by the principal inflammatory
cells infiltrating the GI tract.1 Most of these cell lines can be found
in cases of IBD, but certain ones are more common. Lymphocyticplasmacytic IBD, which infiltrates the lamina propria, is most
common. Eosinophilic IBD and suppurative IBD are less common,
typically invading one of two layers of the intestinal tract. Neutrophilic IBD and granulomatous IBD are rare.
Pathophysiology
No studies have confirmed the etiology of IBD in cats. Therefore,
information on the cause of IBD has been based on human and
Box 1. Immune System Receptors
2–6
Pattern-recognition receptors (PRRs) are proteins that recognize molecules
unique to a specific microorganism. Toll-like receptors (TLRs) and nucleotide
oligomerization domain (NOD) receptor families are PRRs that play a role in
mucosal balance.
Several TLRs exist, and each one is responsible for inciting a response to
microorganisms. Once a TLR recognizes an invader, it signals cytokine
production, which leads to adaptive immunity. If the invader is friendly, the
inflammatory response is suppressed. If a TLR is dysfunctional, a danger signal
is sent, even if the microorganism is a food antigen or commensal bacteria.
Once the signal is sent, the cytokine cascade begins. Subsequent adaptive
responses further damage the mucosal barrier.
NOD2 receptors bind with muramyl dipeptide, which is found in gram-negative
and gram-positive bacteria. This binding protects the host by recognizing
bacteria and activating a cytokine response. When a mutated NOD2 receptor
does not recognize pathogenic bacteria, the mucosal barrier is breached. The
defective NOD2 receptor also allows large quantities of microbes and food
antigens into the lamina propria.
Vetlearn.com | October 2011 | Veterinary Technician
murine studies. Although significant clinical and histologic differences exist between cats and humans, the pathogenesis of IBD
is thought to be similar in both species.1
The development of IBD is hypothesized to be due to interplay
between (1) a disturbance in the GI mucosal barrier, (2) mucosal
immunity, and (3) mucosal microflora.2 In a normal GI tract, a
healthy epithelial lining protects the mucosal barrier with innate
and adaptive immune responses to insults. Receptors on and
within epithelial cells control the innate and adaptive immune
responses and affect the interplay between the mucosal barrier,
immunity, and microflora3–5 (BOX 12–6). Malfunctioning receptors
disrupt homeostasis.1,6 Abnormal numbers of mucosal microflora
may also be involved in the pathogenesis of IBD7 (BOX 27–9). Bacterial
populations that are likely to induce inflammation increase in
number, and commensal bacteria decrease in number. Large
numbers of mucosal bacteria are associated with a faulty mucosal
barrier, a cytokine mRNA response, and increased clinical signs.8
The interactions between the defective mucosal barrier, immunity,
and microflora encourage chronic inflammation and clinical signs.
Clinical Findings
Clinical signs of IBD can vary significantly among patients,
depending on the anatomic location of the associated inflammation.1,10 Signs can appear and disappear sporadically. Vomiting
and diarrhea are the most common signs. If the small intestine is
inflamed, abdominal discomfort may be detected on palpation.
Cats with inflammation of the large intestine may be painful on
rectal palpation. In severe cases, the following can be present:
weight loss, appetite changes, poor haircoat, mucoid feces, tenesmus,
increased frequency of defecation, and hematochezia.
Male and female cats share the same disease predisposition.11
The mean age for development is 5.2 years.11 Siamese and exotic
breeds appear to be at increased risk of developing lymphocyticplasmacytic IBD, but no definitive breed predilection has been
reported.11 The pancreatic and biliary ducts are combined in cats,
Box 2. Abnormal Mucosal Microflora7–9
In one study, mucosal Enterobacteriaceae spp accounted for 66% of total
bacteria in cats with IBD, but 0.3% in healthy cats. In another study involving
mice, germ-free control subjects did not develop IBD, whereas mice with
normal bacterial flora developed the disease.
E1
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Inflammatory Bowel Disease in Cats
Box 3. Ruleouts for IBD
• Endocrinopathies (e.g., hyperthyroidism, diabetes mellitus)
• FeLV, FIV, coronavirus
• Renal disease
• Helminth infection, giardiasis, salmonellosis, campylobacteriosis,
Tritrichomonas foetus infection, Clostridium spp infection)
• Food allergy or intolerance
• Neoplastic growth
• Systemic disease (renal or hepatic)
• Foreign body
• Motility disorder
so IBD, lymphocytic cholangitis, and chronic pancreatitis can be
associated with each other.12,13 Other than the cited breed associations, genetic influences have not been identified in cats; however,
a gene mutation identified in humans may be applicable to cats.14
Diagnosis
IBD is diagnosed by ruling out other causes of inflammation. The
following must be investigated in a step-by-step manner, but not
necessarily in the following order: infectious or parasitic pathologies, food sensitivity or intolerance, endocrine or metabolic disturbances, foreign bodies, or neoplastic diseases of the GI tract
(BOX 3). Empirical treatment should be initiated for suspected
conditions. After the possibility of these diseases and conditions
has been eliminated, the following clinical criteria must be met
to confirm a diagnosis15:
• The cat has shown chronic GI clinical signs for at least 3 weeks
• Other conditions (BOX 3) have been eliminated as likely
causes of the inflammation
• Food trials and antibacterial and anthelmintic treatment
provide incomplete relief of clinical signs
• The cat has responded well to antiinflammatory and/or
immunosuppressant medications
• Biopsy shows evidence of mucosal inflammation consistent
with IBD
Laboratory Findings and Diagnostic Imaging
Laboratory findings can rule out other disorders1,10 and support a
diagnosis of IBD. In IBD of the small intestine, serum biochemistry
panels may show hypercholesterolemia, hypocalcemia, and hypomagnesemia. Hematology may show neutrophilia with or without
a left shift. Anemia may be present because of chronic inflammation
or chronic blood loss. These findings are not as common in IBD
of the large intestine. The C-reactive protein level, which surges
in response to inflammation, may be increased in severe IBD of
the small or large intestine.16 Fecal α1-protease inhibitor activity
Vetlearn.com | October 2011 | Veterinary Technician
tests can be used to detect protein-losing enteropathies before
hypoproteinemia is apparent.17 Cats with IBD often have high
trypsin-like immunoreactivity concentrations, which points toward
simultaneous pancreatic disease. Increased hepatic values are
frequently seen.
Cats with IBD sometimes have low serum folate and cobalamin
concentrations.18–20 Folate is absorbed by the proximal small
intestine, and cobalamin is absorbed in the ileum. These test results are consistent with a diagnosis of IBD and may help determine the location of the inflammation.
Radiography, including contrast studies, has limited value,
except to rule out a foreign body; however, ultrasonography is an
important diagnostic measure. Thickening of the large and small
intestinal walls and enlarged lymph nodes are common ultrasonographic findings.21 They are characteristic of inflammatory
disease processes but are not specific to IBD. Ultrasonography
can provide information on the location and severity of lesions,
suggesting whether a biopsy should be performed endoscopically
or surgically.
Food Trials
To diagnose IBD, food allergies and intolerances must be ruled
out. Except for very mild IBD, the disease does not respond to
dietary manipulation alone. However, idiopathic GI signs resolve
in up to 50% of cats placed on an elimination diet.22 These cats are
presumed to have a food allergy or intolerance instead of IBD. At
presentation, some cats are too fragile to begin a food trial and
need immediate empirical treatment, which eliminates a food
trial as a diagnostic possibility. If a food trial is permissible, a 4- to
6-week trial is recommended, although shorter trials have been
adequate.1,10,22
Histopathology
Histopathology is the only way to confirm IBD. However, histopathologic findings vary significantly among pathologists.23 Until
recently, a lack of standard criteria clouded agreement on the
normal histology of cats with IBD. Guidelines, including pictorial
templates and standard reporting forms advocated by the World
Small Animal Veterinary Association Gastrointestinal Standards
Group (www.wsava.org/StandardizationGroup.htm), aim to reduce
the subjectivity of histology.24 With the use of objective criteria,
a sample of mucosa can be identified as normal or diseased. If
diseased, a sample can show the severity of the disease, morphologic abnormalities, and predominant inflammatory cells.
Biopsy samples are most simply obtained using endoscopy,
which is less invasive, less expensive, and more appropriate for frail
cats. However, endoscopy allows sampling of only the mucosal
layer of the proximal GI tract. Full-thickness and extraintestinal
biopsies are important diagnostic tools25–27; if they are not obtained,
a diagnosis may be missed or a misdiagnosis can be made (e.g.,
IBD can be easily confused with lymphoma). Although surgical
and laparoscopic biopsies are complex, they are preferred.
Clients should be encouraged to allow a biopsy before any other
diagnostic procedure or therapies. Obtaining a biopsy sample is
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Inflammatory Bowel Disease in Cats
sometimes difficult because of financial restrictions or poor
condition of the patient. Clients should be made aware that biopsies
performed after therapy has begun may not be diagnostically accurate. Furthermore, cats with undiagnosed diseases such as
lymphoma may initially respond well to IBD treatment, obscuring
the true diagnosis.
Treatment
Well-controlled studies examining the efficacy of IBD treatment
are absent. Instead, treatment relies on clinical experience. Treatment is aimed at reducing the antigenic source of inflammation
and suppressing the inflammatory response. Treatment focuses
on diet, supplementation, and pharmaceutical therapies.
Diet and Supplementation
According to the definition of IBD, an affected cat has an incomplete
response to dietary modification. However, cats with mild IBD
may be food-responsive because dietary antigens play a role in its
etiology.2,6 Dietary changes can play a key role in IBD therapy.
Food intolerances or allergies may develop secondary to IBD, so
a dietary change may be called for in these situations. In more
severe IBD, dietary changes should be used in combination with
other IBD therapies. Low-antigen, easily digested diets from a single
protein source may decrease the antigen load on the GI tract.
Cats with eosinophilic IBD may respond well to a hypoallergenic
diet, while a high-fiber diet may be helpful in colonic IBD.1,10
The therapeutic use of probiotics and prebiotics is gaining
popularity. Probiotics are live microorganisms that may help
protect the mucosal barrier and balance microorganisms in the
intestines. Prebiotics are nondigestible materials in food that
may support growth of resident gut bacteria and suppress the
immune response.
Human and canine IBD studies support the use of prebiotics and
probiotics.28,29 Little research has been done on cats, but initial studies
and clinical experience have shown the use of probiotics to be of
value.30 The limited feline studies on the use of prebiotics have found
no significant changes to bacterial flora.31 Further feline studies
exploring their use may
document therapeutic value.
Cats with IBD, especially
Key Points
those with weight loss, often
• IBD is diagnosed by ruling out other
have low cobalamin levels
causes of GI distress and is
because of intestinal malconfirmed by biopsy.
absorption. A low cobalamin level affects GI func• IBD is thought to result from
tion, contributing to clinical
dysfunctional interplay between the
signs.18,19,32 Cobalamin demucosal barrier, mucosal immunity,
ficiency can be treated with
and microflora.
subcutaneous injections. If
• Treatment of IBD may involve dietary
this deficiency is not corchange and/or medication. Strict
rected, an affected cat conowner compliance is required, and
tinues to show clinical signs
recurrence is possible.
despite pharmaceutical and
dietary intervention.
Vetlearn.com | October 2011 | Veterinary Technician
Folate deficiency in cats
can result in anemia, anorexia, and lethargy.20 Folate (400
µg PO q24h for 6 weeks)
should be given to compensate for decreased proximal
intestinal absorption.33
Pharmaceutical Treatment
Glossary
Adaptive immune system—
composed of specialized lymphocytes,
this system recognizes pathogens it
has previously encountered, providing
immunity to anticipated pathogens
Innate immune system—a body’s
Although they can have
first line of defense, this system
adverse effects, corticosterdoes not have specialized cells and,
oids are the pharmaceutical
therefore, does not provide long-term
cornerstone of IBD therapy
immunity to challenges
because they disrupt the
Nucleotide-binding oligomerization
inflammatory pathways of
domain containing 2 (NOD2)
the GI tract. Prednisone,
receptor—a type of pattern-recognition
prednisolone, and methylreceptor, NOD2 proteins work
prednisolone are recomintracellularly to activate an immune
mended. Budesonide has
response; NOD2 receptors specifically
been useful in humans and
recognize muramyl dipeptide, which
dogs with IBD, but clinical
is found in certain strains of bacteria
use of the drug in cats has
had variable success.1,10 No
Pattern-recognition receptor (PRR)—
studies have examined the
proteins that recognize molecules
effectiveness or long-term
unique to a specific microorganism
risk of using budesonide
in cats.
Toll-like receptor (TLR)—a type of
Cats with refractory
PRR, TLRs play a critical role in the
clinical signs or steroidbody’s immune system response; they
induced morbidity require
recognize microbes that have invaded
additional management. The
the intestinal tract mucosa and stimulate
cytotoxic drug chlorambua response from the immune system
cil is an adjunct to steroid
therapy and can be given
until remission occurs.1,10 Leukopenia is an uncommon adverse
effect of chlorambucil, so regular blood work is important.34 The use
of cyclosporine has been helpful in dogs, and anecdotal evidence
supports use of this drug in cats. Latent infections such as toxoplasmosis may appear with the use of cyclosporine in cats.1,10,35
Metronidazole is an antimicrobial that affects the innate and
adaptive GI immune responses. Although this drug’s mechanism
of action is not completely understood, the drug is known to help
balance intestinal microflora, reduce obligate anaerobe load, and
reduce inflammation. The use of metronidazole benzoate is recommended because anorexia and hypersalivation have been
linked to the use of metronidazole hydrochloride.36–38 Metronidazole benzoate contains 60% metronidazole, so the drug must
be dosed at 25 mg/kg instead of 15 mg/kg.37 Metronidazole should
not be used indefinitely because of the risk of neurotoxicosis,
genotoxicosis, and liver insufficiency.36–40
Prognosis
The prognosis for cats with IBD is frequently positive. Mild cases
may respond to metronidazole therapy alone, and remission can
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Inflammatory Bowel Disease in Cats
Box 4. Clinical Index for Disease Activity in Cats
With Chronic Enteropathy
The clinical index for disease activity in cats with chronic enteropathy is derived
from a study of 82 cats that had either IBD or food-responsive enteropathy.13,42
Independent factors used in the index include the cat’s attitude, activity level,
and appetite as well as the presence of vomiting, diarrhea, and/or weight loss.
These variables are graded on a numeric scale of 0 to 3. For example, an
appetite score of 0 is normal, while a score of 3 indicates a severe decrease.
These variables are included in the overall feline chronic enteropathy activity
index (FCEAI), along with the following nonsubjective variables: total white
blood cell count, packed cell volume, total protein level, albumin level, alanine
transaminase level, alkaline phosphatase level, phosphorus level, and
presence of endoscopic lesions. These nonsubjective variables are assigned a
score of 0 for normal values or 1 for abnormal values; for endoscopic lesions,
absence is considered normal and presence is considered abnormal. The total
score obtained from adding the variables indicates the severity of the disease
and the effectiveness of the treatment.
extend for long periods.1,10 Cats are unlikely to immediately develop
serious metabolic side effects from steroid use.1 In some cases,
the prognosis is poor. A decreased cobalamin level is associated
with weak response to treatment.18,19,32 C-reactive protein may be
a marker of the prognosis because increased levels in humans
correlate with chronic and refractory inflammation.41 Research
has raised the possibility that alimentary lymphoma in cats is the
result of previous IBD.1,10
Disease markers such as C-reactive protein can be incorporated
into clinical indices, which are valuable for assessing the course
of a disease. Such indices exist for canine and human IBD, and a
clinical index called feline chronic enteropathy activity index (FCEAI)
was recently developed for cats with enteropathies13,42 (BOX 4). The
numeric scores can be used to measure the initial assessment,
predict the response to treatment and the possibility of remission,
and determine a prognosis. The clinical signs and severity of IBD
vary significantly in cats, so numeric scores can more accurately
define disease activity for clinical and research purposes.
Client Education
The technician’s role in educating clients about IBD is a valuable
part of a cat’s recovery. The time-consuming nature of diagnosing
IBD and stabilizing an affected patient makes client communication
particularly important. Technicians should be able to clearly answer
client questions about the diagnostic process, the disease, and the
reasonable expectations. Remissions and setbacks are common
with IBD, so technicians should offer support when clients are
feeling uncertain about their cats’ progress.
Clients may resist changing their pets’ diet and routine. Some
researchers have speculated that cats and dogs with IBD may be
unresponsive to treatment because of client noncompliance with
food restrictions or with administration of medications.43 Clients
may hastily stop drug treatment if adverse effects appear or if
clinical signs of IBD disappear. Technicians should show clients
Vetlearn.com | October 2011 | Veterinary Technician
how to properly medicate their cats, discuss potential adverse effects,
and emphasize the need for long-term treatment. Technicians play
an important role in supporting clients to ensure compliance
with using a new food and/or medication.
Conclusion
Technicians are likely to frequently see cats with IBD. By understanding the pathogenesis and management of this disease (including potential adverse effects and nonmedical supplements),
technicians can support clients in a possibly lifelong commitment
to managing IBD.
References
1. Hall EJ, German AJ. Diseases of the small intestine. In: Ettinger SJ, Feldman EC,
eds. Textbook of Veterinary Internal Medicine. 7th ed. St. Louis, MO: Elsevier Saunders;
2010:1526-1572.
2. Sartor RB. Microbial and dietary factors in the pathogenesis of chronic, immunemediated intestinal inflammation. Adv Exp Med Biol 2006;579:35-54.
3. Abreu MT, Fukata M, Arditi M. TLR signaling in the gut in health and disease. J Immunol
2005;174(8):4453-4460.
4. Gribar SC, Anand RJ, Sodhi CP, Hackham DJ. The role of epithelial toll-like receptor
signaling in the pathogenesis of intestinal inflammation. J Leukoc Biol 2008;83(3):
493-498.
5. Cario E. Bacterial interactions with cells of the intestinal mucosa: Toll-like receptors and
NOD2. Gut 2005;54(8):1182-1193.
6. Cameiro LAM, Magalhaes JG, Tattoli I, et al. NOD-like proteins in inflammation and
disease. J Pathol 2008;214(2):136.
7. Zakharchenko MP, Zakharchenko MM, Zakharchenko VM, et al. A problem in health
rehabilitation in the development of dysbioses under the influence of environmental factors.
Gig Sanit 2005;6:72-75.
8. Janeczko S, Atwater D, Bogel E, et al. The relationship of mucosal bacteria to duodenal
histopathology, cytokine mRNA, and clinical disease activity in cats with inflammatory
bowel disease. Vet Microbiol 2008;128(1-2):178-193.
9. Nell S, Suerbaum S, Josenhans C. The impact of the microbiota on the pathogenesis
of IBD: lessons from mouse infection models. Nat Rev Microbiol 2010;8(8):564-577.
10. Hall EJ, German AJ. Diseases of the large intestine. In: Ettinger SJ, Feldman EC,
eds. Textbook of Veterinary Internal Medicine. 7th ed. St. Louis, MO: Elsevier Saunders;
2010:1573-1594.
11. Dennis JS, Kruger JM, Mullaney TP. J Am Vet Med Assoc 1993;202(2):313-318.
12. Weiss DJ, Gagne JM, Armstrong PJ. Relationship between inflammatory hepatic
disease and inflammatory bowel disease, pancreatitis, and nephritis in cats. J Am Vet
Med Assoc 1996;209(6):1114-1116.
13. Jergens AE, Crandell JM, Evans R, et al. A clinical index for disease activity in cats
with chronic enteropathy. J Vet Intern Med 2010;24(5):1027-1033.
14. Hugot JP. Role of NOD2 gene in Crohn’s disease. Gastroenterol Clin Biol 2002;
26(1):13.
15. World Small Animal Veterinary Association. WSAVA and Committee Projects: GI
Standardization Group. www.wsava.org/StandardizationGroup.htm. Accessed October 2010.
16. Ceron JJ, Eckersall PD, Martýnez-Subiela S. Acute phase proteins in dogs and cats:
current knowledge and future perspectives. Vet Clin Pathol 2005;34(2):85-99.
17. Fetz K, Steiner JM, Broussard JD, et al. Evaluation of fecal alpha1-proteinase inhibitor
concentrations in cats with inflammatory bowel disease and cats with gastrointestinal
neoplasia. J Vet Intern Med 2005;19(3):439.
18. Simpson KW , Fyfe J, Cornetta A, et al. Subnormal concentrations of serum cobalamin
(vitamin B12) in cats with gastrointestinal disease. J Vet Intern Med 2001;15(1):25-32.
19. Reed N, Gunn-Moore D, Simpson K. Cobalamin, folate and inorganic phosphate
abnormalities in ill cats. J Feline Med Surg 2007;9(4):278-288.
20. Suchodolski JS, Steiner JM. Laboratory assessment of gastrointestinal function.
Clin Tech Small Anim Pract 2003;18(4):203-210.
21. Baez JL, Hendrick MJ, Walker LM, Washabau RJ. Radiographic, ultrasonographic,
and endoscopic findings in cats with inflammatory bowel disease of the stomach and
small intestine: 33 cases (1990-1997). J Am Vet Med Assoc 1999;215(3):349-354.
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Inflammatory Bowel Disease in Cats
22. Guilford WG, Jones BR, Markwell PJ, et al. Food sensitivity in cats with chronic
idiopathic gastrointestinal problems. J Vet Intern Med 2001;15(1):7-13.
23. Willard MD, Jergens AE, Duncan RB, et al. Interobserver variation among histopathologic evaluations of intestinal tissues from dogs and cats. J Am Vet Med Assoc
2002;220(8):1177-1182.
24. Washabau R, Day M, Willard M., et al. Endoscopic, biopsy, and histopathologic
guidelines for the evaluation of gastrointestinal inflammation in companion animals.
J Vet Intern Med 2010;24(1):10-26.
25. Kleinschmidt S, Harder J, Nolte I, et al. Chronic inflammatory and non-inflammatory diseases of the gastrointestinal tract in cats: diagnostic advantages of full-thickness
intestinal and extraintestinal biopsies. J Feline Med Surg 2010;12(2):97-103.
26. Evans SE, Bonczynski JJ, Broussard JD, et al. Comparison of endoscopic and fullthickness biopsy for diagnosis of inflammatory bowel disease and alimentary tract lymphoma in cats. J Am Vet Med Assoc 2006;229(9):1447-1450.
27. Zwingenberger AL, Marks SL, Baker TW, Moore PF. Ultrasonographic evaluation of
the muscularis propria in cats with diffuse small intestinal lymphoma or inflammatory
bowel disease. J Vet Intern Med 2010;24(2):289-292.
28. Damaskos D, Kolios G. Probiotics and prebiotics in inflammatory bowel disease:
microflora ‘on the scope.’ Br J Clin Pharmacol 2008;65(4):453-467.
29. Biagi G, Cipollini I, Pompei A, et al. Effect of a Lactobacillus animalis strain on
composition and metabolism of the intestinal microflora in adult dogs. Vet Microbiol
2007;124(1-2):160-165.
30. Marshall-Jones ZV, Baillon ML, Croft JM, Butterwick RF. Effects of Lactobacillus
acidophilus DSM13241 as a probiotic in healthy adult cats. Am J Vet Res 2006;67(6):
1005-1012.
31. Sparkes AH, Papasouliotis K, Sunvold G, et al. Bacterial flora in the duodenum of healthy
cats, and effect of dietary supplementation with fructo-oligosaccharides. Am J Vet Res 1998;
59(4):431-435.
Vetlearn.com | October 2011 | Veterinary Technician
32. Ruaux CG, Steiner JM, Williams DA. Early biochemical and clinical responses to
cobalamin supplementation in cats with signs of gastrointestinal disease and severe hypocobalaminemia. J Vet Intern Med 2005;19(2):155-160.
33. Gaspar M. Supplementing cat with taurine and folate. Veterinary Information Network. Internal Medicine: Feline; June 2009. http://www.vin.com/Members/boards/discussionviewer.
aspx?FirstMsg=1&LastMsg=20&DocumentId=3528344. Accessed August 2011.
34. Kiselow MA, Rassnick KM, McDonough SP, et al. Outcome of cats with low-grade
lymphocytic lymphoma: 41 cases (1995–2005). J Am Vet Med Assoc 2008;232(3):405-410.
35. Barrs VR, Martin P, Beatty JA. Antemortem diagnosis and treatment of toxoplasmosis
in two cats on cyclosporin therapy. Aust Vet J 2006;84(1-2):30-35.
36. Rutland B. New in the pipeline: Updates on feline IBD. Veterinary Information Network;
2010. http://www.vin.com/Members/CMS/Rounds/default.aspx?id=1144.
37. Trepanier L. Idiopathic inflammatory bowel disease in cats: rational treatment selection.
J Feline Med Surg 2009;11(1):32-38.
38. Davidson G. To benzoate or not benzoate: cats are the question. Int J Pharm Comp
2001;5(2):89-90.
39. Sekis I, Ramstead K, Rishniw M, et al. Single-dose pharmacokinetics and genotoxicity
of metronidazole in cats. J Feline Med Surg 2009;11(2):60-68.
40. Olson EJ, Morales SC, McVey AS, Hayden DW. Putative metronidazole neurotoxicosis
in a cat. Vet Pathol 2005;42(5):665-669.
41. Henriksen M, Jahnsen J, Lygren I, et al. C-reactive protein: a predictive factor and marker
of inflammation in inflammatory bowel disease. Results from a prospective populationbased study. Gut 2008;57(11):1518-1523.
42. Crandell JM, Jergens AE, Morrison JA, et al. Development of a clinical scoring index
for disease activity in feline inflammatory bowel disease. J Vet Int Med 2006;20:788-789.
43. Jergens AE. Controversies in canine/feline IBD II. Proc 79th Western Veterinary
Conference 2007.
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Inflammatory Bowel Disease in Cats
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1. Feline IBD is thought to result from interplay between
all of the following except
a. a defective mucosal barrier resulting in an influx of
microbes and food antigens.
b. dysregulation of an immune response.
c. a food intolerance or allergy.
d. poor balance of endogenous microflora.
2. Findings associated with inflammation of the large
intestine may include
a. pain on rectal palpation and an increase in the C-reactive
protein level.
b. thickening of the large and small intestinal walls and
enlarged lymph nodes on ultrasonography.
c. a decrease in the folate concentration.
d. a and b
3. In their role as client educators, technicians should
a. explain the cause of IBD by discussing TLRs, NOD2
receptors, and recent research.
b. show clients how to properly medicate their cats but
refrain from discussing adverse effects because this
information may hurt client compliance.
c. talk to clients about food trials and the amount of time it
may take for their cats to respond.
d. tell clients that many cats respond to metronidazole
therapy alone and that setbacks in recovery are not very
common.
4. Which of the following can be used for long-term
pharmaceutical treatment of IBD without adverse effects?
a. budesonide
b. a combination of prednisolone, prednisone, and
methylprednisolone
c. continued clinical signs and a weak response to treatment.
d. a food allergy, so feeding a novel protein is recommended.
6. Laboratory findings in IBD of the small intestine may
include
a. hypercholesterolemia, hypercalcemia, and hypomagnesemia.
b. erythrocytosis, hypercholesterolemia, and hypercalcemia.
c. an increase in band cells, anemia, and hypermagnesemia.
d. a low cobalamin level, anemia, and hypomagnesemia.
7. The World Small Animal Veterinary Association
Gastrointestinal Standards Group has guidelines aimed
at ______________________ feline IBD.
a. standardizing the use of probiotics and prebiotics for
treating
b. reducing histologic inconsistencies for diagnosing
c. standardizing recording documents for pathologists in
diagnosing
d. b and c
8. The most common clinical signs of feline IBD are
a. lethargy, inappetence, and diarrhea.
b. vomiting and diarrhea.
c. regurgitation, diarrhea, and pain during abdominal palpation.
d. a low cobalamin level and inappetence.
9. A defective NOD2 receptor
a. binds with TLR and pathogenic bacteria.
b. disrupts mucosal immunity by increasing TLR signals
to the cerebellum, which starts a cytokine cascade.
c. does not recognize pathogenic bacteria.
d. b and c
10. A clinical index can
c. metronidazole
a. give clients a score representing their cats’ health.
d. none of the above; all these drugs have adverse effects
b. help determine the location and severity of inflammation.
5. A low cobalamin level in a cat with IBD is associated with
a. poor ileal and colonic absorption.
c. help predict a cat’s prognosis and response to treatment.
d. help determine the cause of IBD.
b. a good response to treatment.
Vetlearn.com | October 2011 | Veterinary Technician
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