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20TH ANNIVERSARY Vol. 21, No.

9 September 1999

CE Refereed Peer Review

Pathophysiology and
FOCAL POINT Management of Canine
★Colonic diseases in dogs are
relatively uncommon compared
with other gastrointestinal
Colonic Diseases
diseases; however, a firm
understanding of colonic Texas A&M University
physiology and diseases greatly Debra L. Zoran, DVM, PhD
aids in the management of large
intestinal disease.
ABSTRACT: Diet and infectious/parasitic agents are the most common causes of large bowel
diarrhea in dogs. A diagnosis of lymphocytic–plasmacytic colitis (the most common form of
KEY FACTS colonic inflammatory bowel disease) should be reserved for patients in which an etiologic
agent or dietary cause cannot be found. The cause of constipation should be established and
■ Signs of colonic disease range aggressively corrected or controlled to prevent progression to megacolon. This article dis-
cusses the basics of colonic physiology, reviews the diseases most commonly associated with
from diarrhea (small or large
colonic disease in dogs, and presents an approach to the management of these disorders.
bowel) to constipation, and these
distinctions are important in

C
ompared with disorders of the stomach or small intestine, colonic disease
formulating a diagnostic and
in dogs is uncommon. The clinical manifestation of colonic disease may
therapeutic approach.
be constipation or diarrhea, depending on the nature of the problem.
The unique physiology and function of the colon must be appreciated before
■ Management of colonic disease
appropriate treatment strategies can be implemented. This article discusses the
usually requires a combination
medical and dietary management of colonic diseases and relates the clinically rel-
of dietary and pharmacologic
evant aspects of colon physiology and function to treatment of those diseases.
interventions.
Although primarily directed at assisting practitioners in managing chronic co-
lonic disease, this information may also be useful in treating acute disease.
■ Lymphocytic–plasmacytic colitis
is a frequent diagnosis in dogs
BASIC COLONIC PHYSIOLOGY
with large bowel diarrhea, but the
The colon’s roles in conservation of water, sodium, and chloride ions and as
inflammatory cells can be from
a storage site of intestinal waste products until they are expelled as feces are
dietary, infectious, parasitic, or
well known. Its role in the final digestion and metabolism of ingesta is equally
immunologic causes.
important and often overlooked. There is ample and increasing evidence that
the microbial population of the colon plays a unique and important role in
■ Constipation must be
digestion and metabolism.1–3 Fermentation of dietary fiber by colonic mi-
aggressively treated in order to
crobes produces short-chain fatty acids (SCFAs), carbon dioxide, water,
prevent progression to chronic,
methane, and hydrogen gas; in turn, these byproducts affect the luminal
irreversible megacolon.
ecosystem and colonocytes.2 Enzymes in the colonic microflora convert pri-
mary bile acids into secondary bile acids, which are colonic epithelial cell irri-
tants and tumor promoters and may contribute to inflammatory bowel disease
(IBD) and neoplasia.4,5
There has been much interest recently in the use of fructooligosaccharides
(FOS) to enhance the colonic microflora and aid in the prevention and treat-
Compendium September 1999 20TH ANNIVERSARY Small Animal/Exotics

ment of colonic disease in humans and dogs.6,7 FOS are in determining the final water content of fecal material.
complex carbohydrates that are not digested by the Because of this storage function, distal colonocytes are
small intestine enzymes; rather, they are fermented by often exposed to bacterial or dietary toxins and other
specific colonic microbes that use them as an energy luminal irritants (e.g., bile acids, ammonia) that can in-
substrate. Because they are not used by pathogenic bac- jure the epithelial cells that line the gut.5,16 Increased
teria for energy, FOS “feed” the beneficial bacteria in amounts of moderately or poorly fermented fiber in the
the colon while inhibiting the growth of other less de- fecal stream result in greater fecal bulk and dilution po-
sirable species.8 Thus FOS are potentially beneficial not tential (i.e., ability to dilute luminal substances via in-
only for their fermentability and production of SCFAs creased fecal mass and water). In addition, increased fe-
but also because they selectively provide an energy sub- cal bulk stimulates colonic motility and reduces the
strate for the normal bacterial flora. retention time of feces in the colonic lumen. Thus the
The proximal colon (i.e., the ascending and trans- best fibers for improving distal colonic function and re-
verse segments) is the primary site of fermentation of ducing the exposure of colonocytes to luminal toxins
undigested carbohydrates and proteins by the bacterial are those that are incompletely fermented by the mi-
flora. Dietary fiber is the primary substrate for bacterial croflora of the proximal colon.
fermentation, but not all dietary fibers are fermented The role of the colon in metabolism and storage of
equally. Fibers are grouped based on their fermentabili- ingesta is clearly important, but colonic motility is an
ty: (1) highly fermentable fibers (e.g., FOS, citrus pec- equally important component of normal gastrointesti-
tin, carrageenan, vegetable gums), (2) moderately ferm- nal (GI) tract function and one that is frequently al-
entable fibers (e.g., beet pulp, oat fiber, rice bran), and tered in disease states. The motor activity of the colon
(3) poorly fermentable fibers (e.g., cellulose, peanut is similar to that of the small intestine (i.e., segmenta-
hulls, lignin).9 The more fermentable the fiber is, the tion and propulsive movements are present).17 Segmen-
more SCFAs are produced; the fermentation process tation is responsible for mixing the contents of the
also reduces fecal bulk. 9 Conversely, the less ferm- colonic lumen by slowing passage of ingesta and is con-
entable a fiber is, the more it retains its structural char- trolled by the slow-wave activity of colonic smooth
acteristics and fecal bulk; however, a lower concentra- muscle. Rhythmic segmentation within the colon is
tion of SCFAs is produced. controlled by local events (e.g., the primary stimulus in
Production of SCFAs (e.g., acetate, propionate, bu- the normal colon is distention by contents) via the in-
tyrate) is important because they are used by colonic trinsic nervous system. The slow-wave activity generat-
epithelial cells as a source of metabolic energy and are a ed in the colon is less than five cycles per minute—the
substrate for cellular lipid synthesis. Butyrate is the pri- slowest activity cycle in the GI tract.17
mary source of metabolic fuel used by the colonic ep- Propulsive motor activity occurs in three patterns in
ithelium in rats, pigs, and humans10; in dogs, however, the colon: peristaltic activity, reverse peristalsis, and
butyrate and glucose appear to be equally important mass peristalsis.17 Peristalsis, or propulsion, is the aborad
substrates for metabolic energy.11 The presence of bu- movement of ingesta through the colon by tonic con-
tyrate in the colonic lumen provides a readily available tractions of smooth muscle. These contractions are
source of energy for colonic epithelial cells, which have stimulated by the presence of ingesta or distention of
a continuous need for metabolic fuel because of their the lumen (e.g., as occurs with poorly fermentable
rapid turnover rate and constant growth and mainte- fiber). Reverse peristalsis is unique to the proximal colon
nance requirements. The production of SCFAs also and is characterized by contractions that move cephalad.
serves several other important purposes: SCFAs are the The motility pattern in the proximal colon is primarily
primary cations in the colonic lumen (which helps a combination of segmentation and reverse peristalsis,
maintain a more acidic pH)12 and are involved in sodi- which serves to thoroughly mix food and allows com-
um and water fluxes in the colon.13 An acidic luminal plete absorption of necessary nutrients, SCFAs, and ions
pH reduces the ionization of long-chain fatty acids and before the remaining contents are slowly moved distally.
bile acids (both are colonic irritants),4 increases the In addition to reverse peristalsis, peristalsis, and seg-
concentration of ammonium ions (which are unable to mentation, the colon has another unique propulsive mo-
cross the cell membrane and thus are excreted in feces),14 tor activity called mass peristalsis17: Spike bursts in the
and reduces the sporulation and overgrowth of path- middle of the colon generate a migrating spike burst that
ogenic bacteria (e.g., Clostridium species).15 is responsible for a mass movement that propels the
Although bacterial population and fermentation ac- colonic contents caudally. In the distal colon, the primary
tivities are the greatest in the proximal colon, the distal motor pattern is segmentation and propulsion; the mass
colon is the major site of fecal storage and is important peristaltic activity occurs during the act of defecation. De-

FOS ■ FIBER FERMENTABILITY ■ SCFAs ■ SEGMENTATION ■ PERISTALSIS


Small Animal/Exotics 20TH ANNIVERSARY Compendium September 1999

creased segmentation and/or propulsion leads to the de- Large Bowel Diarrhea). This section reviews the more
velopment of diarrhea, whereas increased segmentation common causes of large bowel diarrhea and focuses on
results in constipation. The addition of moderately or chronic (i.e., longer than 3 weeks’ duration) colonic dis-
poorly fermentable fibers to the diet normalizes motility eases. A suggested diagnostic approach to evaluate dogs
patterns in animals with large bowel disease by stimulat- with colonic disease is presented in Figure 1.
ing both segmentation and peristalsis18; however, consti-
pation can also occur if excess amounts of dietary fiber are Colitis
given or the animal is not adequately hydrated. Although inflammatory diseases of the colon are
common causes of large bowel diarrhea in dogs, often a
COLONIC DISEASES CAUSING DIARRHEA cause is not identified and the diagnosis is based on
Colonic diseases that cause diarrhea are associated with histopathologic description. Regardless of whether a
signs of tenesmus, increased mucus in the stool, hema- definitive diagnosis is obtained, the end result of in-
tochezia, increased frequency of defecation, and de- flammatory disease in the colon is a reduction in water
creased stool volume and generally occur without vomit- and electrolyte absorption and a change in motility that
ing or weight loss. However, diarrhea with small bowel causes increased frequency and urgency of defecation.
characteristics may occur in dogs with inflammatory or Colonic goblet cells are stimulated to increase mucus
infectious diseases that affect both segments of the GI production; in severe cases, mucosal ulceration occurs,
tract. Colitis (e.g., colonic IBD) is the most common di- resulting in hematochezia.
agnosis in dogs with chronic large bowel diarrhea, but The most common inflammatory response in canine
dietary intolerance or indiscretion and bacterial, parasitic, colitis is an increase in lymphocytes and plasma cells,
and neoplastic diseases are also important causes of and the histologic diagnosis is lymphocytic–plasmacytic
colonic disease that must be considered (see Causes of colitis.19 However, the cellular infiltrate may consist of

Causes of Large Bowel Diarrhea in Dogs

Dietary Indiscretion, Intolerance, (protozoan), Entamoeba histolytica (protozoan),


or Hypersensitivity Balantidium coli (protozoan), Cryptosporidium
■ Indiscretion: Adverse reaction to ingestion of species (protozoan)
unusual foodstuffs such as garbage or table ■ Fungal: Histoplasma capsulatum, Candida species
scraps; abrupt change in diet; excess ingestion of ■ Miscellaneous: Heterobilharzia americana
foodstuffs (gluttony); or ingestion of nonfoods (schistosomiasis), Prototheca species (algae)
(pica) such as bones, hair, plants, or foreign objects
■ Intolerance: Abnormal response to an ingested Miscellaneous
food or food additive that is not an immunologic ■ Metabolic: Pancreatitis, ulceration secondary
reaction; these include metabolic, pharmacologic, to neurologic disease/corticosteroids, vascular
or idiosyncratic reactions ectasia (congenital)
■ Hypersensitivity: Adverse reaction to food that ■ Neoplasia: Adenocarcinoma, leiomyosarcoma,
has a proven immunologic basis lymphosarcoma, mast cell tumors, adenoma,
leiomyoma, fibrosarcoma, extramedullary
Infectious/Inflammatory Agents plasmacytoma, and benign polyps
■ Bacterial: Clostridium perfringens, Salmonella ■ Mechanical: Ileocolic intussusception, cecal
species, Campylobacter species, Yersinia inversion, perianal disease, short colon,
enterocolitica, Escherichia coli, Clostridium enterocysts
difficile, bacterial overgrowth in the small intestine ■ Idiopathic: Lymphocytic–plasmacytic colitis,
■ Parasitic: Trichuris vulpis (whipworm), eosinophilic (entero)colitis, histiocytic ulcerative
Ancylostoma caninum (hookworm), Giardia colitis, granulomatous (regional) colitis,
lamblia (protozoan), Pentatrichomonas hominis suppurative or neutrophilic colitis

TENESMUS ■ HEMATOCHEZIA ■ CHRONIC COLONIC DISEASE ■ COLONIC GOBLET CELLS


Compendium September 1999 20TH ANNIVERSARY Small Animal/Exotics

Diagnostic Approaches in Canine Colonic Disease

Large bowel diarrhea


(tenesmus, increased mucus, hematochezia, increased urgency)

Acute Chronic
(<3 wk duration) (>3 wk duration)

History, Fecal Therapeutic Same initial Imaging


examinations Colonoscopy,
signalment, trial: diet, approach as for studies: proctoscopy
(salt, zinc
physical sulfate, anthelmintics acute cases, but radiography (for direct
examination: direct smear, (broad-spectrum add minimum data (survey, visualization,
Important in cytology; anthelmintic base (complete contrast), aspiration/
focusing conduct treatment), blood count, ultrasonography,
multiple fecal culture,
diagnostics antibiotics routine biochemistry scintigraphy biopsy)
examinations
over 2–3 days) (amoxicillin, profile, urinalysis); (motility)
tylosin, other tests to
metronidazole) consider include
trypsin-like
immunoreactivity
assay, bile
acid assay,
corticotropin
stimulation, food
sensitivity
elimination trials

Figure 1—Algorithm for the diagnosis of acute and chronic large bowel diarrhea in dogs.

eosinophils, neutrophils, lymphocytes, plasma cells, known and likely relates to a combination of dietary,
macrophages, or a combination thereof. The presence infectious, immunologic, and genetic factors.19–22 Un-
of these inflammatory cells in the lamina propria of the like the classic causes of human IBD, ulcerative colitis,
colon or small intestine has been termed inflammatory or Crohn’s disease, lymphocytic–plasmacytic colitis in
bowel disease. The accumulation of inflammatory cells dogs is rarely associated with weight loss or ulcerative
in the colon can occur with many different diseases, lesions and is usually responsive to therapy. Neverthe-
however, and a diagnosis of IBD should be reserved for less, dogs frequently have hematochezia, increased mu-
those patients in which no identifiable cause can be cus in the feces, and an increased urgency to defecate.19
found and in which there is a significant (moderate to In most cases of canine lymphocytic–plasmacytic co-
severe) accumulation of inflammatory cells in associa- litis, a combination of dietary and pharmacologic ther-
tion with epithelial structural changes. apy will relieve clinical signs. Dietary therapy can be
provided by feeding a diet that consists of a novel pro-
Lymphocytic–Plasmacytic Colitis tein and carbohydrate, is highly digestible, or is high in
The most common histologic diagnosis in dogs with fiber (Table I). Each approach has merits, depending
IBD is lymphocytic–plasmacytic colitis. Evidence con- on the clinical situation, but there is no biopsy result or
tinues to point toward an immunologic mechanism in series of tests that will help determine which is likely to
the pathogenesis of this disease, but the cause is not be successful. Thus the rule of thumb is to feed one

INFLAMMATORY BOWEL DISEASE ■ DIETARY THERAPY


TABLE I
Commercial Prescription Diets for the Management of Canine Colonic Diseasesa
Diet Category Trade Name Contents
® ®
Hypoallergenic Hill’s Prescription Diet Canine d/d (canned and dry) Canned: whitefish or lamb, rice; dry: egg, rice
Small Animal/Exotics

(novel protein and (Hill’s Pet Nutrition, Topeka, KS)


carbohydrate sources) Eukanuba Veterinary Diets® Response Formula® FP/Canine Catfish, herring meal, potato
(canned and dry) (The IAMS Company, Dayton, OH)
IVD™ Limited Ingredient Diets™ Canine (canned and dry) Rabbit, venison, lamb, whitefish or duck, potato
(Innovative Veterinary Diets, Newport, KY)
Waltham® Veterinary Diet Canine Selected Protein Canned: lamb, rice; dry: catfish, rice
(canned and dry) (Waltham, Vernon, CA)
CNM HA-Formula® Canine Diet (dry) Modified soy protein, corn starch
(Pro-Visions, Pet Specialty Enterprises, a division of Ralston
Purina Company, St. Louis, MO)
CNM LA-Formula® Canine Diet (dry) (Pro-Visions) Salmon meal, rice
Highly digestible Hill’s Prescription Diet® Canine i/d® (canned and dry) Soy fiber (soluble fiber)
(low fat, low residue) (Hill’s Pet Nutrition)
Eukanuba Veterinary Diets® Low-Residue Formula™/ Beet-pulp fiber (mixed fiber), FOS, fish oil
Canine (dry) (The IAMS Company)
IVD™ Select Care™ Canine Neutral Formula (dry) Duck, potato, oat bran, oat-hulls fiber, FOS
(Innovative Veterinary Diets)
IVD™ Select Care™ Canine Sensitive Formula Canned: chicken, egg, cottage cheese, oat bran, guar fiber (soluble),
(canned and dry) (Innovative Veterinary Diets) FOS; dry: lamb, rice, potato, pea fiber (mixed), FOS
20TH ANNIVERSARY

Waltham® Veterinary Diet Canine Low Fat Canned: fish, meat, rice, cellulose powder, carrageenan, carob fiber
(canned and dry) (Waltham) (mixed fiber); dry: ground wheat fiber (mixed fiber), soy protein, rice
CNM EN-Formula® Canine Diet (canned and dry) Canned: beef, rice, egg product, no fiber, MCTs, fish oil; dry: rice,
(Pro-Visions) corn, no fiber, MCTs, fish oil
High dietary fiber Hill’s Prescription Diet® Canine w/d® (canned and dry Canned: cellulose fiber (insoluble fiber); dry: peanut hulls
(low fat, high fiber) (Hill’s Pet Nutrition) (insoluble fiber)
Hill’s Prescription Diet® Canine r/d® (canned and dry) Canned: cellulose (insoluble fiber); dry: peanut hulls
(Hill’s Pet Nutrition) (insoluble fiber)
IVD™ Select Care™ Canine Hifactor Formula Canned: cellulose, guar fiber (mixed fiber), FOS, fish oil;
(canned and dry) (Innovative Veterinary Diets) dry: poultry byproducts, corn, rice, peanut hulls, rice hulls
(insoluble fiber), FOS, fish oil
Waltham® Veterinary Diet Canine High Fiber (dry) Wheat bran, cellulose (mixed fiber)
(Waltham)
CNM DCO-Formula™ Canine Diet (dry) (Pro-Visions) Beet pulp, pea fiber (mixed), fish oil
CNM OM-Formula® Canine Diet (canned and dry) Canned: pea fiber, beet pulp (mixed); dry: pea fiber (mixed),
(Pro-Visions) soybean hulls (insoluble)
a
This list is not intended to be exhaustive but rather is representative of the wide variety of commercial products available from veterinarians for treatment of gastrointestinal disease.
FOS = fructooligosaccharides; MCTs = medium-chain triglycerides.
Compendium September 1999
Compendium September 1999 20TH ANNIVERSARY Small Animal/Exotics

diet for 3 to 6 weeks; if no beneficial response is seen, containing 5-ASA, combination therapy with pred-
another diet should be tried. A trial using a hypoaller- nisolone, metronidazole, or such immunosuppressive
genic diet (e.g., novel protein and carbohydrate source; agents as azathioprine may be tried (Table II). Most
Table I) is important because of the possible association cases of lymphocytic–plasmacytic colitis are responsive
of IBD with dietary intolerance or sensitivity.23 Alterna- to routine dietary and treatment approaches; for dogs
tively, feeding a high-fiber diet to dogs with colitis is that do not respond to therapy, clinicians should ques-
also a good strategy because of the beneficial increases tion whether the correct diagnosis was made, the ani-
in luminal SCFA concentrations and fecal bulk. mal is receiving the medication and diet as directed,
If feeding a high-fiber or novel-protein diet is not ef- and the dosage and frequency of drug administration
fective, a low-residue diet can be tried (Table I). Low- are adequate.
residue diets that contain FOS may prove to be espe-
cially helpful in dogs with colitis due to overgrowth of Eosinophilic Colitis
bacterial pathogens or reduced numbers of normal flo- Eosinophilic colitis is characterized by accumulations
ra; however, clinical studies reporting the effectiveness of eosinophils in the lamina propria and may also be as-
of FOS in canine colitis are lacking. Because long-term sociated with persistent peripheral eosinophilia.25 This
dietary management may be required in dogs with disorder is a chronic, idiopathic inflammatory disease
IBD, using a commercial diet (rather than a homemade that affects the stomach, small intestine, and/or colon
diet or one supplemented with fiber) is often the best of dogs. Food allergy has been incriminated in some
approach for preventing nutritional deficiencies or im- human patients26 but has not been proven in dogs. Spo-
balances. radic reports have associated the disease with parasites27
The pharmacologic treatment of choice for lympho- and infectious agents,28 but these findings have not
cytic–plasmacytic colitis continues to be sulfasalazine, been corroborated. Nevertheless, although the disease is
which is sulfapyridine linked to 5-aminosalicylic acid uncommon compared with lymphocytic–plasmacytic
(5-ASA; the active drug). Its mechanism of action is be- colitis, it tends to be clinically more aggressive; hema-
lieved to be via its antileukotriene activity24 and free tochezia and dyschezia are commonly observed.
radical scavenging ability. Other actions may include In addition to dietary therapy, treatment of eosin-
inhibition of lymphocyte responsiveness and natural ophilic colitis often requires immunosuppressive doses
killer cell activity and reduced production of cytokines of steroids, alone or in combination with 5-ASA com-
by lymphocytes.24 The azo bond serves as a vehicle to pounds or metronidazole, to achieve clinical remission.25
deliver the active molecule to the colon, where bacterial Efforts to reduce the steroid side effects in humans in-
enzymes (azoreductases) cleave the bond to free the 5- clude use of steroid-containing rectal suppositories or
ASA.24 enemas, newer glucocorticosteroid preparations that
Newer aminosalicylic preparations (mesalamine) are cause fewer systemic side effects (e.g., budesonide), or
available that allow delivery of 5-ASA without the sulfa such drugs as methotrexate to manage the disease.29,30
moiety, which is believed to be responsible for the nu-
merous adverse effects (keratoconjunctivitis, vomiting) Histiocytic Ulcerative Colitis
associated with sulfasalazine use. These newer products Histiocytic ulcerative colitis, a rare cause of large
include oral delayed-release preparations of mesal- bowel diarrhea, has been reported only in boxers31,32
amine, which prevent its absorption in the upper GI and a French bulldog.33 The occurrence of the disease
tract, and products that have an azo bond (e.g., sulfa- also seems to be somewhat regional, suggesting a possi-
salazine) but in which the sulfa component has been re- ble genetic influence. This ulcerative form of colitis is
placed with another amine (balsalazide, a prodrug of often associated with both watery mucoid diarrhea and
mesalamine; not available in the United States) or a marked hematochezia, and patients with severe disease
second 5-ASA (olsalazine).24 Sulfasalazine and olsalazine may exhibit weight loss. The basis for a diagnosis of
are the most common products used in dogs and have histiocytic colitis is the finding of periodic acid-
established dosages (Table II). Because few of the other Schiff–positive histiocytes in the lamina propria in con-
mesalamine-containing drugs have been thoroughly junction with other inflammatory cells.32 The prognosis
evaluated in dogs, dosages are empiric. for this disease is very guarded because the response to
When using 5-ASA in the therapy of colonic IBD, therapy is often poor, and recurrence is common even
the key is to administer high doses until control is in dogs that do respond to aggressive drug therapy.
achieved and then maintain that dose for 3 to 4 weeks
beyond clinical improvement. For patients that are not Granulomatous Colitis
responsive to diet and appropriate therapy with drugs Granulomatous colitis is another rare form of colitis

LOW-RESIDUE DIET ■ SULFASALAZINE ■ 5-ASA ■ MESALAMINE


Small Animal/Exotics 20TH ANNIVERSARY Compendium September 1999

TABLE II
Drugs for Treatment of Colonic Disease
Drug Trade Name Dosage a Indication/Action
Amoxicillin Many 10–20 PO or SC every 12 hr Salmonella, Clostridium
Ampicillin Many 10–40 PO or SC every 6–8 hr Salmonella, Clostridium
Azathioprine Imuran® 1–2 PO every 24–48 hr IBD, colitis
(Glaxco Wellcome,
Research Triangle
Park, NC)b
Barium sulfate Many 10–30 ml/kg PO once Contrast studies
Cefadroxil Cefa-Tabs® 10–30 PO every 12 hr Yersinia
(Fort Dodge,
Ft. Dodge, IA)
Cephalexin Many 10–30 PO every 8–12 hr Yersinia
Chlorambucil Leukeran® 0.2 PO every 24–48 hr IBD
(Burroughs Wellcome,
Research Triangle
Park, NC)
Chloramphenicol Many 40–50 PO every 6–8 hr Campylobacter
Chlordiazepoxide/clidinium Librax® 0.05–0.125 mg PO IBS
(Roche Products, every 8–12 hr
Manati, PR)
Clindamycin HCl Antirobe® 5–11 PO every 12 hr Anaerobes (Clostridium)
(Pharmacia & Upjohn,
Kalamazoo, MI)
Cisapride Propulsid® 0.1 PO every 8–12 hr Prokinetic
(Janssen Pharmaceutica,
Titusville, NJ)
Dicyclomine Many 0.15 PO every 8–12 hr IBS
Diethylcarbamazine/ Filaribits Plus® 5.0 PO every 24 hr Heartworm/whipworm
oxibendazole (Pfizer Animal Health, prevention
Exton, PA)
Diphenoxylate Many 0.1–0.2 PO every 8–12 hr Motility modifier
Docusate sodium Many 50–200 mg PO every 8–24 hr Stool softener
Doxycycline Many 2.5–5 PO every 12 hr Campylobacter, Yersinia
Enrofloxacin Baytril® 2.5–5 PO or SC every 12–24 hr Salmonella, Escherichia
(Bayer Corporation, coli
Shawnee, KS)
Erythromycin Many 10–20 PO every 8–12 hr Campylobacter
Febantel/praziquantel/ Drontal® Plus 1 small tablet/2–4 kg BW Hookworms,
pyrantel pamoate Tablets (Bayer (dogs weighing up to 25 lb) roundworms,
Corporation) or 1 large tablet/12–15 kg BW whipworms
(dogs weighing over 25 lb) PO
once
Fenbendazole Many 25–50 PO every 24 hr for 5 days Hookworms, whipworms,
Giardia
Gastrointestinal lavage Many 10–15 PO two doses every 2 hr Colonoscopy preparation
solution
Hyoscyamine Many 0.0005–0.0015 PO every 8 hr IBS
Lactulose Many 0.25–0.5 PO every 6–8 hr Stool softener
Loperamide Many 0.1–0.2 PO every 8–12 hr Motility modifier
Mebendazole Many 22 PO every 24 hr for 3–5 days Whipworms, hookworms
Mesalamine Many 10–22 PO every 8 hr IBD
Metoclopramide Many 0.2–0.5 PO or SC every 6–8 hr Prokinetic, antiemetic
Metronidazole Many 10–50 PO every 8–24 hr IBD, Clostridium,
Trichomonas, Giardia
Compendium September 1999 20TH ANNIVERSARY Small Animal/Exotics

TABLE II (continued)
Drug Trade Name Dosage a Indication/Action
Milbemycin oxime Interceptor ®
0.5 PO every 30 days Heartworm preventive,
(Novartis Animal whipworms, hookworms
Health, Greensboro, NC)
Olsalazine Dipentium® 10–22 PO every 8 hr IBD
(Pharmacia & Upjohn)
Orbifloxacin Orbax® 2.5–7.5 PO every 24 hr Salmonella, E. coli
(Schering-Plough
Animal Health,
Kenilworth, NJ)
Prednisolone Many 1–3 PO or SC every 12–24 hr IBD
Propantheline Many 0.25–0.5 PO every 8 hr IBS
Psyllium hydrophobic Many 1–3 tbsp/25 kg PO Fiber-responsive diseases
mucilloid every 8–24 hr
Sulfasalazine Azulfidine® 20–30 PO every 8 hr IBD
(Pharmacia & Upjohn)
Trimethoprim/ Many 15 PO every 12 hr Yersinia, Salmonella
sulfadimethoxasole
(or sulfadiazine)
Tetracycline Many 15–20 PO every 6–8 hr Campylobacter, Yersinia
Tylosin Many 7–15 PO every 8 hr IBD, Clostridium
a Dosages
are in mg/kg unless otherwise indicated.
bAlso
available generically.
BW = body weight; IBD = inflammatory bowel disease; IBS = irritable bowel syndrome; PO = orally; SC = subcutaneously.

reported in dogs. The presence of macrophages and environment: (1) a change in the amount of osmotical-
other inflammatory cells within the lamina propria is ly active particles present in the lumen, (2) a change in
similar to histiocytic ulcerative colitis, but these the bacterial flora resulting in an increase in fermenta-
macrophages are not periodic acid–Schiff positive.34 tion products or change in flora (overgrowth of
The cause is usually not identified in this type of coli- Clostridium species), or (3) the presence of physical
tis, but it is very important to rule out histoplasmosis, (abrasive) or chemical materials that induce an inflam-
phycomycosis, and other infectious diseases before matory response and mucosal injury. Diagnosis of this
starting immunosuppressive drug therapy. Like histio- syndrome is primarily based on the history, presenting
cytic colitis in boxers, this form of colitis can be unre- signs, lack of other identifiable causes (Figure 1), and
sponsive to therapy and relapses are common. In one response to dietary change or removal of the offending
reported case, surgical resection of the colon was used substance from the diet.
to control refractory disease.34 One treatment approach for dogs with diarrhea due
to dietary indiscretion is to give nothing by mouth for
Colitis Secondary to Dietary Indiscretion, 24 hours and then feed a low-fat, highly digestible diet
Intolerance, or Sensitivity (Table I). Alternatively, a low-fat, high-fiber diet may
Dietary indiscretion, intolerance, or sensitivity can help restore normal colonic motility. In patients with
also cause large bowel diarrhea in dogs. Dietary indis- significant pain or distress, motility-modifying drugs
cretion is defined as the ingestion of excess quantities of (e.g., loperamide) may be used to promote fluid and
a normal diet, feedstuffs not considered to be part of electrolyte resorption by restoring the normal segmen-
the animal’s normal diet (e.g., table food, garbage, tation contractions of the bowel. If clinical signs persist
treats, new diet), or nonfood substances (e.g., foreign for more than 3 to 5 days or are associated with other
matter, rocks, bones) that cause GI tract disturbances GI tract signs, the dog should be reevaluated and other
and result in vomiting or diarrhea. Dietary intolerance is diagnoses considered. In contrast to dogs with dietary
a nonimmunologic reaction to a substance(s) in food.23 indiscretion, dogs with dietary intolerance must be
Diarrhea due to dietary indiscretion or intolerance switched to a diet that does not contain the offending
can be induced by several effects on the colonic luminal substance(s), typically a hypoallergenic diet (Table I); in

RULE-OUTS FOR GRANULOMATOUS COLITIS ■ MOTILITY-MODIFYING DRUGS


Small Animal/Exotics 20TH ANNIVERSARY Compendium September 1999

some cases, feeding a highly digestible (premium fate flotation techniques. Multiple fecal samples should
brand) dog food rather than a grocery- or feed-store be examined before pronouncing the fecal sample nega-
brand may be effective. tive.
Dietary sensitivity is most commonly associated with Other diagnostic methods include aspiration of lumi-
vomiting, small bowel diarrhea, and dermatologic nal contents via endoscopy or a fecal ELISA marketed
signs; large bowel diarrhea may be rarely observed.35 for human use. 38 In a recent report, however, the
When dietary sensitivity is suspected, a dietary trial ELISA was found to have a 14% false-negative rate in
must be conducted using a controlled diet that is based zinc sulfate–positive dogs39 and thus is not recommend-
on both highly digestible and novel protein and carbo- ed. The long-standing recommended treatment for Gi-
hydrate sources.35 In some cases, commercial hypoaller- ardia has been 10 to 14 days of metronidazole (Table
genic diets will be sufficiently novel to both prove the II), but many Giardia species are resistant to this drug.
diagnosis and treat the disease (Table I). However, Fenbendazole or albendazole administered for 5 consec-
homemade or elemental diets may be required to con- utive days40 (Table II) may be successful in resistant cas-
trol the hypersensitivity.35 Because the risk of inducing es. Client education is essential because of the organ-
nutritional deficiencies is much greater with homemade ism’s zoonotic potential. Finally, a Giardia vaccine
diet preparations, it very important to consult a clinical (GiardiaVax™; Fort Dodge, Ft. Dodge, IA) has recent-
nutritionist (if possible) or, for long-term management, ly been developed and may be an important preventive
choose the most effective commercial diet. in regions with severe Giardia problems; side effects,
duration, and effectiveness in the clinical setting have
Infectious, Inflammatory, not been independently reported.
and Parasitic Disorders Clostridium perfringens is a common cause of acute or
Whipworm (Trichuris vulpis) is the most common par- chronic diarrhea in dogs. This bacterium is a normal
asitic cause of large bowel diarrhea in dogs; however, inhabitant of the GI tract but is typically found in its
whereas whipworm colitis is common in some areas, it vegetative form, which does not produce enterotoxin.15
does not occur in all regions of the world. Problems asso- Enterotoxin, which can be produced when the organ-
ciated with whipworm colitis are related to several factors: ism undergoes sporulation, is responsible for the resul-
(1) diagnosis is difficult because oocysts are shed intermit- tant diarrhea.15 Sporulation tends to occur in the distal
tently, (2) infective stages persist in the environment for small intestine and proximal colon and is enhanced by
months to years, and (3) acquired immunity is apparently an alkaline intestinal luminal environment. Although
lacking.36 the normal proximal colon is relatively acidic, dietary
The treatment of choice for whipworm infection is changes, antibiotics, microorganisms, or stress may al-
the benzimidazole anthelmintics, of which fenbenda- ter this environment, making conditions favorable for
zole is the most well known. Other products, including sporulation and subsequent enterotoxin production.15
febantel and milbemycin oxime (Table II), are also Dogs with clostridial enterotoxin–induced diarrhea
quite effective. The use of milbemycin oxime in month- have signs of either small or large bowel diarrhea. The
ly heartworm preventives has decreased the prevalence definitive diagnosis of clostridial enterocolitis requires
of many intestinal parasites, including whipworm.37 identification of clostridial spores and the presence of
Dogs with whipworm colitis should be retreated with enterotoxin in the feces using either a fecal ELISA or
fenbendazole (or febantel) every 6 to 12 weeks for sev- reverse passive latex agglutination (RPLA) test. Howev-
eral months to destroy the prepatent infection and pre- er, a recent study has shown that the RPLA test does
vent reinfection.36 However, monthly treatment with not correlate well with the number of fecal endospores
milbemycin oxime plus frequent, aggressive cleaning of and thus may not be a reliable test.40a Fecal cytology
kennels, runs, and yards is necessary to control chronic alone is a quick and simple screening test for the dis-
or recurrent clinical disease. ease, and identification of a large number of spores
Giardia species are protozoan parasites of the small (more than five per high-power field) in the feces of
intestine that typically cause small bowel diarrhea, but dogs with typical clinical signs correlates well with a
development of large bowel diarrhea (hematochezia or positive enterotoxin assay. The safety-pin shape of the
increased fecal mucus) is not unusual. Detection of Gi- spores makes them easily identifiable on smears stained
ardia trophozoites or oocysts in the stool is often diffi- with Diff-Quik® (Figure 2).
cult, and treatment based on a presumptive diagnosis In some cases, spores found on fecal cytology may
may be necessary. Trophozoites may be identified on represent a nonenterotoxigenic strain of Clostridium
examination of numerous direct fecal smears. The best species. Alternatively, clostridia may be secondary to
approach, however, is to identify oocysts using zinc sul- other intestinal diseases, such as parvoviral enteritis,

WHIPWORMS ■ BENZIMIDAZOLE ANTHELMINTICS ■ GIARDIA ■ CLOSTRIDIUM


Small Animal/Exotics 20TH ANNIVERSARY Compendium September 1999

hemorrhagic gastroenteritis, Therefore, other causes of


giardiasis, or IBD, 15,41 and large bowel diarrhea should
contribute to the severity of be thoroughly investigated
the disease. If there is a before a diagnosis of IBS is
question as to whether the made.
presence of fecal spores is Because dietary fiber may
clinically significant, clini- normalize myoelectric activ-
cians should either perform ity, motility, and GI transit
the RPLA assay or simply times, dietary fiber supple-
treat for the disease. mentation (especially with
Antibiotics that are effec- poorly fermentable fiber) is
tive against anaerobic bacte- a commonly recommended
ria (e.g., amoxicillin, ampi- treatment in humans. 42 In
cillin, tylosin, clindamycin, dogs in which diarrhea is
metronidazole; [Table II]) Figure 2—Photomicrograph (original magnification ×100) of the primary sign, motility
®
are also effective in reducing a fecal sample stained with Diff-Quik . There is a mixed modifiers (e.g., diphenoxy-
clostridial overgrowth and en- population of bacteria that includes numerous (more than late or loperamide) may re-
five per high-power field) Clostridium species spores. The
terotoxin production. Clini- spores have a characteristic safety-pin shape and are larger sult in significant improve-
cal signs in most dogs with than the other bacterial species present. ment (Table II).42 Dogs that
acute disease will resolve in have abdominal pain or in-
3 to 5 days. For dogs with creased flatulence may re-
chronic or recurrent clostridial enterocolitis, long-term spond to tranquilizer–antispasmotic drugs, such as
(4 to 6 weeks) antibiotic therapy is required.15 Because chlordiazepoxide (a benzodiazepine sedative) and cli-
fermentation of dietary fiber reduces the luminal pH dinium bromide (an anticholinergic; Table II).42 Other
and decreases the sporulation of clostridia, feeding a drugs that may be useful in controlling IBS include
diet that contains moderate or highly fermentable fiber propantheline or dicyclomine (Table II). Any of these
will also be beneficial (Table I). Adding highly fer- drugs should be used on a short-term basis and general-
mentable fibers (psyllium, oat fiber, canned pumpkin) ly only when the disorder flares up. Finally, because
to the diet (1 to 4 tbsp/25 kg body weight) is also bene- clients can easily become frustrated with their pet’s con-
ficial but may decrease the diet’s palatability and should dition, it is essential that good client communication is
not be used long term. established.

Irritable Bowel Syndrome Colonic Neoplasia


Irritable bowel syndrome (IBS) is a poorly defined Tumors of the GI tract represent only 1% of all ca-
disorder in dogs that causes diarrhea, but a histologic nine malignancies; however, the colon and rectum are
lesion or organism cannot be identified. In humans, the the most common sites of GI neoplasia in dogs.43 Ade-
disorder has also been termed spastic colon, nervous nocarcinoma is the most common intestinal tumor in
colon, and spastic colitis.42 It is often a recurrent cause of dogs,43 and leiomyosarcoma is the most common sarco-
large bowel diarrhea in young, hyperactive, or stressed ma.44 Adenomatous polyps of the rectum are the most
dogs and therefore resembles IBS in humans. Animals common benign growths.45 Other tumors affecting the
with IBS have no other outward signs of disease, and colon and rectum include lymphosarcoma, fibrosarco-
the colon is histologically normal; thus IBS is classified ma, leiomyoma, extramedullary plasmacytoma, mast
as a functional disorder. The disease is presumed to cell tumor, and undifferentiated sarcomas. Adenocarci-
have an neurologic component, with altered colonic nomas of the colon typically occur in older dogs (mean
motility or sensation, but this has not been proven in age, 9 years) and may be annular or intraluminal.46,47
dogs. Humans with IBS often have documented motili- Clinical signs include changes in fecal size (due to lu-
ty disorders, but the relationship of these disorders to minal constriction), large bowel diarrhea, and constipa-
the disease itself is still not clear. tion. However, one relatively consistent clinical sign is
Clinically, IBS is characterized by a chronic, intermit- weight loss, which is unusual with other large bowel
tent pattern of signs ranging from increased flatulence, diseases.47 Thus neoplastic disease must be a major con-
nausea, and abdominal pain to dyschezia, mucoid sideration in any older dog with signs of weight loss,
stools, hematochezia (less common), and tenesmus. anorexia, or lethargy.
This uncommon disorder is a diagnosis of exclusion. The most common treatment for large intestinal non-

MOTILITY MODIFIERS ■ TRANQUILIZER–ANTISPASMODIC DRUGS ■ ADENOCARCINOMA


Small Animal/Exotics 20TH ANNIVERSARY Compendium September 1999

Causes of Constipation, Obstipation, or Megacolon in Dogs50

Environmental Metabolic
■ Hospitalization ■ Dehydration
■ Inactivity ■ Hypercalcemia (e.g., neoplasia,
■ Change of habitat hyperparathyroidism, renal secondary
hyperparathyroidism, hypoadrenocorticism,
Extraluminal Colonic Obstruction
renal failure, toxicity [vitamins A and D])
■ Prostatic disease (e.g., hypertrophy, neoplasia,
■ Hypokalemia (e.g., vomiting/diarrhea, renal
abscess, cysts)
failure, hyperadrenocorticism, alkalemia,
■ Fractures involving the pelvic canal
drug-induced)
■ Neoplasia (primary or metastatic)
■ Hypothyroidism
■ Abdominal masses (e.g., abscesses, cysts that
compress the colon) Pain-Induced
■ Obstruction of perineum with hair, feces, or masses, ■ Anorectal diseases (e.g., anal sac impaction/
resulting in decreased ability to evacuate the colon abscess, stricture, perianal fistulas, proctitis)
■ Orthopedic diseases (e.g., pelvic, spinal, or rear
Intraluminal Colonic Obstruction
limb fractures)
■ Foreign material (e.g., hair, bones, plant material,
plastic, toys) Iatrogenic
■ Neoplasia (annular constriction, pedunculated ■ Opioid analgesics
growths, polyps) ■ Antacids
■ Granuloma ■ Anticholinergics
■ Rectal or colonic diverticulum ■ Anticonvulsants
■ Perineal hernia ■ Barium sulfate
■ Carafate
Neuromuscular
■ Diuretics
■ Lumbosacral spinal cord disease or injury
■ Pelvic nerve injury
■ Dysautonomia

lymphoid neoplasia is surgical resection. Postoperative to determine the underlying cause in every case (see
adjuvant chemotherapy appears to be of little benefit in Causes of Constipation, Obstipation, or Megacolon in
dogs with adenocarcinoma.48 Radiation therapy has Dogs50). Either constipation or obstipation may culmi-
shown encouraging results in the treatment of rectal nate in the syndrome of megacolon, which occurs via
tumors.49 In contrast to malignant tumors, colorectal the process of dilation or hypertrophy. Dilation is the
polyps have an excellent prognosis if they are completely endstage of idiopathic megacolon (common in cats,
excised. Recurrence is possible, especially with large le- rare in dogs) or neurologic dysfunction, whereas hyper-
sions that are difficult to excise completely, but not com- trophy develops as a consequence of some obstructive
mon. Polyps, especially those that are most distal and ses- mechanism (intraluminal or extraluminal).51 The pres-
sile, can also be treated by electrosurgery or cryosurgery.47 ence of hardened feces in the colon, termed colonic im-
paction, is a consequence of constipation, obstipation,
COLONIC DISEASES CAUSING CONSTIPATION or megacolon but does not necessarily imply perma-
Infrequent or difficult evacuation of feces is termed nent loss of function. Diagnosis of constipation is rela-
constipation. Obstipation refers to intractable constipa- tively straightforward; however, functional evaluation
tion that is refractory to control or cure and implies a of a dilated colon to assess the reversibility of the condi-
permanent loss of function. The numerous causes of tion requires anorectal manometry, pelvic floor elec-
constipation in dogs often relate to the indiscriminate tromyography, motility assessments, and intestinal
eating habits of the species. An attempt should be made transit time tests, none of which are routinely available.

POLYPS ■ DILATION ■ HYPERTROPHY ■ COLONIC IMPACTION


Compendium September 1999 20TH ANNIVERSARY Small Animal/Exotics

Constipation, Obstipation, and Megacolon The end result is a bulkier, softer stool that is easier to
Constipation is a common but easily managed prob- pass. Alternatively, fiber sources can be added to existing
lem in most dogs. For the more difficult problems of diets in the form of bulk-forming laxatives, such as psylli-
chronic constipation or obstipation, however, the incit- um, but this approach is not recommended for long-term
ing cause must be identified and corrected before treat- management of constipation. The emollient and lubri-
ment will be successful (see Causes of Constipation, cant laxatives, such as DSS and petroleum jelly, result in a
Obstipation, or Megacolon in Dogs). The initial thera- softer stool either by increasing fecal water or simply lu-
py of constipation is aimed at removing feces from the bricating the fecal mass. These laxatives are good for
colon and rectum. In de- short-term management of mild constipation and in soft-
hydrated dogs, fluid thera- ening a fecal mass that contains hair, bones, or the like
MPENDIU py is often necessary to but are not effective for therapy of chronic constipation.
M’

20th
 CO

help soften the stool. Intra- Osmotic laxatives, such as lactulose or polyethylene
S

1 9 7
9 - 1
9 9 9
venous fluid therapy is pre- glycol–electrolyte solutions, increase intraluminal water
ANNIVERSARY
ferred to oral rehydration content via their osmotic properties and are fermented
in most severe cases. Multi- by the colonic microflora (like fermentable fiber),
A LookBack ple enemas will be required
to evacuate the colon in se-
which also increases fecal water content. Stimulant lax-
atives, such as bisacodyl or phenolphthalein, increase
There have been a number of verely constipated or obsti- the propulsive contractions of the colon and decrease
exciting changes in our pated dogs. The type of colonic water absorption. They are very effective laxa-
understanding of colonic diseases enema solution varies, but tives for short-term use but should not be used in dogs
warm water should be used with severe obstipation and are not well tolerated for
of dogs and cats. The role of
initially. Dioctyl sodium long-term (daily) use in dogs. Prokinetic therapy with
different diets (e.g., highly
sulfosuccinate (DSS) is an cisapride will increase colonic smooth muscle contrac-
digestible, high-fiber, novel emollient that can be add- tions and is especially useful in dogs with postoperative
protein) and dietary components ed to warm water solutions ileus or constipation nonresponsive to fiber or laxative
(e.g., fructooligosaccharides, to help soften the stool; supplementation and in some patients with loss of func-
fiber, protein sources) in the however, DSS irritates the tion.52 In severe cases of obstipation or megacolon that
management of colonic diseases colonic epithelium.52 Ene- are unresponsive to fiber and drug therapy, a subtotal
is an especially important area ma solutions (0.5 to 1 L, colectomy may be considered.53 However, there are
of research interest. The depending on the dog’s many complications associated with this procedure in
size) should be adminis- dogs, and it should only be used as a last resort.
increased availability and
tered by gravity flow.52 So-
awareness of endoscopy as a
lutions containing soaps or REFERENCES
diagnostic tool has improved the phosphate salts should be 1. Macfarlane GT, Gibson GR: Microbiological aspects of the
ability to diagnose colonic avoided because of their ir- production of short-chain fatty acids in the large bowel, in
disease. Finally, we have better ritant or toxic effects. In Cummings JH, Rombeau JL, Sakata T (eds): Physiological
and Clinical Aspects of Short Chain Fatty Acids. Cambridge,
drugs to manage motility dogs with severe impac-
UK, Cambridge University Press, 1995, pp 87–106.
disorders (e.g., cisapride) and tion, the fecal mass may be 2. Buddington RK, Sunvold GD: Fermentable fiber and the
are beginning to understand broken down with gentle GI tract ecosystem, in Reinhart GA, Carey DP (eds): Recent
gastrointestinal motility and its digital manipulation or Advances in Canine and Feline Nutrition, vol III. Wilming-
forceps. ton, DE, Orange Frazier Press, 1998, pp 449–463.
role in disease. Nevertheless, we 3. Macfarlane GT, Gibson GR: Carbohydrate fermentation, en-
Management or preven-
still do not understand tion of constipation is di- ergy transduction and gas metabolism in the human large in-
inflammatory bowel disease or testine, in Mackie RI, White BA (eds): Gastrointestinal Micro-
rected at diet changes or biology. New York, Chapman and Hale, 1997, pp 269–318.
the importance of diet and its the addition of laxatives. 4. Reddy BS, Engel A, Simi B, et al: Effects of dietary fiber on
effect on colonic microflora in Increasing fecal bulk with colonic bacterial enzymes and bile acids in relation to colon
health and disease. dietary fiber that is moder- cancer. Gastroenterology 102:1475–1492, 1992.
ately or poorly ferment- 5. Freeman HJ: Effects of dietary fiber on fecal-luminal muta-
able stimulates the defeca- genic activities, in Spiller GA (ed): Dietary Fiber in Human
Nutrition. Boca Raton, CRC Press, 1993, pp 413–418.
tion reflex and shortens
6. Willard MD, Simpson RB, Delles EK, et al: Effects of di-
transit time while increas- etary supplementation of fructo-oligosaccharides on small
ing SCFAs and microbes, intestinal bacterial overgrowth in dogs. Am J Vet Res 55:
thus softening the stool. 654–659, 1994.

FLUID THERAPY ■ ENEMA SOLUTIONS ■ LAXATIVES ■ PROKINETIC THERAPY


Small Animal/Exotics 20TH ANNIVERSARY Compendium September 1999

7. Oli MW, Petschow BW, Buddington RK: Evaluation of 1133.


fructooligosaccharide supplementation of oral electrolyte so- 27. Hayed DW, Van Kruiningen HJ: Eosinophilic gastroenteri-
lutions for treatment of diarrhea. Dig Dis Sci 43:138–147, tis in German shepherd dogs and its relationship to visceral
1998. larval migrans. JAVMA 162:379–384, 1973.
8. Roberfroid MB: Health benefits of non-digestible oligosac- 28. Van der Gaag I, van der Lindi-Sipman JS, van Sluiys FJ, et
charides, in Kritchevsky D, Bonfield C (eds): Dietary Fiber al: Regional eosinophilic coloproctitis, typhilitis and ileitis in
in Health and Disease. New York, Plenum Press, 1997, pp a dog. Vet Quart 12:1–6, 1990.
211–219. 29. Danielsson A, Lofberg R, Persson T: A steroid enema, bu-
9. Sunvold GD, Fahey Jr GC, Merchen NR, et al: Dietary desonide, lacking systemic effects for the treatment of distal
fiber for dogs: IV. In vitro fermentation of selected fiber ulcerative colitis or proctitis. Scand J Gastroenterol 27:9–12,
sources by dog fecal inoculum and in vivo digestion and 1992.
metabolism of fiber supplemented diets. J Ann Sci 73:1099– 30. Aranda R, Horgan K: Immunosuppressive drugs in the treat-
1109, 1995. ment of inflammatory bowel disease. Semin Gastro Dis 9:2–
10. Roediger WEW: Utilization of nutrients by isolated epithe- 10, 1998.
lial cells of the rat colon. Gastroenterology 83:424–429, 1982. 31. Bush BM: Boxer colitis. Vet Rec 170:181, 1992.
11. Drackley JK, Beaulieu AD, Sunvold GD: Energetic sub- 32. Hall EJ, Rutgers HC, Scholes SFE, et al: Histiocytic ulcera-
strates for intestinal cells, in Reinhart GA, Carey DP (eds): tive colitis in boxer dogs in the UK. J Small Anim Pract 35:
Recent Advances in Canine and Feline Nutrition, vol III. 509–515, 1994.
Wilmington, DE, Orange Frazier Press, 1998, pp 463–473. 33. Van der Gaag I, van Toorenberg J, Voorout G, et al: Histio-
12. Newmark HL, Lupton JR: Determinants and consequences cytic colitis in a French bulldog. J Small Anim Pract 19:283–
of colonic luminal pH. Nutr Cancer 14:161–173, 1990. 290, 1978.
13. Binder HJ, Mehta P: Short chain fatty acids stimulate active 34. Bright RM, Jerkins L, De Novo R, et al: Chronic diarrhea in
sodium and chloride absorption in vitro in the rat distal a dog with regional granulomatous enteritis. J Small Anim
colon. Gastroenterology 96:989–996, 1989. Pract 35:423–426, 1994.
14. Reinhart GA, Sunvold GD: New methods for managing ca- 35. Brown CM, Armstrong PJ, Globus H: Nutritional manage-
nine chronic renal failure, in Reinhart GA, Carey DP (eds): ment of food allergies in dogs and cats. Compend Contin
Recent Advances in Canine and Feline Nutrition, vol III. Educ Pract Vet 17(5):637–659, 1995.
Wilmington, DE, Orange Frazier Press, 1998, pp 395–405. 36. Reinemeyer CR: Post-therapeutic management of gastroin-
15. Twedt DC: Clostridium perfringens associated enterotoxicosis testinal parasitisms of small animals. Proc 17th Waltham/
in dogs, in Kirk RW, Bonagura JD (eds): Kirk’s Current Vet- OSU Symp:80–89, 1993.
erinary Therapy XI. Philadelphia, WB Saunders Co, 1992, 37. Blagburn BL, Hendrix CM, Lindsay DS, et al: Efficacy of
pp 602–604. milbemycin oxime against naturally occurring, acquired or
16. Sartor RB: Postoperative recurrence of Crohn’s disease: The experimentally induced Ancylostoma sp. and Trichuris vulpis
enemy is within the fecal stream. Gastroenterology 114:398– infections in dogs. Am J Vet Res 53:513–516, 1992.
399, 1998. 38. Leib MS, Zajac AM: Giardia infection in dogs and cats. Proc
17. Guilford WG: Small and large intestine: Normal structure 17th Waltham/OSU Symp:90–94, 1993.
and function, in Strombeck DR, Guilford WG, Center SA, 39. Barr SC, Bowman DD, Erb HN: Evaluation of two test pro-
et al (eds): Strombeck’s Small Animal Gastroenterology. cedures for the diagnosis of giardiasis in dogs. Am J Vet Res
Philadelphia, WB Saunders Co, 1996, pp 451–486. 53:2028–2031, 1992.
18. Maskell IE, Bauer JE: Role of dietary fiber in gastrointestinal 40. Barr SC, Bowman DD, Heller RL: Efficacy of fenbendazole
function. Proc 17th Ann Waltham/OSU Symp:63–72, 1993. against giardiasis in the dog. Am J Vet Res 55:988–990, 1994.
19. Jergens AE, Moore FE, Haynes JS, et al: Idiopathic inflam- 40a. Marks SL, Melli A, Kass PH, et al: Evaluation of methods to
matory bowel disease in dogs and cats: 84 cases (1987– diagnose Clostridium perfringes–associated diarrhea in dogs.
1990). JAVMA 201:1603–1608, 1992. JAVMA 214(3):357–360, 1999.
20. Gibson PR, Pavli P: Pathogenic factors in inflammatory bow- 41. Tilton RC, Van Kruiningen HJ, Kwasnik I, et al: Toxigenic
el disease. I. Ulcerative colitis. Dig Dis Sci 10:17–28, 1992. Clostridium perfringens from a parvoviral-infected dog. J Clin
21. Sartor RB: Cytokines in inflammatory bowel disease. Prog Microbiol 14:697–700, 1981.
Inflam Bowel Dis 12:5–8, 1991. 42. Tams TR: Irritable bowel syndrome, in Kirk RW, Bonagura
22. Richter KP: Lymphocytic plasmacytic enterocolitis in dogs. JD (eds): Kirk’s Current Veterinary Therapy XI. Philadelphia,
Semin Vet Med Surg 7:134–144, 1992. WB Saunders Co, 1992, pp 604–608.
23. Guilford WG: Adverse reactions to foods: A gastrointestinal 43. Birchard SJ, Couto CG, Johnson S: Nonlymphoid intestinal
perspective. Compend Contin Educ Pract Vet 16(8):957–969, neoplasia in 32 dogs and 14 cats. JAAHA 22:533–537, 1986.
1994. 44. Bruecker KA, Withrow SJ: Intestinal leiomyosarcoma in six
24. Allgayer H: Sulfasalazine and 5-aminosalicylic acid com- dogs. JAAHA 24:281–284, 1988.
pounds. Gastrointest Clin North Am 21:643–658, 1992. 45. Holt PE, Lucke VM: Rectal neoplasia in the dog: A clinico-
25. Johnson SE: Canine eosinophilic gastroenterocolitis. Semin pathological review of 31 cases. Vet Rec 116:400–405, 1985.
Vet Med Surg 7:145–152, 1992. 46. Patnaik AK, Hurvitz AI, Johnson GF: Canine intestinal ade-
26. Heyman MB: Food sensitivity and eosinophilic gastroen- nocarcinoma and carcinoid. Vet Pathol 17:149–163, 1980.
teropathies, in Sleisenger MH, Fordtran JS (eds): Gastroin- 47. Straw RC: Tumors of the intestinal tract, in Withrow SJ,
testinal Disease, Pathophysiology, Diagnosis, and Management, MacEwen EG (eds): Small Animal Clinical Oncology, ed 2.
vol 2, ed 4. Philadelphia, WB Saunders Co, 1989, pp 1113– Philadelphia, WB Saunders Co, 1996, pp 252–261.
Small Animal/Exotics 20TH ANNIVERSARY Compendium September 1999

48. Ogilvie GK, Moore AS: Gastrointestinal neoplasia, in Contin Educ Pract Vet 19(6):721–736, 1997.
Ogilvie GK, Moore AS (eds): Managing the Veterinary Can- 53. Bright RM, Burrows CF, Boring R, et al: Subtotal colecto-
cer Patient, Trenton, NJ, Veterinary Learning Systems, my for treatment of acquired megacolon in the dog and cat.
1995, pp 349–360. JAVMA 188:1412–1416, 1986.
49. Turrel JM, Theon AP: Single high dose irradiation for se-
lected canine rectal adenocarcinomas. Vet Radiol 27:141–
145, 1986.
About the Author
50. Dimski DS: Constipation: Pathophysiology, diagnostic ap-
proach, and treatment. Semin Vet Med Surg 4:247–254, Dr. Zoran is affiliated with the Department of Small Animal
1989. Medicine and Surgery, College of Veterinary Medicine,
51. Washabau RJ, Hasler AH: Constipation, obstipation, and Texas A&M University, College Station, Texas. She is a
megacolon, in August JR (ed): Feline Internal Medicine, vol Diplomate of the American College of Veterinary Internal
3. Philadelphia, WB Saunders Co, 1996, pp 104–112. Medicine.
52. Washabau RJ, Hall JA: Diagnosis and management of gas-
trointestinal motility disorders in dogs and cats. Compend

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