Practical Veterinarian

Parasites of the Liver



• Worldwide distribution in ruminants, pigs, and horses; occasionally in humans; distribution in North America centers on the Gulf Coast/southeastern states, Pacific Northwest (including Montana), and eastern Canada; highly significant to veterinary medicine; low significance to public health.

• Common name: liver fluke.

Life Cycle

• Indirect.

• Intermediate host: lymnaeid snails; require neutral, poorly drained soil.

• Eggs are passed with bile to intestine and out with the feces; miracidia develop in 10-12 days; require water to hatch; penetrate snail, undergo asexual development and produce cercariae in 1-2 months; one miracidium into a snail equals several hundred cercariae out of snail; leave and attach to vegetation where encyst becoming metacercariae; cercariae may also overwinter in snail.

• Definitive host acquires infection by ingesting metacercariae on vegetation; fluke penetrates the small intestine to abdominal cavity, migrates to and penetrates liver in 4 — 6 days; migrates throughout liver for 4 — 7 weeks and then enters bile ducts and matures.

• Prepatent period is 8-12 weeks; may live for several years.

• In temperate regions, carrier animals important in contaminating pastures in the spring; metacercariae appear during late summer into fall.

• In mild regions, infected snails may overwinter; metacercariae may appear during spring to early summer; spring occurrence depends on moisture and snail activity the preceding fall; carrier animals also important in maintaining pasture contamination.

Pathogenesis and Clinical Signs

• Migration of immature flukes causes traumatic hepatitis and hemorrhage; anemia may result; migratory tracts eventually heal by fibrosis.

• Adults ingest blood and may also cause anemia; presence of adults causes extensive proliferation of the bile duct epithelium, cholangitis, and necrosis of the ductal wall; fibrosis of the lamina propria of the bile duct occurs that may eventually calcify.

• Clinical disease occurs in four forms:

1. Acute — caused by short-term intake of massive numbers of metacercariae that invade the liver all at once; clinical signs include inappetence, weight loss, abdominal pain, anemia, ascites, depression, sudden death; course is only a few days; occurs primarily in sheep and goats.

2. Subacute — also caused by intake of massive numbers of metacercariae, but over a longer period of time; clinical signs include inappetence, decreased weight gain or weight loss, progressive hemorrhagic anemia, liver failure, and death; course is 4 — 8 weeks.

3. Chronic — caused by intake of moderate numbers of metacercariae over an extended period of time; clinical signs include decreased feed intake and weight gain, reduced milk yield, anemia, emaciation, submandibular edema, ascites; cattle tend to exhibit chronic disease.

4. Subclinical — caused by intake of low numbers of metacercariae over a long period of time; moderate cholangitis occurs without apparent clinical signs.



• May find eggs on fecal sedimentation during chronic and subclinical infections, possibly subacute infections also.

• Eggs are oval, operculate, yellow, 130-150 x 65-90 um.


• Mature flukes may be found within the bile ducts; flukes are leaf-shaped, greenish-brown, 2-4 x 1-1.5 cm; with conical anterior end and shoulders.

• Immature flukes (up to 7 mm in length) may be difficult to find within the liver parenchyma; requires sequential slicing of the liver and expressing flukes from cut surfaces.

Treatment and Control

• See Table 4-3 for treatment of cattle; albendazole at 7.5 mg per kg in sheep and 15 mg per kg in goats has been used.

• Strategic use of anthelmintics is cornerstone of control programs; purpose is to remove parasites before animal productivity is affected and to prevent egg shedding that subsequentiy contaminates pastures; the timing, frequency, and choice of anthelmintic vary based on the transmission patterns in each geographic region.

• Grazing management should avoid high-risk areas during periods of transmission; may need to fence off areas of snail habitat; control of snails themselves through draining of habitat or use of molluscicides is impractical in most cases.


• Distributed in North America, central Europe, Mexico, and South Africa; cervids are the usual definitive hosts; catde, sheep, and goats may be accidentally infected; low to moderate significance.

• Common name: large American liver fluke.

Life Cycle

• Indirect.

• Intermediate host: freshwater lymnaeid snails.

• In cervid definitive host, life cycle is essentially as for F. hepatica.

• Prepatent period is approximately 8 months.

• Patency is generally not achieved in catde or sheep (see Pathogenesis and Clinical Signs).

Pathogenesis and Clinical Signs

• Cervids: infections are inapparent; flukes are encapsulated by a thin-walled cyst with channels to the bile ducts; eggs leave the cysts via these channels.

• Cattle: infections tend to be inapparent; flukes reach the liver and are encapsulated in cysts that usually do not communicate with the bile ducts; eggs generally are not passed out of cysts.

• Sheep, goats: flukes tend to migrate continuously within the liver as well as to ectopic sites such as the lungs; traumatic hepatitis results, which is fatal before flukes mature.



• May find eggs on fecal sedimentation of deer feces; eggs are oval, operculate, yellow, 110-160 x ~ 75 um.


• Mature flukes may be found in cysts in liver of cervids and cattle or within the liver parenchyma or other organs of sheep and goats; flukes are leaf-shaped with no demarcated anterior cone, thick, up to 10 cm in length by 2.5 cm in width.

Treatment and Control

• Clorsulon at 20 mg per kg in both sheep and cattle has been used.

• Prevention is best achieved by not grazing sheep in endemic areas; avoid grazing cattle in high-risk areas during transmission.


• Worldwide distribution, except Australia, in cattle, sheep, and goats; sporadic occurrence, moderate significance.

Life Cycle

• Indirect.

• First intermediate host: terrestrial snails.

• Second intermediate host: ants.

• Embryonated eggs are passed with the feces and ingested by snails; cercariae develop in 3-4 months, are shed by the snail, and clump together in slime-balls; ants eat slime-balls and metacercariae form in 26-62 days; most develop in the hemocoel, but some lodge in the subesophageal ganglion; this causes tetanic spasms of the mouthparts as temperatures decrease, which locks the ant onto herbage overnight; ants are then available to grazing animals the following morning.

• Definitive host acquires infection by ingesting ant containing metacercariae; flukes enter the liver by migrating up the bile ducts from the small intestine.

• Prepatent period is 47-54 days; may live for 6 years or longer.

Pathogenesis and Clinical Signs

• Pathologic changes increase in severity as infection increases in age; advanced infections can cause hepatic cirrhosis and proliferation of bile duct epithelium.

• Clinical signs in young animals are usually not present; in sheep, may cause anemia, edema, decreased wool production, and lactation.



• Eggs may be found on fecal sedimentation.

• Eggs are brown, operculated, oval, 36-46 x 10-20 um, containing miracidia; operculum may be difficult to see.


• The flukes are flattened, leaf-like, 6-10 x 1.5-2.5 mm; found in bile ducts; because of their small size, they may be missed at necropsy.

Treatment and Control

• Generally do not treat domestic animals for infection; if heavy infections are present, can use albendazole at 15-20 mg per kg once or 7.5 mg per kg once and repeated 2-3 weeks later; fenbendazole at 100-150 mg per kg has also been used.


• Distributed in southern North America through Central and South America, West Africa, Malaysia, and Pacific Islands in cats; usually low significance except in highly endemic areas.

Life Cycle

• Indirect.

• First intermediate host: terrestrial snails.

• Second intermediate host: sowbugs, woodlice, lizards.

• Paratenic host: lizards, frogs.

• Embryonated eggs are passed with the feces and ingested by snails; sporocysts containing cercariae are shed by snail and ingested by second intermediate host in which metacercariae form.

• Cats acquire infection by ingesting infected lizards (hence the name “lizard poisoning disease”); flukes migrate from the small intestine up the common bile duct.

• Prepatent period is 2-3 months.

Pathogenesis and Clinical Signs

• Infections are usually inapparent with only a short-term inappetence occurring.

• Heavy infections can cause proliferative cholangitis and cirrhosis.

• Clinical signs may include anorexia, icterus, enlarged liver, diarrhea, vomiting, and death.



• Eggs may be found on fecal sedimentation; fecal flotation may be ineffective.

• Eggs are brown, operculated, oval, 35-50 x 20-35 um, containing miracidia.


• Adults live in bile ducts, gallbladder, and pancreas; worms are very small and generally not seen at necropsy; rather, may find them on histologic section.

Treatment and Control

• Praziquantel at 20 mg per kg has been used.

• Prevent predation and scavenging whenever possible.



• Worldwide distribution in gallinaceous birds; locally significant in free-ranging birds.

• Common name: blackhead.

Life Cycle

• Direct; indirect with Heterakis gallinarum or earthworm paratenic host.

• Trophozoites are passed in the feces or in the eggs of H. gallinarum (nematodes ingest trophozoites that infect oocytes); primary means of transmission is ingestion of trophozoites in eggs of H. gallinarum or in eggs of H. gallinarum in earthworms; trophozoites die quickly (within hours) but it is possible they can be ingested with contaminated food or water.

• Remains in flagellated form in cecal lumen approximately 1 week; penetrates subepithelial tissues appearing as a round form without flagellum; carried via circulation to liver 10-12 days postinfection.

• Chickens: nonpathogenic.

• Turkeys: causes inflammation and ulcers in the ceca; cores of necrotic tissue, exudate, and parasites plug ceca; in liver, causes characteristic circular, yellow-green areas of necrosis with a depressed center; clinical signs include depression, inappetence, sulfur-colored droppings, cyanosis of the head (hence the common name), death.



• None.


• Examination of fresh or fixed impression smears obtained from the edge of cecal or liver lesions for organisms; may also be able to find organisms in histological sections.

Treatment and Control

• Modern, intensive management has decreased the incidence of this parasite; separate turkeys from chickens and poults from adults; avoid contaminated ground and adhere to strict sanitation; reuse of litter may lead to build-up of H. meleagridis eggs; treat chickens for H. meleagridis.




Cause of Trichuris

Trichuris vulpis is perhaps one of the most common causes of chronic large bowel diarrhea in dogs. Cats are occasionally infected with Trichuris serrata and Trichuris campanula. Clinical signs in Trictouro-infected dogs and cats may vary from asymptomatic infections to mild intermittent episodes of mucousy feces to acute-onset bloody diarrhea with tenesmus and dyschezia.

Pathophysiologyof Trichuris

The fecal-oral route of transmission is the canonical route of infection. After ingestion of infective Trichuris ova, eggs hatch in the small intestine and larvae migrate to the cecum and colon where they attach to the mucosa. The pathogenicity of any infection is generally related to the magnitude of the host immune response. Factors contributing to the pathogenicity and clinical signs include the number of mature worms present, the location of the worms, the degree of inflammation, the severity of anemia or hypoproteinemia, nutritional status of the host, and the presence of other gastrointestinal parasites and micro-organisms.

Clinical examination

Affected animals generally have mild clinical signs of typhlitis and colitis, although some dogs develop a clinical scenario of signs and laboratory findings (e. g., hyponatremia, hypochloremia, hyperkalemia) consistent with hypoadrenocorticism. When tested, Trichuris-infected dogs are normoreactive to adrenocorticotropic hormone stimulation and are instead referred to as pseudo-Addisonian. Eosinophilia, anemia, and hypoalbuminemia are possible, but these are more common laboratory findings with other gastrointestinal helminth infections (e. g., hookworms).

Diagnosis of Trichuris

Trichuris ova can be identified on routine fecal flotation procedures; however, they may be missed because of intermittent shedding. Empiric treatment for occult Trichuris infection should always be performed before moving on to a more detailed, costly, and unnecessary medical investigation.

Treatment of Trichuris

Many safe and effective therapeutic agents are available for Trichuris spp. Fenbendazole, febantel with praziquantel, milbemycin, and ivermectin with pyrantel pamoate all have established efficacy against whipworms. Treatment should be repeated in 3 weeks and again in 3 months, and pet owners should be advised to decontaminate the environment.

Prognosis of Trichuris

The prognosis for recovery and cure is excellent.

Ancylostoma caninum

Hookworms are primary pathogens of the small intestine, but they occasionally infect the cecum and colon with overwhelming infestations. Diagnosis is achieved by demonstrating hookworm ova in the feces, and treatments are similar to those used for whipworm infections.

Heterobilharzia americana

Heterobilharzia americana: Cause

Heterobilharzia americana is considered the primary agent of schistosomiasis in dogs. It is an uncommon infection in dogs and is encountered almost exclusively in the southern Atlantic and Gulf Coast states in the United States. In addition to the dog, nutria, raccoons, rabbits, and mice serve as important reservoir hosts. Although uncommon, heterobilharziasis is an important consideration in the differential diagnosis of acute and chronic large bowel diarrhea in endemic areas.

Pathophysiology of Heterobilharzia americana

The life cycle of Heterobilharzia americana is complex and involves an intermediate (snail) and definitive (dog) host and various life stages. Dogs are infected when motile cercaria from snails penetrate their skin. The schistosomulae migrate from the skin to the liver of the definitive host, where they develop into mature male and female worms. Adult schistsomes lay eggs in the terminal mesenteric venules, and egg migration through the bowel wall elicits an intense granulomatous response. It is usually the host response that gives rise to the clinical symptomatology.

Clinical examination

Clinical signs vary from none to acute signs of vomiting, weight loss, bloody diarrhea, and progressive emaciation. Affected animals may have biochemical evidence of hypoalbuminemia, hyperglobulinemia, hypercalcemia, and liver enzyme elevation.

Diagnosis of Heterobilharzia americana

Diagnosis is confirmed by demonstration of ova on direct fecal examination or tissue biopsy. Serologic tests have not yet been successfully implemented in companion animals.

Treatment of Heterobilharzia americana

Fenbendazole in combination with praziquantel appears to be effective in the treatment of Heterobilharzia americana.

Prognosis of Heterobilharzia americana

The prognosis for acute infections is generally favorable, although severe liver involvement may portend chronic liver disease and cirrhosis.



Balantidium coti

Balantidium coli is primarily a pathogen of sheep. Only one case report of natural infection in the dog has ever been published. In another report, a total of 375 fecal samples of 56 mammalian species belonging to 17 families of 4 orders were examined for the detection of Balantidium coli. B. coli organisms were detected in several animal species, but not in dogs or cats.

Entamoeba histolytica

Two isolated case reports of colitis in dogs and one in cats are associated with recovery of Entamoeba histolytica from the feces. E. histolytica can be recovered from the feces of healthy dogs and cats, but it appears to be of low pathogenicity in dogs and cats.


Giardia: Cause

Giardia spp. are protozoal parasites that primarily infect the small intestine of dogs and cats. The cecum and colon are only occasionally colonized by Giardia. All mammalian isolates are currently classified as Giardia lamblia, although some nomenclature systems use the name G. duodenalis or G. intestinalis. Recent DNA sequence technology suggests that one or two distinct Giardia genotypes can be isolated exclusively from dogs, and a distinct genetic group can be isolated from cats. It is not clear whether differences in pathogenicity exist between these genotypes. Giardia species have a worldwide distribution. Because Giardia is maintained in nature primarily by fecal-oral transmission, more cases are associated with crowded and unsanitary conditions. A recent study showed a prevalence in the dog of 7.2%.

Pathophysiology of Giardia

Giardia spp. are found on the surface of enterocytes, where the trophozoites attach to the brush border of the epithelium. Specific histologic changes have not been reported, but persistence of infection may promote apoptosis and inhibition of re-epithelialization.

Clinical examination

Although infected animals may remain asymptomatic, clinical signs such as acute or chronic diarrhea, weight loss, or even acute or chronic vomiting may develop. Although Giardia cysts and trophozoites have been found in the feces of dogs with both small bowel and large bowel diarrhea, Giardia infection is primarily a problem of the small intestine.

Diagnosis of Giardia

Giardia infections can be diagnosed by demonstrating motile trophozoites on fresh fecal smears or cysts by zinc sulfate sedimentation. Commercial enzyme-linked immunosorbent assay (ELISA) kits have also been used to detect Giardia antigen in fresh fecal samples. Enzyme-linked immunosorbent assay assays may be slightly more sensitive and specific than a single zinc sulfate concentrating technique in diagnosing Giardia infections in dogs. A direct immunofluorescent antibody test has been used in the diagnosis of Giardia infections in humans, but it has not yet been validated in the dog. Duodenal aspirates during gastrointestinal endoscopy appear to be ineffective in diagnosing Giardia infection.

Treatment of Giardia

Metronidazole, ipronidazole, fenbendazole, albendazole, and a praziquantel, pyrantel pamoate, febantel combination have all been used in the treatment of Giardia infections with varying levels of success. A Giardia vaccine has been shown to be effective in prevention and therapy in dogs, but efficacy has not yet been established in cats.

Prognosis of Giardia

The prognosis for long-term health and recovery is generally very favorable.

Isospora cants, Isospora ohioensis, Isospora felis, Isospora neorivoha

The Isospora species are the most common coccidial parasites of dogs (Isospora canis and Isospora ohioensis) and cats (Isospora felis and Isospora neorivoha). The coccidia are primarily parasites of the small intestine, but Isospora ohioensis may induce cecal and colonic pathology in puppies and young dogs. Sulfadimethoxine (50 mg / kg orally, once a day for 10 days) or sulfatrimethoprim (15 to 30 mg / kg orally, once a day for 5 days) may be used where clinical signs warrant treatment.

Tritrichomonas foetus

Tritrichomonas foetus: Cause

Tritrichomonas foetus is a flagellated protozoan parasite that is an important venereal pathogen in cattle. T. foetus has also been identified as an intestinal pathogen in domestic cats from which intraluminal infection of the colon leads to chronic large bowel diarrhea. Infected cats are usually young and frequently reside in densely populated housing such as catteries or animal shelters. Cats often have a history of infection with Giardia spp.; these infections are subsequently identified as trichomoniasis after failure to eradicate the organisms with standard antiprotozoal treatment (e. g., metronidazole or fenbendazole).


After experimental inoculation in cats, Tritrichomonas foetus organisms have been shown to colonize the ileum, cecum, and colon, reside in close contact with the epithelium, and are associated with transient diarrhea that is exacerbated by coexisting cryptosporidiosis.

Clinical examination

Infected animals have clinical signs that are consistent with chronic colitis-type diarrhea.

Diagnosis of Tritrichomonas foetus

Diagnosis of trichomonosis in cats is made by direct observation of trichomonads in samples of freshly voided feces that are suspended in physiologic saline (0.9% NaCl) solution and examined microscopically at x200 to x400 magnification. Tritrichomonas foetus can also be grown from feces via incubation at 37° C. in Diamond’s medium. The sensitivity of direct examination of a fecal smear for diagnosis of T. foetus in naturally infected cats is unknown but is suspected to be poor. A commercially available culture system that is sensitive and specific for culture of Tritrichomonas foetus will improve the diagnostic outcome. These kits are most useful when inoculated with less than or equal to 0.1 g of fresh feces at 25° C. More recently, a single-nested tube polymerase chain reaction technique has been developed that is ideally suited for diagnostic testing of feline lecal samples that are found negative by direct microscopy and by definitive identification of microscopically observable or cultivated organisms.

Treatment of Tritrichomonas foetus

At this time the origin of the infection in most cats is unknown, and no effective antimicrobial treatment exists for Tritrichomonas foetus infection. Metronidazole and fenbendazole may improve clinical signs but generally do not resolve infection. Nitazoxanide eliminates shedding of Tritrichomonas foetus and Gryptosporidium oocysts, but diarrhea and oocyst shedding recur with discontinuation of treatment. A series of cats that were treated with paromomycin for Tritrichomonas foetus infection subsequently developed kidney failure. Consequently, paromomycin should probably not be used in cats.

Prognosis of Tritrichomonas foetus

The prognosis for eradication of the organism is not encouraging at this time.



Cause of Inflammatory Bowel Disease

Inflammatory bowel disease (IBD) may be defined using clinical, histologic, immunologic, pathophysiologic, and genetic criteria.

Clinical criteria Inflammatory bowel disease has been defined clinically as a spectrum of gastrointestinal disorders of an unknown cause that is associated with chronic inflammation of the stomach, intestine, or colon. A clinical diagnosis of inflammatory bowel disease is considered only if affected animals have: (1) persistent (> 3 weeks in duration) gastrointestinal signs (anorexia, vomiting, weight loss, diarrhea, hematochezia, mucosy feces), (2) failure to respond to symptomatic therapies (parasiticides, antibiotics, gastrointestinal protectants) alone, (3) failure to document other causes of gastroenterocolitis by thorough diagnostic evaluation, and (4) histologic diagnosis of benign intestinal inflammation. Small bowel and large bowel forms of inflammatory bowel disease have been reported in both dogs and cats, although large bowel inflammatory bowel disease appears to be more prevalent in the dog.

Histologic criteria Inflammatory bowel disease has been defined histologically by the type of inflammatory infiltrate (neutrophilic, eosinophilic, lymphocytic, plasmacytic, granulomatous), associated mucosal pathology (villus atrophy, fusion, crypt collapse), distribution of the lesion (focal or generalized, superficial or deep), severity (mild, moderate, severe), mucosal thickness (mild, moderate, severe), and topography (gastric fundus, gastric antrum, duodenum, jejunum, ileum, cecum, ascending colon, descending colon). As with small intestinal inflammatory bowel disease, subjective interpretation of large intestinal inflammatory bowel disease lesions has made it difficult to compare tissue findings between pathologists. Subjectivity in histologic assessments has led to the development of several inflammatory bowel disease grading systems.

Immunologic criteria Inflammatory bowel disease (IBD) has been denned immunologically by the innate and adaptive response of the mucosa to gastrointestinal antigens. Although the precise immunologic events of canine and feline inflammatory bowel disease remain to be determined, a prevailing hypothesis for the development of inflammatory bowel disease is the loss of immunologic tolerance to the normal bacterial flora or food antigens, leading to abnormal T cell immune reactivity in the gut microenvironment. Genetically engineered animal models (e. g., IL-2, IL-10, T cell receptor knockouts) that develop inflammatory bowel disease involve alterations in T cell development, function, or both, suggesting that T cell populations are responsible for the homeostatic regulation of mucosal immune responses. Immunohistochemical studies of canine inflammatory bowel disease have demonstrated an increase in the T cell population of the lamina propria, including CD3+ cells and CD4+ cells, macrophages, neutrophils, and IgA-containing plasma cells. Many of the immunologic features of canine inflammatory bowel disease can be explained as an indirect consequence of mucosal T cell activation. Enterocytes are also likely involved in the immunopathogenesis of inflammatory bowel disease. Enterocytes are capable of behaving as antigen-presenting cells, and interleukins (e. g., IL-7, IL-15) produced by enterocytes during acute inflammation activate mucosal lymphocytes. Up-regulation of Toll-like receptor 4 (TLR4) and Toll-like receptor 2 (TLR2) expression contribute to the innate immune response of the colon. Thus the pathogenesis and pathophysiology of inflammatory bowel disease appears to involve the activation of a subset of CD4+ T cells within the intestinal epithelium that overproduce inflammatory cytokines with concomitant loss of a subset of CD4+ T cells and their associated cytokines, which normally regulate the inflammatory response and protect the gut from injury. Enterocytes, behaving as antigen-presenting cells, contribute to the pathogenesis of this disease.

Pathophysiologic criteria Inflammatory bowel disease (IBD) may be defined patho-physiologically in terms of changes in transport, blood flow, and motility. The clinical signs of inflammatory bowel disease, whether small or large bowel, have long been attributed to the pathophysiology of malabsorption and hypersecretion, but experimental models of canine inflammatory bowel disease have instead related clinical signs to the emergence of abnormality motility patterns.

Genetic criteria Inflammatory bowel disease (IBD) may be defined by genetic criteria in several animal species. Crohn’s disease and ulcerative colitis are more common in certain human genotypes, and a mutation in the NOD2 gene (nucleotide-binding oligomerization domain2) has been found in a subgroup of patients with Crohn’s disease. Genetic influences have not yet been identified in canine or feline inflammatory bowel disease, but certain breeds (e. g., German shepherds, boxers) appear to be at increased risk for the dis-

Inflammatory Bowel Disease: Pathophysiology

The pathophysiology of large intestinal inflammatory bowel disease is explained by at least two interdependent mechanisms: (1) the mucosal immune response and (2) accompanying changes in motility.

Immune responses A generic inflammatory response involving cellular elements (B and T lymphocytes, plasma cells, macrophages, and dendritic cells), secretomotor neurons (e. g., vasoactive intestinal polypeptide, substance P, cholinergic neurons), cytokines and interleukins, and inflammatory mediators (e. g., leukotrienes, prostanoids, reactive oxygen metabolites, nitric oxide (NO], 5-HT, IFN-γ, TNF-α, platelet-activating factor) is typical of canine and feline inflammatory bowel disease. Many similarities exist between the inflammatory response of the small and large intestine, but recent immunologic studies suggest that inflammatory bowel disease of the canine small intestine is a mixed Th 1 and Th2 response, whereas inflammatory bowel disease of the canine colon may be more of a Th 1 type response with elaboration of IL-2, IL-12, INF-γ, and TNF-α. Other studies of canine colonic inflammatory bowel disease have demonstrated increased numbers of mucosal IgA- and IgG-containing cells, nitrate, CD3+ T cells, NO, and inducible nitric oxide synthase (iNOS) in the inflamed colonic mucosa (Table Immunologic and Motility Abnormalities in Canine Large Bowel Inflammatory Bowel Disease). Increases in the CD3+ positive T cell population of the inflamed colon are consistent with changes reported in the inflamed canine intestine. Thus important similarities exist, as do differences between small and large bowel inflammatory bowel disease.

Immunologic and Motility Abnormalities in Canine Large Bowel Inflammatory Bowel Disease

Histolocic Findings Immunologic Abnormalities
Lymphocytic-plasmacytic colitis Increased nitric oxide and IgG in colonic lavage fluid
Lymphocytic-plasmacytic colitis Increased expression of inducible nitric oxide synthase mRNA
Lymphocytic-plasmacytic colitis Increases in T cells and B cells in lamina propria
Lymphocytic-plasmacytic colitis Increases in CD3+ T cells and in lgA+ and lgC+ plasma cells
Lymphocytic-plasmacytic colitis Increased IL-2 and TNF-α mRNA expression
Tissue / Cell Type Motility Abnormalities
Colon Loss of spontaneous phasic contractions
Decreased frequency of migrating motor complexes (MMCs)
Increased frequency of giant migrating contractions (CMCs)
Colonic circular smooth muscle cells Decreased amplitude and duration of the slow wave plateau potential
Shift from the M3 to M2 muscarinic receptor subtype
Reduced calcium influx through L-type calcium channel
Reduced L-type calcium channel expression
Decreased open probability of KCa channels
Down-regulation of PKC α, β, ξ expression and activation
Reduced phospholipase A2 expression
Increased NF-κB expression and activation
Colonic enteric neurons Sensitization to substance P during colonic inflammation
Colonic interstitial cells of Cajal Reduced density of interstitial cells
Cytoplasmic vacuolation and damage to cellular processes

IgG, Immunoglobulin G; IgA, immunoglobulin A; IL-2, interleukin-2; TNF-α, tumor necrosis factor alpha; PKC, protein kinase C; M, muscarinic; NF-κB, nuclear factor-icB; KCa, calcium-activated potassium channel.

Motility changes Experimental studies of canine large intestinal inflammatory bowel disease have shown that many of the clinical signs (diarrhea, passage of mucus and blood, abdominal pain, tenesmus, and urgency of defecation) are related to motor abnormalities of the colon. Ethanol and acetic acid perfusion of the canine colon induces a large bowel form of inflammatory bowel disease syndrome indistinguishable from the natural condition. I Inflammation in this model suppresses the normal phasic contractions of the colon, including the migrating motility complex, and triggers the emergence of giant migrating contractions. The appearance of these giant migrating contractions in association with inflammation is a major factor in producing diarrhea, abdominal cramping, and urgency of defecation. Giant migrating contractions are powerful lumen-occluding contractions that rapidly propel pancreatic, biliary, and intestinal secretions in the fasting state (and undigested food in the fed state) to the colon to increase its osmotic load. Malabsorption results from direct injury to the epithelial cells and from ultrarapid propulsion of intestinal contents by giant migrating contractions so that sufficient mucosal contact time is not allowed for digestion and absorption to take place.

Inflammation impairs the regulation of the colonic motility patterns at several levels (i. e., enteric neurons, interstitial cells of Cajal, circular smooth muscle cells; summarized in Table Immunologic and Motility Abnormalities in Canine Large Bowel Inflammatory Bowel Disease). Inflammation-induced changes in the amplitude and duration of the smooth muscle slow wave plateau potentials contribute to the suppression of rhythmic phasic contractions. These alterations likely have their origin in structural and functional damage to the interstitial cells of Cajal. At the same time that inflammation suppresses the rhythmic phasic contractions, inflammation sensitizes the colon to the stimulation of giant migrating contractions by the neurotransmitter substance P. These findings suggest that SP increases the frequency of giant migrating contractions during inflammation and that selective inhibition of giant migrating contractions during inflammation may minimize the symptoms of diarrhea, abdominal discomfort, and urgency of defecation associated with these contractions.

Inflammation suppresses the generation of tone and phasic contractions in the circular smooth muscle cells through multiple molecular mechanisms (see Table Immunologic and Motility Abnormalities in Canine Large Bowel Inflammatory Bowel Disease). Inflammation shifts muscarinic receptor expression in circular smooth muscles from the M3 to the M2 subtype. This shift has the effect of reducing the overall contractility of the smooth muscle cell. Inflammation also impairs calcium influx” and down-regulates the expression of the L-type calcium channel, which may be important in suppressing phasic contractions and tone while concurrently stimulating giant migrating contractions in the inflamed colon. Changes in the open-state probability of the large conductance calcium-activated potassium channels (Kc) partially attenuate this effect. Inflammation also modifies the signal transduction pathways of circular smooth muscle cells. Phospholipase A2 and protein kinase C. (PKC) expression and activation are significantly altered by colonic inflammation, and this may partially account for the suppression of tone and phasic contractions. PKC α, β and ξ isoenzyme expression is down-regulated, PKC i and X isoenzyme expression is up-regulated, and the cytosol-to-membrane translocation of PKC is impaired. The L-type calcium channel, already reduced in its expression, is one of the molecular targets of PKC. Inflammation also activates the transcription factor NF-κB that further suppresses cell contractility.

Clinical Examination The clinical signs of large intestinal inflammatory bowel disease are those of a large bowel-type diarrhea (i. e., marked increased frequency, reduced fecal volume per defecation, blood pigments and mucous in feces, and tenesmus). Anorexia, weight loss, and vomiting are occasionally reported in animals with severe inflammatory bowel disease of the colon or concurrent inflammatory bowel disease of the stomach, small intestine, or both. Clinical signs usually wax and wane in their severity. A transient response to symptomatic therapy may occur during the initial stages of inflammatory bowel disease. As the condition progresses, diarrhea gradually increases in its frequency and intensity and may become continuous. In some cases the first bowel movement of the day may be normal or nearlv normal, whereas successive bowel movements are reduced in volume and progressively more urgent and painful. During severe episodes, mild fever, depression, and anorexia may occur.

There does not appear to be any sex predilection, but age may be a risk factor, with inflammatory bowel disease appearing more frequently in middle-aged animals (mean age approximately 6 years with a range of 6 months to 20 years). German shepherd and boxer dogs are at increased risk for inflammatory bowel disease, and pure-breed cats appear to be at greater risk. Cats more often have an upper gastrointestinal form of inflammatory bowel disease, whereas dogs are at risk for both small and large bowel inflammatory bowel disease.

Physical examination is unremarkable in most cases. Thickened bowel loops may be detected during abdominal palpation if the small bowel is concurrently involved. Digital examination of the anorectum may evoke pain or reveal irregular mucosa, and blood pigments and mucous may be evident on the examination glove.

Diagnosis of Inflammatory Bowel Disease

CBCs, serum chemistries, and urinalyses are often normal in mild cases of large bowel inflammatory bowel disease. Chronic cases may have one or more subtle abnormalities. One review of canine and feline inflammatory bowel disease reported several hematologic abnormalities including mild anemia, leukocytosis, neutrophilia with and without a left shift, eosinophilia, eosinopenia, lymphocytopenia, monocytosis, and basophilia. The same study reported several biochemical abnormalities including increased activities of serum alanine aminotransferase and alkaline phosphatase, hypoalbuminemia, hypoproteinemia, hyperamylasemia, hyperglobulinemia, hypokalemia, hypocholesterolemia, and hyperglvcemia. No consistent abnormality in the complete blood count or serum chemistry has been identified.

A scoring index for disease activity in canine inflammatory bowel disease was recently developed that relates severity of clinical signs to serum acute-phase protein (C-reactive protein (CRP], serum amyloid A) concentrations. The canine inflammatory bowel disease activity index (CIBDAI) assigns levels of severity to each of several gastroen-terologic signs (e. g., anorexia, vomiting, weight loss, diarrhea), and it appears to be a reliable index of mucosal inflammation in canine inflammatory bowel disease. Interestingly, both the activity index and serum concentrations of C-reactive protein improve with successful treatment, suggesting that serum C-reactive protein is suitable for the laboratory evaluation of therapy in canine inflammatory bowel disease. Other acute-phase proteins were less specific than C-reactive protein. One important caveat that should be emphasized is that altered CRP is not prima facie evidence of gastrointestinal inflammation. Concurrent infections or other inflammatory conditions could cause an acute-phase response, including C-reactive protein, in affected patients.

Treatment of Inflammatory Bowel Disease

Dietary therapy The precise immunologic mechanisms of canine and feline inflammatory bowel disease have not yet been determined, but a prevailing hypothesis for the development of inflammatory bowel disease is the loss of immunologic tolerance to the normal bacterial flora or food antigens. Accordingly, dietary modification may prove useful in the management of canine and feline inflammatory bowel disease. Several nutritional strategies have been proposed including novel proteins, hydrolyzed diets, antioxidant diets, medium chain triglyceride supplementation, low-fat diets, modifications in the omega-6 (ω-6) and omega-3 (ω-3) fatty acid ratio, and fiber supplementation. Of these strategies, some evidence-based medicine has emerged for the use of novel protein, hydrolyzed, and fiber-supplemented diets.

Food sensitivity reactions were suspected or documented in 49% of cats presented because of gastroenterologic problems (with or without concurrent dermatologic problems) in a prospective study of adverse food reactions in cats. Beef, wheat, and com gluten were the primary ingredients responsible for food sensitivity reactions in that study, and most of the cats responded to the feeding of a chicken- or venison-based selected protein diet for a minimum of 4 weeks. The authors concluded that adverse reactions to dietary staples are common in cats with chronic gastrointestinal problems and that they can be successfully managed by feeding selected protein diets. Further support for this concept comes from studies in which gastroenterologic or dermatologic clinical signs were significandy improved by the feeding of novel proteins.

Evidence is accruing that hydrolyzed diets may be useful in the nutritional management of canine inflammatory bowel disease. The conceptual basis of the hydrolyzed diet is that oligopeptides are of insufficient size and structure to induce antigen recognition or presentation. In one preliminary study, dogs with inflammatory bowel disease showed significant improvement after the feeding of a hydrolyzed diet, although they had failed to respond to the feeding of a novel protein. Clinical improvement could not be solely attributed to the hydrolyzed nature of the protein source because the test diet had other modified features (i. e., high digestibility, cornstarch rather than intact grains, medium-chain triglycerides, an altered ratio of ω-6 to ω-3 polyunsatu-rated fatty acids). Additional studies will be required to ascertain the efficacy of this nutritional strategy in the management of inflammatory bowel disease.

Fiber-supplemented diets may be useful in the management of irritable bowel syndrome (IBS) in the dog. IBS is a poorly defined syndrome in the dog that may or may not bear resemblance to IBS in humans. Canine irritable bowel syndrome has been defined as a chronic large bowel-type diarrhea without known cause and without evidence of colonic inflammation on colonoscopy or biopsy. Dogs fulfilling these criteria were successfully managed with soluble fiber (psyllium hydrophilic mucilloid) supplementation of a highly digestible diet.

Exercise Experimental inflammatory bowel disease (IBD) in the dog is accompanied by significant abnormalities in the normal colonic motility patterns. Physical exercise has been shown to disrupt the colonic MMCs and to increase the total duration of contractions that are organized as nonmigrating motor complexes during the fed state. Exercise also induces giant migrating contractions, defecation, and mass movement in both the fasted and fed states. The increased motor activity of the colon and extra giant migrating contractions that result from physical exercise may aid in normal colonic motor function.

Pharmacologic therapy Animals with mild to moderate forms of large bowel inflammatory bowel disease generally respond favorably to dietary modification alone, but pharmacologic therapy will be required with more severe forms of large bowel inflammatory bowel disease. Medical therapy includes anti-inflammatory (sulfasalazine and other 5-aminosalicylates, metronidazole, prednisone, budesonide), immunosuppressive (azathioprine, cyclosporine, chlorambucil), and motility-modifying (loperamide) drugs (Table Drug Index — Large Bowel Diarrhea).

Drug Index — Large Bowel Diarrhea

Drug Classification And Examples Dose Indication
Anthelmintic Drugs
Albendazole 25 mg / kg PO SID x 2 days Ciardia infection
Febantel 10 mg / kg PO SID x 3 days — adult dogs Trichuris infection
15 mg / kg PO SID x 3 days — puppies Trichuris infection
Fenbendazole 50 mg / kg PO SID x 3 days Trichuris, Ancylostoma, Ciardia infection
Ivermectin 200 μg / kg SQ once Larvicidal for Trichuris canis
Mebendazole 22 mg / kg PO SID x 3 days Trichuris infection
Metronidazole 25 mg / kg PO BID x 5 days Ciardia infection
Milbemycin oxime 0.5 mg / kg PO once per month Trichuris preventive
Praziquantel 44 mg / kg PO once Heterobilharzia
Pyrantel pamoate 5 mg / kg PO dog, 20 mg / kg cat Ancylostoma, Toxocara
Ampicillin 22mg / kg PO IV TID Salmonella, E. coli, Clostridium perfringens
Cefadroxil 22 mg / kg PO BID Salmonella, E. coli
Chloramphenicol 44 mg / kg PO TID — dogs Campylobacter
11 mg / kg PO BID — cats Campylobacter
Enrofloxacin 5 mg / kg PO IM SQ BID Salmonella, E. coli
Erythromycin 15-20 mg / kg PO TID Campylobacter, C. perfringens
Metronidazole 10-20 mg / kg PO BID-TID C. perfringens
Orbifloxacin 2.5-7.5 mg / kg PO SID Salmonella, E. coli
Trimethoprim sulfonamide 30 mg / kg PO IM SQ BID Salmonella
Tylosin 40-80 mg / kg PO SID Inflammatory bowel disease, C. perfringens
Antifungal Drugs
Amphotericin B 2-3 mg / kg IV QOD administered to a cumulative dose of 24-27 mg / kg Histoplasmosis, pythiosis, protothecosis
Itraconazole 5 mg / kg PO BID for several months Histoplasmosis, pythiosis, protothecosis
Ketoconazole 10-15 mg / kg PO BID several months Histoplasmosis, pythiosis. protothecosis
Anti-Inflammatory Drugs
Budesonide 1 mg / cat or 1 mg / dog PO SID Inflammatory bowel disease
Meselamine 10 mg / kg PO TID IBD
Metronidazole 10-20 mg / kg PO BID-TID for 4-6 weeks Inflammatory bowel disease
Olsalazine 5-10 mg / kg PO TID for 4-6 weeks IBD
Prednisolone 4.0-6.0 mg / kg PO SID for 4-6 weeks Feline eosinophilic colitis
Prednisone 1.0-2.0 mg / kg PO SID for 4-6 weeks IBD
Sulfasalazine 10-25 mg / kg PO TID for 4-6 weeks — dogs inflammatory bowel disease, ulcerative colitis
5-12.5 mg / kg PO TID for 2-4 weeks — cats Refractory IBD
Immunosuppressive Drugs
Azathioprine 2 mg / kg PO SID for 4-6 weeks — dogs Inflammatory bowel disease
Chlorambucil 2 mg / m PO every other day for 4-6 weeks IBD
Cyclosporine 3-7 mgAg PO BID for 4-6 weeks IBD
Motility-Modifying Drugs
Loperamide 0.08 mgAg PO TID-QID IBD, IBS
Propantheline 0.25 mg / kg PO BID-TID Irritable bowel syndrome
Aminopentamide 0.01-0.03 mg / kg PO BID-TID IBS
Enterococcus faecium (SF68) 5 x 10 colony-forming units / day IBD
Lactobacillus rhamnosus GC 1 x 10 to 5 x 10 colony-forming units / day Inflammatory bowel disease

PO, per os; SID, once per day; IV, intravenous; TID, three times per day; BID, twice per day; QOD, every other day.

Sulfasalazine Sulfasalazine is a highly effective prostaglandin synthetase inhibitor that has proven efficacy in the therapy of large bowel inflammatory bowel disease in the dog. Sulfasalazine is a compound molecule of 5-aminosalicylate (meselamine) and sulfapyridine linked in an azochemical bond. After oral dosing, most of the sulfasalazine is transported to the distal gastrointestinal tract where cecal and colonic bacteria metabolize the drug to its component parts. Sulfapyridine is largely absorbed by the colonic mucosa but much of the 5-aminosalicylate remains in the colonic lumen where it inhibits mucosal cyclooxygenase and the inflammatory cascade. Sulfasalazine has been recommended for the treatment of canine large bowel inflammatory bowel disease at doses of 10 to 25 mg / kg orally, three times a day for 4 to 6 weeks. With resolution of clinical signs, sulfasalazine doses are gradually decreased by 25% at 2-week intervals and eventually discontinued while maintaining dietary management. Salicylates are readily absorbed and induce toxicity in cats; therefore this drug classification should be used with great caution in cats. If used in cats, some authors have recommended using half of the recommended dog dose (i. e., 5 to 12.5 mg / kg orally, three times a day). Sulfasalazine use has been associated with the development of keratoconjunctivitis sicca in the dog, so tear production should be assessed subjectively (by the pet owner) and objectively (by the veterinarian) during use.

Other 5-aminosalicylates This drug classification was developed to reduce the toxicity of the sulfapyridine portion of the parent molecule (sulfasalazine) and to enhance the efficacy of the 5-aminosalicylate portion. Meselamine (Dipentum, Asachol) and dimeselamine (olsalazine) are available for use in the treatment of canine large bowel inflammatory bowel disease. Olsalazine has been used at a dose of 5 to 10 mg / kg orally, three times a day in the dog. Despite the formulation of sulfa-free 5-aminosalicylate preparations, instances of keratoconjunctivitis sicca have still been reported in the dog.

Metronidazole Metronidazole (10 to 20 mg / kg orally, twice a day to three times a day) has been used in the treatment of mild to moderate cases of large bowel inflammatory bowel disease in both dogs and cats. Metronidazole has been used either as a single agent or in conjunction with 5-aminosalicylates or glucocorti-coids. Metronidazole is believed to have several beneficial properties, including antibacterial, antiprotozoal, and immunomodulatory effects. Side effects include anorexia, hypersalivation, and vomiting at recommended doses and neurotoxicity (ataxia, nystagmus, head title, and seizures) at higher doses. Side effects usually resolve with discontinuation of therapy, but diazepam may accelerate recovery of individual patients.

Glucocorticoids Anti-inflammatory doses of prednisone or prednisolone (1 to 2 mg / kg orally, once a day) may be used to treat inflammatory bowel disease in dogs that have failed to respond to dietary management, sulfasalazine, or metronidazole, and as adjunctive therapy to dietary modification in feline inflammatory bowel disease. Prednisone or prednisolone are used most frequendy, because both have short durations of action, are cost-effective, and are widely available. Equipotent doses of dexamethasone are equally effective but may have more deleterious effects on brush border enzyme activity. Prednisone should be used for 2 to 4 weeks depending upon the severity of the clinical signs. Higher doses of prednisone (e. g., 2 to 4 mg / kg orally, once a day) may be needed to control severe forms of eosinophilic colitis or hypereosinophilic syndrome in cats.

Combination therapy with sulfasalazine, metronidazole, or azathioprine may reduce the overall dose of prednisone needed to achieve remission of clinical signs. As with sulfasalazine, the dose of glucocorticoid may be reduced by 25% at 1- to 2-week intervals while (it is hoped) maintaining remission with dietary modification.

Because of steroid side effects and suppression of the hypothalamic-pituitary-adrenal axis, several alternative glucocorticoids have been developed that have excellent topical (i. e., mucosal) anti-inflammatory activity but are significantly metabolized during first pass hepatic metabolism. Budesonide has been used for many years as an inhaled medication for asthma, and an enteric-coated form of the drug is now available for treatment of inflammatory bowel disease in humans (and animals). Little clinical evidence supports of the use of this medication in canine or feline inflammatory bowel disease, but doses of 1 mg / cat or 1 mg / dog per day have been used with some success in anecdotal cases.

Azathioprine Azathioprine is a purine analog that, after DNA incorporation, inhibits lymphocyte activation and proliferation. It is rarely effective as a single agent and should instead be used as adjunctive therapy with glucocorticoids. Azathioprine may have a significant steroid-sparing effect in inflammatory bowel disease. Doses of 2 mg / kg orally, every 24 hours in dogs and 0.3 mg / kg orally every 48 hours in cats have been used with some success in inflammatory bowel disease. It may take several weeks or months of therapy for azathioprine to become maximally effective. Cats particularly should be monitored for side effects, including myelosuppression, hepatic disease, and acute pancreatic necrosis.

Cyclosporine Cyclosporine has been used in the renal transplantation patient for its inhibitory effect on T cell function. In more recent times, cyclosporine has been used in a number of immune-mediated disorders, including keratoconjunctivitis sicca, perianal fistula (anal furunculosis), and IMHA. Evidence-based medicine studies will be needed to establish efficacy, but anecdotal experience would suggest that cyclosporine (3 to 7 mg / kg orally, twice a day) may be useful in some of the more difficult or refractory cases of inflammatory bowel disease.

Chlorambucil Chlorambucil (2 mg / m orally, every other day) has been used in place of azathioprine in some difficult or refractory cases of feline inflammatory bowel disease.

Motility-modifying drugs The mixed μ, δ-opioid agonist, loperamide, stimulates colonic fluid and electrolyte absorption while inhibiting-colonic propulsive motility. Loperamide (0.08 mg / kg orally, three times a day to four times a day) may be beneficial in the treatment of difficult or refractory cases of large bowel-type inflammatory bowel disease.

Probiotic therapy Probiotics (see Table Drug IndexLarge Bowel Diarrhea) are living organisms with low or no pathogenicity that exert beneficial effects (e. g., stimulation of innate and acquired immunity) on the health of the host. The gram-positive commensal lactic acid bacteria (e. g., Lactobacilli) have many beneficial health effects, including enhanced lymphocyte proliferation, innate and acquired immunity, and anti-inflammatory cytokine production Lactobacillus rhamnosus GG, a bacterium used in the production of yogurt, is effective in preventing and treating diarrhea, recurrent Clostridia difficile infection, primary rotavirus infection, and atopic dermatitis in humans. Lactobacillus rhamnous GG and Lactobacillus acidophilus (strain DSM13241) have been safely colonized in the canine gastrointestinal tract, although probiotic effects in the canine intestine have not been firmly established. The probiotic organism, Enterococcus faecium (SF68), has been safely colonized in the canine gastrointestinal tract, and it has been shown to increase fecal IgA content and circulating mature B (CD21+ / MHC class 11+) cells in young puppies. It has been suggested that this probiotic may be useful in the prevention or treatment of canine gastrointestinal disease. This organism may, however, enhance Campybbacter jejuni adhesion and colonization of the dog intestine, perhaps conferring carrier status on colonized dogs. Two recent studies have shown that many commercial veterinary probiotic preparations are not accurately represented by label claims. Quality control appears to be deficient for many of these formulations. Until these products are more tightly regulated, veterinarians should probably view product claims with some skepticism.

Behavioral modification Inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) very likely have underlying behavioral components. Abnormal personality traits and potential environmental stress factors were identified in 38% of dogs in one study. Multiple factors were present in affected households, including travel, relocation, house construction, separation anxiety, submissive urination, noise sensitivity, and aggression. The role of behavior in the pathogenesis and therapy of canine and feline gastrointestinal disorders remains largely unexplored.

Prognosis of Inflammatory Bowel Disease

Most reports indicate that the short-term prognosis for control of inflammatory bowel disease is good to excellent. After completion of drug therapy, many animals are able to maintain remission of signs with dietary management alone. Treatment failures are uncommon and are usually due to (1) incorrect diagnosis (it is especially important to rule out alimentary lymphosarcoma), (2) presence of severe disease such as histiocytic ulcerative colitis and protein-losing enteropathy or irreversible mucosa lesions such as fibrosis, (3) poor client compliance with appropriate drug and dietary recommendations, (4) use of inappropriate drugs or nutritional therapy, and (5) presence of concurrent disease such as small intestinal bacterial overgrowth or hepatobiliary disease. The prognosis for cure of inflammatory bowel disease is poor, and relapses should be anticipated.


Small Intestinal Disease



Diarrhea is an increase in fecal mass caused by an increase in fecal water and / or solid content. It is accompanied by an increase in frequency and / or fluidity and / or volume of feces. Yet it must be remembered that the absence of recognizable diarrhea does not preclude the possibility of significant small intestine disease.

Classifications of Diarrhea


  • Osmotic
  • Secretory
  • Permeability (exudative)
  • Dysmotility
  • Mixed


  • Acute
  • Chronic


  • Extraintestinal
  • Small intestinal
  • Large intestinal
  • Diffuse


  • Biochemical
  • Allergic
  • Inflammatory
  • Neoplastic


  • Diet; bacterial, viral, parasitic causes; other


  • Exocrine pancreatic insufficiency, salmonellosis, lymphoma, other


  • Acute, nonfatal, self-limiting
  • Acute potentially fatal
  • Acute systemic disease
  • Chronic

Diarrhea can be classified in several ways (Box Classifications of Diarrhea). These categories are not mutually exclusive, and they allow the problem to be viewed from different perspectives, facilitating diagnosis and the choice of appropriate treatment. A mechanistic approach is simple, and many small intestine diseases have a component of osmotic diarrhea, but even in a situation as simple as lactase deficiency, other mechanisms become involved. Osmotic diarrhea in lactose malabsorption causes intestinal distension, which induces peristalsis and rapid transit, and bacterial fermentation products in the colon cause secretion. Bacterial fermentation of unabsorbed solutes is often a complicating factor in malabsorption. The fecal pH is often low because of the production of volatile fatty acids, and some products of fermentation (e. g., hydroxylated fatty acids, unconjugated bile acids) can cause colonic inflammation and secretion, and therefore signs of large intestinal diarrhea frequently accompany prolonged small intestine disease.

Osmotic diarrhea Excess water-soluble molecules in the intestinal lumen retain water osmotically and overwhelm the absorptive capacity of the small intestine and colon (e. g., sudden diet change, overeating, and malabsorption). The diarrhea typically resolves when food or laxatives are withheld.

Secretory diarrhea Stimulation of small intestine secretion such that the reserve absorptive capacity is overwhelmed results in diarrhea even though the absorptive ability of the small intestine and colon may not actually be impaired. Treatment with oral rehydration fluids containing glucose and amino acids (e. g., glycine) to increase water absorption is appropriate.

Typically secretory diarrhea does not resolve with fasting but does not cause weight loss unless anorexia, vomiting, or additional small intestine damage is a factor. Morbidity and even mortality are associated with the dehydration that results from excessive fluid loss. Secretory diarrhea typically is caused by chemical toxins and toxins elaborated by enteric bacteria (Box Causes of Secretory Diarrhea).

Causes of Secretory Diarrhea
  • Bacterial enterotoxins and endotoxins (e. g., Clostridium perfringens, Escherichia coli. Salmonella spp., Shigella spp., Yersinia enterocolitica)
  • Unconjugated bile acids from bacterial fermentation
  • Hydroxylated fatty acids from bacterial fermentation
  • Ciardia infection
  • Possibly hyperthyroidism
  • Laxatives (castor oil, dioctyl sodium sulfosuccinate, bisacodyl)
  • Cardiac glycosides
  • Amine precursor uptake and decarboxylation (APUD) neoplasms (excess vasoactive intestinal polypeptide, serotonin, prostaglandins, substance P)
  • Intestinal inflammation

Permeability (exudative) diarrhea Intestinal inflammation can stimulate increased fluid and electrolyte secretion and impair absorption. Leakage of tissue fluid, serum proteins, blood, and mucus may occur from sites of inflammation, ulceration, or infiltration or if portal hypertension or lymphatic obstruction is present. Increased permeability severe enough to cause loss of plasma proteins in excess of their rate of synthesis results in a protein-losing enteropathy.


Failure of food assimilation is sometimes classified as primary failure to digest (maldigestion) or primary failure to absorb (malabsorption). However, such a classification is misleading, because failure of absorption is an inevitable consequence of failure to digest. The preferred use of the term malabsorption is to describe defective absorption of dietary constituent resulting from interference with the digestive and / or absorptive phases in the processing of that molecule.

Within this broad definition, the site of the primary abnormality may be found in the luminal, mucosal, or transport phase (Table Pathophysiologic Mechanisms of Malabsorption). Also, the reserve capacity of the distal small intestine and colon may prevent overt diarrhea despite significant malabsorption and weight loss. The clinical manifestations of malabsorption, namely diarrhea, weight loss, and altered appetite (polyphagia, coprophagia, pica), are largely a result of the lack of nutrient uptake and the losses in feces. Animals are often systemically healthy and have an increased appetite unless an underlying neoplastic or a severe inflammatory condition is present. Only when the patient is quite malnourished or develops hypoproteinemia does it become ill.

Pathophysiologic Mechanisms of Malabsorption
Mechanism Example
Luminal Phase
Rapid intestinal transit Hyperthyroidism
Defective substrate hydrolysis
Enzyme inactivation Gastric hypersecretion
Lack of pancreatic enzymes Exocrine pancreatic insufficiency
Fat maldigestion
Decreased bile salt delivery Cholestatic liver disease, biliary obstruction
Increased bile salt loss Heal disease
Bile salt deconjugation Bacterial overgrowth
Fatty acid hydroxylation Bacterial overgrowth
Impaired release of CCK, secretin Impairment of pancreatic secretion due to severe small intestine disease
Cobalamin malabsorption
Intrinsic factor deficiency Exocrine pancreatic insufficiency Giant schnauzer defect
Competition for cobalamin Bacterial overgrowth
Mucosal Phase
Brush border enzyme deficiency
Congenital Trehalase (cats)
Acquired Relative lactose deficiency
Brush border transport protein deficiency
Congenital Intrinsic factor receptor
Acquired Secondary to diffuse small intestine disease
Enterocyte defects
Enterocyte processing defects Abetalipoproteinemia
Reduction in surface area Villus atrophy
Immature enterocytes Increased enterocyte turnover
Mucosal inflammation Inflammatory bowel disease
Transport Phase
Lymphatic obstruction
Primary Lymphangiectasia
Secondary Obstruction caused by neoplasia, infection, or inflammation
Vascular compromise
Vasculitis Infection, immune mediated
Portal hypertension Hepatopathy, right heart failure, cardiac tamponade

The presence of dark, tarry, oxidized blood in feces, a condition called melena, reflects either swallowed blood or generalized or localized gastrointestinal bleeding, which usually occurs proximal to the large intestine (Table Causes of Melena). Medication with ferrous sulfate or bismuth subsalicylate (Pepto-Bismol) also can impart a black color to the feces. It has been estimated that the loss of 350 to 500 mg / kg of hemoglobin into the gastrointestinal tract is required for melena to be visible. The presence of microcytosis with or without thrombocytosis is suggestive of iron deficiency secondary to chronic blood loss. An increased blood urea nitrogen (BUN) to creatinine ratio (from bacterial digestion of blood) provides supporting evidence. Hypoproteinemia may indicate significant blood loss or the presence of a protein-losing enteropathy.

Causes of Melena
Mechanism Source
Ingestion of blood Oral, nasal, pharyngeal, or pulmonary bleeding
Coagulopothies Thrombocytopenia, factor deficiencies, DIC
Gastrointestinal erosion / ulceration
Metabolic Uremia, liver disease
Inflammatory Gastritis, enteritis, hemorrhagic gastroenteritis
Neoplastic Leiomyoma, adenocarcinoma, lymphosarcoma
Paraneoplastic Mastocytosis, hypergastrinemia and other APUDomas
Vascular A-V fistula, aneurysms, angiodysplasia
Ischemia Hypovolemic shock, hypoadrenocorticism, thrombosis / infarction, reperfusion
Drug induced Nonsteroidal and steroidal anti-inflammatory agents
Foreign objects

APUD, amine precursor uptake and decarboxylation tumor; A-V, arteriovenous; DIC, disseminated intravascular coagulation

The general approach to melena is to rule out bleeding diatheses, ingestion of blood, and underlying metabolic disorders before pursuing primary gastrointestinal causes. Ultrasonography is particularly useful for detecting gastrointestinal masses and thickening. The next step for investigating upper gastrointestinal blood loss is endoscopy. If the source of gastrointestinal bleeding is still undetermined, lagged red cell scintigraphy, exploratory laparotomy, angiog-raphy. and enteroscopy may be used to localize the site.

Borborygmi and Flatulence

Borborygmus is a rumbling noise caused by the propulsion of gas through the intestines. Swallowed air and bacterial fermentation of ingesta are the main causes of borborygmi and flatulence. Feeding a diet that is highly digestible, with a low fiber content (e. g., cottage cheese and rice in a 1:2 ratio) leaves little material present in the intestine for bacterial fermentation and can effect a cure in some cases. If borborygmi or flatulence continues despite dietary modification, the animal may be excessively aerophagic or may have malabsorption, especially if diarrhea or weight loss are also present.

Weight Loss or Failure to Thrive

General causes of weight loss are reduced nutrient intake, increased nutrient loss, and increased catabolism or ineffective metabolism. The history should reveal whether the type and amount of diet fed is adequate and whether anorexia, dysphagia, or vomiting is a potential cause. Weight loss or failure to thrive accompanied by diarrhea often is a feature of mal-absorption, and the diagnostic approach is the same as for chronic diarrhea. However, diarrhea does not invariably accompany malabsorption that causes weight loss.

Protein-Losing Enteropalhy

When small intestine disease is severe enough for protein leakage into the gut lumen to exceed protein synthesis, hypoproteinemia develops. Chronic diarrhea associated with hypoproteinemia usually requires intestinal biopsy to define the cause of the protein-losing enteropathy (Table Protein-Losing Enteropathies). Nonintestinal diseases, which may potentially be associated with intestinal protein loss (e. g., portal hypertension), usually present with ascites before diarrhea. Hypoproteinemia associated with gastrointestinal disease is much less common in cats than in dogs and most often accompanies gastrointestinal lymphoma.

Protein-Losing Enteropathies
Causes Examples
Lymphangiectasia Primary lymphatic disorder, venous hypertension (e. g., right heart failure, hepatic cirrhosis)
Infectious Parvovirus, salmonellosis, histoplasmosis, phycomycosis
Structural Intussusception
Neoplasia Lymphosarcoma
Inflammation Lymphocytic-plasmacytic, eosinophilic, granulomatous
Endoparasites Ciardia, Ancylostoma spp.
Gastrointestinal hemorrhage hemorrhagic gastroenteritis, neoplasia, ulceration


Clinical presentation Breeds that appear to be predisposed to protein-losing enteropathy are the basenji, lundehund, soft-coated wheaten terrier, Yorkshire terrier, and Shar Pei. Clinical signs associated with protein-losing enteropathy include weight loss, diarrhea, vomiting, edema, ascites, and pleural effusion. Weight loss frequently is the predominant feature, and diarrhea is not invariably present, particularly with lymphangiectasia and focal intestinal neoplasia. Physical findings may include edema, ascites, emaciation, thickened intestines, and melena. Thromboembolism is a feature of some cases of protein-losing enteropathy.

Diagnosis The serum concentrations of both albumin and globulin are reduced in most patients with protein-losing enteropathy. Exceptions are raised hyperglobulinemia with hypoalbuminemia found in histoplasmosis and immunoproliferative small intestine disease in the basenji. Renal and hepatic causes of hypoalbuminemia are eliminated by assay of serum bile acids and urinary protein loss respectively. Hypocholesterolemia and lymphopenia are common in protein-losing enteropathy. Hypocalcemia and hypomagnesemia are also reported. Measurement of fecal loss of alpha, -protease inhibitor may be a sensitive test for protein-losing enteropathy.

Survey abdominal radiographs often are normal in patients with protein-losing enteropathy, but ultrasound scans may reveal intestinal thickening, mesenteric lymphadenopathy, or abdominal effusion. Thoracic radiographs may show pleural effusion, metastatic neoplasia, or evidence of histoplasmosis. Although intestinal function tests may confirm the presence of malabsorption, they rarely provide a definitive diagnosis, and intestinal biopsy is more appropriate. Because many intestinal causes of protein-losing enteropathy are diffuse, endoscopy is the safer way to obtain biopsies, but surgical biopsy may be required to obtain a definitive diagnosis for lymphoma and for diseases that cause secondary lymphangiectasia (Box Relative Advantages of Endoscopic and Surgical Intestinal Biopsy).

Relative Advantages of Endoscopic and Surgical Intestinal Biopsy



  • Minimally invasive
  • Allows visualization and biopsy of focal lesions
  • Permits multiple biopsies
  • Minimal adverse reactions
  • Allows steroids to be started early


  • Requires general anesthesia
  • Permits access only to duodenum (and distal ileum?)
  • Allows only small, superficial (and crushed) biopsies
  • Requires expensive equipment
  • Technically demanding



  • Allows biopsy of multiple sites
  • Permits large, full-thickness biopsies
  • Allows inspection of other organs
  • Offers potential for corrective surgery


  • Requires general anesthesia
  • Poses a surgical risk
  • Requires convalescence
  • Requires delay before steroids can be started

Treatment Plasma transfusion may be indicated during the perioperative period when collecting biopsy specimens, and diuretics may reduce ascites. Spironolactone (1 to 2 mg / kg given orally twice daily) may be more effective than furosemide for treating ascites. Thromboembolism is a feature of some cases of protein-losing enteropathy. Specific treatments are discussed later.

Diagnosis of Small Intestinal Disease

Occult blood

These tests are used to search for intestinal bleeding from ulcerated mucosa and benign or malignant tumors. Unfortunately, all versions nonspecifically test for hemoglobin and are very sensitive, reacting with any meat diet and not just patient blood. Therefore the patient must be fed a meat-free diet for at last 72 hours for a positive result to have any reliability.

Alpha1-protease inhibitor This test assays the presence in feces of a naturally occurring endogenous serum protein that is resistant to bacterial degradation if it is lost into the intestinal lumen. To improve diagnostic accuracy, three fresh fecal samples should be sampled. The assay is valid only if used on fecal samples collected after voluntary evacuation, because abrasion of the colonic wall during manual evacuation is enough to elevate alpha1-protease inhibitor (alpha1-PI) concentrations. It appears to be of value for the diagnosis of protein-losing enteropathy and may prove to be more a sensitive marker than measurement of serum albumin for the detection of early disease.

Rectal cytology At the end of the rectal examination, the recta] wall is mildly abraded, the gloved finger rolled on a microscope slide, and the smear stained. Although the result is often negative and, when positive, probably more representative of large intestinal disease, an increased number of neutrophils may be suggestive of a bacterial problem, indicating the need for fecal culture. Clostridial endospore elements (Histoplasma, Aspergillus, Pythium, and Candida spp. ) may be identified. The test is fast and simple but in all cases confirmatory tests are indicated.

Small Intestine: Imaging

Small Intestine: Special Tests


Flexible endoscopy allows gross examination of the small intestine mucosa and collection of tissue samples without the need for invasive surgery. The proximal small intestine can be viewed during gastroduodenoscopy, and the distal small intestine often can be visualized by passing the endoscope retrograde through the ileocolic valve. Therefore only the midjejunum cannot be satisfactorily examined by routine endoscopy. However, given that most cases of malabsorption involve diffuse disease, this limitation may not be significant. Enteroscopy, which was developed in humans and which uses a much narrower, thinner endoscope, may allow examination of most of the jejunum.

Abnormal findings on gross endoscopic examination include mucosal granularity and friability, erosions / ulcers, retained food, mass lesions, and hyperemia / erythema. However, none of these characteristics is pathognomonic for particular disease conditions, and gross findings frequendy do not correlate with those of the histopathologic examination. A milky white appearance or a milky exudate is suggestive of lymphangiectasia, and the presence of intraluminal parasites may be diagnostic in some cases.

Small Intestine: Intestinal Biopsy

Acute Small Intestinal Disease

Viral Enteritides

Bacterial Enteritides

Rickettsial Diarrhea (Salmon Poisoning)

Neorickettsia helminthoeca and Neorickettsia elokominica are found in the metacercariae of the fluke Nanophyetus salmonicola, which is present in salmon in the western regions of the Cascade Mountains from northern California to central Washington. About a week after ingestion of infected salmon by dogs, the rickettsiae emerge from the mature fluke and cause a disease characterized by high fever, hemorrhagic gastroenteritis, vomiting, lethargy, anorexia, polydipsia, nasal-ocular discharge, and peripheral lymphadenopathy. Mortality is extremely high in untreated patients.

The diagnosis is based on a history of ingestion of raw fish in an endemic area, the detection of operculated fluke eggs in feces, and the presence of intracytoplasmic inclusion bodies in macrophages from lymph node aspirates. Oxytetracycline (7 mg / kg given intravenously three times a day) is the treatment of choice and should be continued for at least 5 days. The trematode vector is eradicated with praziquantel.

Algal Infections

Toxic algal blooms can lead to acute gastroenteritis and death in animals that drink contaminated water. Blue-green algae can synthesize an anticholinesterase that induces vomiting, diarrhea, ataxia, and rapid death in dogs. Prototheca spp. are achlorophyllous algae that cause protothecosis. Typically a cutaneous infection in cats, in dogs it can involve the intestine. Large intestinal disease is more common, but fatal disseminated disease affecting the small intestine has been reported.

Fungal Infections



Chronic Idiopathic Enteropathies

Adverse Reactions To Food

Small Intestinal Bacterial Overgrowth

Inflammatory Bowel Disease


Miscellaneous Causes Of Protein-Losing Enteropathy

Common causes of protein-losing enteropathy include lymphoma and IBD. However, there have also been recent reports of protein-losing enteropathy associated with intestinal crypt lesions without evidence of lymphangiectasia or inflammation in most cases. The underlying etiology of such lesions is not known. Response to therapy with antibacterials and immunosuppressive medication is variable; some dogs deteriorate suddenly and can die from thromboembolic disease

Intestinal Neoplasia

Adynamic Ileus And Intestinal Pseudo-Obstruction

Adynamic ileus is a common sequel to parvoviral enteritis, abdominal surgery, pancreatitis, peritonitis, endotoxemia, hypokalemia, and dysautonomia. The term intestinal pseudo-obstruction describes a condition in which patients show clinical evidence consistent with an obstruction, but no mechanical cause can be found. The condition has been associated with both visceral neuropathies and myopathies in humans, and such causes may occur in small animals. Most canine cases are associated with idiopathic sclerosing enteropathy, with fibrosis and a mononuclear cell infiltrate of the tunica muscularis. A case of feline intestinal pseudo-obstruction occurred secondary to intestinal lymphoma. After the possibility of a mechanical obstruction has been eliminated, management of both adynamic ileus and intestinal pseudo-obstruction is aimed at identifying any underlying cause and providing specific treatment. Symptomatic therapy to stimulate intestinal motility is also indicated. Suitable prokinetic agents include the 5-HT4 receptor agonist cisapride, the D2 dopaminergic antagonist metoclopramide, and motilin-like drugs such as erythromycin. In dogs and cats cisapride appears to be the most effective agent, but it is no longer marketed in many countries. Antibacterials may also be appropriate, given the probability of secondary SIBO, and immunosuppressive medication may be appropriate if an underlying inflammatory bowel disease is suspected. Feeding is beneficial in humans, and nutritional support can be continued indefinitely, although vomiting, constipation, and diarrhea usually continue. Unfortunately, most cases reported in the veterinary literature responded poorly to therapy, and the prognosis is grave.

Intestinal Obstruction

Intestinal obstruction can be classified as acute or chronic, partial or complete, and simple or strangulated. Obstruction can be the result of extraluminal, intramural, or intraluminal mass lesions. The most common extraluminal cause of obstruction is intussusception. Younger animals are more likely to develop intussusception after a case of gastroenteritis or after having intestinal surgery, although an increased risk in postparturient queens has also been reported. Intestinal neoplasia is the more frequent cause of intussusception in middle-aged and older animals. Intramural causes include intestinal neoplasia (most common), hematomas, granulomas (e. g., focal FIP), inflammatory bowel disease, stricture, and phycomycosis. Most intraluminal obstructions are caused by foreign objects, such as stones, fruit pits, and toys in dogs and linear foreign objects in cats. Intestinal volvulus describes a condition in which the intestines rotate around the mesenteric axis, compromising the cranial mesenteric artery, and complete vascular obstruction may lead to strangulation. Reports are sporadic, but a predisposition in German shepherds has been reported.

The prognosis depends on the cause of the obstruction and the severity of associated abnormalities. The outcome is likely to be favorable with simple foreign bodies, but it is grave for animals with volvulus or metastatic intestinal neoplasia. The patient may be at risk of developing short bowel syndrome if a significant length of intestine must be removed.

Short Bowel Syndrome

Irritable Bowel Syndrome

Irritable bowel syndrome (IBS) is characterized by recurrent, usually acute, episodes of abdominal pain, borborygmi, and diarrhea. In the absence of morphologic changes, a functional disorder is considered the cause of this enigmatic problem. Disordered intestinal motility may be of primary importance, and a number of mechanisms have been proposed for irritable bowel syndrome in humans (Box Causes of Irritable Bowel Syndrome). However, it is not known whether any are responsible in dogs and cats. A variety of treatments, including antispasmodics (anticholinergics and also smooth muscle relaxants, such as mebeverine), anxiolytics (e. g., diazepam, chlordiazepoxide) and dietary modification (low-fat diet, increased fiber) have been tried with no consistent results. IBS probably will remain a frustrating condition to diagnose and treat successfully until its etiology is better understood.

Causes of Irritable Bowel Syndrome

  • Primary motility disorders
  • Visceral hyperalgesia
  • Psychosomatic disorders
  • Food intolerance
  • Undiagnosed inflammatory disease


Helminthic infestation is common in dogs and cats. Some species are pathogenic in large numbers, and others are nonpathogenic.

Roundworm Ascarids

Toxocara canis and Toxascaris leonina are found in dogs, and Toxocara can and Toxascaris leonina are found in cats. T. canis can be transmitted across the placenta and T. canis and T. cati through the milk. Infection is also caused by ingestion of the ova or of other hosts, such as rodents. The adult nematodes live in the small intestine. Migrating juvenile T. canis can cause hepatic, pulmonary, and occasionally ocular damage. T. canis presents a public health problem (i. e., visceral and ocular larva migrans).

Clinical Findings

Roundworms most often cause disease in young animals, and common signs are diarrhea, weight loss, or failure to thrive. A poor haircoat and a potbelly may be evident in puppies or kittens. Intestinal obstruction and perforation have been described in severe cases.


Almost all puppies can be presumed to have T. canis infection. The diagnosis is made by fecal flotation.


A wide range of anthelmintics is effective against roundworms (Table 222-10). Treatment should be repeated at 2- to 3-week intervals in affected animals. Young animals should be routinely wormed at 2, 4, 6, 8, 12, and 16 weeks of age and then at least at 6-month intervals. It is important to ensure proper hygiene to stop reinfection or spread. T. canis can be controlled by administering fenbendazole to pregnant bitches at an oral dosage of 50 mg / kg given daily from day 40 to 2 days after whelping.


Ancylostoma caninum is the most important hookworm of dogs and is associated with blood loss and hemorrhagic enteritis. Ancylostoma tubeforme is the most common hookworm in cats but is less pathogenic. Ancylostoma braziliense occurs in dogs in the southern United States.

Uncinaria stenocephala is the hookworm of dogs in western Europe, although it also occurs in the northern United States and in Canada. Infection is most commonly reported in kenneled dogs, particularly greyhounds, and can be acquired prenatally, during lactation, by ingesting larvae, by migration of larvae through the skin, and by ingestion of a paratenic host.

Clinical Findings

Diarrhea, weakness, pallor, vomiting, dehydration, poor growth, and anemia are common in puppies with A. caninum infection. The infection can cause a rapid and fatal anemia or a more chronic iron deficiency anemia. U. stenocephala does not suck large quantities of blood and cause anemia, although severe infestations may be associated with diarrhea. Larval migration of U. stenocephala causes pedal pruritus.


The diagnosis is made by demonstrating ova in feces.


Appropriate anthelmintics are detailed in Table Common Anthehnintic Medications for Dogs.For Ancylostoma infection in anemic puppies, pyrantel pamoate has been suggested as the treatment of choice because it acts very rapidly and is comparatively safe. Anemic puppies may require blood transfusion and supportive care. Monthly administration of milbemycin or ivermectin plus pyrantel pamoate has been approved for the prevention or control of hookworm in dogs.

Common Anthehnintic Medications for Dogs

Drug Dosage Usual Formulation Spectrum Of Activity
Nematode Cestode
Piperazine 83.2-300 mg / kg Tablet Yes No
Pyrantel 5 mg / kg Paste Yes No
Selamectin 6 mg / kg monthly Topical Spot-on Yes No
Fenbendazole 20-100 mg / kg for 1-3 days Granules, paste, suspension Yes Toenia sp.
Mebendazole 50 mg / kg for 2 days Tablet Yes Taenia, Echinococcus spp.
Nitroscanate 50 mg / kg Tablet Yes

(not Trichuris sp. )

Taenia, Dipylidium caninum, (Echinococcus) spp.
Pyrantel, febantel, praziquantel (combination) 1 tablet / 10 kg Tablet Yes Taenia, Echinococcus spp., D. caninum
Pyrantel, febantel (combination) 1 mL / kg Suspension Yes Taenia sp., D. caninum
Dichlorophen 200 mg / kg Tablet No Taenia sp., D. caninum
Praziquantel 5 mg / kg Injection, tablet No Taenia, Echinococcus spp., D. caninum



Dipylidium caninum is the most common tapeworm infecting dogs and cats in the United States and Europe. Fleas are the intermediate host. Echinococcus granulosus is a tapeworm that uses dogs as definitive hosts, but humans and sheep are intermediate hosts. E. granulosus infection is not associated with clinical signs in dogs but is an important zoonosis. Various other Taenia spp. are also common in dogs and cats.

Clinical Findings

Heavy infestations of D. caninum are only rarely associated with diarrhea, weight loss, and failure to thrive. There are usually no clinical signs except “rice grains” (proglottids) in the perineal area or feces.


A diagnosis of D. caninum infection is made by demonstrating characteristic egg capsules, contained in proglottids, obtained from the perineal area or feces.


Treatment of D. caninum infection involves adequate flea control (the animal and the environment) and administration of an appropriate anthelmintic (see Table Common Anthehnintic Medications for Dogs). E. granulosus and other Taenia spp. are best controlled by routine administration of praziquantel (see Table Common Anthehnintic Medications for Dogs).

Strongyloides sp.

Strongyloides stercoralis is a small nematode that may cause hemorrhagic enteritis in young puppies. Infective larvae are ingested, transmitted transmammary or through penetration of the skin, and after migration through the lung develop in the small intestine.

Clinical Findings

Signs of hemorrhagic enteritis occur in young puppies.


Fecal evaluation using the Baermann technique or demonstration of motile first-stage larvae in smears of fresh feces helps differentiate larvae from Filaroides and mature hookworms.


Infection is treated with thiabendazole or possibly fenbendazole or ivermectin (see Table Common Anthehnintic Medications for Dogs).




Isospora spp.

hospora spp. are the most common coccidial parasites of dogs (Isospora canis, Isospora ohioensis) and cats (Isospora felis, Isospora rivolta). Transmission occurs by ingestion of ova or paratenic hosts. Sporozoites are liberated in the small intestine and enter cells to begin development. The prepatent period ranges from 4 to 11 days, depending on the species. Isospora organisms are rarely associated with clinical signs. Puppies and kittens kept in unhygienic conditions or immunosuppressed animals may develop heavy infestations, which occasionally are associated with diarrhea that is often mucoid but sometimes bloody. Isospora oocysts are found on direct examination of a fecal smear or by flotation. The infection is often self-limiting, but sulfadimethoxine (50 mg / kg given orally once daily for 10 days) or trimethoprim-sulfa (15 to 30 mg / kg given orally once daily for 5 days) can be used when clinical signs warrant treatment. The prognosis for recovery is good.

Cryptosporidium sp.

Cryptosporidium parvum, a significant pathogen in humans, is not a single species but is composed of genetically distinct genotypes. Transmission occurs by the fecal-oral route. Molecular studies have shown that dogs may transmit the catde genotype to humans but that specific cat and dog genotypes also exist. C. parvum has been associated with self-limiting diarrhea in dogs and cats and severe hemorrhagic diarrhea in immunocompromised animals.

Cryptosporidial oocysts are extremely small (approximately 1 / 10 the size of Isospora oocysts) and require identification by fecal flotation and oil immersion microscopy or by intestinal biopsy.

Paromomycin was reported to be effective against Cryptosporidium organisms in a cat. However, more recent studies have demonstrated that the drug’s efficacy is poor and that it may cause acute renal failure. No other drugs are consistently efficacious, although nitazoxanide may prove to be effective. Fortunately, the disease is usually self-limiting in immunocompetent animals.

Giardia sp.

Giardia sp. can affect both dogs and cats. The prevalence of infection in canine studies ranges from less than 2% to 100% in kennels. Cats are less commonly infected than dogs. The parasite is usually transmitted via the fecal-oral route. Ingested oocysts excyst in the upper small intestine, and trophozoites attach to the intestinal mucosa from the duodenum to the ileum. After multiplication of trophozoites, oocysts are passed in the feces at 1 to 2 weeks after infection. Molecular epidemiologic studies indicate that giardiasis may be a zoonosis.

Clinical Findings

Most infections are not associated with clinical signs. Clinical signs range from mild, self-limiting, acute diarrhea to severe or chronic small bowel diarrhea associated with intestinal protein loss and weight loss.


Giardia infection can be diagnosed by demonstration of motile trophozoites in duodenal juice or on a fresh fecal smear or by demonstration of cysts by zinc sulfate fecal flotation. Shedding of cysts occurs intermittendy, and three fecal analyses are 95% sensitive. Giardia antigen can also be detected by means of a fecal enzyme-linked immunosorbent assay, and this is the preferred method of diagnosis compared to zinc sulfate flotation performed by inexperienced technicians.


Metronidazole is the drug most commonly used to treat Giardia infection in small animals. The standard dosage recommended for dogs is 25 mg / kg given orally twice daily for 5 days; the standard dosage for cats is 10 to 25 mg / kg given orally twice daily for 5 days. The drug is effective at eliminating Giardia infection in two thirds of infected dogs but may cause side effects at these high doses.

Albendazole (25 mg / kg given orally twice daily for 2 days) and fenbendazole (50 mg / kg given orally twice daily for 3 days) also eliminate Giardia infection. Fenbendazole is preferred, because albendazole has been associated with bone marrow toxicosis. Febantel (in a combination product with praziquantel and pyrantel pamoate) is also effective in dogs.

Decontamination of the patient’s coat by bathing and the patient’s habitat by steam cleaning or cleaning with quaternary ammonium compounds is advised to prevent reinfection. A Giardia vaccine is available for use in high-risk areas, and it has been shown to be effective in clearing infection from dogs that failed to respond to standard drug therapy.


The prognosis is usually good. Some patients may require several treatments to eliminate infection, because reinfection is a significant problem.


Chronic Enteropathies

Chronic Idiopathic Enteropathies

Chronic enteropathies have historically been defined by histologic description of the tissue, which provides little information as to the nature of the intestinal dysfunction or its etiology.

Furthermore, tissue samples collected from many cases have no obvious morphologic changes. In the future, new methods of investigation may better characterize functional and immunologic abnormalities.

Management of Chronic Enteropathies

The management of idiopathic enteropathies is essentially symptomatic if a specific diagnosis is made (e. g., lymphangiectasia, severe inflammatory bowel disease, lymphoma), specific treatment modalities can be used. However, in many circumstances the diagnosis is not obvious, often because of a lack of specific or marked histopathologic changes, and it usually is most appropriate to perform treatments sequentially. It is safest to commence with antiparasiticides, then a dietary trial, followed by an antibacterial trial, before finally attempting immunosup-pression. Such an approach may identify occult parasitism, antibiotic-responsive diarrhea (antibiotic-responsive diarrhea) and diet-responsive conditions. However, because different treatments also lack specific activities, caution should be exercised in using treatment trials for diagnosis without prior investigation.

Antiparasiticides An appropriate trial of an antiparasiticide should eliminate the possibility of parasitic diseases, such as chronic giardiasis, that are difficult to diagnose. Fenbendazole (50 mg / kg given orally every 24 hours for 3 days) is the most appropriate drug for these circumstances, although alternatives exist (e. g., metronidazole or a febantel / pyrantel / praziquantel combination). Given the highly infectious nature of Giardia organisms, all in-contact animals may need to be treated concurrendy or reinfection may occur, which might suggest apparent treatment failure.

Dietary management Dietary management is a very important treatment modality in most chronic enteropathies and can be used in different ways. For diagnosis and treatment of adverse food reactions, an antigen-limited exclusion diet is most appropriate. Dietary management also can be important in the symptomatic management of many idiopathic enteropathies. The ideal diet is highly digestible, moderately fat restricted, lactose free, gluten free, not markedly hypertonic, nutritionally balanced, and palatable.

Inclusion of moderately fermentable fiber (e. g., psyllium, ispaghula) is known to promote colonic health, and soluble fiber also promotes small intestinal health. However, because dietary fiber can delay intestinal transit, its inclusion may be contraindicated for some intestinal diseases. Feeding the daily requirement in divided meals (usually between two and four) reduces the load on a compromised intestine. Feeding more frequendy is unnecessary, because the rate of gastric emptying imposes natural trickle feeding of the intestine.

Additional supplements include prebiotics such as fructo-oligosaccharides (FOS) and mannanoligosaccharides. FOS has been shown to alter the constituents of the fecal flora, but the effect on the small intestine flora is limited.

Antibacterials Antibacterials are indicated for specific conditions in which a bacterial pathogen has been documented (see above), in the treatment of antibiotic-responsive diarrhea or secondary SIBO, and in other chronic enteropathies, such as inflammatory bowel disease, in which modulation of the flora may be required. The drugs most commonly used in these circumstances are oxytetracycline, metronidazole, and tylosin. The beneficial effects of such drugs may go beyond their antibacterial activity, with potential effects on the mucosal immune system.

Immunosuppressive medication Immunosuppressive or anti-inflammatory drugs are indicated when evidence of mucosal inflammation is present and no underlying cause is found. However, given that immunosuppression may lead to clinical deterioration in some cases, the diagnosis should be reviewed before institution of such therapy, especially if the diagnosis was made on the basis of endoscopic biopsy alone.



Tapeworms are considered segmented flatworms, belonging to a class of organisms called Cestoda. One important characteristic of this class is that all utilize intermediate hosts in their transmission cycle. Intermediate hosts can include rodents, fleas, and other insects, rabbits, sheep, swine, cattle, and in some instances, even humans!

Tapeworm segments containing eggs are shed in fecal material. When these eggs are accidentally or voluntarily consumed by an intermediate host, they hatch and the resulting larvae migrate into the body tissues and begin their development. Yet they won’t reach their adult stage inside the tissues of this intermediate host. Instead, the life cycle is completed when this host or portions thereof are consumed by another, called the definitive host. Inside this new host environment, the larvae then proceed to develop into adult tapeworms, which attach to the intestinal wall, eat, and repeat the life cycle all over again.

The extent of disease caused by tapeworms depends on the type of worm involved, and if the affected individual is an intermediate or final host. As a rule, adult tapeworms living within the intestines of a definitive host are seldom life-threatening, causing varying degrees of gastroenteritis and malnutrition. Larval forms, on the other hand, tend to do more damage, simply because they migrate through the body tissues. Furthermore, if these larvae gain entrance into the tissues of an animal (or human) that is not a normal intermediate host for that tapeworm, the results can sometimes be deadly.

By far the most prevalent species of tapeworm seen in dogs and cats is Dipylidium caninum, the double-pored tapeworm. It is so common because it uses the flea as an intermediate host (the dog louse can also be a carrier).

Segments from the tapeworm are passed in the feces or actually “crawl” out onto the haircoat of an infested animal. Once outside, the segments dry out and release egg baskets into the environment. Flea larvae looking for food then ingest these eggs, and a new tapeworm begins its development. If the flea happens to be ingested by a pet during chewing or self-grooming episodes, the tapeworm larvae will continue to develop into adult worms within the pet’s small intestine.

Although less frequently, dogs and cats can become infected with other types of tapeworms besides Dipylidium, depending on potential exposure to intermediate hosts. For instance, dogs fed raw meat or garbage are at risk. Echinococcus granulosus, the tapeworm responsible for hydatid cyst disease, is often transmitted to dogs in this way. The hunting habits of outdoor domestic cats put them at high risk of exposure to this parasite as well.

Dogs and cats infested with adult tapeworms may or may not exhibit the typical signs associated with gastroenteritis, such as vomiting and diarrhea. Weight loss certainly can occur as the worms absorb nutrients from within the gut. Often, scooting and other signs related to anal sac discomfort might also tip off an owner as to the presence of these pesky parasites.

Diagnosis of a tapeworm infestation can be confirmed by actually seeing the white, moving, wormlike segments in fresh fecal material or on the haircoat around the hind region. Segments might also be seen on anal sac expression. If dried, the segments will take on a brownish, “ricelike” appearance.

Microscopic examination of the stool might be helpful as well; however, because the shedding of the segments is sporadic, a negative finding cannot totally rule out an infestation.

Tapeworms can be difficult pests to treat and totally eliminate. Praziquantel and epsiprantel are two effective medications used by veterinarians to eliminate tapeworms from the intestines. Other drugs are available as well. Repeating the treatment in 2 to 3 weeks helps ensure thorough elimination.

Flea control is the best way to prevent Dipylidium caninum. Other tapeworms, including Echinococcus, can be prevented by denying access to garbage and/or raw meat, and discouraging the hunting habits of felines.