Dietary-responsive disease is an all-inclusive term that includes dietary allergy (a hyperimmune response to a dietary antigen) and dietary intolerance (a nonimmune¬ mediated response to a dietary substance). From a clinical standpoint, there is minimal value in distinguishing between the two unless there are concurrent cutaneous signs of allergic disease.

Clinical Features
Affected patients may have vomiting and/or diarrhea (large and/or small bowel) as well as allergic skin disease.

iagnosis consists of showing response to feeding an elimination diet that is appropriate for the patient (see the discussion of dietary management in !hapter "#). $here is typically minimal value in distinguishing between allergy and intolerance. $ests for %g& antibodies i n the patient's blood to specific antigens are not as valuable as seeing the response to an elimination diet. $he diet must be carefully chosen( it must consist of nonallergenic substances or foods to which the patient has not previously been e)posed. *ost animals respond to an appropriate diet within " weeks, although some take longer.

*ost patients that respond can simply be fed the diet to which they responded in the dietary trial (assuming that it is balanced). +are patients develop allergies to the elimination diet and re,uire different elimination diets to be fed on rotating -- to "-week cycles.

$he prognosis is usually good.

%. involves idiopathic intestinal inflammation. %. can affect any portion of the canine or feline intestine. Although the cause of %. is unknown, it is speculated to involve an e)aggerated or inappropriate response by the immune system to bacterial and/or dietary antigens as at least part of the mechanism. $he clinical and histologic features of %. can closely resemble those of alimentary lymphoma (see p. /01). 2ymphocytic-plasmacytic enteritis (23&) is the most commonly diagnosed form of canine and feline %. . !hronic small intestinal diarrhea is common, but some patients have weight loss with normal stools. %f the duodenum is severely affected, vomiting may be the ma4or sign, and diarrhea can be either mild or absent. 3rotein-losing enteropathy can occur with the more severe forms. &osinophilic gastroenterocolitis (&5&) is usually an allergic reaction to dietary substances (e.g., beef, milk) and as such is not %. . 6owever, the clinical signs do not always respond to dietary change and may represent true %. in some dogs. %t is less common than 23&. 7ome cats have eosinophilic enteritis as part of a hypereosinophilic syndrome (6&7). $he cause of feline 6&7 is unknown, but immune-mediated and neoplastic mechanisms may be responsible. 2ess severely affected cats without 6&7 seem to have a condition similar to canine &5&.

.ecause %. is idiopathic intestinal inflammation, it is a diagnosis of e)clusion( it is not 4ust a histologic diagnosis. 8o physical e)amination, historic, clinical pathology, imaging, or histologic findings are diagnostic of %. . iagnosis re,uires elimination of known causes of diarrhea plus histology showing mucosal inflammatory infiltrates, architectural changes (e.g., villus atrophy, crypt changes),

. 6istologic diagnosis of mucosal inflammation is unfortunately sub4ective. A:athioprine is not used in cats( instead. and methylprednisolone is typically more effective than prednisolone.uate therapy.uality (either from the standpoint of si:e or artifacts present).g. either alone or in combination with corticosteroids and diet. may also be effective. 6ighly digestible elimination diets may be curative if what was thought to be %. . prednisolone. *ucosal cytologic evaluation is unreliable for diagnosing lymphocytic inflammation because lymphocytes and plasma cells are normally present in intestinal mucosa. *ore severe disease. and biopsy samples are fre. is actually dietary intolerance or A+&. -. iagnosis of &5& is similar to diagnosis of 23&. usually re. 5erman 7hepherd dogs seem to be overrepresented. or misdiagnosis (i. owner noncompliance. it is also more e)pensive. +ecent data document that biopsy of more than one site (e.. lymph node..g. &ven descriptions of 9moderate9 or 9severe9 23& may be dubious because of substantial inconsistency among pathologists. those with diabetes mellitus). hepatic. chlorambucil is used for cats with biopsy-proven. !yclosporine seems to be reasonably effective and works faster than a:athioprine administered every other day( however. 9 * i l d 9 23& often refers to essentially normal tissue.. %f the biopsy specimens are of marginal . but it is important to note that cats with %.<-h). severe 23& that does not respond to other therapy (see !hapter 1>) or for cats with well-differentiated lymphoma. 6igh doses of corticosteroids are typically administered early in cats because of their beneficial effects and the cat's relative resistance to iatrogenic hyperadreno¬ corticism. Treatment !anine 23& treatment begins with elimination diets and antibiotics in case what appears to be %.. is actually food intolerance. &lemental diets. can be invaluable in severely emaciated or severely hypopro¬ teinemic patients with severe inflammation as a way to feed the patient and the intestinal mucosa without causing more mucosal irritation.. splenic. 3rednisolone is preferred to prednisone in the cat.uires immunosuppressives (e. a:athioprine or cyclosporine).g. ogs with &5& may have eosinophilia and/or concurrent eosinophilic respiratory or cutaneous dietary allergies with pruritus. Feline 23& treatment is somewhat similar to that for canine 23&. iagnosis of feline &5& centers on finding intestinal eosinophilic infiltrates( however. duodenum and ileum. 2ow-dose metronida:ole (<# to <= mg/kg administered orally . . and therapeutic diets should always be used i f the cat will eat them. it is easy to mistakenly diagnose 23& instead of lymphoma if the latter is causing a secondary tissue reaction. %t can be e)tremely difficult to distinguish a well-differentiated lymphocytic lymphoma from severe 23&. especially if associated with hypoalbuminemia. as opposed to 4ust duodenum) is sometimes critical in finding inflammatory (and neoplastic) changes.e. iagnosis of feline 23& is similar to that of canine 23&. 7omewhat more severe disease warrants metronida:ole with or without high-dose corticosteroid therapy (e. may have mild to moderate mesenteric lymphadenopathy. 7ome animals with intense dietary reactions have biopsy findings that resemble lymphoma.udesonide is primarily indicated in cats that cannot tolerate the systemic effects of steroids (e.g. and bone marrow infiltrates and peripheral eosinophilia are common.uently overinterpreted. &nteral or parenteral nutritional supplementation may be useful in emaciated cats (see . even with full-thickness samples.and/or epithelial changes.ther therapy depends on the severity of the 23&. and such lymph¬ adenopathy is not diagnostic of intestinal or budesonide in steroid-intolerant patients). although e)pensive. diagnosing 23& when the problem is lymphoma). Failure of a dog to respond to 9appropriate9 therapy can be the result of inade.

an animal i n i tially responds to dietary management but relapses while still eating this diet because it becomes allergic to one of the ingredients. LARGE INTESTINAL INFLAMMATORY . but that is uncertain.e. turkey and potato).g. $his situation necessitates administration of another elimination diet. . which should be tapered cautiously. %f the cat responds to this therapy. then the therapy should be continued without change for another . it may be 4ust as likely that either the initial diagnosis of " weeks. the elimination diet should be continued while the medications are gradually tapered one at a time. fish and potato. %f signs do not resolve with dietary therapy. !anine &5& treatment should focus on a strict hypoal¬ lergenic diet (e. . %atrogenic !ushing's syndrome should be avoided. was wrong (i. %t is important to determine what the dog was fed previously when selecting the dietary therapy.) Feline &5& associated with hypereosinophilic syndrome usually re. the animal should be slowly weaned from the drugs. $here is no obvious benefit to rebiopsying patients that are clinically improving. A markedly low serum cobalamin concentration in the dog might be a poor prognostic sign. if possible. 3arenteral administration of cobalamin to cats with severely decreased serum concentrations may aid or be necessary for remission of diarrhea. *any with moderate to severe disease will need prolonged medical therapy. 7ometimes. starting with those that have the greatest potential for adverse effects./ to 0. %f a dog or cat with a prior diagnosis of 2 3& is later diagnosed as having lymphoma. !ats with eosinophilic enteritis not caused by 6&7 often respond favorably to elimination diets plus corticosteroid therapy. switching back and forth from one elimination diet to another at --week intervals helps to prevent this relapse from happening.0 mg/kg/day)( response is often poor. %f the dog or cat responds clinically. then the lowest effective dose of each should be slowly determined.nce the clinician is convinced that the prescribed therapy is responsible for the improvement seen.uired. but they are not a panacea for all 5% dietary allergies/intolerances.. %n some animals that are very prone to developing such intolerances. Animals usually respond better to elimination diets than to corticosteroids.. %f antiinflammatory or immunosuppressive therapy was initially re.asen4is)( however. balanced commercial elimination / weeks to ensure that the clinical improvement is the result of the therapy and not an unrelated transient improvement. if therapy is begun before the patient is emaciated. .nly one change should be made at a time. *any animals will need to be on a special diet for the rest of their lives. 7evere hypoalbuminemia and a very poor body condition are thought to be suggestive that the patient may have more difficulty responding. ietary and antibiotic therapy are usually the last to be altered. %f a homemade diet was used initially. (7ee !hapter "# for more information on these therapies. and the dose should not be decreased more fre. %f that regimen is successful. the addition of corticosteroid therapy is usually curative. Although the relationship is unclear. 3artially hydroly:ed diets may also be helpful. this is uncertain. the patient had lymphoma) or that the lymphoma developed independently of the %.e. /0# for immunopro¬ liferative enteropathy in . the clinician should seek to transition the patient to a complete. 23& has been suggested to be a potentially prelymphomatous lesion (see p.. the clinician should attempt to maintain the pet on every-otherday corticosteroid and a:athioprine therapy.uires high-dose corticosteroid therapy (i. 7everely affected animals may initially benefit from enteral or parenteral nutritional therapy. prednisolone. Prognosis $he prognosis for dogs and cats with 23& is often good. /.!hapter "#).uently than once every .

sulfasala:ine (A:ulfidine). tends to be better than for small bowel %. whereas canine large bowel %. . disease).e. GRANULOMATOUS ENTERITIS/ GASTRITIS !anine granulomatous enteritis/gastritis is uncommon. Feline granulomatous enteritis is a rare type of %. %n cats hematoche:ia is the most common clinical sign.e. . a:athioprine. Affected cats seem to respond to high-dose corticosteroid therapy.9 !anine lymphocyticplasmacytic colitis (23!) typically causes large bowel diarrhea (i. and diarrhea is the second most common sign. %n general. and/or gastric mucosal atrophy. $he clinician should search diligently for an etiology (e. %t probably has a genetic basis or predisposition. $oo few cases have been described and treated to allow generali:ations. e)cluding other causes and finding mucosal histologic changes) is similar to that for small bowel %. . %f the disease is locali:ed.g.uires histopathologic confirmation. affected dogs are fundamentally healthy e)cept for soft stools. or olsala:ine may be used in dogs with moderate to severe 23!. metronida:ole. vomiting.g. Clostridium colitis. traveling. fungal).. $he prognosis is poor. and it can be diagnosed only histopathologically. Although compared to !rohn's disease in people. but attempts to reduce the dose of glucocorticoids may cause recurrence of clinical signs.g.. and intestinal bacteria may play an important role. and sulfasala:ine is rarely needed. metronida:ole. corticosteroids. 6igh-fiber and hypoallergenic diets are also often beneficial in cats( in fact. 6ypoallergenic and fiber-enriched diets are often very helpful. antibiotics.. and dietary therapy should be considered. most 9intractable9 feline 2 3 ! cases seen in the author's practice are ultimately determined to be related to diet. that causes weight loss. *ost cats with 23! respond well to prednisolone and/or metronida:ole. surgical resection should be considered i f the clinician is sure that there is not a systemic cause (e. %f it is diffuse. dietary intolerance. and perhaps diarrhea( it also re.BOWEL DISEASE Clinical Features %n the author's practice.. small intestinal diarrhea. and fiber-responsive diarrhea are responsible for most cases referred and previously diagnosed as having 9intractable9 large bowel 9%. . $he prognosis is guarded. Diagnosis iagnosis (i. protein-losing enteropathy. mesala¬ mine. Treatment 7teroids. IMMUNOPROLIFERATIVE ENTEROPATHY IN BASENJIS Etiology %mmunoproliferative enteropathy in . particularly as the animal is stressed (e. seems to be infre. parasites. Clinical Features $he disease tends to be a severe form of 23& that wa)es and wanes.. the two are dissimilar. !linical signs are similar to those of other forms of %. . soft stools with or without blood or mucus( no appreciable weight loss). %n particular. gastric rugal hypertrophy. . Feline 2 3 ! may occur by itself or concurrently with 23&. %t is critical to eliminate colonic fungal infections before begining immunosuppressive therapy. lymphocytic gastritis. ?eight loss. Tritrichomonas can cause substantial mononuclear infiltrates into feline colonic mucosa. fungal).uently associated with small bowel %. m i l d lacteal dilation. Prognosis $he prognosis for patients with colonic %. !orticosteroids and/or metronida:ole may be effective by themselves and/or allow lower doses of sulfasala:ine to be successful.asen4is is an intense lymphocytic-plasmacytic small intestinal infiltrate often associated with villous clubbing.

o) -@-<#).e. lymphoma. it is usually a severe form of 23&.uently have 32&.ue to them or may be a severe form of %. $he prognosis is poor for recovery. especially in advanced cases. it is usually .to " years after diagnosis. 2ymphangiectasia appears to be more common (in dogs) than was once thought( the problem is that it can be difficult to diagnose. 5% ulceration/erosion. %mmunopro¬ liferative enteritis of . and alimentary tract lymphoma have been suggested as particularly common causes in adult dogs.g. because other diseases (e. %. (i. 6owever. Diagnosis 7mall intestinal biopsy is necessary for diagnosis. +esponse to therapy is variable. but when it occurs. and affected dogs that respond are at risk for relapse. although &5& or granulomatous disease may be responsible. 7erum cobalamin concentrations are often . especially if stressed. /=1)( high-dose corticosteroids( metronida:ole( and a:athioprine.uite low. is responsible. or bleeding can produce a proteinlosing enteropathy (32&( or gastropathy if it affects the stomach( see . . not enough is known to be able to confidently recommend a breeding program. ENTEROPATHY IN CHINESE SHAR-PEIS Etiology !hinese 7har-3eis have a poorly characteri:ed enteropathy that may be uni. or elemental diets( antibiotics for A+& (see p. small intestinal dysfunction) are the main clinical signs. Prognosis Affected !hinese 7har-3eis have a guarded prognosis. whereas hookworms and chronic intussusception are common causes in very young dogs. elimination diets and immunosuppressive drugs) and A+&. and bleeding tumors may also produce 32&. ?hen %. although the changes tend to be milder.. Prognosis *any affected animals die . histoplasmosis) may mimic immunoproliferative enteropathy. congestion. %n advanced cases the clinical signs are so suggestive that a presumptive diagnosis is often made without biopsy. *ost affected . Treatment $herapy may include highly digestible. Clinical Features iarrhea and/or weight loss (i.asen4is start showing clinical signs by " to / years of age.asen4is may have lesions similar to those of dogs with diarrhea and weight loss.. PROTEIN-LOSING ENTEROPATHY CAUSES OF PROTEIN-LOSING ENTEROPATHY Any intestinal disease that produces sufficient inflammation.asen4is. Treatment $he animal is treated for %. alimentary tract biopsy is needed before aggressive immunosuppressive therapy is begun. !hinese 7har-3eis have immune system abnormalities that may predispose them to e)aggerated inflammatory reactions. elimination. &osinophilic and lymphocytic-plasmacytic intestinal infiltrates are typically found.and/or anore)ia are commonly seen. $he early stages of the disease resemble many other intestinal disorders. infiltration. Diagnosis *arked hypoalbuminemia and hyperglobulinemia are common. but some dogs can be maintained for prolonged periods of time with careful monitoring and care.e. 3erforming biopsy of the intestines of asymptomatic dogs to identify animals in which the disease will develop is dubious because clinically normal . Although a genetic basis is suspected.. !ats infre. %n a few dogs lymphoma later develops.

*onitoring serum albumin concentration may be the best way of assessing response to therapy. Treatment $he underlying cause of %2 is rarely determined.g.. although some re. 2ymphopenia is common but inconsistent. %ntestinal lipogranulomas (i. and lumen.e. %f full-thickness surgical biopsies are performed. animals that were initially hyperglobulinemic may lose most of their serum proteins and still have normal serum globulin concentrations. 7oft !oated ?heaten $erriers also have an unusually high incidence of protein-losing nephropathy.uired. and 2undehunds appear to be at higher risk than other breeds. and chylomicrons) into the intestinal or a:athioprine (-. pericarditis. &ndoscopic biopsies are often diagnosFIG 33-8 Endoscopic image of the duodenum of a dog with lymphangiectasia The large white !dots! are dilated lacteals in the tips of the "illi tic if done appropriately. lymphatic obstruction. 7oft !oated ?heaten $erriers. but hypoalbuminemia and hypocholesterolemia are e)pected. congenital malformations)./@h) or cyclosporine ("-= mg/kg . 2eakage of lymphatic fat into the intestinal wall may cause granuloma formation.. *ost cases of symptomatic %2 are idiopathic.. INTESTINAL LYMPHANGIECTASIA Etiology %ntestinal lymphangiectasia (%2) is a disorder of the intestinal lymphatic system of dogs. iagnosis re. ""-@).e. infiltrative intestinal mucosal disease. Although these proteins may be digested and resorbed. %f the animal improves with dietary therapy.caused by 23& or lymphoma.uent protein loss. Diagnosis !linical pathologic evaluation is not diagnostic. but surgical biopsies are sometimes re. thus resulting in hypoalbuminemia. Although panhypoproteinemia is classically attributed to 32&.. $hey are probably secondary to %2 (i.uire prednisolone in addition to the diet. serosal patch grafting and nonabsorbable suture material may decrease the risk of dehiscence. white nodules in the intestinal serosa or mesentery) are sometimes found at surgery. A few dogs die despite dietary and prednisolone . which e)acerbates lymphatic . infiltrative mesenteric lymph node disease. Feeding the animal fat the night before the biopsy seems to make lesions more obvious. $herapy should be directed at managing the underlying cause. but most dogs respond well to ultra-low-fat diets. 8ot reported in cats. Prognosis $he prognosis is variable. if at all.. lamina propria. A:athioprine or cyclosporine therapy might help solidify response to dietary therapy and maintain remission. the condition has many potential causes in dogs (e. $he first sign of disease caused by %2 may be transudative ascites.l-h) sometimes lessens inflammation around the lipogranulomas and improves lymphatic flow.e. ileum).-/h to .g.< to -. %2 may be locali:ed to one area of the intestines (e.uires intestinal histopathology. and classic mucosal lesions may be seen endo¬ scopically (Fig. e)cessive loss e)ceeds the intestine's ability to resorb them. fat leaking out of dilated lymphatic vessels). iarrhea is inconsistent and may occur early or late i n the course of the disease.uent leakage of lymphatic contents (i. Clinical Features Aorkshire $erriers. it should probably be fed that diet indefinitely. lymphocytes.. necessitating reliance on symptomatic therapy. A n ultra-low-fat diet essentially devoid of long-chain fatty acids helps to prevent further intestinal lacteal engorgement and subse. but they might worsen e)isting %2 by further obstructing lymphatics. protein. 3rednisolone (<. 2ymphatic obstruction causes dilation and rupture of intestinal lacteals with subse..

and inflammatory causes have been eliminated.7) i n people is characteri:ed by diarrhea. Diagnosis iagnosis consists of eliminating known causes by physical e)amination. with most dying within a year of diagnosis. *any animals must receive fiber chronically to prevent relapse. chronic large bowel diarrhea in which parasitic. although food hypersensitivity has been reported to be present in some affected dogs. #. propantheline. and appropriately performed therapeutic trials. and weight loss is very rare. $ypical clinical signs may include vomiting.<= mg/kg up to ..e. %t is an idiopathic large bowel disease in which all known causes of diarrhea have been eliminated and a 9functional9 disorder is presumed. Clinical Features %ndividual dogs may have 32& or protein-losing nephropathy (or both).. clinical pathologic data. and ascites. or supposedly %. as needed). ">@). FUNCTIONAL INTESTINAL DISEASE IRRITABLE BOWEL SYNDROME Etiology %rritable bowel syndrome (%. bacterial. Prognosis $he prognosis is good( in most animals the signs are controlled by diet or medical management. especially 5erman 7hepherd ogs). diarrhea. 7ome dogs with %. . $here are probably various causes of this syndrome in dogs..therapy. $he cause uncertain. !linical signs may develop following separation of the dog from the favored person. Diagnosis 3anhypoproteinemia and hypocholesterolemia are common. weight loss. %. police or guard dogs. lymphangitis. PROTEIN-LOSING ENTEROPATHY IN SOFT-COATED WHEATEN TERRIERS Etiology 7oft !oated ?heaten $erriers (7!?$s) have a predisposition to 32& and protein-losing nephropathy. Fecal mucus is common.@h.-= mg/kg( or dicyclomine. and/or cramping (usually of the large intestines) in which an organic lesion cannot be identified. #. 7ome dogs have no apparent initiating cause. B1C to >C fiber on a dry matter basis) is often helpful (see p. as with any 32&. Treatment#Prognosis $reatment is typically as for lymphangiectasia and/or %.g. Clinical Features !hronic large bowel diarrhea is the principal sign. dietary. .g. colonoscopy/ biopsy. 6istopathology of intestinal mucosa may reveal lymphangiectasia. Treatment $reatment with fiber-supplemented diets (i. Affected dogs are often middle aged when diagnosed.uent. fecal analysis.7 in dogs is different and primarily involves an idiopathic.ther dogs with %.7 are nervous and high-strung (e. Anticholinergics occasionally are useful (e. . . $he prognosis appears guarded to poor for clinically i ll animals. constipation.7 are small breeds that are heavily imprinted on a single family member. blood in the feces is infre.