Approach and Management of Chronic Enteropathies in Dogs
World Small Animal Veterinary Association Congress Proceedings, 2018
F. Gaschen
School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA, USA


The general term “chronic enteropathies” (CE) has been used frequently in recent years to describe dogs and cats with chronic intestinal diseases of unknown origin. Diet-responsive diarrhea (DRD), antibiotic-responsive diarrhea (ARD), and inflammatory bowel disease (IBD) are different forms of chronic enteropathies. They may form a continuum, with DRD being a mild form of CE, and IBD representing the severe form of the disease.


The following definitions apply to diseases affecting the small and/or the large intestine:

  • Chronic enteropathies (CE): A term encompassing all chronic inflammatory intestinal diseases of unknown origin. This includes diet-responsive CE, antibiotic-responsive diarrhea or intestinal dysbiosis, and inflammatory bowel disease (IBD).
  • Diet-responsive CE: A form of CE that responds to a dietary trial with an elimination diet based on a novel protein source or the use of hydrolyzed peptides.
  • Antibiotic-responsive diarrhea or idiopathic small intestinal dysbiosis: A form of CE associated with a severe imbalance of intestinal microbiota that responds to treatment with select antimicrobials.
  • Inflammatory bowel disease (IBD): A term used by some as synonymous to CE. Other authors prefer to use IBD to define a more severe form of CE that does not respond to a dietary trial or to a course of antimicrobials, and requires the use of immunosuppressive drugs. IBD is associated with moderate to severe infiltration of the intestinal mucosa with inflammatory cells (such as lymphocytes, plasma cells, eosinophils, neutrophils, macrophages and/or a combination of 2 types). In addition, changes in mucosal architecture such as stunting of the small intestinal villi are also common. Severe IBD may cause protein-losing enteropathy (PLE). Granulomatous colitis of boxers is a particular form of IBD that affects young boxers and bulldogs.


Canine CE are thought to occur as a consequence of a combination of factors that include dysregulation of the intestinal mucosal immune system and its interactions with intestinal microbiota and/or dietary components, and compromised integrity of the intestinal mucosal barrier.

Clinical Presentation

CE are characterized by chronic or chronic-intermittent diarrhea of more than 3 weeks duration. Mild CE may cause intermittent clinical signs, whereas progressive and severe clinical signs are common in severe cases. Poor body condition with poor hair coat is frequent with severe disease. Some animals may regularly vomit and dehydration is possible. Thickened small intestinal loops may occasionally be palpated. Animals may show pain or discomfort on abdominal palpation. Ascites, hydrothorax and peripheral edema may occur in case of significant protein loss (PLE).


Diagnosis of CE consists in an elimination process. The aim is to rule out other diseases of known etiology that may cause similar clinical signs: fecal flotation and a Giardia antigen test should be performed in all dogs. Alternately, empiric parasiticide treatment can be administered (e.g., fenbendazole 50 mg/kg q 24 h for 3–5 days). Subsequently, the diagnostic process is different for dogs with mild clinical signs and no evidence of systemic complication such as hypoproteinemia, and for dogs that are more severely affected.

Dogs with mild to moderate disease can undergo a treatment trial with a novel protein or hydrolyzed peptide diet, while severely affected dogs showing significant systemic repercussions of their intestinal disease should be evaluated more thoroughly with collection of a minimal database including CBC, serum biochemistry and urinalysis. Presence of hypoalbuminemia, often accompanied by hypoglobulinemia, suggests PLE. Sensitivity of abdominal ultrasound is intermediate, and scans may be normal or show focal or diffuse loss of wall layering, presence of mucosal striations or spicules, wall thickening, enlarged and/or hypoechoic mesenteric lymph nodes. If lesions are present, localization to a specific intestinal segment may be helpful.

Procurement of biopsy samples with upper GI endoscopy or exploratory celiotomy is necessary to further evaluate disease severity in dogs undergoing an in-depth work up. Each method offers different advantages and drawbacks. A biopsy specimen of adequate quality and quantity are required for accurate interpretation by pathologists. The most important justification for histology is to rule out a neoplastic infiltrate. However, it is also useful to evaluate the magnitude of intestinal mucosal inflammation based on the severity and type of the infiltrate and on the severity of the architectural mucosal changes. Current scoring systems are based on results from a WSAVA working group, and take both architectural and inflammatory mucosal changes into account. Inflammatory infiltration may be of varying severity and consist of lymphocytes and plasma cells (lymphoplasmacytic enteritis), eosinophils, neutrophils or macrophages or combinations thereof. Examples of small intestinal mucosal architectural changes include: villus stunting, surface epithelial injury, crypt distension, lacteal dilation, and mucosal fibrosis.

Differential Diagnoses

General differentials include intestinal parasitic diseases, bacterial enteritis, fungal enteritis, chronic intestinal foreign body, and diseases originating outside the GI tract such as chronic kidney disease, chronic liver disease, chronic pancreatitis, exocrine pancreatic insufficiency, and atypical hypoadrenocorticism.


In most instances, the goal of treatment is to manage the clinical signs. Full recovery may be possible in mild cases.

After endoparasites have been ruled out (see above), the standard approach for a dog with mild to moderate chronic recurrent diarrhea of unknown origin without significant systemic repercussions is to initiate a food trial with a novel protein or hydrolyzed peptide diet. It is important to collect a detailed dietary history in order to identify the best-suited diet which may be different for each animal. At this time, many clinicians prefer hydrolyzed diets to novel protein diets to treat their patients with diet-responsive CE, although there is no evidence to support their superiority. A thorough discussion about the implementation of the dietary trial with the animal’s owners is an indispensable prerequisite. During the trial, the dog should not receive any other food or treats other than the prescribed diet. All dogs with diet-responsive CE show at least a partial response within 10 to 14 days. In dogs with partial or complete response, the dietary trial should be pursued for several months. There does not appear to be any benefit in adding probiotics to the treatment, although the studies published to date included only small numbers of dogs.

In dogs that do not respond to the elimination diet, the next step may consist of another treatment trial with another novel protein or hydrolyzed peptide diet. Antimicrobials may also be used in conjunction with the new diet. Small intestinal dysbiosis (change in the composition of the intestinal microbiota) occurs in most dogs with IBD. Young large breed dogs with CE (particularly but not exclusively German Shepherd dogs) respond to prolonged treatment with antimicrobials such as tylosin (20 mg/kg PO BID) or metronidazole (10–15 mg/kg PO BID). This may result from an inability of these dogs’ immune system to interact adequately with their intestinal microbiota. Clinical experience accumulated over the past decades indicates that prolonged treatment (4–8 weeks) is necessary, and that relapses are common. In refractory cases, and in dogs with severe disease and evidence of systemic involvement a more thorough work up with acquisition of a minimal database should be initiated (see Diagnosis above).

Dietary management is also an essential part of the treatment for most other forms of canine CE. Feeding a novel protein or hydrolyzed diet may also contribute to decreased mucosal inflammation in dogs with IBD receiving immunosuppressive treatment. In dogs with lymphangiectasia, a cause of protein-losing enteropathy, treatment with a highly digestible diet with low to very low-fat content (10–15% on a dry matter basis) may prevent further dilation and rupture of lacteals by reducing the flow of chyle. This diet significantly contributes to the success of treatment, which often includes anti-inflammatory doses of glucocorticoids. Additionally, the diet should contain highly bioavailable dietary proteins and be low in crude fiber.

All dogs with chronic small intestinal inflammation have limited absorptive capacity, and feeding them with a highly bioavailable diet is necessary in order to improve metabolic state and stop ongoing catabolism. As stated above, the goal of treatment in dogs with various forms of IBD is to successfully manage the disease. Therefore, appropriate dietary therapy should be administered long term and regularly adapted to the dog’s condition in order to decrease the risk of recurrences.


The prognosis for diet-responsive CE is good. It appears that 77–80% of these dogs are still controlled only with an elimination diet one year after diagnosis. However, several studies showed that the prognosis of dogs with CE that do not respond to a dietary treatment trial is significantly worse, with up to 1/3 of patients euthanized within 3 months of diagnosis. Moreover, severe hypoalbuminemia (serum albumin < 2 g/dL or < 20 g/L) at the time of presentation was identified as a negative prognostic factor.

Value of Diet in Other Chronic Enteropathies


1.  Dandrieux JRS. Inflammatory bowel disease versus chronic enteropathy in dogs: are they the same? J Small Anim Pract. 2016;57:589–599.

2.  Honnefer JB, Minamoto Y, Suchodolski JS. Microbiota alterations in acute and chronic gastrointestinal inflammation in cats and dogs. World J Gastroenterol. 2015;20(44):16489–16497. doi: 10.3748/wjg.v20.i44.16489.


Speaker Information
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F. Gaschen
School of Veterinary Medicine
Louisiana State University
Baton Rouge, LA, USA

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