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Ask Dr. Michael Salkin Your Own Question
Dr. Michael Salkin
Dr. Michael Salkin, Veterinarian
Category: Dog Veterinary
Satisfied Customers: 28522
Experience:  University of California at Davis graduate veterinarian with 45 years of experience
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Customer Question

Submitted: 1 year ago.
Category: Dog Veterinary
Customer: replied 1 year ago.
7 yr old German Shepherd dx'd with lymphangiectasia. Started 1 wk ago on Flagy 250mg twice daily, Prednisone 20 mg twice daily, Plavix 75 mg once daily; and changed to Purina HA diet. Since tx started, retaining more abd fluid, diarrhea now completely liquid, low energy/interest, drinking > 1 gal/day and peeing large quantities frequently. Most concerning: dog is now refusing all food (new HA diet, previous Royal Canin potato/venison, original ProNature turkey/cranberry). Could the meds need adjusting?
Customer: replied 1 year ago.
Oops - Flagyl is two 250mg tabs (500 mg total) twice daily.
Expert:  Dr. Michael Salkin replied 1 year ago.

I regret that your question doesn't have a simple answer. Can you upload a copy of his latest test results to our conversation? I understand that you might not have a copy of the results at home but his vet should be able to give you one which you could scan into your computer and give me the link or you can photograph the page(s) and upload the images by using the paperclip icon in the toolbar above your message box (if you can see such an icon) or by using an external app such as or Here's a synopsis of IBD/lymphangiectasia/PLE for you taken from Clinical Veterinary Advisor, 3rd Ed., Cote', 2015. Note the various treatment protocols:

Inflammatory Bowel Disease

 Basic Information


Common intestinal disease of dogs and cats. Characterized by chronic (>3 weeks) gastrointestinal (GI) signs of idiopathic origin, with inflammatory infiltration of small- and/or large-intestinal mucosa.


IBD. Depending on the infiltrating cell type: lymphocytic-plasmacytic, eosinophilic, suppurative, or granulomatous enteritis, colitis, or enterocolitis. Chronic enteropathy (CE).


Species, Age, Sex

Most prevalent among middle-aged and old dogs and cats but can affect patients of all age categories

Genetics and Breed Predisposition

A UK study showed that German shepherd dogs, Weimaraners, rottweilers, Border collies, and boxers are at high risk of developing IBD in that country. IBD with protein-losing enteropathy (PLE) occurs frequently in soft-coated wheaten terriers, Yorkshire terriers and other small breeds, rottweilers, and lunde­hunds. Granulomatous colitis affects boxers and French bulldogs.

Associated Disorders

  • Dog: severe IBD may cause PLE and/or intestinal lymphangiectasia.
  • Cat: “triaditis” with concurrent IBD, cholangiohepatitis, and pancreatitis; relatively common

Clinical Presentation

Disease Forms/Subtypes

Clinical signs vary depending on which segment of the intestine is involved. In cats, suspect concomitant small-intestinal involvement even in patients showing exclusively large-bowel signs.

History, Chief Complaint

  • Mild IBD may cause intermittent clinical signs, whereas severe IBD is characterized by progressive and severe clinical signs.
  • Dogs are presented for evaluation of chronic diarrhea, which can be of small- and/or large-bowel origin (see p. 1271).
    • Small-intestinal disease may be associated with decreased appetite, weight loss, vomiting, and lethargy.
    • Large-intestinal disease is usually limited to typical diarrhea; occasional vomiting may also occur.
  • Cats are usually presented for evaluation of chronic vomiting, which may or may not be associated with diarrhea. Inappetence/anorexia, weight loss, and lethargy are common.

Physical Exam Findings

Small-intestinal disease:

  • Poor body condition with poor haircoat is frequent with severe disease.
  • Dehydration is possible.
  • Thickened small-intestinal loops may occasionally be palpated.
  • Animals may occasionally show pain or discomfort on abdominal palpation.
  • Ascites, pleural effusion, and peripheral edema may occur in case of significant protein loss.

Large-intestinal disease:

  • Usually unremarkable; may be associated with abdominal discomfort in severe cases
  • Mucoid and/or bloody stool during rectal exam

Etiology and Pathophysiology

  • Abnormal interactions between intestinal microbiome and innate/adaptive immune systems
  • Breakdown of the intestinal mucosal barrier and exposure of lamina propria to luminal antigens, with subsequent uncontrolled immune response
  • Inflammation causes changes in the mucosal architecture and ultracellular structure of enterocytes, and ultimately abnormal function of the affected intestinal segment.
  • Protein loss reflects poor absorptive function or inflammatory exudation or ulceration.
  • In some instances, IBD is associated with the presence of mucosa-adhesive bacteria such as Escherichia coli (e.g., canine histiocytic ulcerative colitis, feline IBD).


Diagnostic Overview

The diagnosis of IBD is reached by exclusion.

Differential Diagnosis

General differentials

  • Chronic intestinal foreign body
  • Intestinal parasites: hookworms, whipworms, Giardia, Tritrichomonas (cat)
  • Chronic kidney disease
  • Chronic liver disease
  • Chronic pancreatitis
  • Endocrine diseases (hypoadrenocorticism [dog], hyperthyroidism [cat])
  • Cecal intussusception (dog, rare)

Differentials that may result in GI signs and histologic evidence of GI inflammation:

  • Adverse reactions to food (food intolerance, food allergy)
  • Intestinal dysbiosis/antibiotic-responsive diarrhea (dog)
  • Infiltrative intestinal neoplasia (alimentary lymphoma, particularly cat)
  • Fungal enterocolitis (e.g., Histoplasma)
  • Bacterial enterocolitis (e.g., in dogs, Campylobacter spp., C. perfringens, C. difficile)
  • Colitis associated with Pythium insidiosum infection
  • Granulomatous/histiocytic ulcerative colitis in boxer and other dogs

Differentials to consider for intestinal protein loss:

  • Intestinal lymphangiectasia (Yorkshire terrier, lundehund), histoplasmosis, alimentary lymphoma
  • Hepatic, renal, or dermal origin

Initial Database

  • Fecal parasitologic examinations to rule out nematodes, protozoa
  • Fecal Giardia antigen test to rule out giardiasis
  • In endemic areas for fungal diseases: rectal scraping (see p. 1222)
  • CBC, especially in dogs and cats with small-intestinal signs; useful to rule out differential diagnoses
  • Serum biochemistry: panhypoproteinemia may be associated with severe disease (dog), hypocalcemia reflects hypoalbuminemia and possibly malabsorption of fat-soluble vitamin D, concomitant liver disease (cat); useful to rule out differential diagnoses.
  • Serum thyroxine concentration (cat)
  • Consider ACTH stimulation test (dog).
  • Abdominal radiographs to rule out intestinal obstruction (e.g., in vomiting cats)
  • Abdominal ultrasound: may be normal or show focal or diffuse loss of intestinal wall layering, presence of mucosal striations or spicules, wall thickening, enlarged and/or hypoechoic mesenteric lymph nodes. Localization of lesions may help decide best approach for biopsies (endoscopy or celiotomy). Ultrasound-guided fine-needle aspiration of abnormal lymph nodes or intestinal wall can be useful to rule out neoplasia.
  • Serum trypsin-like immunoreactivity, cobalamin, and folate concentrations: recommended to identify concurrent pancreatic disease and cobalamin deficiency (especially in cats and in dogs with PLE)

Advanced or Confirmatory Testing

  • Upper and/or lower gastrointestinal endoscopy: assess mucosa, sample at least eight deep biopsies (ideally including upper submucosal layer) per anatomic site.
  • Celiotomy if lesions are inaccessible by endoscopy or if full-thickness biopsies are desirable (e.g., to rule out lymphoma in cats)
  • Histopathologic analysis: beware of inter-pathologist variability in interpretation; objective is to confirm and evaluate severity of mucosal lesions (inflammation, architecture) and to rule out neoplastic infiltration.


Treatment Overview

  • Dietary treatment with novel protein sources or hydrolyzed peptides is a key component.
  • Modification of the intestinal microbiome with antimicrobials may also be helpful.
  • Treatment of moderate to severe IBD most commonly centers on immune suppression with glucocorticoids. Other immune-suppressive drugs can be added as needed.
  • The goal of therapy is to control the clinical signs, as a cure may be unattainable.

Acute and Chronic Treatment

  • Supportive treatment as necessary if patient not stable (IV fluids, antiemetics, etc.)
  • Empirical deworming (e.g., with fenbendazole 50 mg/kg PO q 24h × 3 days)
  • Elimination diet: see Nutrition/Diet, below.
  • Antimicrobial treatment with metronidazole (10-15 mg/kg PO q 12h), tylosin (25 mg/kg PO q 12h), or tetracycline (20 mg/kg PO q 8h) for 2-6 weeks
  • In case of canine colitis (not granulomatous/histiocytic ulcerative colitis:
    • Sulfasalazine (10-30 mg/kg PO q 8h) for 2 weeks, then taper to same dose q 12h for 2 weeks, then half dose q 12h for 2 weeks, and so on. Alternatively, olsalazine (10-20 mg/kg PO q 12h). Monitor tear production (risk of keratoconjunctivitis sicca with sulfa drugs).
    • Consider adding soluble fiber (psyllium 1-2 teaspoons/10 kg body weight per meal).
  • In severe cases, in cases with PLE, or in cases in which the above approaches have failed, treatment with immune-suppressive doses of glucocorticoids is indicated:
    • Prednisone 2 mg/kg PO initially q 12h for a few days, then q 24h for 2-4 weeks. If remission of signs is achieved, decrease to 1 mg/kg PO q 24h, then 1 mg/kg q 48h, then decrease dosage by half every 2 weeks. Treatment and weaning period usually last for at least 8-12 weeks. Cats may respond better to prednisolone (up to 4 mg/kg PO q 24h in the initial 10- to 14-day phase).
    • Budesonide (dog, 3 mg/m2 PO q 24h [see p. 618 for body surface area conversion]; cat, 1 mg/cat PO q 24h) can be substituted for prednisone. Budesonide undergoes some first-pass hepatic metabolism, and low systemic drug concentrations may cause fewer side effects.
  • In glucocorticoid-refractory cases:
    • Cyclosporine A 5 mg/kg PO q 24h can be helpful (dog, cat); or
    • Dogs only: azathioprine 2 mg/kg PO q 24h for 2 weeks, then q 48h (can be decreased to 1 mg/kg q 48h), or
    • Chlorambucil: may be used as supplemental immune-suppressive therapy in dogs with associated PLE (4-6 mg/m2 PO q 24h for the first 7-21 days, then taper to q 48-72h), and in cats (2 mg/cat PO q 48h).
  • Supplement hypocobalaminemic patients with SQ vitamin B12 (see p. 202).
  • Dogs with PLE can be at increased risk for thromboembolism. Low-dose aspirin (0.5 mg/kg PO q 12h) may be used, although evidence confirming efficacy is lacking.
  • Gastroprotection with omeprazole (0.5-1 mg/kg PO q 24h) or famotidine (0.5 mg/kg PO q 12-24h) is recommended.
  • Probiotics may have beneficial effects, as recently documented using a multistrain preparation.

The ultimate goal is to wean the patient off immunosuppressive therapy. If this is not feasible, the goal becomes finding the lowest-dose regimen that will allow reasonable control of clinical signs.


  • An elimination diet with novel proteins (requires good nutritional history) or hydrolyzed peptides is recommended in most dogs and cats with IBD and is often successful as a sole treatment in mild cases.
  • Alternatively, an easily digestible diet with low fat content may be preferable in cases with severe IBD and PLE.

Possible Complications

  • High doses of glucocorticoids may cause multiple systemic side effects (e.g., polyuria/polydipsia, iatrogenic hyperadrenocorticism).
  • Side effects reported with cyclosporine use in dogs include decreased appetite and vomiting. Administering frozen capsules may help.
  • Azathioprine may cause bone marrow suppression, and has been associated with acute pancreatitis and hepatotoxicosis in dogs. Avoid use in patients with previous history of pancreatitis and liver disease. As with chlorambucil, regular monitoring of CBC is advised; additionally, monitoring of serum liver enzyme levels is recommended at the beginning of treatment.
  • Immunosuppressive medications predispose animals to secondary infections.
  • Metronidazole toxicosis may cause neurologic signs.

Recommended Monitoring

Regular evaluation of the body weight and overall clinical condition is essential to adapt treatment. Recheck abnormal parameters to evaluate treatment effect (e.g., serum albumin, cobalamin).

 Prognosis & Outcome

  • Short-term prognosis is usually good in mild to moderate cases of IBD.
  • In dogs, negative prognostic factors include hypoalbuminemia and hypocobalaminemia, as well as severe mucosal lesions in the duodenum (noticed during endoscopy).
  • Lack of response to glucocorticoid treatment is not uncommon in dogs with moderate to severe IBD.
    • Treatment failures may be due to incorrect diagnosis, severe disease, presence of concurrent disease, or poor owner compliance. In cats, lack of response to treatment should motivate the clinician to reconsider the possibility of alimentary lymphoma.

 Pearls & Considerations


IBD is a diagnosis of exclusion that requires a systematic approach. In mild cases, initiate dietary elimination trial in animals with chronic GI signs before starting glucocorticoid treatment. Additionally, in dogs, consider antimicrobial treatment. Severe cases require a more intensive approach.

Client Education

  • A realistic goal for treatment is to manage the intestinal disease. As a definitive cure may not be attainable, our goal is to control the clinical signs while limiting the side effects of therapy.
  • A pet's diet is of central importance for the treatment. Please make every effort to adhere closely to our dietary recommendations.

Please respond with further questions or concerns if you wish.