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Canine Lymphocytic-Plasmacytic Gastroenteritis

Canine lymphocytic-plasmacytic gastroenteritis(LP) is one disease in a group of idiopathic, chronic intestinal diseases collectively termed inflammatory bowel disease (IBD), and is considered to be the most common cause of chronic vomiting and diarrhea in dogs.  LP gastroenteritis is characterized by a diffuse infiltration of lymnphocytes and plasma cells into the lamina propria of the stomach and/or the small intestine resulting in diffuse mucosal inflammation.  Lymphocytic-plasmacytic is the most prevalent form of IBD.  Other forms of IBD may be due to other cellular infiltrates (i.e. eosinophilic gastroenteritis, granulomatous enteritis, chronic histiocytic ulcerative colitis in Boxers).

  The definitive cause and pathogenesis of this disease remains unknown.  It is thought that an abnormal mucosal immune response to various environmental antigens, potentially dietary or parasitic in origin, results in a host hypersensitivity reaction that is  responsible for the recruitment of inflammatory cells.  Continued exposure to the antigen perpetuates the gastrointestinal inflammation.  Subsequent damage results from the elaboration of cytokines, release of proteolytic and  lysosomal enzymes, complement activation secondary to immune complex deposition, and the generation of oxygen free radicals.  Delayed gastric emptying can then occur secondary to the inflammation.  Hereditary factors may also influence the development of IBD.  Basenjis and Ludenhunds are known to have familial forms of IBD; German shepherd dogs and Shar-peis have been reported to be  predisposed to LP gastroenteritis specifically. Typically, middle aged to older dogs are affected and no sex predilections have been described.

  Chronic small bowel diarrhea is the most common clinical sign of lymphocytic-plasmacytic gastroenteritis.  If only the stomach is involved, vomiting might be the most common sign in dogs.  Initially, the chronic diarrhea and vomiting is intermittent, but eventually increases in frequency over time.  Additionally, weight loss with a waxing and waning appetite is usually reported.  On physical exam, poor BCS, dehydration, ascites, thickened bowel loops, fluid filled intestines, or abdominal pain may be noted.  Initial diagnostic  findings may include a neutrophilic leukocytosis with a left shift, microcytic anemia, hypoproteinemia,  hypoalbuminemia, and hypocholesterolemia. Additionally, extra-intestinal manifestations of IBD to be aware of include growth retardation, thrombo-embolic episodes, polyarthritis, nephrolithiasis, dermatologic disease, and immune-mediated anemia.
  The exclusion of diseases that mimic IBD along with histopathology is the primary way to diagnosis LP gastroenteritis.  A differential diagnosis list should include infectious diseases such as histoplasmosis Intestinal bacterial overgrowth, other infiltrative inflammatory bowel conditions (e.g. eosinophilic enteritis, granulomatous IBD), neoplastic  conditions (e.g. lymphoma), and other diseases such as lymphagiectasia, gastrointestinal motility disorders, and exocrine pancreatic insufficiency.  Additional diagnostic tests that should be performed to rule out these diseases may include urinalysis to rule out a renal cause for protein loss, zinc sulfate fecal flotation (Giardia sp.), fecal culture (Salmonella sp., Campylobacter sp, Clostridium sp.), folate/cobalamin assays (bacterial overgrowth), TLI or trypsin-like immuno-reactivity test (exocrine pancreatic insufficiency), abdominocentesis to classify any abdominal effusions (IBD typically  results in a pure transudate), and  diagnostic imaging including abdominal radiographs and ultrasound and/or contrast studies to help define the disease distribution.

  Following a diagnostic exclusion protocol, upper gastrointestinal endoscopy and biopsy is the diagnostic test of choice.  Studies indicate that increased granularity, increased friability, and erosions are the predominant mucosal lesions seen endoscopically.  Grossly, the stomach and intestine may also appear edematous, thickened, or completely normal.  Focal gastric ulceration alone is not frequently seen in dogs with LP gastroenteritis.  Some reports indicate that visible endoscopic lesions on the gut mucosa are present in only 50% of canine IBD cases.  Histologic findings reveal an infiltrate of lymphocytes and plasma cells in the lamina propria.  Less commonly, the cellular infiltrates may extend into the submucosa and muscularis tissue layers.  Villous clubbing, atrophy and fusion can be seen on biopsy in some severe cases.  The distribution may be irregular, so several biopsy specimens need to be collected.

  Even though endoscopic biopsies of the gastro-intestinal tract are less invasive with minimal  complications, limitations of this procedure include a requirement for expensive equipment and highly skilled personnel, the entire bowel is not accessible, and the small sample size can occasionally cause problematic diagnostic interpretations.  Since the diagnosis of IBD is subjectively based on the evaluation of the cellularity of the lamina propria, there can be considerable variability in biopsy interpretation.  This may be due to technical constraints of specimen size along with procurement and processing artifacts involved in collecting endoscopic samples.  Studies have shown that significant interobserver variation exists when  attempting to describe histopathologic lesions of intestinal biopsy specimens from dogs with and without inflammatory intestinal diseases.  The alternative to endoscopic biopsies is full thickness surgical biopsies of the gastrointestinal tract acquired through a laparotomy.  Large, full thickness biopsies obtained are reported to provide definitive histopathologic diagnosis more readily than endoscopic biopsies, especially to rule out gastrointestinal lymphoma.  Disadvantages of surgery in an IBD patient include increased morbidity and a necessary delay before initiating steroid therapy.

 Standardization of histopathologic descriptions of intestinal tissues that correlate with clinical signs would be ideal for clinicians attempting to diagnose lymphocytic-plasmacytic gastroenteritis.  However, unlike in human medicine, uniform and objective morphological criteria for IBD lesions have not been established.  Attempts have been made at creating a system of clinical indices to assess and classify mild, moderate, and severe cases of IBD in dogs.  Factors such as attitude/activity, appetite, vomiting, stool consistency, stool frequency, and weight loss have been used to correlate clinical signs with histologic lesions.  Through the development of a standardized scoring index, not  only can an accurate diagnosis be made histologically, but, by knowing the extent of the disease, the appropriate therapy can be correctly  instituted.

  Finally, if finances are a concern to the client, a hypoallergenic diet trial may be started first in order to rule in or out dietary allergy or intolerance.  Dietary management is the most important aspect of the treatment of LP gastroenteritis and it is sometimes  possible to control the disease with diet alone.  Therefore, if clinical signs resolve, no further work-up is necessary and dietary manipulations should not be overlooked as a diagnostic tool in some patients. Controlled diets are the most common dietary manipulation used for the treatment of IBD cases.  Prescription or homemade controlled diets include a highly digestible carbohydrate source, are gluten-free, low in lactose and fat, and contain a novel protein source. Prescription low residue diets with a hydrolyzed protein source may also be effective.  Additional aspects in the treatment of LP gastroenteritis may include providing immunosuppression using corticosteroids, azathioprine, budesonide, cyclophosphamide, or cyclosporine, treatment with immunomodulators and antibiotics such as metronidazole, tylosin, and salicylates, and empirical treatment with fenbendazole and cobalamin supplementation.

  There are several possible routes to reach a  diagnosis of lymphocytic-plasmacytic gastroenteritis, making it a challenge to quickly and accurately diagnose.  Once a diagnosis is established, the short term for prognosis is good for control, but poor for a cure.  Chronic therapy is usually indicated making owner compliance important.

-by Scott Trapp, Class of 2007
-edited by Dr. Robert Johnson, ADDL Graduate  Student


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  3.  German AJ, Hall EJ, Day MJ: 2003.  Chronic intestinal inflammation and intestinal disease in dogs. J Vet Intern Med 17:8-20.

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  6.  Jergens AE: 2004.  Clinical assessment of disease activity for canine inflammatory bowel disease.  J Am Anim Hosp Assoc 40: 437-445.

  7. Kleinschmidt S, Meneses F, Nolte I, Hewicker-Trautwein M: 2006.  Retrospective study on the diagnostic value of full-thickness biopsies from the stomach and intestines of dogs with chronic gastrointestinal disease symptoms.  Vet Pathol 43: 1000-1003.

  8. Rousseau M: 2005.  Severe lymphocytic-plasmacytic and atrophic gastritis, as well as predominantly eosinophilic, severe enteritis, in a 19-month old Labrador retriever.  Can Vet J 46: 264-267.

  9. Willard MD, Jergens AE, Duncan RB et al: 2002.  Interobserver variation among histopathologic evaluations of intestinal tissues from dogs and cats. JAVMA 220:1177-1182.




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