Inflammatory Bowel Disease

Introduction: Inflammatory bowel disease (IBD) is characterized by an infiltration of inflammatory cells in the intestinal lamina propria that results in recurrent GI signs such as diarrhea, vomiting, and weight loss. IBD is idiopathic and is a common cause of chronic diarrhea and vomiting in both dogs and cats. Clinical signs may vary depending on the severity of the inflammation and the location in the GI tract (large intestine or small intestine). The predominant inflammatory cell type present further classifies IBD. The three forms of IBD are lymphocytic-plasmacytic enteritis (LPE), eosinophilic enteritis, and granulomatous enteritis. LPE is the most common form in small animals. It is important to note that inflammation can occur secondarily to a number of intestinal diseases including infection with various pathogens, food allergy, and neoplasia, and must be differentiated from primary IBD.

Pathophysiology: IBD can cause both an exudative and malabsorptive diarrhea. However the exact etiology of IBD is unknown. It is most likely due to multifactorial mechanisms. Some of these mechanisms include:

genetic influence	Boxer’s with histiocytic ulcerative colitis or Basenji’s with immunoproliferative enteropathy
immunological mechanisms	possible food or chemical antigen stimulus or malfunctioning mucosal immune system
infectious agents	so far unidentified
environmental factors	stress

Whatever the underlying cause, inflammation is the source of the clinical signs seen with IBD. Release of inflammatory mediators by the infiltrating cells causes increased permeability of the intestinal mucosa, resulting in the loss of water and electrolytes into the lumen. If inflammation is severe, larger protein molecules may also be lost into the lumen, causing a protein losing enteropathy that results in weight loss and wasting. The physical presence of the infiltrating inflammatory cells in the lamina propria also interferes with absorption of nutrients. Villous atrophy may occur (stunted villi), which decreases the surface area of the intestinal mucosa, and further decreases the absorption of nutrients.

Figure: Small bowel malabsorption due to chronic mucosal inflammation and villous atrophy.

Signalment: Middle-aged dogs and cats. Some breeds may be more susceptible to LPE, including the Basenji, Chinese Shar-Pei, and German Shepherd. A similar disease process, equine granulomatous enteritis, occurs in horses.

Clinical signs: Signs are associated with lesion location along the GI tract, i.e. vomiting occurs when inflammation involves the proximal small intestine or stomach. Large bowel signs are present if the large intestine is affected.

Gross pathology: Intestinal mucosa may appear thickened or no obvious gross lesions are apparent. Hyperemia may be evident on endoscopy.

Histopathology: Cellular infiltrate in the lamina propria may be a predominance of lymphocytes and plasma cells (LPE), eosinophils (eosinophilic enteritis), or activated macrophages and/or multinucleated giant cells (granulomatous enteritis). Stunted villi (villous atrophy) may also be present. Lymphangiectasia and edema may occasionally be present. It may be difficult to differentiate LPE from diffuse intestinal lymphosarcoma in some cases.

Lymphoplasmacytic enteritis in a dog: Infiltration of the lamina propria with lymphocytes and plasma cells is accompanied in this case by blunting and fusion of villi. The epithelium is also hyperplastic.

Diagnosis: Clinical pathology for these cases is fairly non-specific and may show the following.

IBD can be diagnosed by biopsy after other conditions causing intestinal inflammation have been ruled out. Biopsies obtained by endoscopy are less invasive than those obtained by laparotomy, however, IBD may occur anywhere along the GI tract and endoscopy cannot access the jejunum and ileum.