Chapter 1 Digestive Diseases final PDF

Chapter 1:PATHOLOGY OF DIGESTIVE SYSTEM Outlines I-Pathology of Mouth cavity II-Pathology of Esophagus III-Pathology of Stomach IV- Pathology of Intestines 1  I- Pathology Of Mouth Cavi...

Chapter 1:PATHOLOGY OF DIGESTIVE SYSTEM Outlines I-Pathology of Mouth cavity II-Pathology of Esophagus III-Pathology of Stomach IV- Pathology of Intestines 1  I- Pathology Of Mouth Cavity Stomatitis is the inflammation of mucosa of oral cavity (causes irritation, redness and swelling ). It includes: Gingivitis: Inflammation of gums. Glossitis: Inflammation of tongue. Cheilitis: Inflammation of lips. Tonsilitis: Inflammation of tonsil. Palatitis : Inflammation of palates. → Etiology : Trauma due to nails, wire, or any sharp object like needle. Physical due to hot milk Chemical : Alkali or acids and medicines Microorganisms : Bacteria, virus, fungi. 2  Macroscopic features Catarrhal stomatitis: Mucous exudation in oral cavity. Vesicular stomatitis: Vesicles in oral mucosal Erosive stomatitis: Erosions in oral mucosa Fibrinous stomatitis: False membrane in oral mucosa. Ulcerative stomatitis: Presence of ulcers in oral mucosa Vesicular stomatitis Erosive stomatitis 3  II-Diseases of the Esophagus 1. Cricopharyngeal Achalasia 2. Dilatation of the Esophagus 3. Esophageal Strictures 4. Esophagitis 5. Esophageal Diverticula 6. Hiatal Hernia 7. Esophageal Obstruction 4  1. Cricopharyngeal Achalasia Achalasia = “failure to relax” It is characterized by inadequate relaxation of the cricopharyngeal muscle, which leads to a relative inability to swallow food or liquids. It is seen primarily as a congenital defect but is occasionally seen in adult dogs. Associated with acquired neuromuscular disorders. Repeated attempts to swallow are followed by regurgitation. Aspiration pneumonia is a common complication : Stasis of food may produce inflammation and ulceration and there is danger of aspiration of esophageal contents into the lungs. 5  2. Dilatation of the Esophagus Megaesophagus = Dilatation of the esophagus, it stays enlarged and does not push the food down to the stomach → the food fails to enter the stomach and often stays in the esophagus, and is eventually regurgitated, or enters the lungs through breathing. Megaesophagus may be due to a congenital defect or may be an adult-onset, acquired disorder (an esophageal stricture, foreign body, neoplasia) Aspiration pneumonia is a complication with associated signs of cough, fever, and sometimes nasal discharge. 6  3.Esophageal Strictures Esophageal stricture is a pathologic narrowing of the lumen that may develop after anesthesia, trauma (foreign body), exposure to certain drugs, esophagitis, gastroesophageal reflux, vascular ring anomalies or tumor invasion. Most strictures develop in the thoracic portion of the esophagus. Clinical signs regurgitation, dysphagia, and pain. 7  4.Oesophagitis Oesophagitis is the inflammation of oesophagus and is characterized by catarrhal inflammation and ulceration. Etiology o Trauma due to foreign bodies. o Chemicals - drugs and gastroesophageal reflux o Infection - Spirocerca lupi, sarcosporidiosis o Nutritional- Vit. A deficiency. Regurgitation is the classic sign of esophagitis; others include ptyalism (Hypersalivation ), repeated swallowing attempts, pain, anorexia, dysphagia. 8  Gastroesophageal reflux : the backward movement of gastric contents into the esophagus, a condition that causes heartburn. Gastroesophageal reflux is usually associated with anesthesia and acute or chronic vomiting. Feeding tubes that traverse the gastroesophageal junction may result in gastroesophageal reflux. 9  5.Esophageal Diverticula Diverticula are pouch-like dilatations of the esophageal wall and may be congenital or acquired. Acquired diverticula are of two types: A- pulsion or B- traction. A- Pulsion diverticula are caused by increased intraluminal pressure or deep esophageal inflammation, which can lead to mucosal herniation. It involves the esophageal epithelium and connective tissue. Predisposing conditions include esophagitis, esophageal stricture, foreign bodies, vascular ring anomalies, megaesophagus, and hiatal hernia. 10  Esophageal Diverticula B-Traction diverticula result from inflammation in the chest cavity in close proximity to the esophagus. Fibrous tissue is produced, which then contracts, pulling the esophageal wall outward. This diverticulum involves all layers of the esophagus. Small diverticula may be subclinical. Large diverticula allow food to become trapped in the pouch, leading to postprandial dyspnea, regurgitation, and anorexia. 11  6.Hiatal Hernia Hiatal hernia is characterized by a protrusion or herniation of the stomach through the esophageal hiatus of the diaphragm. There are 2 types: axial or sliding, and nonaxial or paraesophageal. 12  Hiatal Hernia A-The sliding hiatal hernia is characterized by a bell-shaped protrusion of the stomach above the diaphragm 13  Hiatal Hernia B- In paraesophageal hiatal hernias, a separate portion of the stomach, usually along the fundus of the stomach, enters the thorax through a widened opening. The hernia progressively enlarges and increases in size. 14  7. Esophageal Obstruction In Large Animals: Esophageal obstruction (choke) occurs when the esophagus is obstructed by food or foreign objects. It is the most common esophageal disease in large animals. Esophageal obstruction can also occur after a general anesthesia. Horses most commonly obstruct on grain or hay. Cattle tend to obstruct on a single solid object: apples, potatoes, corn stalks. In horses, clinical signs associated with esophageal obstruction include nasal discharge of feed material or saliva, dysphagia, coughing, or ptyalism. 15  Esophageal Obstruction in small Animals Esophageal foreign bodies are more common in dogs than cats. Bones are the most common foreign body, but needles, wood, and dental chew may also become lodged in the esophagus. Objects usually lodge in the areas of the esophagus with the least distensibility: the thoracic inlet, over the heart base, or the caudal esophagus just cranial to the diaphragm. Ptyalism, dysphagia, regurgitation, and repeated attempts to swallow are signs of an esophageal foreign body. The signs depend on the location of the foreign body and on the degree and duration of obstruction. A partial obstruction may allow fluids but not food to pass. With a chronic obstruction, anorexia, weight loss, and lethargy are common 16  Pathology Of Digestive System Outlines Pathology of Mouth cavity Pathology of Esophagus Pathology of Stomach -Bloat in Ruminants (Ruminal tympany) -Gastritis -Gastric Dilation and Volvulus in Small Animals -Gastrointestinal Ulcers - Rumenitis and traumatic gastritis -Diseases of the Abomasum Pathology of Intestines 17  Bloat in Ruminants (Ruminal tympany) Tympany = Bloat : is an overdistention of the rumenoreticulum with the gases of fermentation, (CO2,H2S and CO) either – A primary or frothy bloat : persistent foam mixed with the ruminal contents – A secondary or free-gas bloat: free gas separated from the ingesta. It is predominantly a disorder of cattle but may also be seen in sheep. The susceptibility of individual cattle to bloat varies and is genetically determined. 18  Bloat in Ruminants (Ruminal Tympany) In primary ruminal tympany, or frothy bloat, the cause is entrapment of the normal gases of fermentation in a stable foam. Soluble leaf proteins and hemicelluloses (sudden change in animal feed with high content of legumes) are believed to be the primary foaming agents and form a monomolecular layer around gas rumen bubbles forming foams that is not easily removed. Several factors, both animal and plant, influence the formation of a stable foam. The major factor that determines if bloat will occur is the nature of the ruminal contents. Intraruminal pressure increases because eructation cannot occur. 19  Bloat in Ruminants (Ruminal tympany) In secondary ruminal tympany, or free-gas bloat, physical obstruction of eructation is caused by esophageal obstruction due to a foreign body (choke): Lesions of the wall of the reticulum may interrupt the normal reflex that is essential for escape of gas from the rumen. Ruminal tympany also can be secondary to the acute onset of ruminal atony that occurs in grain overload; this causes a reduction in rumen pH and possibly an esophagitis and rumenitis that can interfere with eructation. Bloat is a common cause of sudden death. 20  Lesions of Ruminal Tympany Distended rumen compresses the lungs, and intrabronchial hemorrhage may be present. The cervical esophagus is congested and hemorrhagic, but the thoracic portion of the esophagus is pale. The liver is pale due to expulsion of blood from the organ and rupture of the diaphragm. 21  Gastritis Gastritis is the inflammation of the stomach in non-ruminant animals. 22  Gastritis Irritation, infection, antigenic stimulation, or injury (chemical, erosion, ulceration) of the gastric mucosa stimulates the release of inflammatory and vasoactive mediators with subsequent disruption of gastric epithelial cells, increased gastric HCl secretion, and impaired gastric barrier function. Visceral receptors sensitive to gastric distention, gastric inflammation, and tonicity of gastric contents send impulses via vagal and sympathetic nerves to the vomiting center of the medulla oblongata, thereby stimulating the vomiting reflex. 23  Acute Gastritis Causes: include dietary intolerance (ingestion of contaminated foods), drug or toxin ingestion (antibiotics, NSAIDs, corticosteroids), systemic illness ( pancreatitis), endoparasitism (Physaloptera sp [dog], Ollulanus sp [cat]), or bacterial (Helicobacter pylori ) or viral (canine parvovirus gastroenteritis) infection. In acute gastritis, vomiting of sudden onset is presumed or confirmed to be secondary to inflammation of the gastric mucosa. The vomitus may contain bile, food, froth, blood or evidence of an ingested substance (eg, grass, bones, foreign material, etc). 24  Chronic Gastritis Chronic gastritis should be considered in animals with intermittent or persistent vomiting that lasts >7 days and that cannot be attributed to dietary intolerance; drug, toxin, or foreign body ingestion; systemic illness; endoparasitism; infection (bacterial or viral); or neoplasia. The most common clinical sign is intermittent vomiting of food or bile. Systemic illness, weight loss, and GI ulceration are infrequent and should raise suspicion of a more serious condition or diffuse GI inflammation (eg, inflammatory bowel disease) 25  Gastric Dilation and Volvulus in Small Animals Gastric Dilation and Volvulus (GDV) is an acute, life-threatening condition that primarily affects large- and giant-breed dogs (Bloat = stomach dilatation = gastric torsion). The exact causes of GDV are unknown. A variety of factors, including genetics, anatomy (Large and giant-breed dogs may be at higher risk), and environment are in suspect. No sex predisposition exists and dogs appear to be at increased risk with advancing age. Other reported predisposing factors include lean body condition, stress (delayed emptying of the GI), once daily feeding, dry food, rapid consumption of food, and increased gastric ligament laxity. 26  Gastric Dilation and Volvulus in Small Animals It is unclear whether dilation or volvulus (malrotation) occurs first during the development of GDV. Dilation of the stomach results from accumulation of gas and/or fluid, and volvulus prevents the normal release of these contents. During volvulus, the pylorus and duodenum first migrate ventrally and cranially. 27  The stomach may rotate from 90° to 360° in a clockwise fashion about the distal esophagus. This rotation displaces the pylorus entrapping the duodenum between the distal esophagus and the stomach. Depending on the degree of volvulus, the spleen may vary in position from the left caudodorsal to the right craniodorsal abdomen. A volvulus of >180° causes occlusion of the distal esophagus. 28  Gastric Dilation and Volvulus in Small Animals After volvulus of the stomach, gas is trapped within this compartment and intragastric pressure rises. Gastric outflow obstruction may be caused by compression of the duodenum by the distending stomach against the body wall. 29  Gastric Dilation and Volvulus in Small Animals The progressively distending stomach compromises venous return by compression of the caudal vena cava →GI tract ischemia, hypovolemia, and systemic hypotension. Dogs may present with a history of restlessness, hypersalivation, and faster breathing. Acute or progressive abdominal distention may be noted and unsuccessful trying to vomit. Progression from gastric dilation to volvulus predisposes to hypovolemic shock. Signs of shock are common and can include weak peripheral pulses, tachycardia, pale mucous membranes, and dyspnea. Additionally, the expanding stomach may compress the thoracic cavity and inhibit diaphragmatic movement, leading to respiratory distress. 30  Gastrointestinal Ulcers Ulceration or disruption of the GI mucosal barrier can be a consequence of several drugs and diseases. The gastric mucosal barrier is a complex defense mechanism that protects the normal mucosa from the harsh chemical environment of the gastric luminal contents. The acids, pepsin, and proteolytic enzymes normally present in the gastric lumen have a pH of 2. The mucous layer provides a weak buffer, maintaining a pH of 4–6 and neutralizing the acidic luminal contents. 31  Gastrointestinal Ulcers The GI barrier is maintained by a protective layer that includes: mucosal cells, tight junctions, elaboration of Prostaglandins and a thick layer of mucus. High blood flow to this area supports cellular metabolism and rapid renewal of injured cells. Tight junctions seal the cellular layers of the gastric mucosa, ensuring that the luminal contents do not leak into or around these cells. 32  Gastrointestinal Ulcers Prostaglandins help maintain the GI mucosal blood flow and integrity, increase secretion of mucus and bicarbonate, and decrease acid secretion 33  Gastrointestinal Ulcers A defect in the GI mucosal barrier leads to a self-perpetuating cycle of mucosal damage. Injury to this barrier allows HCl, acids, and proteolytic enzymes to degrade the epithelial cells, disrupt lipid membranes, and induce inflammation and apoptosis. Diffusion of luminal contents through the tight junctions leads to inflammation and hemorrhage of the GI cells, with further acid secretion mediated by inflammatory cells and their products. 34  Gastrointestinal Ulcers Mast cell degranulation occurs, causing histamine release that perpetuates further gastric acid secretion. The inflammatory environment also causes decreases in blood flow, ability for cellular repair, and secretion of mucus and cytoprotective prostaglandins. Mucosal ulceration can result, exposing the submucosa or deeper layers of the GI tissue to the luminal contents. 35  Gastrointestinal Ulcers NSAID administration, neoplasia, and hepatic disease are the most common causes in dogs. NSAIDs can cause direct topical damage to the GI mucosa and inhibition of COX-1→ decreases production of protective prostaglandins. The use of COX-2-specific NSAIDs is thought to decrease GI ulceration. Corticosteroids potentiate the effects of mucosal damage by decreasing cell mucus production and by stimulating acid production. Hepatic disease is associated with increased gastric acid secretion and alterations in mucosal blood flow, potentially leading to ulcer formation. Other drugs and diseases associated with GI ulceration in dogs include renal disease, stress, extreme exercise shock, and sepsis. Neoplasia (eg, lymphoma, adenocarcinoma) has been associated with GI 36 ulceration in cats, but the cause is often unknown.  Grain Overload in Ruminants (Lactic acidosis, Carbohydrate engorgement, Rumenitis) Grain overload is an acute disease of ruminants that is characterized by rumen hypomotility to atony, dehydration, acidemia, diarrhea, and in severe cases, death. Etiology and Pathogenesis The disease is most common in cattle that accidentally gain access to large quantities of readily digestible carbohydrates, particularly grain. Grain overload also is common in feedlot cattle when they are introduced to heavy grain diets too quickly. Less common causes include engorgement with apples, grapes, bread, dough, potatoes. The amount of feed required to produce acute illness depends on the kind of grain, previous experience of the animal with that grain, the nutritional status and condition of the animal, and the nature of the ruminal microflora. Adult cattle accustomed to heavy grain diets may consume 15–20 kg of grain and develop only moderate illness, while others may become acutely ill and die after eating 37 10 kg of grain.  Grain Overload in Ruminants Ingestion of toxic amounts of highly fermentable carbohydrates is followed within 2–6 hr by a change in the microbial population in the rumen. The number of gram-positive bacteria (Streptococcus bovis) increases markedly, which results in the production of large quantities of lactic acid. The rumen pH falls to ≤5, which destroys protozoa, cellulolytic organisms, and lactate-utilizing organisms, and impairs rumen motility. The low pH allows the lactobacilli sp. to utilize the carbohydrate and to produce excessive quantities of lactic acid Metabolic acidosis 38  Grain Overload in Ruminants The superimposition of lactic acid and its salts, L-lactate and D-lactate, on the existing solutes in the rumen liquid causes osmotic pressure to rise substantially, which results in the movement of excessive quantities of fluid into the rumen, causing dehydration. The low ruminal pH causes a chemical rumenitis, and the absorption of lactate results in lactic acidosis and acidemia. In addition to metabolic acidosis and dehydration, the pathophysiologic consequences are hemoconcentration, cardiovascular collapse, renal failure, muscular weakness, shock, and death Animals that survive may develop hepatic abscesses several weeks or months later. 39 40  Traumatic Reticuloperitonitis (Hardware disease, Traumatic gastritis) Traumatic reticuloperitonitis develops as a consequence of perforation of the reticulum. Cattle commonly ingest foreign objects because they do not discriminate against metal materials in feed and do not completely masticate feed before swallowing. The disease is common when hay are made from fields that contain old rusting fences or wire, or when pastures are on areas or sites where buildings have recently been constructed. 41  Traumatic Reticuloperitonitis Swallowed metallic objects fall directly into the reticulum or pass into the rumen and are carried over the ruminoreticular fold into the cranioventral part of the reticulum by ruminal contractions. 42  Traumatic Reticuloperitonitis Contractions of the reticulum promote penetration of the wall by the foreign object. Perforation of the wall of the reticulum allows leakage of ingesta and bacteria, which contaminates the peritoneal cavity. The resulting peritonitis is generally localized and frequently results in adhesions. The object can penetrate the diaphragm and enter the thoracic cavity (causing pleuritis) and the pericardial sac (causing pericarditis, sometimes followed by myocarditis). Occasionally, the liver or spleen may be pierced and become infected. 43 Clinical Findings The initial penetration of the reticulum is characterized by the sudden onset of ruminoreticular atony and a sharp fall in milk production. Fecal output is decreased. The rectal temperature is often mildly increased. The heart rate is normal or slightly increased, and respiration is usually shallow and rapid. Initially, the cow exhibits an arched back; an anxious expression; a difficulty to move and an uneasy, careful walk. 44  Diseases of the Abomasum Abomasal disorders include : – Left Displaced Abomasum (LDA) – Right Displaced Abomasum (RDA) – Abomasal Volvulus (AV) – Abomasal ulceration. 45  Left or Right Displaced Abomasum and Abomasal Volvulus Because the abomasum is suspended loosely by the greater omentum and lesser omentum, it can be moved from its normal position on the right ventral part of the abdomen to the left or right side over a relatively short period (LDA, RDA), AV can develop rapidly or slowly from an uncorrected RDA. 46  Diseases of the Abomasum A) Normal topography of left abdominal viscera, cow. B) Left displacement of abomasum 47  Left or Right Displaced Abomasum and Abomasal Volvulus The etiology is multifactorial, although abomasal hypomotility and dysfunction of the intrinsic nervous system are thought to play an important role in development of displacement or volvulus. Important contributing factors include : – Abomasal hypomotility associated with hypocalcemia and possibly hypokalemia. – Concurrent diseases (mastitis, metritis) associated with endotoxemia and decreased rumen fill. – Periparturient changes in the position of intra-abdominal organs – Genetic predisposition, particularly in deep-bodied cows. 48  Left or Right Displaced Abomasum and Abomasal Volvulus In LDA, as a result of abomasal hypomotility and gas production, the partially gas-distended abomasum becomes displaced upward along the left abdominal wall lateral to the rumen → Causes displacement of the pylorus and duodenum. The omasum, reticulum, and liver are also rotated to varying degrees. The abomasal obstruction is partial, and although the segment contains some gas and fluid, a certain amount can still escape, and the distention rarely becomes severe. Because there is minimal interference with blood supply unless the gas distention is marked, the effects of displacement are entirely due to interference with digestion and passage of ingesta, which lead to decreased appetite and dehydration. 49  Abomasal Ulcers The causes of abomasal ulceration are not well understood. Although abomasal ulcers can be seen any time during lactation, they are common in high-producing, mature dairy cows within the first 6 wk after parturition. The most likely cause is prolonged inappetence, which results in sustained periods of low abomasal pH → Ulcers. Abomasal ulcers may also arise in association with lymphosarcoma of the abomasum, abomasal disorders (displacement or volvulus), or increased luminal pressure causing ischemia of abomasal mucosa and the erosions of the abomasal mucosa that develop in viral diseases such as bovine viral diarrhea. 50  Abomasal Ulcers Clinical Findings The syndrome varies, depending on whether ulceration is complicated by hemorrhage or perforation and by the severity of such hemorrhage or peritonitis. A system of classification is based on the depth of penetration or the degree of hemorrhage or peritonitis caused by the ulcer: Type I is an erosion or ulcer without hemorrhage Type II is hemorrhagic Type III is perforated with acute localized peritonitis Type IV is perforated with acute diffuse peritonitis 51  Abomasal Ulcers Type V is perforated with peritonitis within the omental bursa. The omental bursa, also known as the lesser sac, is the cavity in the abdomen that is formed by the lesser and greater omentum 52  Chapter 3: PATHOLOGY OF DIGESTIVE SYSTEM Outlines Pathology of Mouth cavity Pathology of Esophagus and crop Pathology of Stomach Pathology of Intestines -Bovine Viral Diarrhea and Mucosal Disease Complex -Colic in Horses -Inflammatory Bowel Disease 53  Intestinal Diseases in Cattle Bovine Viral Diarrhea and Mucosal Disease Complex Bovine viral diarrhea (BVD) is most common in young cattle (6–24 mo old). The clinical presentation can range from inapparent or subclinical infection to acute and severe enteric disease to the highly fatal mucosal disease complex characterized by profuse enteritis in association with typical mucosal lesions. BVD produces diarrhea and mucosal lesions. Bovine viral diarrhea virus (BVDV), the causal agent of BVD and mucosal disease complex, is classified in the genus Pestivirus in the family Flaviviridae. 54  Intestinal Diseases in Cattle Clinical Findings and Lesions Acute clinical disease may range from mild disease of high morbidity and low mortality to severe enteric disease with considerable mortality. Biphasic fever (~ 40°C), decreased milk production, rapid respiration, excessive nasal secretion, excessive lacrimation, and diarrhea are typical signs of acute clinical BVD. Clinical signs of disease usually are seen 6–12 days after infection and last 1– 3 days. Transient leukopenia may be seen with onset of signs of disease. Gross lesions rarely are seen in cases of mild disease. Lymphoid tissue is a primary target for replication of BVDV, which may lead to immunosuppression and enhanced severity of infections. 55  Colic in Horses The term “colic” means abdominal pain. Throughout the years, it has become a broad term for a variety of conditions that cause a horse to exhibit clinical signs of abdominal pain. 56  Colic in Horses A diagnosis can be made and appropriate treatment begun only after determining which part of the intestinal tract is involved, and identifying the cause of the particular episode of colic. Colic develops for 1 of 4 reasons: 1) The wall of the intestine is stretched excessively by either gas, fluid, or ingesta. This stimulates the stretch-sensitive nerve endings located within the intestinal wall, and pain impulses are transmitted to the brain. 2) Pain develops due to excessive tension on the mesentery, as might occur with an intestinal displacement. 3) Ischemia develops, most often as a result of severe twisting of the intestine. 4) Inflammation develops and may involve either the entire intestinal wall (enteritis) or the covering of the intestine (peritonitis),erosion of the intestinal lining (ulceration), and “unexplained colic.” 57  Clinical Findings The most common include pawing repeatedly with a front foot, looking back at the flank region, curling the upper lip and arching the neck, repeatedly kicking at the abdomen, lying down, rolling from side to side, sweating, stretching out as if to urinate, distention of the abdomen, loss of appetite, and decreased number of bowel movements. It is uncommon for a horse with colic to exhibit all of these signs. Although they are reliable indicators of abdominal pain, the particular signs do not indicate which portion of the GI tract is involved. 58  Inflammatory Bowel Disease Inflammatory Bowel Disease (IBD) constitutes a group of GI diseases characterized by persistent clinical signs and histologic evidence of inflammatory cell infiltrate of unknown etiology. The various forms of IBD are classified by anatomic location and the predominant cell type involved. Disease is characterized by infiltration of the small and large intestine with inflammatory cells, including lymphocytes, plasma cells, macrophages, and eosinophils. This collection of diseases includes granulomatous enteritis (GE), lymphocytic- plasmacytic enterocolitis (LPE), multisystemic eosinophilic epitheliotropic disease (MEED), and idiopathic focal eosinophilic enterocolitis (IFEE). The inflammatory condition may be limited to only a short segment of the bowel 59 or be more diffuse.  Inflammatory Bowel Disease Several factors may be involved, such as GI lymphoid tissue (GALT); permeability defects; genetic, ischemic, biochemical disorders; infectious and parasitic agents; dietary allergens; and drug reactions. The intestinal mucosa has a barrier function and controls exposure of antigens to GALT. The latter can stimulate protective immune responses against pathogens, while remaining tolerant of harmless environmental antigens (eg, commensal bacteria, food). 60  Inflammatory Bowel Disease There is no apparent age, sex, or breed predisposition associated with IBD The mean age reported for development of clinical disease is 6.3 yr in dogs and 6.9 yr in cats. Lymphocytic-plasmacytic enteritis is the most common form in dogs and cats, followed by eosinophilic inflammation. Clinical signs are often chronic and sometimes cyclic or intermittent. Vomiting, diarrhea, changes in appetite, and weight loss may be seen. Pulmonary thrombo-embolism is a rare complication; however, it can occur if there is severe intestinal protein loss (loss of antithrombin III). 61  Inflammatory Bowel Disease Clinical signs of large-intestinal diarrhea, including anorexia and watery diarrhea, are not uncommon. Malabsorption and a protein-loss result. Inflammatory bowel disease should be considered in the differential diagnosis of horses with weight loss, recurrent colic, or hypoproteinemia, as well as in some horses with generalized skin disease. 62