Chapter 5B DIGESTIVE SYSTEM LOWER ALIMENTARY TRACT

5.1 TERMINAL OBJECTIVES

At the conclusion of this section, each student should be able to perform the following tasks.

5.3 GENERAL CONSIDERATIONS

The intestine plays an important role in the propulsion, secretion, digestion, absorption, storage and excretion of material. The small intestine consist of the duodenum, jejunum and ileum. The duodenum is the most critical site, in terms of the development of lesions, in the entire small intestine. This is true because it contains the common bile and pancreatic ducts as well as its proximity to other critical constituents of the digestive system such as the pancreas, liver, gallbladder and colon. There is no sharp line of demarcation between the jejunum and ileum. Customarily, the proximal two fifths is considered jejunum.

Histologic identification of the parts of the small intestine depends largely on the recognition of villi which are most numerous and prominent in the duodenum. These structures become progressively less well defined toward the terminal ileum. The surface covering of intestinal villi is made up of three types of cells. These are principally composed of absorptive cells interspersed with goblet cells and a few endocrine cells. These cells are fused together by "tight junctions" which maintain a virtually impermeable barrier between the luminal content and the subepithelial lamina propria. Thus, most molecules must pass through the surface mucosal cells (except for the smallest, such as sodium, chloride, water, etc.). The differentiated absorptive cells have finger-like microvilli along their luminal aspects which expands their surface 25 to 30 fold. Microvilli are covered by glycocalyx which is produced by absorptive cells. Injury to the microvillous structure may have serious absorptive consequences and give rise to malabsorption.

The intestinal crypts are lined by undifferentiated cells, paneth's cells, goblet cells and endocrine cells. The undifferentiated crypt epithelial cells are most numerous and they are the progenitors of the absorptive and other intestinal epithelial cells. These cells exhibit a high level of mitotic activity and migrate toward the intestinal surface as they mature. The undifferentiated crypt cells go through the entire process of cell division, migration and maturation in 2 to 6 days. This rapid renewal of surface epithelial cells provides a remarkable capacity for repair of intestinal injuries. On the other hand, this renders the small intestine particularly susceptible to agents that interfere with cell replication (radiation, etc.). The lamina propria in the small intestine contains phagocytic cells as well as lymphocytes and plasma cells. Immunoglobulins, particularly IgA, are synthesized by these plasma cells (secretory piece of IgA is added to the molecule during transit through undifferentiated crypt cells on its way to the lumen to participate in host defense).

Specific diseases that selectively affect absorptive epithelial cells of the small intestine include transmissible gastroenteritis of pigs, neonatal calf and pig diarrhea caused by rotavirus, epizootic diarrhea of infant mice, and lethal intestinal virus infection of mice. In swine dysentery (caused by Treponema hyodysenteriae) and in Shigella infections, the absorptive cells of the colon are much more susceptible to invasion by the causative agent than crypt cells. Also, some protozoa, such as coccidia, cause enteric disease by penetrating, multiplying, and destroying intestinal absorptive cells. The undifferentiated crypt epithelial cells are the target for destruction by the parvoviruses and intestinal radiation injury.

Remember, some intestinal diseases are characterized by destruction and loss of a specific cell type (as mentioned above), while others may affect several types of epithelial cells. Also, the early target cell may be rather selective, but as the lesion progresses there may be nonselective extension to all elements of the mucosa, submucosa, and tunica muscularis. Not all intestinal diseases are characterized by cell destruction, some are characterized by primary abnormalities of subcellular organelles (the affected target cells remaining viable). Furthermore, some diseases are characterized by profound functional alterations with little or no associated morphologic abnormalities.

DIARRHEA

is a common sign associated with diseases of the intestinal tract. It is characterized by the excretion of abnormally fluid feces , which is usually accompanied by increased volume and increased frequency of defecation. In addition to primary enteric diseases, diarrhea occurs in some primary gastric, pancreatic, and endocrine diseases. Mechanisms by which primary enteric diseases lead to diarrhea include:

• (1) malabsorption or malabsorption accompanied by bacterial fermentation, which in turn leads to osmotic diarrhea as in transmissible gastroenteritis of pigs,
• (2) hypersecretion by a structurally intact mucosa as in enteric colibacillosis and
• (3) exudation in diseases characterized by increased capillary and/or epithelial permeability such as salmonellosis. Remember, more than one mechanism may be involved in some diseases. The systemic consequences of diarrhea are dehydration, acidois, and electrolyte imbalance. 

5.4 THE INTESTINE 

5.4.1 INFLAMMATION OF THE INTESTINE:

The term enteritis refers to inflammation of any portion of the intestinal tract. However, the term is commonly used to refer to inflammation of the small intestine. Inflammation of the cecum, colon and rectum are more specifically referred to as typhlitis, colitis and proctitis, respectively. The term gastroenteritis refers to inflammation of the stomach and intestine. The causes of enteritis are numerous and may involve primary factors such as bacteria, virus, fungi, protozoa and helminths or more secondary predisposing factors i.e., immunoglobulin deficiency in the newborn, therapy with oral antibacterial agents and stress due to transportation. Clinically, diarrhea is the major manifestation. Remember,diarrhea may occur in the absence of a classical enteritis e.g., enteric colibacillosis. In addition, dehydration, abdominal pain, septicemia, toxemia and fever are clinical signs that may be observed in cases of enteritis. Enteritis may be classified as either primary or secondary or it may be referred to in a temporal sense as acute or chronic. All of the types of exudates that you studied in General Pathology may be found. Acute catarrhal enteritis is quite common and a variety of gross appearances may be observed. It is also often misdiagnosed. Physiologic hyperemia and postmortem maceration of the mucosa are commonly confused with acute catarrhal enteritis. Grossly, catarrhal enteritis is characterized by hyperemia of the mucosa, which may be mild enough to be overlooked or severe enough to confuse with hemorrhage. Although, in this condition there is usually no blood in the gut lumen. The mucosa is swollen due to exudation into the lamina propria. The wall is usually flaccid and the lumen may be dilated. The contents of the intestinal lumen will vary in appearance depending on the relative amounts of fluid, cells and mucus in the exudate. Microscopically, acute catarrhal enteritis is characterized by hyperemia, edema, infiltration of neutrophils and desquamation of epithelial cells. Chronic enteritis is characterized by thickening of the mucous membranes, increases in the quantity of connective tissue and by a marked increase in the secretion of mucus by goblet cells. Hemorrhagic enteritis is actually a more fulminant type of catarrhal enteritis, and it is common in a number of septicemic diseases caused by bacteria and viruses. Hemorrhagic enteritis is characterized by superficial extravasation of erythrocytes and staining of ingesta with blood. Fibrinous enteritis is characterized by an exudation of fibrin (croupous or diphtheritic forms may occur). The fibrin is deposited in strands or as thick yellowish membranes which may form "casts" in the lumen. 

Remember,

Villous absorptive epithelial cells are involved, directly or indirectly, in almost every type of enteritis. These cells are involved in absorption of fluids, electrolytes, monosaccharides, amino acids, and in the transport of fat. Absorptive cells are replaced every 2 to 4 days in most animals 3 weeks of age or older. However, their replacement time is 7 to 10 days in the newborn. This may explain the relatively greater susceptibility of the newborn to viral enteritides, such as TGE in piglets and rotavirus infection in all newborn farm animal species. Also, the constant migration and loss of absorptive cells require constant proliferation to produce new cells and this occurs in the crypts.

5.4.2 OBSTRUCTION OF THE INTESTINE:

Intestinal obstruction refers to the partial or complete occlusion of the lumen of the bowel. The result is interference with peristaltic contractions and the passage of intestinal contents. Important causes of intestinal obstruction are: stricture (congenital or acquired), obturation (from within), compression (from outside), volvulus, torsion, intussusception, hernias, embolism and thrombosis. 

A strangulated obstruction (occlusion of blood vessels as well as the intestine) always leads to catastrophic consequences. There is congestion, hemorrhage into the gut lumen, necrosis and gangrene of the affected segment. The infarcted gangrenous intestinal wall is readily permeable to putrefactive bacterial and their products and the near by peritoneum provides an excellent absorptive surface for these toxic products. Death is usually due to the combined effects of blood loss into the gut lumen and toxemia. Death in these instances occurs very rapidly. A simple obstruction (occlusion of an intestinal segment in the absence of vascular occlusion) may cause varying clinical and pathologic effects. In general however, the higher the obstruction (duodenum, etc.), the more acute the clinical signs are and the more rapid the course becomes. In other words, obstructions in the upper portion of the intestine (including the pyloric portion of the stomach) is likely to be acute and very serious, whereas the large intestine is more capable of supporting a chronic obstruction. 

5.4.3 SIMPLE ACUTE UPPER INTESTINAL OBSTRUCTIONS

Result in local as well as systemic disturbances. The large volume of fluid normally produced in the upper alimentary tract and its accompanying electrolytes are prevented from reaching the absorptive surfaces of the lower intestine. Thus, these fluids and electrolytes are largely lost to the body by vomition and hydration cannot be maintained. Significant changes in the blood include hemoconcentration, loss of electrolytes, alkalosis and uremia. Hemoconcentration develops subsequent to reduced plasma volume. The changes in electrolyte balance primarily affect chloride, sodium, and potassium. During vomition, the effect is usually more pronounced on chloride than it is on sodium. This favors the development of metabolic alkalosis. The uremia is due primarily to reduced renal blood flow and glomerular filtration. Immediately following an acute upper intestinal obstruction, there is increased peristalsis both proximal and distal to the point of obstruction. This is responsible for the early episodes of acute pain. Shortly thereafter, reverse peristalsis arises above the point of obstruction. Also, the segment of intestine anterior to the point of obstruction becomes distended with fluid and gas. Death is due to fluid and electrolyte loss. 

5.4.4 SIMPLE ACUTE OBSTRUCTION OF THE LOWER INTESTINE

(Distal jejunum, ileum, cecum, and upper colon) generally results in less fluid and electrolyte loss than an upper intestinal obstruction since more absorptive surface is available. However, as gas and fluid pressures build up anterior to the obstruction, there is increased permeability of the intestinal mucosa and bacterial toxins readily escape from the damaged bowel and enter the bloodstream. In this instance, death is largely a result of toxemia. 

5.4.5 SIMPLE ACUTE OBSTRUCTION OF THE LOWER COLON AND RECTUM

May allow the animal to survive for a considerable period of time because sufficient absorption of fluids may take place in the anterior colon to prevent the damaging distention. In such cases, death is due primarily to starvation. Remember, when strangulation occurs, there is initially venous obstruction with development of a hemorrhagic infarct. However, arterial occlusion only occurs if the strangulation is severe. 

5.4.6 SIMPLE CHRONIC INTESTINAL OBSTRUCTIONS

Are seldom encountered. However, they are more likely to occur in the large than in the small intestine. Proximal to the chronic obstruction, hypertrophy of the bowel wall and ulcerations are likely to occur. 

5.4.7 INTESTINAL OBSTRUCTION DUE TO STENOSIS AND OBTURATION:

Stenosis of the intestinal lumen may be associated with a chronic inflammatory process (scar tissue), neoplasm, abscess, etc. Stenosis usually develops slowly with a course like that described for simple chronic obstructions. In swine, functional stricture of the rectum in the absence of organic causes may occur. It has been suggested that these strictures may be hereditary or congenital. All kinds of foreign bodies (sand, grass, strings, enteroliths, etc.) may be found in the intestinal tract of animals. Small rounded foreign bodies may pass through the intestinal tract without causing problems, but sharp pointed objects may perforate the intestinal wall and result in a peritonitis. Compression of the intestinal wall from outside is commonly caused by neoplasms, chronic inflammatory processes, abscesses and adhesions. 

5.4.8 INTESTINAL OBSTRUCTION DUE TO VOLVULUS:

The rotation of a loop of intestine around its mesenteric base of attachment is referred to as volvulus. The twist is usually more than 180 degrees which results in acute intestinal obstruction and strangulation. Thus, severe congestion, hemorrhage and gangrene develop rapidly. In most cases, the twist involves most of the freely suspended mesenteric intestine sparing only a portion of the duodenum and terminal ileum. Volvulus is most common in young ruminants and swine. It occurs less frequently in adult horses and swine. Adult ruminants and carnivores are virtually exempt from this phenomenon. Clinically, the condition is manifested by severe abdominal pain. At necropsy, the affected loops of intestine are dark red, the veins are engorged and the intestinal wall and mesentery are edematous. The intestinal lumen contains gas and considerable quantities of blood. If the animal lives long enough, the infarction gives way to gangrene and perforation. Subsequently, peritonitis develops. Death usually occurs within 6-12 hours. 

5.49 INTESTINAL OBSTRUCTION DUE TO TORSION:

The rotation of a segment of intestine on its long axis is referred to as torsion. Such a twist results in acute intestinal obstruction and strangulation. Therefore, the same clinical and pathological alterations described for volvulus (severe abdominal pain, congestion, hemorrhage, gangrene, etc.) are expected. Torsion is most commonly reported in horses, cattle and swine. In the horse, torsion of the left colon occurs frequently. The left dorsal colon is usually twisted because of its relative mobility. The left dorsal colon can rotate medially or laterally down over the ventral colon which lies immediately below it. The twist occurs at the level of the transverse flexure. A rotation through 180 degrees results in intestinal occlusion and strangulation; death usually occurs within 12 hours after the onset of clinical signs. Torsion of the cecum occurs rather commonly in cattle, but rarely in horses and swine. The twist occurs at the base of the cecum and encroaches upon the terminal ileum and coiled colon.

NOTE: The terms volvulus and torsion are used as synonyms by many authors. 

5.4.10 INTESTINAL OBSTRUCTION DUE TO INTUSSUSCEPTION:

In an intussusception, a segment of the intestine is forced inside the segment just posterior to it. The condition occurs in all animal species, but is more common in dogs, young horses, adult cattle and lambs. Intussusception is most common in the jejunum, proximal ileum and at the ileocecal junction. The causes are not clear cut, but this malposition tends to accompany enteritis and/or increased peristalsis. There is interference with venous drainage and or arterial blood flow to the affected part resulting in congestion, hemorrhage and gangrene. The amount of telescoped intestine is limited by the mesenteric attachment of the affected segment. In dogs and cats, 5 to 10 cm of the intestine may be involved, whereas in large animals, 20 to 30 cm may be telescoped.

• -- An intussusception is believed to develop subsequent to constriction of the circular muscular layer and contraction of the longitudinal muscular layer of the intestine just posterior to the constricted circular muscular layer. As a result, the anterior segment of the intestine is reduced in diameter. However, the posterior segment is shortened but not reduced in diameter. Thus, it is possible for the constricted segment of the gut to move into the lumen of the posterior segment. This occurs because contraction of the posterior segment pulls the constricted segment into its lumen.

Remember,

once an intussusception starts, it has a tendency to increase in severity rather than correct itself. Agonal intussusceptions are readily recognized by the ease with which they can be reduced and the absence of inflammation.

5.4.11 INTESTINAL OBSTRUCTION DUE TO THROMBOEMBOLISM:

The mesenteric veins may be occluded by thrombi and the arteries may be occluded by thrombi or emboli. All animal species may be affected. Occlusion of the mesenteric vessels that results in severe intestinal injury (infarction, etc.) will lead to partial or complete paralytic obstruction of the affected intestine. Verminous thromboarteritis of the anterior mesenteric artery due to Strongylus vulgaris larvae occurs with frequency in horses (please refer to the cardiovascular system section). Large and fatal intestinal infarcts develop when portions of the main thrombus detach and occlude a large branch of anterior mesenteric artery. An infarcted segment of the intestine becomes congested, hemorrhagic, edematous and gangrenous. 

5.4.12 INTESTINAL OBSTRUCTION ASSOCIATED WITH HERNIATION:

The term hernia refers to the protrusion of an organ or tissue through a natural or artificial body opening with the organ being covered by skin, etc. An external hernia refers to displacement of an organ outside the body cavity but with the displaced portion contained within a hernial sac. Such a hernia typically consists of a hernial sac, hernial ring and the hernial contents. An internal hernia refers to the displacement of an organ through normal or pathological openings within a cavity without the formation of a hernial sac. The intestine is oftentimes included as a portion of the hernial contents. If a segment of the intestine becomes strangulated or incarcerated, serious consequences may occur, including intestinal obstruction. However, as long as the hernial contents remain freely movable and the hernia is reducible, there may be no serious consequences. The following are the important types of hernias:

5.4.12.1 ABDOMINAL OR VENTRAL HERNIA

Occurs when there is a tear in the abdominal wall that allows the escape of the intestine from the confinement of the normal wall. An outpouching is visible grossly.

5.4.12.2 UMBILICAL HERNIA

Occurs when there is failure of the umbilical ring to close after birth. The condition is seen with frequency in pigs, calves, colts and dogs.

5.4.12.3 INGUINAL HERNIA

Occurs at the internal inguinal ring. The viscera (usually a loop of the intestine) remains in the inguinal canal. Among females of all species, this condition occurs only in the bitch. The bitch has an internal inguinal ring and a small inguinal canal.

5.4.12.4 SCROTAL HERNIA

Occurs when a loop of intestine passes through the inguinal canal into the scrotum. This occurs frequently in stallions on the right side. It is common in swine on both sides.

5.4.12.5 FEMORAL HERNIA

occurs when a loop of intestine escapes through the femoral ring (site where vessels pass through).

5.4.12.6 PERINEAL HERNIA

Occurs when the contents of the abdominal cavity passes back through the weakened pelvic structures and eventually migrate through the pelvic canal. It appear as a large, soft bulge under the skin around the anus or vulva. This condition is commonly observed in old dogs of both sexes. The intestine, urinary bladder or uterus may be herniated

5.4.12.7 DIAPHRAGMATIC HERNIA (RUPTURE)

occurs when there is a tear in the diaphragm that allows abdominal visceral organs to enter the thoracic cavity. This condition may be congenital or acquired. When abdominal organs herniate into the thoracic cavity (usually the intestine, stomach or one or more lobes of the liver) the animal becomes uncomfortable, is reluctant to lie down, its respiration is increased and there is some interference with the passage of ingesta through the intestine. If the condition is severe, death occurs.

5.4.12.8 OMENTAL HERNIA

Occurs when a loop of the intestine passes through a tear in the omentum. This condition is most common in horses.

5.4.13 THE EPIPLOIC FORAMEN

is a site where hernias (which contain a loop of gut) occur occasionally. The epiploic foramen is a small opening that lies above the liver and forms the communication between the two peritoneal sacs. Its dorsal wall is formed by the vena cava and the ventral wall is formed by the portal vein. 

5.4.14 ULCERATION OF THE INTESTINE:

Ulcers in the intestinal tract may be associated with infectious, toxic or mechanical factors. They are usually irregular in shape and may be single or multiple. Microscopically, ulcers extend into the submucosa but rarely beyond. They are associated with edema, arteritis and infiltration of inflammatory cells which are primarily neutrophils, but mononuclear cells and eosinophils are also present. Hyperplasia of the submucosal lymphoid follicles may be prominent. In some instances, ulcers may perforate leading to the escape of ingesta into the peritoneal cavity and subsequently peritonitis.

In dogs, duodenal ulcers and/or erosions have been associated with uremia, neoplasia and cirrhosis of the liver. It has been suggested that hypersecretion of gastric acid may play an etiologic role.

Remember,

Intestinal ulcers occur in several of the specific erosive diseases, i.e., bovine virus diarrhea, etc.

5.4.15 CONGENITAL ANOMALIES OF THE INTESTINAL TRACT:

The most frequently reported congenital anomalies of the intestinal tract are those associated with agenesis, atresia and hypoplasia. Atresia occurs most commonly in calves and pigs, where either the anus, rectum, or colon may be involved.

• -- Atresia ani simplex occurs when the anal membrane fails to perforate or disappear. Thus, the exterior opening of the intestinal tract is effectively closed. Affected animals usually die at 7 to 10 days of age if the condition is not surgically corrected. The intestine becomes grossly distended and the abdomen is swollen. Evidence suggests that atresia ani is inherited in Yorkshire swine.
• -- Atresia ani et recti refers to congenital closure of both the anus and rectum. Thus, during fetal development, the lumen of the posterior segment of the rectum as well as the anal opening fail to develop. Consequently, the closed segment of the intestine extends deeper into the body than in atresia ani simplex.
• -- Atresia recti simplex refers to the condition in which the lumen of the rectum failed to develop, but the anal opening is normal.
• There may be malformation of the genitourinary tract associated with anomalies of the colon and rectum. For example, the terminal portion of the intestine may empty into the vagina or urinary bladder.

5.4.16  MECKELS' DIVERTICULUM

Refers to a remnant of the omphalomesenteric duct. This duct is a fetal structure commonly known as the yolk stalk. In mammals, the omphalomesenteric duct atrophies and disappears soon after birth. If it persists, it is referred to as Meckel's diverticulum. The condition is reported most commonly in pigs and foals. Remnants of the yolk stalk are common in baby chicks. 

5.4.17 NEOPLASMS OF THE INTESTINE:

Primary neoplasms of the intestine are rare; however, they may arise from any of the tissue components of the intestine. The malignant lymphoma is the most commonly reported metastatic neoplasm. 

5.4.18 EMPHYSEMA OF THE INTESTINE

Intestinal emphysema is characterized by the presence of numerous small air-filled vesicles in the serosa, submucosa and mucosa of the small intestine and in the mesentery and mesenteric lymph nodes. Microscopically, the gas bubbles occupy lymphatics. The air (gas) is probably derived from the lungs via interstitial leakage. Intestinal emphysema is occasionally seen in healthy swine at slaughter. 

5.4.19 LIPOFUSCINOSIS OF THE INTESTINE (BROWN DOG GUT):

Intestinal lipofuscinosis is characterized by the accumulation of a pigment (which is similar or identical to "ceroid") in smooth muscle cells. In heavy concentrations, this pigment will impart a visible brown color to the intestine. The pigment is sometimes referred to as "leimyometoplasts." The condition can be experimentally induced by causing vitamin E deficiency. 

5.5 SPECIFIC DISEASES OF THE INTESTINAL TRACT

5.5.1 COLIBACILLOSIS

Is one of the most common diseases of newborn farm animals. It is caused by pathogenic strains of Escherichia coli. There are two different patterns of the disease:

• (1) enteric colibacillosis which is manifested primarily by varying degrees of diarrhea and
• (2) septicemic colibacillosis which is manifested by septicemia and rapid death.

Certain serotypes of E. coli are associated with the development of diarrhea and other serotypes are responsible for septicemia. Factors which influence the development of colibacillosis include insufficient colostrum at birth, inclement weather, hygiene practices, etc. The immune status of the animal is considered to be the most important predisposing factor.

5.5.2 ENTERIC COLIBACILLOSIS

Results from strains of E. coli that possess the ability to colonize and proliferate in the upper-part of the small intestine. In these situations, enterotoxins are produced. The enterotoxins result in net secretion of fluid and electrolytes from the systemic circulation into the lumen of the intestine. This results in varying degrees of dehydration, diarrhea, electrolyte imbalances and acidosis. When acidosis is severe, circulatory failure, shock and death occurs.

Enterotoxins of E. coli stimulate adenyl cyclase activity in the intestinal mucosa which leads to increased cyclic AMP. Cyclic AMP is thought to increase intestinal fluid secretion.

Grossly, the intestinal tract is distended with yellowish watery ingesta and gas. In uncomplicated cases, there are no significant gross lesions. Microscopically, no significant lesions are usually present. However, in prolonged cases in pigs, villous atrophy (similar to that described for transmissible gastroenteritis) has been described. A definitive diagnosis is dependent on laboratory isolation of the causative agent.

5.5.3 SEPTICEMIC COLIBACILLOSIS

Results from stains of E. coli that invade the systemic circulation (usually via the portal system of the intestine). Animals deficient in immunoglobulins are most susceptible to septicemic colibacillosis. Clinical signs and lesions are attributed to the effects of endotoxin which causes shock. Grossly, no lesions are observed in peracute cases. In more prolonged cases, serosal petechial hemorrhages may be observed. A diagnosis usually depends upon isolation of the causative organisms from abdominal viscera or heart blood. Animals which recover from the septicemic phase may develop lesions due to E. coli localization in various organs and tissues (arthritis, meningitis, etc.).

Remember,

Diarrhea in calves under 2 weeks of age is a major cause of economic loss in cattle herds. In addition to E. coli. several viral agents have been incriminated as important primary causes of acute diarrhea in calves. Rotavirus (reovirus-like agent) and a coronavirus-like agent are considered to be the most important. Grossly, no significant lesions are observed in calves affected with these viruses. Microscopically, there is shortening of the intestinal villi. The rotavirus produces changes in the small intestine, while the coronavirus-like agent produces changes in both the small and large intestine.

5.5.4 TRANSMISSIBLE GASTROENTERITIS OF SWINE:

Transmissible gastro-enteritis of swine (TGE) is a contagious viral disease characterized by profuse diarrhea and vomiting. All age groups are susceptible, but there is a very high morbidity and mortality in pigs infected during the first 2 weeks of life. In older swine, mortality is low, but morbidity may be high. The incubation period is from 4 hours to 4 days and most deaths occur 2 to 6 days after onset. Death is unusual in pigs over 4 to 5 weeks of age. The characteristic lesions are loss of intestinal epithelial cells and extreme shortening of the intestinal villi (which are best seen in the distal ileum). A diagnosis of TGE can be confirmed on fluorescent antibody tests. The disease is caused by a coronavirus that grows within and destroys absorptive epithelial cells. The virus does not affect crypt cells or the lamina propria directly. As the virus disappears, the crypt cells rebuild the villi in a matter of days. The lesions are rapidly and completely reversible. The functional defect in TGE is malabsorption because of reduced villous surface area and decreased numbers of absorptive cells. Ingesta and normal intestinal secretions are unabsorbed. Therefore, they undergo bacterial degradation and fermentation within the lumen of the intestinal tract. This degradation and fermentation increases the osmolarity of the intestinal contents and fluid is drawn into the gut lumen by the resultant osmotic gradient. Absorptive cells of the large intestine are not affected by the TGE virus. However, thee absorptive capacity of the large gut is exceeded and diarrhea results.

Gross lesions are minimal or absent; the intestinal wall is usually thin and transparent. The lumen is distended with fluid ingesta. Microscopically, shortening of the intestinal villi is the most prominent lesion. The marked reduction in villous size can be detected at low magnification using a stereomicroscope.

5.5.5 INFECTIOUS FELINE ENTERITIS (PANLEUKOPENIA):

Infectious feline enteritis or feline panleukopenia is a highly contagious parvovirus infection of cats. It is characterized by sudden onset, fever, severe panleukopenia, enteritis and high mortality. The virus attacks all members of the cat family (felidae) as well as the raccoon, coati mundi and kinkajou. Significant clinical signs include fever, anorexia, vomition, weakness, depression, diarrhea, dehydration and decreased circulating leukocytes. The virus tends to attack rapidly proliferating and undifferentiated cells. In the intestinal tract, the target cells for infection and destruction by the parvovirus of panleukopenia are rapidly proliferating crypt cells. Villous absorptive cells are not attacked. However, these cells are not replaced by crypt cells as they are sloughed from the tips of villi. Eventually, diarrhea is manifested due to a lack of absorptive cells (remember, radiation destroys rapidly proliferating and undifferentiated cells in a manner similar to the panleukopenia virus). Significant gross lesions consist of lymphoid hyperplasia and edema followed by necrosis. The bone marrow of long bones becomes semifluid and may appear fatty. There is a hemorrhagic and fibrinous enteritis which involves the ileum most extensively. Microscopically, there is hyperplasia of reticuloendothelial elements of lymph nodes followed by lymphoid necrosis. The villous epithelial cells are eroded and the intestinal crypts are dilated and filled with debris. Intranuclear inclusion bodies are found occasionally in intestinal epithelial cells and in cells of lymph nodes. There is a marked decrease or depletion of bone marrow myeloid elements. In germ-free cats, the enteric lesions of panleukopenia do not develop.

5.5.6 SALMONELLOSIS:

Salmonellosis is caused by many species of salmonellae and occurs in all animal species. The disease is manifested by four major syndromes:

• (1) peracute septicemia,
• (2) acute enteritis,
• (3) chronic enteritis and
• (4) asymptomatic carriers.

The species of salmonellae which commonly cause disease in mammals are S. typhimurium and S. dublin in cattle, S. cholerasuis and S. typhimurium in swine and S. typhimurium in horses. Ingestion is the principal means of infection.

5.5.6.1 PERACUTE SEPTICEMIC FORM OF SALMONELLOSIS

Occurs primarily in young calves, foals and pigs (from birth up to 4 months of age). There is depression, dullness and high fever. Death occurs within 24 to 48 hours. Grossly, there may be an absence of lesions, or petechial hemorrhages may be observed in various tissues.

5.5.6.2 ACUTE ENTERIC FORM OF SALMONELLOSIS

is common in adult animals of all species. Clinically, a watery diarrhea is the most prominent sign. Grossly, inflammation that varies from a catarrhal enteritis to a severe hemorrhagic enteritis may be present in the small and large intestine. Mesenteric lymph nodes are enlarged, edematous and hemorrhagic. The gallbladder wall may be thickened and inflamed.

5.5.6.3 CHRONIC FORM OF SALMONELLOSIS

Is common in pigs and occurs occasionally in cattle. Clinically, there is persistent diarrhea, severe emaciation and intermittent fever. The feces may contain spots of blood or fibrinous casts. The chronic form is often preceded by an attack of the acute enteric form. In swine, enteric salmonellosis (fibrinous enteritis, necrotic enteritis, fibrinonecrotic enteritis, "necro") is usually chronic and characterized by thick, rough, brownish or grayish diphtheritic fibrinous exudate in the ileum, cecum and colon. In some cases, well defined "button ulcers" are present. Salmonella choleraesuis and Fusobacterium necrophorum are usually recovered from affected portions of the intestine. Poor sanitation and a deficiency of nicotinic acid are predisposing factors. Initially, salmonella organisms attack and destroy villous absorptive cells but they rapidly move deep into the mucosa.

Remember,

salmonella organisms frequently localize in the gallbladder and mesenteric lymph nodes and survivors intermittently shed organisms into the intestine and thus into the feces. In cattle, the chronic form is usually manifested by discrete areas of necrosis in the wall of the cecum and colon. The wall is thickened and covered by a yellowish-grey fibrinous exudate.

In septicemic and acute enteric forms, salmonella are present in heart blood, spleen, bile, mesenteric lymph nodes and intestinal contents. In the chronic form, the bacteria may be isolated from intestinal lesions, but seldom from other tissues.

5.5.7SWINE DYSENTERY:

Swine dysentery is an acute infectious disease of young pigs, characterized by bloody diarrhea. Treponema hyodysenteriae (a spirochete) is considered to be the primary etiologic agent. However, anaerobic bacteria which are normally found in the colon of pigs are necessary in order for Treponemia hyodysenteriae to produce the disease in gnotobiotic pigs. The characteristic lesion is a hemorrhagic typhilitis and colitis. In some cases, the terminal ileum may be involved. In later stages, the mucosa may be covered by thick fibrinous pseudomembranes. Diagnosis can be confirmed by fluorescent antibody tests.

5.5.8 ENTEROTOXEMIA (COLOSTRIDIUM PERFRINGENS INFECTION)

Clostridium perfringes is widely distributed in the soil and in the gastrointestinal tract of animals. This organism produces potent endotoxins (types A, B, C and D) . Clostridium perfringes type B is the cause of lamb dysentery and a similar disease in calves and foals. Clostridium perfringes type D may cause severe enterotoxemia in lambs and calves. The disease is often peracute and affected animals are found dead without having exhibited any signs. In adult sheep, the lesions are the same as in the lambs, but they are more constant and more developed. Clostridium perfringes type C causes a highly fatal intoxication characterized by hemorrhagic enteritis in calves, lambs and piglets under two weeks of age. The clinical course varies from 2 to 24 hours.

In the early stages of Clostridium perfringens infection, the causative agent adheres to absorptive cells in the small intestine and the toxins cause necrosis of these cells. As the disease progresses, the necrotic process extends non-selectively to involve all elements of the lamina propria, crypt epithelium, submucosa and even the muscular layers.

In sheep that survive the acute form of enterotoxemia, type D brain lesions may occur. The lesions are of two basic morphologic patterns. Both of these types are bilaterally symmetrical. The more common pattern is hemorrhage and softening in the basal ganglia, internal capsule, dorsal lateral thalamus and substantia nigra. The second pattern is characterized by lysis and liquefaction of the white matter of the frontal gyri sparing only the communicating "U" fibers. The gray matter overlying the affected areas is edematous.

Remember,

Clostridium perfringens type D is an important disease of sheep (especially lambs). The disease may also occur in calves. In most cases, the disease is peracute in lambs and calves; i.e., animals are found dead without signs having been observed. Diarrhea may be observed in animals that survive for 1 to 2 days. In sheep, glycosuria (blood glucose may reach 400 mg% and spill into the urine) may occur, providing very good circumstantial evidence for the diagnosis of the disease. However, bacterial growth in the urine will destroy the glucose via fermentation within a few hours after death. Thus, the absence of glycosuria in lambs that have been dead for a few hours is of no significance. Glycosuria is not a feature of enterotoxemia in calves.

5.5.9 BOVINE VIRUS DIARRHEA:

Bovine virus diarrhea is an infectious virus disease of cattle characterized by erosions and hemorrhages of the alimentary tract and manifested clinically by diarrhea and dehydration. The classical enteric form of the disease occurs primarily in young cattle (up to 2-8 years). Clinically, affected animals are dull, depressed and anorexic. There is a profuse watery diarrhea and the feces may contain mucous and blood. Oral erosions (stomatitis) are usually prominent. The course of the disease varies from 2 to 3 days up to 3-weeks; however, affected cattle may die within 48 hours. The basic lesion in bovine virus diarrhea is focal degeneration of epithelial cells resulting in erosions and ulcers. Grossly, erosions and/or ulcers are observed in the oral cavity, esophagus, forestomachs, abomasum and intestine. In chronic cases, necrosis of intestinal Peyer's patches is a prominent feature (necrosis of intestinal lymphoid tissue).

Abortions may occur in affected animals following acute attacks. Septic metritis following abortion may result in death. In the fetus, lesions similar to those described for adults may be observed in the oral cavity, esophagus and abomasum. Also calves born alive may exhibit signs and lesions described for bovine virus diarrhea in adults.

Cerebellar hypoplasia may occur in calves when they are infected in-utero before 165 days of gestation.

5.5.10 INFECTIOUS BOVINE RHINOTRACHEITIS:

Infectious bovine rhinotracheitis is considered in detail in the Respiratory System section of this syllabus. In very young calves, however, infectious bovine rhinotracheitis is characterized by lesions that may involve the digestive system. These lesions consist of erosions and ulcers in the esophagus, rumen, omasum, abomasum, cecum, colon, as well as multiple necrotic foci in various visceral organs, including the liver. Rather high mortality occurs in affected calves.

5.5.11 JOHNE'S DISEASE (PARATUBERCULOSIS)

Johne's disease is a chronic infectious disease of sheep, cattle and goats caused by Mycobacterium paratuberculosis and characterized by thickening of the intestinal wall, diarrhea and dehydration. In addition to the intestine, the causative organism has been recovered from the mesenteric lymph nodes, udder and reproductive tracts of both sexes. Calves are highly susceptible, but because of the very long incubation period most clinical cases are seen in 2 to 6 year old animals. Characteristic lesions are most commonly found in the lower portion of the small intestine (even though the entire small intestine, the large intestine and mesenteric lymph nodes may be involved). Grossly, the affected intestinal wall is thickened and the mucosa is thrown up in folds. Microscopically, the intestinal mucosa is closely packed with epithelioid cells that have abundant cytoplasm. These epithelioid cells contain "acid fast" organism (bacilli). Clinically, the chief sign is a persistent or recurrent diarrhea.

5.5.12 EDEMA DISEASE OF SWINE:

Edema disease of swine is an acute disease of young pigs (4 to 15 weeks) which is characterized by edema and paresis. The disease is usually associated with weaning or some management change. Rapid proliferation of beta hemolytic strains of E. coli in the upper small intestine with elaboration of endotoxin has been incriminated as the cause of edema disease. Clinical signs may not be present in peracute cases. In some cases, however, eyelid edema and pitting edema over the forehead may be prominent. Grossly, edema may be present in the stomach wall, coiled colon, gallbladder wall, mesentery, etc. Microscopically, there is a necrotizing arteritis in most organs and tissues. Central nervous system lesions consist of focal symmetrical and bilateral malacia which primarily involves the thalamus, basal ganglia and nuclei of the brain stem.

5.5.13 COLITIS-X OF HORSES:

So called colitis-X is a fatal enteric disease of horses in which the causative mechanism is unknown. Affected horses range from 1 to 10 years. Suggestive causes are

• (1) Salmonella species,
• (2) E. coli toxin, and
• (3) exhaustion shock or stress.

Grossly, lesions are confined primarily to the cecum and colon. In the early stages, petechial hemorrhages and severe edema are prominent. Later, necrosis of the gut wall occurs. Intestinal contents are watery, foul-smelling and may be foamy or blood-tinged.

5.5.14 HEMORRHAGIC BOWEL SYNDROME OF SWINE:

Hemorrhage bowel syndrome encompasses the sudden death of pigs resulting from massive hemorrhage into the intestine. The causative mechanism is unknown. However, it has been suggested that vitamin E deficiency, intestinal hypersensitivity to some agent, and mycotoxins in feed may serve as initiating agents. The disease occurs primarily in post-weaned pigs, and it is a major problem in "specific pathogen free" herds. Grossly, there is massive hemorrhage into the intestinal lumen (free blood). The hemorrhages are most severe in the ileum, cecum and colon. Although the intestinal wall is hemorrhagic, there may be no obvious point of hemorrhage. In chronic cases, necrotic enteritis due to secondary bacterial invasion may develop.

Remember,

when presented with sudden death in pigs associated with hemorrhage into the gastrointestinal tract and extreme skin pallor, there are 4 major conditions that should be considered:

(1) hemorrhagic bowel syndrome,

(2) gastric ulcers, (3) acute swine dysentery, and

(4) acute salmonellosis.

5.5.15 ENTERITIS IN RABBITS (MUCOID ENTERITIS):

Enteritis resulting in diarrhea is one of the most important causes of morbidity and mortality in domestic rabbits. It is usually a complex problem rather than a simple disease entity. This enteritis (diarrhea) of unknown cause has been referred to as mucoid enteritis, mucoid enteropathy, enterotoxemia and scours. Several known causes of diarrhea in the rabbit include salmonella, Bacillus piliformis (Tyzzer's disease), E. coli (colibacillosis), clostridia (enterotoxemia) and intestinal coccidiosis. The cause of mucoid enteropathy is unknown although it can be classified as an "enterotoxin-induced secretory diarrhea." The incidence is a function of age with most cases occurring in rabbits 7 to 10 weeks old. Occasional infections occur as early as 2 weeks or as late as 20 weeks of age. The disease runs an acute course (up to 8 days). Clinical signs include anorexia, lassitude, subnormal temperature, rough hair coat and diarrhea with weight loss. There may be polydipsia and the abdomen is bloated because of intestinal gases and fluids. The perineum is stained with mucus and feces. At necropsy, the colon often contains gelatinous mucoid material.

5.5.16 PROLIFERATIVE ILEITIS OF HAMSTERS;

This is a specific, apparently infectious and contagious disease of unknown cause and is characterized by marked hyperplasia of the ileal epithelium. The disease is usually enzootic but may reach epizootic proportions. Clinical signs include diarrhea, dehydration, anorexia and depression. Grossly, lesions are usually found in the ileum, but occasionally the jejunum and colon may be involved. The involved portion of gut is dilated, thickened, studded with small white subserosal foci and often adhered to other viscera. Microscopically, there is hyperplasia of the intestinal epithelium (forming small glands or cysts) accompanied by purulent inflammation and coagulative necrosis extending into the submucosa, muscularis and often to the serosa. Weanlings are most often affected. The condition responds to oral therapy with neomycin sulfate.

5.5.17 TYZZERS DISEASE:

This is principally a disease of mice caused by Bacillus piliformis. The condition has been reported in rats, hamsters, gerbils, rabbits and foals. Bacillus piliformis is a slender gram-negative rod which is also an obligate intracellular parasite that can only be grown in tissue culture. The organism appears to live as a saprophyte in many mouse colonies, producing disease under various forms of stress. Clinical signs include diarrhea, humped back and poor hair coat. Gross lesions consist of focal necrosis of the liver and inflammation of the terminal ileum and cecum. In rabbits, myocardial hemorrhage and necrosis is a significant lesion. Microscopically, organisms (B. piliformis) are present in the vicinity of the necrotic liver foci which can be demonstrated by special stains (Giemsa, etc.).

5.5.18 ULCERATIVE ENTERITIS OF BIRDS (QUAIL DISEASE):

This is an acute or chronic infection of the lower intestinal tract of quail, chickens, turkeys, pheasants, pigeons and probably other species. The condition is caused by Clostridium colinum and it is particularly severe in quail. Susceptible quail may suffer an explosive disease with virtually 100% mortality in a few days. In other species, mortality usually does not exceed 10%. Significant lesions are found in the ceca and intestine. Acute cases are characterized by hemorrhagic enteritis in the duodenum and punctate hemorrhages in the wall of the lower intestine. In chronic cases, lesions are more extensive and ulcers may occur in any portion of the intestine and ceca. Small yellow foci with hemorrhagic borders may be seen on the serosal and mucosal surfaces. Ulcers may coalesce to form large necrotic diphtheritic patches. Liver lesions occur as large irregular yellow areas of necrosis. The spleen may be enlarged and hemorrhagic.

5.5.19 HISTOMONIASIS:

Histomoniasis (sometimes referred to as blackhead or infectious enterohepatitis) is a protozoan disease of the lower digestive tract (ceca and liver) of turkeys, chickens and several other gallinaceous birds. The disease is caused by the protozoan Histomonas meleagridis, in combination with any one or more of a group of common bacterial inhabitants of the intestinal tract of chicken and turkeys. The protozoan does not seem capable of producing the disease in the absence of bacteria. Histomonas meleagridis may be transmitted directly from one bird to another by ingestion of infected feces. However, it is more commonly transmitted by ingestion of the embryonated eggs of the cecal worm, Heterakis gallinae, which harbor H. meleagridis. The primary lesions are found in the ceca, but the liver may also be involved. The ceca are inflamed, thickened and ulcerated. Necrotic liver lesions are circular, yellowish-green and depressed.

5.5.20 HISTOPLASMOSIS:

Histoplasmosis is an infectious mycotic disease of man and lower animals caused by Histoplasma capsulatum. A benign unapparent form and a fatal systemic form may occur. In dogs, the fatal systemic form occurs most commonly, and various organs and tissues may be affected. Histoplasmosis is characterized by extensive proliferation of cells which belong to the mononuclear phagocytic system (macrophages, etc.). Many of these cells contain "yeast forms" of the causative organism. The yeast-like bodies are cytoplasmic, irregular, egg-shaped and measures approximately 2 microns in diameter. Histoplasmosis is one of the most frequent systemic fungal diseases encountered in dogs and man. The fungus grows in soil and infection is acquired by inhalation or rarely by the oral route. Acute disseminated histoplasmosis usually is fatal.

5.5.21 PARASITIC DISEASES OF THE INTESTINAL TRACT:

Parasitic diseases of the intestinal tract are discussed in detail in your parasitology course. However, the student should be familiar with those parasites covered in this section.

5.5.21.1 ANCYLOSTOMIASIS:

This is an important parasitic disease in man and animals. Ancylostoma caninum is the principal hookworm in dogs in the USA. These small parasites are 12 to 15 mm in length. Most infections are ingested, but larvae may penetrate the skin. Also, larvae may appear in the milk where it can infect suckling young. Adult hookworms attach themselves to the mucosa of the small gut, produce an anticoagulant and suck blood. Clinical signs include pallor of the mucosa, hypoproteinemia, weakness, diarrhea, emaciation, etc. Larval migration may occur. The most severe effect of this type is usually seen in the lungs.

5.5.21.2 ASCARIASIS:

Ascarids are extremely common in the gastrointestinal tract of mammals and birds. Young animals are particularly susceptible to infection. Many adult animals lose their ascarid parasites spontaneously. Adult ascarids live free in the intestinal tract and feed on intestinal contents. They may obstruct the intestinal lumen, bile ducts and pancreatic duct. Occasionally, adults may penetrate the intestinal wall or liver and produce a fatal peritonitis. Inanition and retardation of growth of the young animal are the most common effects produced. Ascarids cause disease by depriving the host of food and interfering with its digestive processes. There is a tendency for ascarid larvae to wander in the body of the host. The lesions produced are determined by the migratory pattern (liver, lungs, brain, etc.) that the specific larvae follow.

5.5.21.3 CESTODIASIS:

Adult tapeworms apparently produce little serious effect upon the host except in very heavy infections in which they interfere with digestion or cause partial obstruction of the gut lumen. However, the intermediate stages of tapeworms may cause serious damage to the host.

5.5.21.4 OESOPHAGOSTOMIASIS:

Oesophagostomiasis (nodular worm infection) is an important parasitic disease in sheep, goats and cattle. Ingested larvae penetrate the intestinal mucosa become encysted and molt in the submucosa. Eventually, they return to the intestinal lumen where they reach maturity. The adults cause minimal tissue damage and do not suck blood. The larvae, however, produce intense tissue reaction in susceptible animals. Nodules develop in the intestinal wall subsequent to this phenomenon. These nodules may interfere with peristalsis and with absorption.

5.5.21.5 EQUINE STRONGYLOIDOSIS:

The large strongyles in the horse are Strongylus vulgaris, S. equinus and S. edentatus. They are slender worms which measure from 1 to 2 inches in length. They are primarily found in the cecum and large colon. Strongylus vulgaris (the common or double-tooth strongly) larvae are believed to penetrate the gut wall, enter the bloodstream and pass through the liver and lungs. Larvae frequently localize in the anterior mesenteric artery resulting in arteritis, thrombosis and aneurysmal dilation. Less frequent localization occurs in the aorta, iliacs and renal arteries. The adults of Strongylus equinus (the triple-tooth strongyle) are found primarily in the cecum. Ingested larvae of S. equinus are believed to penetrate the gut wall, enter the bloodstream and migrate through the liver, heart and lungs. Subsequently, large numbers of nearly mature worms may be found in tissues of the pancreas, spleen, lungs, liver and abdominal fat (just under the parietal peritoneum). The adults of Strongylus edentatus are found in the cecum and colon. Ingested larvae of S. edentatus are believed to penetrate the wall of the colon and encyst in abdominal fat for 3 to 4 months. Subsequently, larvae reach the serosa of the jejunum and ileum and produce elevated nodules oftentimes referred to as haemonomelasma ilei. Large strongyles are very active bloodsuckers. Therefore, production of anemia is the most characteristic sign of infection with one of these parasites.

Small strongyles may be numerous in the cecum and colon. This group of parasites is represented by many species within several genera. Generally, they are less injurious to the host than the large strongyles. However, one species, Triodontophorus tenuicollis, produces rather severe ulcers in the wall of the colon.

5.5.21.6 TRICHURIASIS:

Trichuriasis (whipworm infection) occurs in many animal species. Light to moderate infections produce little detectable effects. However, heavy parasitic loads may lead to erosion of the cecal mucosa, typhilitis and deleterious effects on the host.

5.5.21.7 OXYURIS EQUI INFECTION:

Oxyuris equi (pinworms) are found mainly in the cecum, colon and rectum. Gravid females pass toward the rectum, where some are passed in the feces, while others crawl out of the anal opening into the perineum where they deposit their eggs. Clinical signs include pruritus, which is probably induced by the egg laying.

5.5.21.8 COCCIDIOSIS:

In cattle,

Eimeria zuernii and Eimeria bovis are the species associated with most clinical cases of coccidiosis. Light infestations are characterized by watery feces with little or no blood. Severely infected animals may develop a diarrhea consisting of thin, bloody fluid, or thin feces containing streaks or clots of blood, shreds of epithelium and mucus. Grossly, the mucosa may be thickened and hemorrhagic.

In sheep and goats,

E.arloingi and E.parva are considered to be important. They may cause focal hyperplasia of the intestinal mucosa in chronic cases. The hyperplastic nodules can be observed from both the mucosal and serosal surfaces.

In poultry,

E. tenella causes severe lesions in the ceca. There is an accumulation of blood in the ceca as well as bloody feces. E. necatrix produces major lesions in the anterior or midpoint of the small intestine which are recognizable by the spotted appearance of the unopened intestine. In severe cases, the intestinal wall is thickened and the involved area is dilated. Large quantities of blood may also be present in the lumen in these cases. While the damage is in the small intestine (E. necatrix oocyst are not found in the small intestine), the sexual phase of the life cycle is completed in the ceca. E. acervulina and E. mivati infections are characterized by numerous gray or whitish transverse patches in the upper half of the small intestine. The clinical course in a flock is usually protracted. E.brunetti occurs in the lower small intestine, ceca, rectum and cloaca. In moderate infections, there is catarrhal enteritis and thickening of the intestinal wall. Severe infections may cause extensive necrosis and sloughing of the mucosa throughout the entire intestinal tract.

5.6 THE PERITONEUM

The peritoneal surface is the serous membrane which lines the abdominal cavity and covers the visceral surfaces of the abdominal organs. Its primary functions are protective and absorptive. The peritoneum protects the peritoneal cavity by walling off areas of inflammation. It also permits the absorption, exudation or transudation of fluids. The normal peritoneum is a smooth and shiny membrane which is covered with just enough fluid to keep it moist. Free fluid (in quantities which are easily detected) in the peritoneal cavity is abnormal. Accumulation of fluid in either abnormal amounts (transudates), or of abnormal character (blood, fibrin, etc.), along with inflammation are the most common and important conditions affecting the peritoneum.

5.6.1 INFLAMMATION OF THE PERITONEUM:

Inflammation of the peritoneum is referred to as peritonitis. The condition may occur in any species. The exudate may be either fibrinous, serofibrinous, purulent, fibrinopurulent or hemorrhagic. Peritonitis can be caused by a variety of agents (bacterial, parasitic, viral, etc.) but most are bacterial in origin. Bacterial peritonitis may result when bacteria are implanted directly on the peritoneum by perforating lesions or when organisms reach the peritoneum via the bloodstream or lymphatics. In addition, a severe peritonitis develops when bile or pancreatic enzymes are released into the cavity. In horses, generalized peritonitis is nearly always fatal. In this species, rupture or perforation of the stomach or intestine is the most common cause. Corynebacterium equi (oftentimes associated with an umbilical infection) is a frequent cause of purulent peritonitis in foals. In cattle generalized peritonitis is usually the result of a perforation (especially of the reticulum and uterus). In swine, Corynebacterium pyogenes is oftentimes recovered from cases of peritonitis. Glasser's disease (Hemophilus suis infection in the porcine) produces a fibrinous or serofibrinous peritonitis which is considered to be its characteristic feature. Clinically, peritonitis is accompanied by abdominal pain, tenderness on palpation, rigidity of the abdominal wall and a systemic reaction. Peritonitis may result in toxemia, septicemia, paralytic ileus, accumulation of fluid/exudate and adhesions.

5.6.2 ABNORMAL CONTENTS IN THE PERITONEAL CAVITY:

A variety of material may be found in the peritoneal cavity of animals, including ingesta, foreign bodies, blood and transudate.

5.6.3 HEMOPERITONEUM

Refers to the presence of blood in the peritoneal cavity. The condition is seen most commonly in the dog and cat as a result of traumatic injury to the liver, spleen and kidneys. In addition, hemoperitoneum may be associated with neoplasms (hemangiosarcoma etc.), infectious canine hepatitis (rupture of liver), toxic plants (sweet clover poisoning) and uterine rupture. The blood within the cavity may be completely liquid or partially clotted. The outcome will depend on the rate and volume of bleeding, site of the hemorrhage, the cause and the initial health status of the animal. Remember, the amount of blood present in the peritoneal cavity at necropsy is not an accurate indication of the volume of bleeding because, during life, extravasated blood is removed quite rapidly by the lymphatic channels. Hemorrhage on or beneath the peritoneum without free blood in the cavity is commonly associated with toxemias.

5.6.4 FELINE INFECTIOUS PERITONITIS:

Feline infectious peritonitis is a chronic debilitating disease of cats characterized by an insidious onset, fever, anorexia, depression, weight loss and an accumulation of fluid within body cavities. Evidence suggests that the disease is caused by a coronavirus. Clinically, feline infectious peritonitis may be manifested in one or more different forms. The classical "wet form" (effusive form) is characterized by an accumulation of fluid in the abdominal, thoracic, and/or pericardial cavities and by the presence of small, discrete foci of necrosis (pyogranulomas) over the surface of the liver, spleen, pancreas, kidneys, lungs, brain, iris and testes. Fluid within body cavities is excessive, yellowish, viscid and has a high specific gravity. A granular, grayish-white, fibrinous exudate or whitish flakes of fibrin are suspended in the fluid. The fibrinous exudate gives the peritoneal and pleural surfaces a dull, granular appearance. The "dry form" (non-effusive form) is characterized by the presence of necrotic pyogranulomas in organs and tissues (visceral organs, eyes, brain etc.), but there is an absence of fluid in the body cavities. In most cases of feline infectious peritonitis, there is a hyperproteinemia caused by hypergammaglobulinemia. Treatment is ineffective. The most recent information relative to pathogenesis is based on immune mediated phenomenon.

5.6.5 POST-INSTRUCTIONAL SELF EXAMINATION

PART B: LOWER ALIMENTARY TRACT

Once this section is completed, the student should be in a position to provide appropriate answers for the following questions. Please review the instructional materials carefully prior to embarking on this task.

SLIDE SESSION 5

PART B

LOWER ALIMENTARY TRACT