PATHOLOGY OF THE ALIMENTARY SYSTEM The alimentary system is a common site for significant pathological changes.

For example, it may be affected by the ingestion of spoiled food or foreign bodies, viral, bacterial, protozoal and helminth infections as well as 'accidents' such as volvulus. The clinical signs of alimentary tract disease include dysphagia, halitosis, vomiting and diarrhoea. Finally, the consequences of alimentary tract disease are important as they include severe pain, death and chronic ill health.

THE ORAL CAVITY Inflammations May be diffuse (stomatitis) or localised in the pharynx (pharyngitis), tongue (glossitis), gums (gingivitis) or tonsils (tonsillitis). Systemic illness and nutritional imbalances may modify salivary secretions and thus interfere with the normal mechanical cleaning of the oral cavity. This in turn may lead to changes in the bacterial population of the oral cavity, impairment of the integrity of the oral epithelium and to stomatitis. Stomatitis may be caused by direct injury to the oral mucosa, for example by ingested chemicals (detergents, caustics) or sharp foreign bodies (bones, grass seeds). Stomatitis is also a local manifestation of some particularly important infectious diseases particularly viruses (foot and mouth disease, blue tongue, rinderpest), autoimmune diseases and systemic diseases. The morphological forms of stomatitis are: 1. Catarrhal stomatitis The mucosae are hyperaemic and covered by a tenacious grey catarrhal exudate (that is, a mucus-rich exudate containing shed epithelial and some inflammatory cells). This is a common non-specific form of stomatitis found in debilitated animals suffering from conditions such as severe anaemia, malnutrition and advanced neoplasia. Catarrhal stomatitis resolves quickly with a return to good health. 2. Vesicular stomatitis Vesicles develop as accumulations of serous fluid in the deeper layers of the epithelium or between the epithelium and lamina propria. These coalesce and the elevated epithelium is then rubbed off to leave raw eroded patches with shreds of epithelium attached. Unless complicated by bacterial infection, healing is rapid. The most important causes of this lesion are the viruses which cause foot and mouth disease (Picornavirus - ruminants and pigs), vesicular stomatitis (Rhabdovirus - horses, cattle and pigs) and vesicular exanthema (Calicivirus - pigs). The mortality rate in foot and mouth disease in cattle is not generally high, but the morbidity rate is very high and productivity is drastically reduced because of poor weight gain and sometimes
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abortions (possibly secondary stress). The oral lesions begin on the lips, buccal mucosa, and tongue and often acquire secondary bacterial infections (which can result in endotoxaemia) and take about two weeks to heal. Similar lesions may occur in the inter-digital skin and coronet, teats and udder. Vesicular stomatitis and vesicular exanthema are important primarily because they resemble foot and mouth disease. 3. Erosive or Ulcerative stomatitis Circumscribed losses of epithelium occur in this form of stomatitis but there is no vesicular stage. Erosions spare the stratum germinativum but there is an acute inflammation in the underlying lamina propria. The lesions tend to heal quickly but may become secondarily infected and develop into ulcers. Ulcers are deeper lesions and extend into the lamina propria. Oral erosions and ulcers may be seen in small animals with dental disease or uraemia. In uraemia, ulceration probably follows the formation of ammonia from urea in the secretions by bacterial action. Oral erosions, associated with upper respiratory tract disease may also be seen in Feline Herpes virus and Calicivirus infections, mucosal disease of cattle (or Bovine Viral Diarrhoea), and Bovine Malignant Catarrhal Fever. They also occur in two major viral diseases - Rinderpest and Blue Tongue. Rinderpest is an acute, highly contagious disease of cattle characterized by erosive and haemorrhagic lesions of the mucous membranes. Blue Tongue is an insect-transmitted viral infection of sheep and cattle. The disease is characterised by swelling and cyanosis then ulceration of the lips and tongue. 4. Necrotizing stomatitis It follows infection with the ubiquitous organism Fusobacterium necrophorum, a gram negative anaerobe normally present in the gut and environment. This infection is common in calves kept in conditions of poor hygiene and nutrition and is referred to as `calf diphtheria'. The lesions are well-demarcated yellowish-grey dry areas of necrosis surrounded by a zone of hyperaemia. F necrophorum can cause rumenitis sometimes with extension to the liver where abscesses develop. It is also involved in the aetiology of the very important disease, ovine foot rot. 5. Granulomatous stomatitis A deep chronic granulomatous reaction with micro-abscesses, particularly affecting the tongue, follows the entry of Actinobacillus lignierisi into the sub-epithelial tissues. This disease is referred to as 'wooden-tongue' in cattle when the tongue is fibrosed. Actinomyces bovis causes a progressive granulomatous osteomyelitis of the mandible and adjacent soft tissue in cattle. Both microorganisms are members of the normal oral flora of cattle. 6. Papular stomatitis Contagious ecthyma or scabby mouth is a viral condition of sheep and goats characterised by macules, papules, vesicles, pustules, scabs, scars and nodules in skin abrasions in the mouth, udder, coronary bands and anus. The condition is zoonotic and in humans is called orf.

7. Eosinophilic granuloma complex Also called rodent ulcers. This is a group of related lesions in the skin and oral cavity of cats. The oral lesions are raised, yellow-red, frequently ulcerated and contain large numbers of eosinophils. They occur most frequently on the lips but can also occur in the gingiva, palate, pharynx and tongue. The aetiology of these disorders is unknown but the lesions are suggestive of an immune-mediated mechanism.

Circulatory Disturbances Examination of the mucous membranes is an essential detail of clinical and post-mortem examinations. Pallor may indicate anaemia; and congestion and cyanosis may be associated with ulceration in dogs with uraemia. Haemorrhages may be seen in septicaemias or accompanying local inflammation and trauma. Petechial haemorrhages may occur with clotting disorders. Hyperaemia may be seen in diffuse stomatitis. Post-mortem changes may modify the expression of changes present at the time of death.

Pigmentations Melanotic pigmentation of the oral mucosa is normal and common. In animals where the oral mucosa is heavily pigmented, assessment of the circulatory function (eg capillary refill time) is difficult. Diffuse yellow discolouration may be seen in jaundice.

Developmental abnormalities Defects may follow failure of integrated growth and fusion in the face and oral cavity. For example failure of mid-line fusion leads to cleft lip (cheiloschisis) and/or palate (palatoschisis). Cleft palate can be genetic or toxic in origin and results from a failure of fusion of the lateral palatine processes. Important sequelae can include starvation due to an inability to create negative pressure in the mouth and hence suckle; and aspiration pneumonia since no effective separation exists between the oral and nasal cavities. Brachygnathia refers to shortening of the mandible (parrot mouth) and prognathia to elongation of the mandibles.

Hyperplasia and Neoplasia

Gingival hyperplasia is overgrowth of the gum tissues and is most common in brachycephalic breeds such as boxers. The term epulis (plural: epulides) is a non-specific term for common tumour-like masses in the gums. They are commonly solitary lesions and are frequently located adjacent to the carnassial tooth. They are most common in dogs, especially boxers and bulldogs. There are several different types of epulis that can be distinguished by histopathological examination including fibrous epulis, fibromatous epulis and acanthomatous epulis. All epulides are considered benign except for acanthomatous epulis which can invade bone and lead to loss of teeth and is prone to re-occurrence following attempts at surgical removal. Squamous cell carcinomas are common in small animals, particularly in the cat where they often occur on the tongue. In dogs they more commonly occur on the tonsils. Oral melanomas are often malignant in the dog. The melanoma begins as a black macule and develops into a rapidly growing firm mass. Some melanomas are non-pigmented and may be difficult to diagnose. Viral papillomas (or warts) occur on the lips and oral mucosa of young dogs, often affecting all dogs in a litter. They are caused by papovavirus. They develop first as smooth papular elevations, which later develop an irregular surface and cauliflower-like shape. Fibrosarcomas arise from collagen-producing fibroblasts and are most common in the cat.

THE TEETH AND DENTAL TISSUES Conformation of the teeth, especially in herbivores, depends on the outcome of opposed growth and wear. Abnormalities in wear may lead to impairment of jaw movements or damage to the oral mucosa by protuberant portions of poorly worn teeth. In rodents and rabbits, the teeth continue to grow throughout the animals lifetime and can result in difficulty eating.

Inflammation

Inflammation of the teeth and gums may involve the pulp (pulpitis) or periodontal tissue (periodontitis). The latter may be superficial (gingivitis) or involve deeper structures in the dental alveolus (pyorrhoea). Pulpitis generally follows entry of bacteria through fractures of, or defects in, the hard tissues of the teeth and may spread to involve the jaws. Gingivitis is often associated with diseased teeth and may follow impaction of food at the gum-tooth margin. When the process spreads to deep alveolar tissue (pyorrhoea) the periodontal membrane may be destroyed and the tooth shed. Chronic gingivitis may be associated with hyperplastic proliferation of the gingival tissues. Caries is a decalcification of the enamel and lysis of the organic matrix. Relatively common in herbivores, especially on the occlusive surface of molars where deep recesses may trap food particles. Plaque is a layer of solid debris and bacteria attached to the surface of teeth. Calculus is mineralized plaque. Calculus is common in all species and closely associated with inflammation of the gums.

Developmental Anomalies Odontodystrophy refers to defects in the formation of the special mineralised connective tissue of the tooth (enamel, dentine and cementum). Systemic conditions which depress blast cell function can lead to such defects, for example canine distemper, fluorine poisoning, Vitamin A deficiency, malnutrition. Dentigerous cysts are epithelium-lined cystic structures in the bone or soft tissue structures of the jaw due to abnormal tooth development. They are rare and may be asymptomatic or cause destructive diseases of the jaw or neoplasia. They can present in the horse as a draining fistulous lesion.

THE SALIVARY GLAND Ptyalism refers to increased secretion of saliva and should be differentiated from the accumulation of saliva in the mouth due to difficulty in swallowing normal secretions. It is common in stomatitis. Foreign bodies may be present in the salivary ducts, especially the parotid duct. These include grass seeds and calculi (sialoliths) and may lead to blockages with stagnation of flow. Ranula refers to the cystic distension of the sublingual or submaxillary ducts in the floor of the mouth. They may occur secondarily to sialoliths. Accumulations of salivary secretions in single or multiloculated cavities adjacent to the salivary ducts are referred to as salivary mucocoeles. They are not true cysts
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as they are not lined by epithelium and they can occur secondarily to rupture of the salivary duct due to trauma. Inflammation of the salivary glands (sialoadenitis) is uncommon in animals but may follow ascending bacterial infections and with rabies and canine distemper. Benign and malignant salivary gland neoplasms are uncommon but can occur in all species.

THE OESOPHAGUS Oesophagitis Erosive and ulcerative oesophagitis accompanies these forms of stomatitis. The only other common form of oesophagitis follows ingestion of corrosive chemicals. Improper use of stomach tubes may lead to linear erosions. Stenosis of the oesophagus may be a developmental defect or be acquired, following scarring of the wall or growth of a tumour. Foreign body impaction (or choke) may follow stenosis or follow ingestion of such things as insufficiently chewed potatoes or apples, masses of grain or bones. Most frequently occurs at anatomical locations where the oesophagus cannot fully expand (e.g. thoracic inlet, heart base and diaphragmatic hiatus). A consequence of impaction is pressure necrosis of the oesophagus, perforation into the adjacent tissue and cellulitis. Foreign bodies such as bones and fish hooks or chop bones may lodge in the oesophagus of dogs. Frequently the thoracic portion is affected and secondary complications may involve the mediastinum and lungs. Dilation of the oesophagus (generally called mega-oesophagus) may be congenital or acquired, generally proximal to a point of stenosis. It has been described in dogs, cats and horses. Congenital mega-oesophagus is usually due to partial blockage of the lumen of the oesophagus by a persistent right aortic arch. In this form, the obstruction occurs cranial to the heart. In acquired mega-oesophagus, the stenosis and dilation occurs cranial to the stomach. Causes are idiopathic or secondary to inflammation of the oesophageal muscle, myasthenia gravis (an autoimmune disease directed against acetyl choline receptors of the neuromuscular junction), hypothyroidism (results in muscle atrophy) and lead poisoning. Mega-oesophagus is recognised clinically by regurgitation of food. Dilations should be differentiated from diverticula, which are local and involve only one side of the oesophagus. Dysphagia or difficulty in swallowing is the cardinal clinical sign of oesophageal disease but it is also common in diseases of the mouth and pharynx, for example cleft palate, pharyngitis or tonsillitis. Achalasia (an inability to relax the oesophagus) leads to progressive dilation and elongation of the oesophagus.

THE RUMINANT FORESTOMACHS

Inflammations Traumatic reticuloperitonitis (or TRP or hardware disease), following penetration of the stomach wall by ingested sharp foreign bodies, is very common in cattle. Foreign bodies may include ingested nails or wire from hay bales (hence the term hardware disease). It is often precipitated by increased intra-abdominal pressure during late pregnancy or parturition. The suppurative or granulomatous inflammation which develops may be confined to the wall of the reticulum or extend to peritonitis and pericarditis. Extension beyond the wall leads to adhesions between the reticulum and adjacent structures. Rumenitis (or lactic acidosis) may follow overeating of grain or a dietary change from hay to a more easily fermentable food. This promotes the growth of bacteria producing lactic acid which drops rumenal pH and alters the normal rumenal flora. Bacterial rumenitis occurs when lactic acidosis or mechanical rumenal damage becomes complicated by overgrowth of Fusobacterium necrophorum or Actinobacillus pyogenes in the changed rumenal environment with subsequent invasion of the rumenal epithelium. Necrosis of large areas of the epithelium follows with occasional metastatic abscesses forming in the liver. Recovery is followed by scarring of the rumenal wall, as its villi do not regenerate completely. Administration of antibiotics can reduce the numbers of normal flora allowing fungi to proliferate and mycotic rumenitis to develop. Inflammatory lesions in the forestomachs occur in some specific erosive diseases, such as mucosal disease.

Other diseases of the forestomachs Bloat or tympany refers to over-distension of the rumen with gas or foam (produced during fermentation) and may lead to respiratory and circulatory failure. Animals that have died from bloat are often found on their back and show subcutaneous emphysema. The blood is dark and does not clot (consequence of anoxia) and there may be haemorrhages in the lymph nodes draining the respiratory tract. Primary bloat occurs following a change of diet, whereas secondary bloat is caused by an obstruction or stenosis of the oesophagus resulting in a failure to eructate. Examples of causes of secondary bloat include vagal indigestion, oesophageal neoplasia or foreign body. Neoplasms, apart from papilloma, are rare in the ruminant forestomach. Conical flukes (paramphistomes) are
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important rumenal parasites. The adult flukes appear to be harmless but immature flukes can cause disease as they migrate up the duodenum and through the abomasum to the forestomachs.

THE STOMACH, INCLUDING THE ABOMASUM General comments Interpretation of post-mortem findings of the lower alimentary tract is complicated by physiological variations in the organ and rapid post-mortem changes such as maceration of the epithelium, congestion of dependent blood vessels and staining by biliary constituents. Histological changes in the gastro-intestinal tract also present problems. For example the normal lamina propria contains many inflammatory cells, particularly plasma cells, and although neutrophils may be migrating into the organ in large numbers they may pass into the lumen quickly without accumulating in the mucosa. In addition the epithelium, particularly over the upper parts of the intestinal villi, is quickly shed after death. Nevertheless, important lesions occur in the lower alimentary tract and it should be systematically examined.

Inflammation of the stomach (gastritis) Gastritis implies inflammation of the stomach alone. Frequently gastritis is associated with inflammation along the length of the intestine, the term gastroenteritis then being applicable. Gastritis is often caused by the ingestion of foreign bodies, consumption of poor quality or spoiled food and various parasitic infections. Catarrhal gastritis is most common. The mucosa is hyperaemic and swollen and covered by a mucus-rich exudate. The upper small intestine may be similarly affected. Reflux of bile may colour the exudate yellow-green. In chronic gastritis the mucosa becomes grey and thickened due to epithelial hyperplasia, oedema and cellular infiltration. Ulcerations of the gastric mucosa in which the entire epithelial thickness down to the basement membrane is lost are common. Penetration through the remaining tissues to the abdominal cavity is termed a perforating ulcer. Ulcers may be complicated by bacterial and fungal invasion. The aetiology of gastric ulceration in animals is poorly understood, but poor diet and stress are believed to predispose to ulcer formation. Steroids and nonsteroidal antiinflammatory drugs (NSAIDs) can also precipitate ulcer formation (especially in horses). In small animals, gastric ulcers may occur in uraemic animals, animals bearing mast cell tumours elsewhere in the body and rarely in dogs with gastrin secreting pancreatic islet cell neoplasms.
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Displacements of the stomach and related abnormalities. Diaphragmatic hernia The stomach may enter the thoracic cavity through a ruptured diaphragm. This is a common consequence of car accidents in dogs and cats. Simple gastric dilation Usually associated with overeating. Especially significant are readily fermented foods which produce gas or which themselves swell, e.g. grains. In dogs the disorder usually resolves spontaneously but in horses gastric rupture and death may occur. Gastric dilation and rupture may occur after death. To distinguish between that occurring in life and death, look for the presence of haemorrhage and inflammation since inflammation can only occur in a live animal. Chronic gastric dilation is usually secondary to diseases such as a gastric ulcer, neoplasia, uraemia, pyloric stenosis, acute gastric dilation, intervertebral disc disease or vagal damage. Gastric dilation with torsion or volvulus (GDV) Seen in dogs when the dilated stomach undergoes a complex rotation and both cardia and pylorus become twisted. The rotation prevents eructation and vomiting and obstruction of the pylorus prevents passage of gastric contents into the duodenum. Vomiting, overeating, postprandial exercise, genetics, trauma, surgery and duodenal obstruction have been incriminated in the aetiology of this condition. It is life-threatening as obstruction of the portal vein and vena cava produces severe cardiovascular effects and shock. Abomasal displacement in cattle The abomasum may become displaced to occupy a position up the left abdominal wall. It tends to become distended with gas and the condition may persist. It may occur in high producing dairy cows post-calving. A much smaller percentage displace to the right. Pyloric stenosis may be congenital or acquired. Generally it is characterised by projectile vomiting associated with feeding. Congenital pyloric stenosis is associated with hypertrophy and fibrosis of the pyloric tissues. It is especially common in boxers. Acquired stenosis is seen in older animals generally following neoplasia in the region of the pylorus. Circulatory changes Active gastric hyperaemia occurs during digestion and in acute gastritis. Passive hyperaemia is associated with portal hypertension and the venous congestion of central and peripheral circulatory failure. There may be accompanying congestive haemorrhages and oedema. Severe congestion and oedema of the gastric mucosa is also seen in dogs suffering from chronic uraemia. Neoplasia Neoplasms, apart from adenocarcinoma in dogs and lymphosarcoma in cats, are uncommon gastric lesions. Leiomyomas and leiomyosarcomas may arise from the tunica muscularis. Squamous cell carcinomas of the stratified squamous portion of the stomach occur in horses.
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THE INTESTINE

General comments While propelling material along its lumen, the intestine carries out secretory, digestive, absorptive, storage and excretory functions. There is a continuous large scale movement of water and electrolytes across the intestinal mucosa. Intestinal pathology upsets the balance between secretion and absorption. Folds, villi, crypts and microvilli increase the effective area of the epithelium lining the intestine. The epithelial cells arise in the crypts, and mature structurally and functionally as they slide to the tips of the villi and are then shed into the lumen. The intestinal lamina propria is a loose, vascular connective tissue, normally containing many lymphocytes and plasma cells with variable numbers of neutrophils and eosinophils. The intestinal lamina propria often responds to injury by shortening and fusion of the villi, and congestion and infiltration of the lamina propria with inflammatory cells. This may compromise the function of the organ. However, the high turnover of the epithelium may lead to rapid regeneration unless the germinal cells in the crypts are damaged. The normal intestine has a vast flora of microorganisms. Some of these may be potential pathogens kept in check by the normal flora. Disturbances of the latter by changes in diet or by drug administration may allow pathogens to flourish and cause disease. The intestinal mucosa secretes antibodies, both locally formed (especially IgA) and serum derived, into the intestine where they resist invasion by pathogens. Newborn animals are deficient in this regard and depend on antibodies in the colostrum until their own local immune system matures.

Intestinal obstruction Intestinal obstruction is acute and catastrophic in the small intestine but may become chronic in the large intestine. Strangulation refers to the additional occlusion of the affected portion's blood vessels. Intestinal obstruction may be due to ingested foreign bodies, tumours, parasites, impacted feed or faeces, volvulus, intussusception or herniation. Anthelmintic administration may result in the rapid death of a large number of nematodes causing impaction. Large amounts of ingested sand may accumulate anywhere in the equine colon, also causing impaction. Enteroliths are stones usually formed of struvite around a small nidus or foreign body. They are rare in species other than the horse
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where they generally lodge at the pelvic flexure or transverse colon. Renosplenic entrapments may occur in the horse in which segments of colon are displaced between the spleen and left body wall, becoming entrapped over the renosplenic ligament. Volvulus refers to the twisting of a length of intestine about its mesenteric attachments. This twisting blocks the intestine and its venous drainage leading to necrosis then gangrene and death of the affected loop. Torsion is a rotation of a tubular organ along its long axis e.g caecum. Volvulus of the left colon is common in the horse and may be secondary to overfilling of the colon with faeces or sand. Also seen in the horse is intestinal strangulation secondary to pedunculated intra-abdominal lipomas wrapping around the mesentery or the intestine. Intussusception refers to the telescoping of a length of intestine into an adjacent length. Acute effects similar to those seen in volvulus may follow but affected animals may survive many days particularly when the lesion is in the large bowel. The aetiology is unknown but may be associated with intestinal irritability and hypermotility. Intussusception may occur secondary to foreign bodies (especially linear foreign bodies), surgical manipulation of the small intestine, intestinal neoplasia or parasitic infestation. Paralytic Ileus This is the non-mechanical hypomotility resulting in a functional obstruction to the bowel. It can be due to paralysis of the bowel wall, which can follow peritonitis, shock, severe painful stimuli elsewhere in the body, toxaemia and electrolyte deficits among other causes. It can also result from sympathetic nerve inhibition secondary to surgical manipulation. Herniation refers to protrusion of an organ through congenital or acquired faults in the surrounding tissues. Herniation of the intestine is described as external if the displacement is through the abdominal wall, e.g. the umbilicus, inguinal canal or beside the rectum in the perineal region. Internal herniation may be through the diaphragm (often following a car accident). The sequelae of intestinal herniation depend on the intestine remaining freely moveable in the hernial sac and maintaining normal circulation. If the intestine becomes incarcerated (or trapped), intestinal obstruction may follow or if the venous drainage is impaired, oedema and venous stasis may lead to incarceration. One of the most common forms of internal herniation occurs in the horse when intestine herniates through the epiploic foramen or mesenteric tears. Eventration refers to displacement outside the abdominal cavity without a covering of parietal peritoneum. Post operative wound dehiscence may result in eventration. The immediate consequences of intestinal obstruction are not solely local. The large volume of fluid normally produced in the upper alimentary tract is prevented from reaching the absorptive surfaces of the lower intestine. Further reflex secretion occurs and to make matters worse fluid and electrolytes may be lost from the body by vomiting. The final results are
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disastrous disturbances in fluid and electrolyte balances. In addition severe cardiorespiratory depression may follow acute distension of the intestinal wall.

Inflammation of the intestine (enteritis) Strictly speaking, enteritis refers to inflammation of the small intestine, colitis to the colon, typhlitis to the caecum and proctitis to the rectum. In many diseases the changes involve the entire intestine and the stomach and in these inflammations the term gastro-enteritis is used. The cardinal clinical manifestation of enteritis is diarrhoea. Enteritis may occur in bacterial, viral, protozoal and helminth infections and chemical poisonings. There are a number of morphological forms of enteritis - catarrhal, haemorrhagic, fibrinous and granulomatous. Catarrhal enteritis is a very common form of intestinal inflammation. It tends to be diffuse rather than patchy with varying degrees of hyperaemia, swelling of the mucosa and enlargement of lymphoid patches. The lumen contains an exudate which varies in appearance according to the ratio of fluid : cells : mucus. If the condition persists the exudate becomes increasingly creamy and opaque. Histologically there is mucosal vascular engorgement with swelling of the lamina propria, loss of epithelial cells and leucocyte infiltration. As neutrophils migrate rapidly into the lumen, they do not accumulate in large numbers in the mucosa. Fusion of villi and dilation of the crypts with inflammatory products may occur (crypt abscesses). The gross appearance of acute catarrhal enteritis can be confused with physiologic hyperaemia combined with postmortem autolysis which sets in very rapidly in the small intestine. Catarrhal enteritis may become chronic, in which case there is a mucus rich exudate, with fusion of villi, increased numbers of goblet cells in the epithelium and increased infiltration of the lamina propria. There may be a cystic dilation of the crypts. Mesenteric lymph nodes may become hyperplastic in chronic enteritis. Acute catarrhal enteritis may be seen in bacterial and protozoal infections while the chronic form is common in helminth infections. In the latter case eosinophils are common in the lamina propria infiltrate. Haemorrhagic enteritis is a more acute and severe inflammation, the exudate containing whole blood. This type of inflammation occurs in severe bacterial and viral infections (for example, rinderpest and mucosal disease). Fibrinous enteritis is a very severe inflammation where there is a fibrin-rich exudate, superficial necrosis of the mucous membrane and possibly formation of a pseudomembrane. The term diphtheritic is applied when there is deep necrosis and a particularly thick pseudomembrane. Before opening, the inflamed intestine feels turgid - due to hyperaemia and exudation into the intestinal wall. Histologically, the exudate lying on the mucosal surface is a
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mixture of fibrin, shed epithelial cells and inflammatory cells. If especially severe, the superficial layers of the intestinal wall may become a structureless mass with the viable part of the wall heavily infiltrated with inflammatory cells. Fibrinous enteritis is seen in severe bacterial and viral infections of the gut (e.g. infectious feline enteritis) and is fatal if extensive. Granulomatous enteritis occurs when there is extensive infiltration and proliferation of chronic inflammatory cells. The reactions are frequently transmural. The best known entity of this type is Johne's disease of ruminants, caused by Mycobacterium avium subsp. paratuberculosis. In well developed cases there is gelatinous thickening and wrinkling of the mucosa throughout most of the gut. Microscopically this can be seen to be due to infiltration by many macrophages in which the organisms can be demonstrated (acid-fast). Giant cells and other chronic inflammatory cells are numerous. The reaction also involves the regional lymph nodes and may affect the liver. Focal nodular granulomas under the serosa develop around the parasite Oesophagostomum columbianum in sheep. Hence the popular name 'nodule worm'.

Some Specific Intestinal Infections Infectious feline enteritis panleukopaenia and Parvoviral enteritis in dogs are contagious, highly fatal viral diseases. The viruses appear to be particularly pathogenic for dividing cells leading to a precipitous fall in the number of circulating leucocytes and a loss of intestinal epithelial cells. Grossly the intestine is turgid and contains a foetid, watery, yellow-grey fluid. Histologically there is loss of epithelium, fusion of villi and dilation of the crypts with fluid and degenerate cells. Kittens infected in utero may be born with cerebellar hypoplasia. The canine virus may cause non-suppurative myocarditis in young pups. Clostridial enterotoxaemias are a group of important fatal diseases which occur when toxigenic types of Clostridium perfringens proliferate in the intestine, their toxins being absorbed and causing severe systemic disturbances. Proliferation follows changed conditions in the gut, generally the result of dietary change especially increased carbohydrate content. C. perfringens Type D is responsible for 'pulpy kidney' disease of sheep and calves. Gastrointestinal inflammation in this disease is mild, the important lesions being the result of toxic damage to the kidney, myocardium and brain. Helminth infections of the intestine are a major cause of ill health in animals. The pathogenesis of the diseases they cause depends on the species of host and parasite, the rate of infection and the immune status and general health

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and nutrition of the host. In general, chronic infections lead to chronic catarrhal enteritis with villus atrophy, increased mucus production and infiltration of the intestinal lamina propria with eosinophils. Regional lymph node hyperplasia generally occurs. Colibacillosis Escherichia coli is a normal inhabitant of the gastrointestinal tract, but may cause significant enteric disease. Factors such as age, immune and nutritional status, host environment and strain of organism influence the course of events. A number of different syndromes have been attributed to E. coli. These include: a) Enterotoxic Colibacillosis. Here the toxin causes net loss of water and electrolytes due to what is essentially a biochemical lesion in the intestinal epithelial cells. Absorption proceeds normally and microscopically the intestine is normal. b) Enterotoxaemic Colibacillosis. In addition to alimentary tract disease, exotoxin is absorbed, spreads haematogenously and causes lesions elsewhere in the body. This is best known in pigs where oedema of the forehead, eyelids, throat, ventral abdominal wall, stomach wall and tissue between the coils of the colon may develop - hence the name "oedema disease". c) Enteroinvasive Colibacillosis in which the organisms invade the intestinal wall causing severe enteritis with absorption of endotoxins causing generalised illness. d) Septicaemic Colibacillosis. Widespread invasion of the body leading to inflammatory lesions such as arthritis and meningitis. This is not necessarily an intestinal infection - for example, newborn animals may become infected via the umbilicus. Seen in young animals with insufficient colostral immunity. Salmonellosis it refers to infectious diseases caused by Salmonella serovars. There are several hundred types of salmonellae and many cause disease in humans and/or other animals. The disease often occurs as an enteritis that develops into a septicaemia and toxaemia. Salmonellosis can be a nosocomial infection (ie. acquired in hospital) and may be fatal following the stress of surgery and antimicrobial therapy. Eosinophilic gastroenteritis it is a poorly understood disease of dogs in which the gastrointestinal mucosa is infiltrated by eosinophils. It may be characterised by episodes of diarrhoea accompanied by a peripheral blood or tissue eosinophilia. It may be associated with development of hypersensitivity to dietary antigens or parasites. Chronic colitis in dogs This is a poorly understood group of diseases often associated with ulceration. One form of the disease occurs in Boxers, in which the colonic mucosa is infiltrated by macrophages containing PAS-positive material. Generally, the colon becomes ulcerated, fibrosed and infiltrated with inflammatory cells.

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Duodenitis - Proximal jejunitis (also known as DPJ, anterior enteritis, gastroduodenojejunitis) this is an idiopathic clinical syndrome seen in the horse. It is characterised by submucosal oedema and a neutrophilic infiltrate in the submucosa and lamina propria resulting in excessive fluid and electrolyte secretion by the small intestine. The horses present clinically with copious gastric reflux through a nasogastric tube, abdominal pain and intestinal distension (palpated rectally) due to the development of a small intestinal ileus. Lesions are always present in the duodenum, often present in the jejunum, and occasionally present in the pyloric portion of the stomach. Enteric infection with Salmonella or clostridial species is frequently speculated as a cause, but neither organism is consistently or frequently isolated from gastric reflux or faecal samples taken from horses with the disease. Complications include adhesions, laminitis and endotoxaemia due to the absorption of toxins through the gut wall. Bovine Viral Diarrhoea (or Mucosal Disease) BVD it is caused by a pestivirus and can present clinically with profuse diarrhoea. In the intestine, the characteristic lesions are areas of necrosis in the epithelium over areas of gut associated lymphoid tissue. Erosions and ulcerations also occur on the tongue, gingiva, oesophagus, abomasum, rumen and coronary bands. Diarrhoea Diarrhoea, which may be defined as the frequent passage of loose or watery faeces, is characteristic of many intestinal disorders. Hypermotility is of dubious importance in the pathogenesis of diarrhoea whereas changes in permeability of the mucosa, secretion and absorption by the mucosa are of major importance. There are continuous fluxes of water and electrolytes across the normal intestinal mucosa. Enteritis can lead to an increased flux into the intestine. If the increase exceeds the intestine's absorptive capacity, diarrhoea ensues. A similar result may follow hypersecretion. On the other hand, malabsorption following damage to the intestinal absorption cells may lead to diarrhoea even when normal quantities of fluid are entering the intestine. Neoplasia Intestinal carcinomas are common and dangerous in human beings. Intestinal carcinomas, and some other neoplasms such as leiomyomas and leiomyosarcomas, rarely occur in the alimentary tracts of domesticated animals. Adenocarcinomas of the intestine are common in sheep. Benign neoplasms of the intestinal tract include adenomas or polyps. Alimentary lymphosarcoma is common in domesticated animals, especially cats. Mastocytomas also occur in cats.

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