Alimentary

• Oral developmental abnormalities:

  • Brachygnathia (shortening of the mandible and maxilla)
  • Prognathia (lengthening of the mandible and maxilla)
  • Palatochisis (cleft palate) – insufficient growth of the paletine shelves results in a midline defect in the hard and/or soft palate. Leads to problems with ingestion and swallowing and commonly aspiration pneumonia
  • Cheilochisis (hare lip) – absence of a segment of the lip, ventral to the nasal septum
• Oral inflammation:

  • Stomatitis – inflammation of the mucosa lining the oral cavity
  • Gingivitis – inflammation of the gingiva
  • Glossitis – inflammation of the tongue
  • Cheilitis – inflammation of the lips
• Vesicular stomatitis is where vessels form in the epithelium where there id degradation of tissues. May be caused by:

  • Viral infections which target stratified squamous epithelial cells e.g. foot and mouth
  • Autoimmune diseases which target mucocutaneous junctions e.g. pemphigus vulgaris in dogs, cats and horses
  • Thermal injury i.e. burns from ingestion of hot food or liquid. Causes full thickness epithelial necrosis.

  Vesicles often progress to erosions and ulcers, particularly in areas of high mechanical contact or bacterial infection.
• Ulcerative stomatitis can be caused by:

  • feline calicivirus in cats, causing vesicle formation, then oral ulceration as the vesicles rupture.
  • mucosal disease caused by bovine viral diarrhoea virus (BVDV) in cows. Causes ulceration of the oral cavity, muzzle and more distal ulcers in the alimentary tract.
• Calf diphtheria is an example of necrotising stomatitis, caused by the bacteria fusobacterium necrophorum. Causes necrosis with formation of a diphtheritic membrane in the oral cavity.
• Wooden tongue (actinobacillosis) is an example if a granulomatous stomatitis, caused by actinobacillus lignieresii in cattle and is an example of granulomatous stomatitis. It causes glossitis (firm swelling of the tongue) with fibrosis, yellow gritty foci and sinus tracts. Histologically, form splendore-hoeppli bodies which are colonies with pyogranulomatous nets. Actinocacillus is a gram negative bacillus.
• Actinomycosis (lumpy jaw) is a form of granulomatous stomatitis caused by actinomyces bovis in cattle. Causes chronic osteomyelitis of the mandible or maxilla, with club colonies of gram positive filamentous bacillus seen histologically.
• Eosinophilic stomatitis is an inflammtation of the mucosa lining the oral cavity in cats. This forms oral eosinophilic granulomas which are immune mediated
• Orf is a proliferative inflammatory lesion, (parapoxvirus) AKA contagious ecthyma, contagious pustular dermatitis, affecting the mouths of sheep and goats. Forms papules and pustules of the skin on the lips and on the oral mucosa, but can affect the teats, hoof coronet, vulva and inguinal region. A mixed inflammatory cell reaction is seen with infiltration of many neutrophils, especially if there is secondary bacterial invasion.

   

  On histology, a thick crust is seen around a lesion where the squamous epithelial layer has many cytoplasmic inclusions and ballooning degeneration (empty pockets)
• Papillomas are a type of oral neoplasia: benign epithelial tumours which appear as raised folded or papillary frond lesions on the lips and oral mucosa. Made up of thick squamous epithelium lining a fibrovascular stroma. In cows these are caused by bovine papillomavirus type 4
• Squamous cell carcinomas are a type of oral neoplasia: A malignant tumour of the squamous epithelium. Seen in dogs and horses but is the most common oral malignancy in cats, often seen on the ventrolateral tongue. These are locally invasive and may metastasise (but this often only happens at a late stage). Histologically appear as irregular cords and island of squamous epithelium invading local stroma, and central concentric keratin foci.
• Malignant melanoma is a tumour of pigment-producing melanocytes. This is the most common oral neoplasm in dogs and is almost always malignant, spreading to lymph nodes and distant sites such as the lungs. These grow rapidly and may not always appear pigmented (amelanotic melanoma ). Histologically appears as oval or spindle shaped melanocytes with varying melanin content.
• Fibrosarcomas are common oral mesenchymal (fibroblastic) tumours which are malignant and most commonly seen in the oral cavity of dogs.
• Anomalies of tooth development:

  • Agenesis
  • Supernumary teeth
  • Dentigerous cysts – most commonly seen in horses
  • Enamel hypoplasia – seen in canine distemper virus
  • Tooth discolouration from adminiseation of tetracyclines to you animals or congenital porphyria
  • Fluoride toxicosis – causes soft, chalky, discoloured teeth in cattle and sheep.
  • Malocclusion- tooth and jaw misalignment
• Dental attrition  is wearing of the teeth, which is usually age related but can be accelerated by abrasive diets in sheep (high in silica) or dogs who chew rocks.
• Degenerative and inflam conditions of teeth

  • Periodontal disease: caused by dental plaque (bacteria and fungi), mineralisation (tartar or dental calculus) and gingivitis. Atrophy of the periodontal ligament is seen, causing loosening and loss of teeth, root abscesses and alveolar osteomyelitis
  • Feline external resorptive neck lesions where the junction between enamel and dentine begin to reabsorb
  • Infundibular impaction or caries: seen in ruminants and horses, but otherwise uncommon. The infundibulum impacts with food material, leading to infection and a foreign body inflammatory response
• An epulis describes a tumour from a group of benign neoplasias which originate in the periodontal ligament, affecting the gingiva. They form firm lesions on the gums, especially in the carnassial region. Tissue makeup is dense collagenous and sometimes ossified tissue covered in stratified squamous epithelium. More specifically they may be called peripheral odonootogenic fibroma.

   

  Odontogenic tumours may arise from rests of Malassez (embryonal remnants) or serres
• Congenital anomalies of the oesophagus:

  • Segmental aplasia where there is a rare failure for the segments of the oesophagus to fuse. There are bands of fibrous connective tissue where the distal oesophagus should be, but no tube. These are difficult to stretch and connect to correct.
  • Achalasia: failure of the cardiac sphincter (the sphincter between oesophagus and stomach) to open so food cannot enter the stomach.
• Megaoesophagus describes a dilated oesophagus which lacks peristalsis. This results in accumulation of ingesta and obstruction, even if the lower oesophageal sphincter is normal. Aspiration pneumonia is a common sequel.

  This may occur due to a function (neuromuscular) disorder, be idiopathic due to a developmental disorder of the vagus nerve (or its motor nucleus) or be acquired (neurological, muscular or toxic). This is especially common in great danes, GSD and Siamese cat
• Causes of acquired megaoesophagus:

  Neurological:

  • Dysautonomias – degeneration of neurones in the autonomic plexus. Caused by equine grass sickness, feline/ canine dysautonomia.
  •   Myasthenia gravis – autoimmune production of antibodies against ACh receptors

  Muscular:

  • Myodegeneration (muscle cells degenerate) e.g. due to nutritional myopathy in cattle (vitamin E/ selenium deficiency)

  Toxicity:

  • Lead poisoning (damages normal nerve cell function)
• An intraluminal obstruction of the oesophagus usually occurs due to a foreign body, examples including food or bones. They commonly occur at narrow sites such as the thoracic inlet, near the base of the heart and at the level of the cardiac sphincter.

  May cause inflammation, pressure necrosis, ulceration and risks of perforation. In ruminants, obstruction can cause bloat as they are left unable to eructate.

  Healing of the oesophagus after an obstruction can cause narrowing (stricture) and increase risk of re-obstruction.
• Intramural oesophagus obstructions occur due to a lesion within the wall of the oesophagus. These may be inflammatory lesions (including abscesses, granulation tissue), fibrosis or a neoplasia

   

  An extrinsic obstruction of the oesophagus occurs due to pressure from outside the oesophageal wall. This may be a vascular ring anomaly ( such as a persistent right aortic arch) constricting the oesophagus and causing cranial megaoesophagus; or pressure from an abscess, haematoma or neoplasm.
• An intraluminal oesophagus obstruction occurs IN the centre of the oesophagus. An intramural obstruction is within the wall of the oesophagus. An extrinsic obstruction is outside the wall of the oesophagus.
• Oesophagitis (inflammation of the oesophagus) may be due to:

  • Reflux. Damage by gastric acid due to gastro-oesophageal reflux or vomiting
  • Infectious bacteria or viruses. Include actinobacillus lignieresii, feline calicivirus and BVDV
  • Parasites, especially spirocerca lupi in dogs
• Common oesophageal neoplasias:

  Papilloma:

  • In cattle : bovine papilloma virus type 4
  • Papillomas have the ability to transorm into squamous cell carcinomas  when exposed to bracken fern toxins

  Squamous cell carcinoma:

  • Particularly in cats, forming concentric (ring) carcinomas around the oesophagus

  Leiomyoma

  • A benign tumour of the oesophageal smooth muscle.  
• The correct name for bloat is ruminal tympany. It occurs due to a failure to expel fermentation gases (eructate). There are two forms:

  Primary (frothy) bloat, where ingestion of high protein clover or low roughage diets causes formation of stable foam on top of the liquid layer in the rumen.

  Secondary (obstructive) bloat where a mechanical or functional obstruction of the oesophagus (including diseases or lesions) leaves the animal unable to expel gas.
• The pathological findings of ruminal tympany (bloat) include a rumen distended with gas and fermenting feed. The blood appears dark due to being hypoxic and clots poorly due to the resulting metabolic acidosis
• Ruminal acidosis can occur due to grain overload i.e there is excess carbohydrate in the diet. This leads to an increased population of gram positive lactobacillus cocci in the rumen. Lactobacillus increases the amount of volatile fatty acids produced but also produces a lot of lactic acid, decreasing the pH below 5 and causing acidosis. Rumenitis may then develop due to damage to the mucosa, with fungi or bacteria then able to colonise. A bacterial or fungal thromboembolism may then spread in the blood vessels to the liver and cause hepatic abscessation.
• On histology, ruminal acidosis appears as microvesicles containing mainly neutrophils in the epithelia of papillae in early stages. Neutrophils may then form pustules as segmental erosion and ulceration occurs.  
• Traumatic reticulitis describes a sharp object ingested and entering the reticulum. They may be insignificant but a contraction may force them through the reticular wall causing local peritonitis. The foreign body may migrate cranially and penetrate the diaphragm and pericardium (traumatic reticulopericarditis). Inflammation of the reticulum can cause ruminal stasis due to ‘vagus indigestion’.

   

  May be suppurative or granulomatous reticuloperitonitis, leading to local fibrous adhesions. If progresses through the diaphragm, fibrinopurulent pleuritis, pericarditis and pneumonia can occur.
• The rumen is lined by stratified squamous epithelium. Ruminal neoplasias include papillomas (bovine papillomavirus type 4) and squamous cell carcinoma (develops from papillomas when bracken fern, which is a carcinogen, is ingested )
• Gastric obstructions may be physical or functional:

  • Physical – foreign bodies including bones, stones, hair and wool (trichobezoars) or plant material (phytobezoars)
  • Functional – neurological (including dysautonomia), end-stage liver disease and vagal indigestion
• Pyloric stenosis is delayed gastric emptying with persistent vomiting and regurgitation, most common in dogs, foals and cats. It is usually acquired from healed ulcers but also is sometimes from congenital hypertrophy of the pyloric muscle. This is a largely functional not lesional issue.
• Herniation of the stomach through the diaphragm can be congenital (e.g. in Persian cats) or acquired (e.g. dog/cat after RTC)
• Gastric dilation and volvulus occurs mostly in large, deep-chested dogs, and sometimes pigs.

  The aetiology and pathogenesis are uncertain but may include exercise after feeding and aerophagia.

  The stomach becomes distended with gas, increasing pressure on the thoracic viscera and blood vessels- resulting in venous drainage obstruction.

  The stomach rotates clockwise to the RHS, bringing the spleen with it. The oesophagus becomes occluded and venous return is blocked, leading to oedema, necrosis of the gastric mucosa and potential rupture of the stomach.
• Gastric rupture can be a post-mortem event due to buildup of putrefactive gases in the stomach. In an ante-mortem gastric rupture, there will be evidence of haemorrhage and peritonitis
• Abomasitis + gastritis = inflammation of the glandular stomach.

  Haemorrhagic – caused by clostridia, e.g. clostridium septicum in sheep. Causes acute necrotising haemorrhagic abomasitis w/ emphysema of the abomasal wall.

  Hypertrophic – chronic hypertrophic gastropathy or gastritis in dogs. Causes chronic retention of gastric fluid, thickened ruggae (hyperplasia of the epithelium)
• Ostertagiasis is a form of parasitic abomasitis / gastritis. In cattle (ostertagia ostertagi) and sheep (teladorsagia circumcincta) causes nodules on the mucosa, giving it a cobblestone appearance. Encysted larvae cause glandular hyperplasia, a loss of parietal/chief cells and chronic inflammation (many lymphocytes, plasma cells and eosinophils seen). Grossly appears reddened due to inflammation with hyperaemia and oedema.
• Gastric ulceration is caused by hypersecretion of acid and/or an impairment to the mucosal barrier. Pepsin and gastric acid causes necrosis, leading to erosion and then ulcers. If erosion is deep enough to reach the underlying blood vessels then haemorrhage can be seen.
• In the dog, gastric ulcers can be caused by use of NSAIDs, mast cell tumours (even at distant sites due to histamine release inducing HCl hypersecretion), azotaemia, Zollinger-Ellison syndrome (due to a pancreatic tumour secreting gastrin), cirrhosis of the liver and bile reflux.