Category:Stomach and Abomasum - Inflammatory Pathology

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()Map ALIMENTARY SYSTEM (Map) STOMACH AND ABOMASUM

• Gastritis refers to inflammation of the stomach.

Catarrhal gastritis

Clinical

• Catarrhal gastritis can be fatal since it makes the animal vomit and can produce rapid dehydration.
  • May die in day or two if vomiting is persistent and untreated.
• Extracellular fluid (isontonic) is lost, and so blood very quickly becomes viscous.
  • Death may occur from hypovolaemic shock
    • Particularly in young animals (can be very quick).

Pathology

• The mucosa appears swollen and hyperaemic, with thickened rugae.
  • Mild inflammation, hyperaemia, and oedema
  • Infiltration of inflammatory cells
  • No fibrin or haemorrhage.
• The surface of the mucosa is covered by a white, sticky catarrhal exudate which lines the stomach.

Pathogenesis

• There are numerous causes of catarrhal gastritis
  1. Ingestion of mild irritant
  2. Systemic bacterial diseases
  3. Infectious enteric diseases e.g.
     • Transmissible gastro enteritis (TGE)
     • E.coli
     • Salmonella etc.
• Dogs are very prone catarrhal gastritis.
  • Anything that affects dogs tends to produce vomiting.
  • Dogs eat almost anything and this can make them vomit for a short time.

Oedema Disease In The Pig

• Catarrhal gastritis is an important characterisitic of this condition
• Oedema disease is a sporadic condition that can become important on some farms.

Clinical

• Generally occurs in young pigs, though sometimes in older pigs
  • 7-10 days after major change in diet e.g. weaning.
• Signs include
  • No diarrhoea
  • Puffy eyelids
  • High-pitched voice (oedema of larynx)
  • Sitting on haunched
  • "Star-gazing" due to cerebral oedema (hallucinations?).
• Animals usually die.
• Disease develops very quickly so pigs do not have time to go off food.

Pathogenesis

• Oedema disease is an enterotoxaemia associated with infection by enterotoxigenic E.coli.
• Verotoxin/ shiga toxin- producing E. coli proliferate in the small intestine
  • Especially O138, O139, and O141.
  • Organisms remain in the gut (are not invasive).
• Labile shiga-like toxin II is absorbed into body, producing effects everywhere.
• Blood vessel walls are damaged and become very leaky, producing oedema everywhere.
  • Histological blood vessel changes are subtle.
  • Fibrinoid degeneration of media in small arteries.

Pathology

• An important characteristic of oedema disease is the occurrence of catarrhal gastritis and marked oedema in the stomach mucosa and wall.
• Also oedema of various organs, particularly between coils of spiral colon.

Diagnosis

• Clinical signs are characteristic.
• Also by culture and typing of E. coli from gut

Erosive and Ulcerative Gastritis

• Causes gastric ulcers
• Seen
  • Commonly in the dog and pig.
  • In young calves weaned onto a coarse diet.
  • These usually heal as animal gets older.
  • In the horse, associated with parasites.
• Once started, gastric ulcers can erode deeply.
  • May penetrate gastric wall leading to peritonitis.
  • May erode a blood vessel to cause haemorrhage.

Pathology

Gross

• Round or oval lesions from 1-4 cm in diameter.
• Sharply “punched out” lesions with perpendicular or slightly overhanging walls.
• Borders are level with, or slightly raised above, the surrounding mucosa.
• Depth is variable.
  • Some penetrate the superficial mucosa only.
  • Some deeply penetrate the muscularis externa.
• Base may be markedly haemorrhagic.
  • In advanced chronic cases, scarring may result in a puckered appearance.

Histological

• Appearance varies with the degree aggressiveness of the ulcer and the amount of healing which has occurred.
  • Rapidly excavating ulcers have minimal granulation tissue and collagen deposition.
  • Others may have a necrotic base with a framework of granulation tissue and collagen.
• The blood vessels at the base of the ulcer may be thickened and thrombosed.
• In the bovine, the ulcer may have a superimposed fungal infection.

Pathogenesis

• There are differences in pathogenesis between species.

Cattle

• Management-related in young calves and dairy cows.
• May also be caused by infectious agents, e.g. mucosal disease/ bovine viral diarrhoea virus.
• Ulcers have a tendency to bleed and perforate.

Horse

• Affects the pars oesophagea (margo plicatus) in adults and foals.
• Due to parasites - Gasterophilus (Bots).
• Bots are not as common as they once were.
• Look like big pink maggots.
• Killed by Ivermectin.
• Gasterophilus leave large ulcers in glandular regions of the stomach.
  • Ulcers / erosions are quite deep.
• The parasites are believed to be non-pathogenic, but in large numbers they probably produce some discomfort and poor growth.
• Carcinoma can also produce ulceration in the stomach of the horse as, in other species.

• In foals, the glandular area may sometimes be affected.
  • This may be e.g. stress-related, or due to used of NSAIDs.

Dog

• Although ulcers are often secondary to other diseases, primary idiopathic peptic ulcers do occur, due to
  • Hyperacidity
  • Gastric carcinoma in older dog

• Secondary ulcers are often associated with systemic diseases particularly uraemia and mast cell tumours. Gastric ulcer may be the cause of death but is not the primary disease.
  1. Mast cell tumours
     • Boxers and Labradors are predisposed to these.
     • Vomit continually together with abdominal pain.
     • Ulcers are usually near the duodenum.
       • Frequently secondarily infected.
       • Often penetrate deeply.
     • Actively secreting mast cell tumours produce histame, leasing to gastric hyperacidity and therefore secondary peptic ulcers.
  2. Uraemia
     • Gastric lesions usually occur with chronic renal disease.
       • Gastrin is produced by the G cells of the gastric antrum during the gastric phase of digestion .
         • Acts on H2 receptors on parietal cells to increase production of HCl.
         • Increases release of histamine from gastric mucosal mast cells to increase HCl release.
       • Serum levels of gastrin are increased in chronic renal disease in dogs and cats.
     • In acute renal failure death ensues before gastric ulceration develops.
     • Pathogenesis
       • Loss of nephron and medullary concentration gradient in chronic interstitial nephritis mean collecting ducts cannot resorb fluid.
         • A common cause of interstitial nephritis in the dog was leptospirosis.
       • Consequently, the animal drinks and urinates in enormous quantities, and urea is washed out with large quantities of fluid ("compensated renal failure").
       • If fluid is restricted, urea cannot be washed out and the animal becomes uraemic.
         • Urea is excreted into stomach, giving it a horrible ammoniacal smell and filling it with brown smelly liquid.
         • Urea is also excreted into the colon.
       • Urea in the stomach breaks down to ammonia, irritating the mucosa and contributing to gastric ulcer.
       • Uraemia also causes arteriolar degeneration in the submucosa, leading to hypoxic damage to the mucosa. This is another contributing factor to gastric ulcer.
       • Vomiting causes dehydration and further raises blood urea.
         • A vicious circle is produced- ends in death by vomiting, dehydration and shock.
       • Note: If an animal in compensated renal failure is given anaesthetic, it will not drink much. It then may start to vomit and die due to uraemia.

• NSAIDs, Zollinger-Ellison syndrome (due to pancreatic gastrin-secreting tumour), cirrhosis and bile reflux can all also cause gastric ulcers in the dog.

Pig

• Gastic ulceration is quite common in the pig- May be seen in 50-60% of pigs arriving at slaughterhouses.
• Has serious economic consequences.

• Clinical
  • Occasionally a well-grown pig will drop dead.
    • Deep ulcers have eroded into a blood vessel, causing massive haemorrhage into the stomach from and producing death very rapidly.
  • If long standing ulcers do not result in death, they do produce pain and discomfort.
    • Give low growth rate and poor feed conversion.

• Pathogenesis
  • Gastric ulceration is associated with modern pig rearing, but the exact cause is unknown.
  • Causes are associated with gastric hyperacidity, and gastric ulceration is probably a multifactorial disease.
  • The following are suggested as possible causes:
    • Infection, e.g. Candida albicans, Streptococci, Staphylococci and mixes of these.
    • Copper toxicity- this is probably more significant.
      • Pigs are fed copper as growth promoter; 50 ppm is know to be toxic, and animals are often fed 250 ppm.
    • Vitamin E / Selenium deficiency.
    • Feeding on concrete floors.
      • Sand is licked up whe pigs eat.
    • Feeding finely milled cereal.
    • Stress
    • Possibly genetic factors.

• Pathology
  • Most commonly affects pars oesophagea (squamous or non-glandular portion).
  • Starts with hyperkeratosis in the stratum corneum
    • Appears rough and thickened
    • May stop at this stage.
  • In approximately 30% of animals, the lesion starts to erode and quite deep ulcers may develop.
  • In a significant small number ,very deep ulcers develop and may affect virtually all of pars oesophagea.
  • Histologically, ulcers are large and flask-shaped ulcer with fibrin, necrosis, erosion and fibrosis at base.

Fibrinous/ Diptheric Gastritis

• Not very common, but has severe consequences.
• Dirty-white, crumbly fibrin is seen on the surface of mucosa.
• Causes
  • Toxic
    • From drinking battery acid or other caustic material.
      • Also gives with stomatitis and oesophagitis as well.
    • Poisons such as mercuric chloride and carbolic acid also cause fibrinous/ diptheric gastritis.
  • Severe systemic disease
    • e.g. septicaemic Erysipelas and Swine Fever in pigs, or septicaemic Salmonellosis.
    • Not usually a primary problem but part of more severe generalised disease problem.

Haemorrhagic Gastritis

Clinical

• Usually only seen post mortem.
• Stomach full of thick tarry clots.
• Occasionally will vomit blood in life.

Pathology

Gross

• Wall of stomach is blacked and ulcerated.
  • Red, thickened, necrotic, haemorrhagic mucosa.

Histologically

• Coagulative necrosis with fibrin, oedema, haemorrhage, and sometimes emphysema.
• May extend deep into submucosa/muscle.

Pathogenesis

• There are several causes of haemorrhagic gastritis
  1. Aspirin and non-steroidal anti inflammatory drug toxicity.
  2. Peracute / acute infections, e.g.
     • Swine Fever
     • Anthrax
     • Leptospirosis in dogs (Leptospira icterohaemorrhagiae).
  3. Clostridial disease
     • e.g. Braxy (Clostridium septicum)
       • Affects older lambs or yearlings producing sudden death.
       • Usually seen on sheep grazing on frosted grass so more common in colder areas.
       • Bacterial exotoxin causes acute abomasitis.
       • Pathology- At post mortem the stomach is grossly distended with partially clotted blood. The wall of the stomach is thickened,reddened and oedematous.
       • Diagnosed by isolation of organism from the stomach wall.
       • Is now usually vaccinated against (Heptovac 7 in 1 clostridial vaccine).
  4. Warfarin poisoning.

Vesicular Gastritis

• Is not seen, as the stomach has no stratum spinosum.

Chronic gastritis

• Chronic gastritis is usually proliferative rather any other type of gastric inflammation.
• Usually a parasitic cause.
• Occurs mostly in the pig and in cattle.

• Pig
  • Redworms (Hyostrongylus)
  • Seen mostly in sows, and are present in up to 30% of pig herds.
  • Small numbers produce little pathology, but large numbers cause thin sow syndrome.
    • Animals eat well but slowly lose condition.

• Cattle
  • Ostertagiasis produces a condition similar to thin sow syndrome.

Chronic Hypertrophic Gastritis In The Dog

• Clinically see anorexia, weight loss, anaemia and associated hepatic disease.
• Associated with protein loss into gut.

Pathology

• Hyperplasia of mucosa.
  • Mucosa thrown up into folds.
  • Reduced numbers of parietal cells and increased numbers of goblet cells.

Chronic Atrophic Gastritis In The Dog

• Aetiology uncertain.
• Grossly: (may be difficult to appreciate)
  • Reduced mucosal thickness.
  • Loss of rugae.
• Histologically
  • Mucosal thinning.
  • Loss of gastric glands.
  • Diffuse inflammatory infiltrate of lymphocytes and plasma cells.
  • Fewer eosinophils in lamina propria.