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Category:Stomach and Abomasum - Inflammatory Pathology (view source)
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|linkpage =Alimentary System - Pathology
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<br>
* '''Gastritis''' refers to inflammation of the [[Forestomach - Anatomy & Physiology|stomach]].
==Catarrhal gastritis==
===Clinical===
* Catarrhal gastritis can be fatal since it makes the animal [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomit]] and can produce rapid dehydration.
** May die in day or two if [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|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 [[Forestomach - Anatomy & Physiology|stomach]].
===Pathogenesis===
* There are numerous causes of catarrhal gastritis
*# Ingestion of mild irritant
*# Systemic bacterial diseases
*# 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 [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomiting]].
** Dogs eat almost anything and this can make them [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|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''' [[Intestine Diarrhoea - Pathology|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 [[Escherichia coli|''E.coli'']].
* Verotoxin/ shiga toxin- producing ''E. coli'' proliferate in the [[Small Intestine - Anatomy & Physiology|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 [[Forestomach - Anatomy & Physiology|stomach]] mucosa and wall.
* Also oedema of various organs, particularly between coils of spiral [[Colon - Anatomy & Physiology|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====
[[Image:gastric ulcer.jpg|thumb|right|150px|Gastic ulcer- gross (Courtesy of BioMed Image Archive)]]
* 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====
[[Image:gastric ulcer histopath.jpg|thumb|right|150px|Gastric ulcer- histological (Courtesy of BioMed Image Archive)]]
* 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. [[Bovine Viral Diarrhoea Virus|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 [[Forestomach - Anatomy & Physiology|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 [[Forestomach - Anatomy & Physiology|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.
*# '''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.
*# '''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 [[Forestomach - Anatomy & Physiology|stomach]], giving it a horrible ammoniacal smell and filling it with brown smelly liquid.
*#*** Urea is also excreted into the [[Colon - Anatomy & Physiology|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.
*#** [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] causes dehydration and further raises blood urea.
*#*** A vicious circle is produced- ends in death by [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|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 [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|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 [[Forestomach - Anatomy & Physiology|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.
* [[Forestomach - Anatomy & Physiology|Stomach]] full of thick tarry clots.
* Occasionally will vomit blood in life.
===Pathology===
[[Image:haemorrhagic gastritis.jpg|thumb|200px|right|Haemorrhagic gastritis (Courtesy of BioMed Image Archive)]]
====Gross====
* Wall of [[Forestomach - Anatomy & Physiology|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
*# Aspirin and non-steroidal anti inflammatory drug toxicity.
*# Peracute / acute infections, e.g.
*#* Swine Fever
*#* Anthrax
*#* Leptospirosis in dogs (''Leptospira icterohaemorrhagiae'').
*#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 [[Forestomach - Anatomy & Physiology|stomach]] is grossly distended with partially clotted blood. The wall of the [[Forestomach - Anatomy & Physiology|stomach]] is thickened,reddened and oedematous.
*#** Diagnosed by isolation of organism from the [[Forestomach - Anatomy & Physiology|stomach]] wall.
*#** Is now usually vaccinated against (Heptovac 7 in 1 clostridial vaccine).
*# [[Stomach and Abomasum Toxicology - Pathology#Warfarin Poisoning| Warfarin poisoning]].
== Vesicular Gastritis==
* Is not seen, as the [[Forestomach - Anatomy & Physiology|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'''
** [[Stomach and Abomasum Parasites - Pathology#Ostertagiasis|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.
[[Category:Stomach and Abomasum - Pathology]]
{{toplink
|backcolour =BCED91
|linkpage =Alimentary System - Pathology
|linktext =Alimentary System
|maplink = Alimentary System (Content Map) - Pathology
|pagetype =Pathology
|sublink1=Stomach and Abomasum - Pathology
|subtext1=STOMACH AND ABOMASUM
}}
<br>
* '''Gastritis''' refers to inflammation of the [[Forestomach - Anatomy & Physiology|stomach]].
==Catarrhal gastritis==
===Clinical===
* Catarrhal gastritis can be fatal since it makes the animal [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomit]] and can produce rapid dehydration.
** May die in day or two if [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|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 [[Forestomach - Anatomy & Physiology|stomach]].
===Pathogenesis===
* There are numerous causes of catarrhal gastritis
*# Ingestion of mild irritant
*# Systemic bacterial diseases
*# 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 [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomiting]].
** Dogs eat almost anything and this can make them [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|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''' [[Intestine Diarrhoea - Pathology|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 [[Escherichia coli|''E.coli'']].
* Verotoxin/ shiga toxin- producing ''E. coli'' proliferate in the [[Small Intestine - Anatomy & Physiology|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 [[Forestomach - Anatomy & Physiology|stomach]] mucosa and wall.
* Also oedema of various organs, particularly between coils of spiral [[Colon - Anatomy & Physiology|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====
[[Image:gastric ulcer.jpg|thumb|right|150px|Gastic ulcer- gross (Courtesy of BioMed Image Archive)]]
* 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====
[[Image:gastric ulcer histopath.jpg|thumb|right|150px|Gastric ulcer- histological (Courtesy of BioMed Image Archive)]]
* 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. [[Bovine Viral Diarrhoea Virus|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 [[Forestomach - Anatomy & Physiology|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 [[Forestomach - Anatomy & Physiology|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.
*# '''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.
*# '''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 [[Forestomach - Anatomy & Physiology|stomach]], giving it a horrible ammoniacal smell and filling it with brown smelly liquid.
*#*** Urea is also excreted into the [[Colon - Anatomy & Physiology|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.
*#** [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] causes dehydration and further raises blood urea.
*#*** A vicious circle is produced- ends in death by [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|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 [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|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 [[Forestomach - Anatomy & Physiology|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.
* [[Forestomach - Anatomy & Physiology|Stomach]] full of thick tarry clots.
* Occasionally will vomit blood in life.
===Pathology===
[[Image:haemorrhagic gastritis.jpg|thumb|200px|right|Haemorrhagic gastritis (Courtesy of BioMed Image Archive)]]
====Gross====
* Wall of [[Forestomach - Anatomy & Physiology|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
*# Aspirin and non-steroidal anti inflammatory drug toxicity.
*# Peracute / acute infections, e.g.
*#* Swine Fever
*#* Anthrax
*#* Leptospirosis in dogs (''Leptospira icterohaemorrhagiae'').
*#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 [[Forestomach - Anatomy & Physiology|stomach]] is grossly distended with partially clotted blood. The wall of the [[Forestomach - Anatomy & Physiology|stomach]] is thickened,reddened and oedematous.
*#** Diagnosed by isolation of organism from the [[Forestomach - Anatomy & Physiology|stomach]] wall.
*#** Is now usually vaccinated against (Heptovac 7 in 1 clostridial vaccine).
*# [[Stomach and Abomasum Toxicology - Pathology#Warfarin Poisoning| Warfarin poisoning]].
== Vesicular Gastritis==
* Is not seen, as the [[Forestomach - Anatomy & Physiology|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'''
** [[Stomach and Abomasum Parasites - Pathology#Ostertagiasis|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.
[[Category:Stomach and Abomasum - Pathology]]