Category:Enteritis, Fibrinous/Haemorrhagic

Pathology

• The mucosa eroded to produce lesions of darkish-red submucosa covered in dry, crumbly fibrin.
• Is usually caused by severe damage due to secondary bacterial infection following an earlier milder insult.
• Tends to be more severe in the lower small intestine and upper large intestine.
  • Many severe infections tend to get worse further down the gut.
    • Catarrhal change may be seen in the upper small intestine and fibrinous change in the lower small intestines.
  • In the lower aprt of the bowel, where the inflammation is more severe, disease is more anaerobic.
    • Lesions are caused by anaerobic organisms- convert mild diseases into more serious disease.

Salmonellosis

• There are many different serotypes of Salmonella.
  • All can produce disease BUT only a few commonly produce illness in UK.
  • Salmonella poses a serious risk to man.
  • Some serotypes tend to be more species specific, whereas others can affect a wide range of species. For example:
    • Salmonella enteritidis
    • Salmonella typhimurium
      • Widespread in most species.
    • Salmonella dublin
      • Cattle
    • Salmonella cholerae suis
      • Pigs
      • Usually speticaemic.
      • Not very common now.
    • Salmonella montevideo
      • Produces outbreaks from contaminated imported meat and bone meal.
  • Strains are often named after where they were first isolated.
  • Typing is important for epidemiology.
  • All strains can occur epizootically, enzootically and sporadically.
  • All strains can also produce very similar changes.
• Salmonellosis is NOT very common in the dog and cat.
• However, the horse is often a carrier.
  • Stress may precipitate the disease, meaning Salmonellosis is seen often in veterinary hospitals.

Pathogenesis

• Disease is often seen associated with stress.
• organisms penetrate enterocytes before crossing the mucosa and entering macrophages.
  • After entering macrophages, organins may then either remain localised to the gut, or are carried round the body to cause disease.
• There are 2 main types of disease- septicaemic and enteric.
  • Each outbreak causes only one type of disease.
  • Type of disease is linked to serotype- some serotyopres produce septicaemia, whereas others remain localised in the gut.

Septicaemic Salmonellosis

• Septicaemic salmonellosis is very dramatic and produces death quite suddenly.
• diarrhoea is often not seen before death.
• This form of the disease is unusual in the very young.

Pathogenesis

• The organism colonises bowel epithelium, where it affects the Peyers patches.
  • It then invades macrophages, which enable it to invade across the epithelium to the submucosa. It may then either
    • Remain localised to submucosa, or
    • Spread to the lymph nodes and enter the circulation to become septicaemic.
• Animals may die at this stage (30%), but this depends on such factors as the infecting dose and strain.
• Is similar to septicaemic E. Coli.

Clinical

• Is usually post-weaning (is unusual in the very young animal).
  • 6 to 9 months in calves.
  • 6 to 10 weeks in piglets.
• Animals suffer from pyrexia, and occasionally a little bit of diarrhoea.
• Skin is reddened diffusely
  • Bruise-like dark purplish-red blotched may be seen.

Pathology

• Intestines
  • May show mild catarrhal enteritis, becoming fibrinous lower down.
  • The bowel is generally flaccid, reddened and filled with fluid.
  • Ecchymotic and petechial haemorrhages on serosa and mucosa.
  • Enlarged, haemorrhagic mesenteric lymph nodes.
• Excessive blood-tinged peritoneal fluid.
• Lungs are collapsed and frothy.
• Heart is often dilated with ecchymotic haemorrhages.
• Viscera have a "half-cooked appearance"
  • Pale in colour.
  • The liver and kidneys are also flabby and may have subcapsular haemorrhages.
  • The liver may contain small white foci of necrosis known as paratyphoid granulomas.

Diagnosis

• By culture of blood and from mesenteric lymph nodes (which are oedematous and red).

Enteric Salmonellosis

• Enteric Salmonellosis shows differences in clinical presentation between species.
  • Horse - acute fatal colitis.
  • Cows - lingering febrile diarrhoea with passage of pseudomembranes.
  • Calves - acute diarrhoea like colibacillosis.
  • Dogs - acute bouts of diarrhoea.
  • Cats - febrile enterocolitis.
  • Pigs - septicemia or enterocolitis.

Clinical

• Affected animals produce acute diarrhoea, which causes many deaths.
  • Watery and yellow.
  • May be tinged with a little blood.
• Animals may die from dehydration.
• In some outbreaks, particularly in pigs, chronic low-grade diarrhoea only is seen.
• Calves usually die in acute stage, but may also recover.

Pathology

• Enteritis is seen throughout the gut, but is worse further along the gut.
  • Inflammation is catarrhal in the duodenum.
  • By the ileocaecal junction enteritis is often fibrinous, sometimes with formation of diptheric membranes on the mucosal surface.
• The necrotic and fibrinous changes particularly affect the Peyers patches and the caecal and colonic lymphoid nodules.
  • May lead to "button ulcers" in the terminal ileum and colon.
    • These ulcers rupture very rarely.
• Focal necrosis may also be seen.
  • Particularly in the liver, but also in the spleen.
  • Histologically, foci show a central zone of necrosis, surrounded by macrophages and lymphocytes- paratyphoid granulomas.
    • Although this indicates the animal has had a systemic incfection, paratyphoid granulomas may be present without showing signs of septicaemia.
    • Enteric cases of salmonella infection nearly always show some evidence of systemic spread.
• Septicaemic form may relocalise in the gut, resulting in enteric disease.

Sequelae

• Animals can remain carriers for months/years following recovery from the acute diarrhoea phase.
  • Bacteria is shed from the bile duct and mesenteric lymph nodes.
    • A source of infection for other animals and people.
    • Shed particularly in times of stress.
• Stricture of the rectum.
  • A possible sequel to acute salmonellosis, especially in the piglet.
  • Just a few centimetres in from the [[anus - Anatomy & Physiology|anus]].
  • Gives rise to:
    1. Difficulty in passing faeces.
    2. Megacolon
    3. thin watery diarrhoea in small 'pencils'.
    4. blown up abdomen
  • Animals eventually die from the stricture if they are not first destroyed.

Swine Dysentery

• Swine dysentery gives rise to fibrinous/ haemorrhagic enteritis.
• A quite common and important disease.
• The disease is caused by Brachyspira hyodysenteriae.
  • Is not seen in gnotobiotic animals - other enteric pathogens such as Fusobacterium or Bacteroides may therefore also be required in order to produce disease.
• The disease is NOT systemic.
  • Localised to the large intestine- in particular, the spiral colon.
• Swine dysentery is spread by the faeco-oral route, and is carried by pigs and rodents.

Clinical

• Affects post weaning pigs at approximately 4 months of age.
• White scour becomes a liquid dirty red / brown scour with a foul smell.
  • Contains poorly digested focal shreds of mucosa and fibrin strands.
    • Mucoid covered faeces.
• There are three outcomes to infection; the animal may:
  • Die
  • There is a morbidity up to 90% in the herd, with up to 50% mortality.
  • Recover
  • Become chronically infected.
• Symptoms are due to loss of absorption in colon.
  • The colon is normally a key site of absorption for water and electrolytes in the pig.

Pathology

• The serosa of the spiral colon may appear shiny from the outside.
  • Is turgid and oedematous.
  • In severe cases, haemorrhage may be seen.
• The small intestine NOT affected.
• Fibrinous deposits are seen on the mucosa as the disease progresses.
  • The mucosa underneath is eroded to expose blood vessels in lamina propria.
    • Accounts for the bleeding.
• Animals often recover, but have a low feed conversion ratio for sometime.

Diagnosis

• Silver stains show organisms in the epithelium of the mucosa.
• Also by immunofluorescence or electron microscopy.

Parvovirus Enteritis

• Parvovirus enteritis is also know as feline infectious enteritis or feline panleucopenia
• Since a vaccine is available, this disease is now uncommon.
• Over the last 10/15 years this has been seen primarily in the cat, but it is now also seen in the dog.

Clinical

• Manifests mainly in cats under 6 months old.
• Common in groups of unvaccinated cats.
  • Produces big outbreaks, with vomiting and pyrexia.
• Severe vomiting and diarrhoea occur.
  • diarrhoea is thin, watery and foul-smelling, and may also be blood-tinged.
    • Animals usually die despite treatment- die from dehydration.
• Animals suffer from fever.
• Pancytopaenia also occures.
  • White blood cell count drops very low so as to become almost non-existent.
    • Drops to 1/ml from 10000/ml.
  • Animals may therefore also die from other infections.

Pathology

Gross

• Virus targets crypt cells and lymphoid areas.
  • Causes villus atrophy.
• In the cat, the intestine is thickened, turgid and swollen.
  • Has a pale, dull and mottled appearance.
  • The contents are rather dry - this gets worse lower down the gut.
• Areas of depression in the mucosa can be seen in the upper small bowel.
  • Due to necrosis of tissue overlying Peyers patch.
• Lower down in the gut, enteritis is apparent.
  • Cat- fibrinous.
  • Dog- haemorrhagic.
    • Blood in lumen.
  • Inflammation sometimes doesn't appear very severe.
• There may be very few lesions
  • Histology is usually required for diagnosis.
• A radiomimetic virus.
  • Affects all rapidly dividing cells and destroys them.
    • E.g. epithelium in the base of the crypts of small intestine are killed.

Histological

• The crypt lining cells undergo complete necrosis, but very little inflammation occurs.
  • Collapse of villous architecture.
• May be fibrinous exudates on surface of mucosa.
• The submucosa and lamina propria are not affected and are left intact.
  • Many neutrophils in the lamina propria.
• Cyst-like structures are seen in the deepest parts of the glands of the intestinal mucosa, if the animal survives for more than a few days.
  • Flattened epithelial cells line these cystic glands.
    • Are enterocytes trying to repair the damage.
    • However, animals usually die from dehydration or secondary infection before the mucosa recovers.
• Inclusion bodies may be seen, but these are very hard to find.
• May get lymphocyte invasion of mucosa.
• Lymph nodes appear pale and oedematous, and almost aplastic.
• Bone marrow appears pale and fatty looking and is depleted of cells.

Canine Disease

• Until 1978 Parvovirus enteriris was totally unknown in dogs.
• First seen in dogs in Australia.
  • Apeared very similar but perhaps slightly worse than the disease seen in the cat.
  • A new and distinct disease, but the virus is very closely related to the feline virus.
    • Viral DNA is 98% homologous to the feline virus.
  • The canine virus does NOT cause disease in cats.
• Clinical
  • Causes enteritis in young dogs over 6 weeks old.
  • Causes myocarditis in puppies.
  • Mainly affects the small intestine.
• Vaccines are very effective, but the virus is hardy and survives in the environment.
• Diagnosis:
  • Look for viral antigen in the faeces by the red cell agglutination test.
  • Immunoflurescence.
  • ELISA.
  • Serology.

Bacterial septicaemia and enteritis

• Some severe acute septicaemias cause very severe acute haemorrhagic enteritis with bleeding into the alimentary tract.
• Death is usually rapid.
• Fairly easy to diagnose
  • small intestine is full of dark, tarry, partly clotted blood (like black currant jelly).
• Associated with severe systemic disease, e.g.
  • Anthrax in cattle (Bacillus anthracis).
  • Leptospirosis in dogs.
    • Especially L. icterohaemorrhagiae.
• Do not confuse with warfarin poisoning.
  • Also gives blood in stomach and intestine BUT there are no signs of inflammatory disease.

Lamb Dysentery (Enterotoxaemia with Blood)

• Clostridium perfringens causes very severe acute haemorrhagic enteritis.
  • Usually affects young farm animals
    • May also be seen in pets.
• Type B Clostridium perfringens infection of lambs leads to lamb dysentery.

Clinical

• Lamb dysentery is usually seen in lambs under 2 weeks of age.
  • Related to being kept in a cold, dirty environment, with build-up of infection during the lambing season.
• Lambs may produce bloodstained diarrhoea before death, but they often die before this effect is apparent.
• Diagnosed by culturing contents of gut.

Pathology

Gross

• The gut is blown and distended with foamy ,bloody contents.
• Sometimes ulceration with perforation and fibrinousperitonitis is seen.
• Focal or diffuse congestion and haemorrhages.

Histological

• Coagulative necrosis of villi.
• Oedema.
• Haemorrhage.
• Influx of inflammatory cells in the lamina propria and submucosa.

Similar Conditions

• Piglets show similar disease caused by Clostridium perfringens type C (and sometimes type B)
  • May look similar to a volvulus but with no twist present.
• In adult sheep Clostridium perfringens type B infection causes Struck.
  • Enterotoxigenic gastritis.
  • Acute sudden death with haemorrhagic enteritis
  • Haemorrhagic enteritis is not as severe as in lambs, and tends to be more patchy.

Colitis X

• Affects the horse.
• Sudden onset with haemorrhages throughout body (shock) and sometimes acute foul smelling diarhoea.
• colon is acutely haemorhagic and oedematous with mucosal necrosis.
• Associated with Clostridium perfringens.
• Possibly an enterotoxaemia.