Category:Enteritis, Proliferative

Paratuberculosis (Johne's Disease)

Proliferative Enteritis in Other Species

Granulomatous Colitis

• Affects the horse.
  • Usually young to middle age adults.
• Unknown cause.
• Is a one-off occurence rather than a herd problem.
• As in Johnes Diseaase, there is chronic ongoing diarrhoea with eventual death.
• Thickening of mucosa is seen mainly in the caecum and colon.
  • Lamina propria contains granulomatous inflammatory tissue (as in Johnes Disease).
  • Sometimes large numbers of eosinophils are seen.
• Mesenteric lymph nodes are very large.
• At laparotomy lymph node appears like lymphosarcoma (very large).
• Cannot do much to remedy the condition once it has started.
  • Progresses to death.

Proposed Pathogenesis

• Hypersensitivity reaction to trichoneme parasite?
  • Possibly an idiosyncratic response to the encysted larvae.
• Dysbacteriosis or disordered immune response?

Porcine Adenomatosis Complex

• Characteristic proliferation of mucosa.
• Known as PIA - porcine intestinal adenomatosis.

Clinical

• Really only seen in the pig.
  • Can affect all ages of pig.
• Clinical signs are variable.
  • Anything from poor weight gain to diarrhoea, weight loss, cachexia and death.
• Seen often as problem in closed, low infection herds.
  • Not seen in pigs with lots of other pathogens in guts.

Pathogenesis

• Caused by Lawsonia intracellularis.
  • A spirochete that does not grow well except in tissue culture.

Pathology

• The terminal small intestine and colon are affected by proliferation of the mucosal epithelium.
• Gross
  • Thickened mucosal epithelium.
  • Has almost polypoid-like nodules several millimetres in diameter.
  • Undifferentiated epithelium replaces goblet cells.
    • Appears almost neoplastic.
• Histologically
  • Very similar to a virus induced proliferation.
  • Organisms seen in the apical part of epithelial cells lining glands of terminal ileum, colon and caecum.
  • May produce mild ulceration in mucosa and mild inflammatory infiltration.

• Porcine adenomatosis complex can be divided into four distinct syndromes:
  1. Intestinal adenomatosis
     • THe basic hyperplastic and metaplastic changes are seen in the epithelium.
       

       Campylobacter mucosalis in intracellular porcine intestinal adenomatosis (Courtesy of Bristol BioMed Image Archive)
     • Causes chronic weight loss and diarrhoea.
  2. Necrotic enteritis
     • Predominately affects the colon and terminal ileum.
     • Parts of the hyperplastic mucosa develop erosions and ulcerations.
       • These areas become colonised by Fusiformis baceria.
         • Gives areas of coagulative necrosis covered by a thick diptheretic membrane.
  3. Terminal ileitis
     • Characterised by marked hypertrophic thickening of the muscular portion of the wall of the terminal ileum.
     • Gives an attendant stenosis of the lumen of the ileum.
     • There is associated thickening of the mucosa due to hypertrophy and secondary granulomatous inflammation.
       • This is presumably caused by a degree of obstruction to the passage of ingesta along the bowel caused by the mucosal hypertrophy.
     • Appears very similar to Johnes disease
       • Lots of mononuclear cells and a chronic granulomatous type of inflammation.
  4. Proliferative haemorrhagic syndrome.
     • The bowel shows proliferation but with ulceration and copious haemorrhage into the bowel lumen.
     • Animals are often be found dead.
     • The pathogenesis is unclear.
       • May involve a type of hypersensitivity reaction or secondary infection of some type.

Sequelae

• Resolution.
• Necrotic enteritis.
• Secondary chronic infection (regional enteritis).
• Porcine haemorrhgaic enteritis (PHE).