Stephen Lister Crowshall Veterinary Services

1. Review of cholangiohepatitis: gross pathology, histopathology and pathophysiology - the whats and the whys! Stephen Lister Crowshall Veterinary Services

3. Big livers - big words! • Necrotic enteritis (NE) • Clostridium perfringens (CP) • Cholangiohepatitis (CH)

4. Necrotic enteritis • First described in 1961 in England • reproduced by infecting chickens with clostridia • was a significant clinical disease • “disappeared” • now re-emerging as the disease of the moment

5. Necroticenteritis • Necrotic = dead • enteritis = inflamed intestine

6. The intestines • An important organ • interface between feed and ability to transform this into £.s.d • works best in a state of homeostasis

7. Homeostasis • Homeo = same • stasis = state • i.e. keeping everything in balance

8. The intestines • Chick hatches with a sterile gut • gut is receptive to colonisation with bacteria • development of a balanced gut microflora • numerous bacteria

9. clostridia E coli streptococci staphylococci proteus pseudomonas lactobacillus enterococcus citrobacter eubacterium veillonella fusobacterium bacteroides propionobacteria bifidobacteria etc etc Gut bacteria

10. Necrotic enteritis • A consequence of the loss of this balance • Enterotoxaemia of chickens caused by toxigenic strains of Clostridium perfringens types A • reproduced by infecting chickens with clostridia • mostly affecting broilers, • but also turkeys, occ. layer and breeder replacements, ducks, geese

11. But why? • Models for creating necrotic enteritis - how to do it! • feed clostridia • feed contaminated with clostridia • change gut pH + clostridia • coccidial challenge + clostridia • high wheat + coccidia + clostridia

12. But why? • Clostridial proliferation • damage to the gut • changes in the gut • loss of homeostasis

13. Effects • Mortality • loss of performance

14. Loss of performance

15. Effects • Mortality • loss of performance • diarrhoea • wet litter • need to treat • and …..

16. ….. if that’s not enough! • Carcase rejects and bad colour • liver damage and jaundice • cholangiohepatitis (CH)

19. What is it? • cholangiohepatitis or fibrosing cholehepatitis or septic intrahepatic choleostasis • hepatitis = liver inflammation • septic = infection • intrahepatic = in the liver • choleostasis = bile stops

20. Findings on the processing line • Bad colour • jaundice • ascites? • Enlarged liver • tan coloured • knobbly appearance • speckled liver

21. What is happening? • It is costing money through downgrading • 3 to 5% downgrades not unusual • We know there is an association with NE & CP • often no disease reported on farm • so why do I see CH without seeing NE or any significant increase in mortality?

25. Experimental work • Not a lot of published literature • Onderka et al (1990) in Canada • Experimental reproduction of the problem • ligating the bile ducts • injecting CP into the bile duct

26. Ligating bile ducts • 21 to 28 days of age • 6 days p.l.: intensely yellow droppings • 5 days p.l.: bile duct proliferation • 10 to 14 days p.l.: liver changes • 28 days p.l.: enlarged tan coloured liver, speckled appearance

28. Injecting CP • 5 to 7 days p.i.: swollen mottled livers • 12 days p.i.: pale, firm mottled livers • 17 days p.i.: enlarged, firm, tan coloured, speckled liver

29. What is happening? • Clinical or subclinical NE can lead to CH at processing • clostridial infection of liver/bile ducts can be “silent”, or associated with very small lifts in mortality but still lead to considerable downgrading • timing of clostridial proliferation is not precisely known, but can be <10 days of age

30. But why? • Clostridial proliferation • damage to the gut • changes in the gut • loss of homeostasis

31. cereal content cereal type use of barley use of whole wheat loss of GPs loss of MBM changes in raw materials least cost rations shorter turnaround times Lighting programmes Less routine antibiotics coccidiostat choice chemical shuttles longer withdrawl times gumboro disease Chick anaemia virus But what has changed?