Western Meeting of Poultry

 Clinicians and Pathologists 

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Further Investigations of the Hemorrhagic Hepatitis Syndrome in Layers

D.K. Onderka

Hemorrhagic hepatitis is a syndrome that has in recent years been recognized in Western Canada in adult leghorns and broiler breeders. It is characterized by extensive intrahepatic hemorrhages mixed with areas of necrosis. In some cases, splenomegaly was also described as part of this syndrome. In a previous report we attempted to establish a possible relationship between piperazine overdose and hemorrhagic liver syndrome, however, no hepatic lesions were induced with repeated 10-fold therapeutic doses of piperazine hydrochloride. Bacterial cultures of affected livers are usually negative, however, from a number of cases we did isolate Clostridium perfringens particularly from the gall bladder. It is possible, that Clostridium perfringens establishes itself in the gall bladder post mortem. A pilot study indicated that this is possible when carcasses were stored at room temperature for 24 hours or longer. Nonetheless it was thought to be worthwhile to explore a possible role of Clostridium perfringens in the pathogenesis of hemorrhagic liver syndrome:

20 week old white layer hens were inoculated via a cannulated bile duct with 10¹¹ saline-washed Clostridium perfringens organisms contained in 0.5 ml normal saline. Control birds were inoculated only with saline and as a positive control; a 3-week-old broiler was also inoculated with Clostridium perfringens.

After 19 days post inoculation, the birds showed no clinical signs. The broiler had a firm, swollen liver with a slight film of fibrin on the surface. It was brown discolored and the gall bladder was edematous. On histology, there was inflammation and bile duct proliferation and reticulin stain showed a marked increase in reticular fibres typical of the lesions described with cholehepatitis in broilers.

The layers were examined 27 days post inoculation. There were no clinical signs and no gross lesions. Microscopic lesions consisted of a mild to moderate increase in periportal lymphocytes with occasional heterophils and a slight widening between hepatic cords. Reticulin stain clearly demonstrates increased reitcular fibres suggesting a lesion similar to the one seen in broilers, although fibrosis was less extensive.

This seems to be a fairly convincing argument that simple invasion of the liver through the bile system by gut clostridia is likely not the underlying cause of hemorrhagic hepatitis.

In a recent mortality survey of leghorns, a significant cause of mortality was hemorrhagic liver syndrome or ruptured liver. There were only a few birds that had lesions suggestive of hemorrhagic hepatitis. It was intriguing to speculate that these two conditions might be related and hemorrhagic hepatitis may be amore chronic sequel to ruptured liver and hemorrhagic liver syndrome. H & E stained histologic sections are not convincing against or for such a hypothesis. In "mild" forms of hemorrhagic hepatitis there are areas in which there seems to be lyses of hepatic cords and pooling of proteinaceous fluid. While chronic cases result in granulomas and extensive necrosis, ruptured liver may also result in necrosis of the surrounding tissue and an inflammatory response to the resolving blood clot. Reticulin stains suggest possibly a lyses of reticular fibres in the area of acute lesions of either case, however, as the lesion becomes more chronic, reticulin fibres increase as a predicable sequel of a chronic tissue response in a healing phase. It might be that the two syndromes have a similar mechanism by which the tissue injury and changes occur.

It would be interesting to study the lipid metabolism in livers from these birds to see if excessive cytoplasmic lipidosis might be an underlying cause for a possibly spontaneous occurrence of these syndromes.

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Last modified: 5/28/2009