March 2014

Case A


Tissue from an ill-thrifty adult horse which had failed to respond to a variety of treatments. The horse was euthanized and at necropsy the liver was reported to be abnormal.

Example Histopathological Description:

The section is of liver including a capsular surface. The latter has been damaged and distorted before processing, but some cuboidal metaplasia is apparent in the few isolated segments of capsular mesothelium that remain.

Most of the parenchyma is partially replaced by florid bile-ductule and stem cell proliferation and extensive fibrosis that is pan-acinar in distribution and tends to isolate remaining hepatocytes, most of which show pronounced enlargement of both nuclei and cytoplasm (megalocytosis). The cytoplasm often has a coarsely granular appearance and a faintly basophilic tinge, particularly peripherally. Some megalocytes contain golden brown pigment and hyaline cytoplasmic inclusions (cytosegresomes), and canaliculi are sometimes manifest by bile casts. As well as being remarkably enlarged, and often multiple, megalocyte nuclei are hyperchromatic with prominent nucleoli and coarse heterochromatin, and many nuclei contain globular, pale, membrane-bound inclusions (pseudo-inclusions/intranuclear cytoplasmic invaginations). No mitoses are visible.

Mixed inflammatory cells are scattered fairly randomly throughout; these are mostly mononuclear and include lymphocytes and macrophages.

Spherical nodules of uniformly smaller hepatocytes are distributed randomly across the section. These vary in size, are devoid of bile-duct proliferation or fibrosis and appear to be expanding and compressing the adjacent, more degenerate, parenchyma. One such nodule contains a small focus of intense suppuration.

Morphological Diagnosis:

Hepatopathy; severe, diffuse, chronic with biliary hyperplasia, megalocytosis, diffuse dissecting fibrosis, canalicular cholestasis and multifocal nodular hepatocellular regeneration.

Aetiological Diagnosis:

Chronic pyrrolizidine alkaloid hepatopathy


While pyrrolizidine alkaloid (PA) poisoning is considered the most likely cause of this condition, it should be remembered that chronic poisoning by other agents such as methylazoxymethanol (MAM, the toxic metabolite of the cycad azoxyglucoside cycasin), aflatoxins and phomopsin can quite convincingly mimic PA poisoning.

Prior exposure to PAs can be confirmed by chemical assay for bound pyrroles in tissues (preferably fresh, but fixed liver can be used). The disadvantages of this diagnostic assay is that (a) it is expensive and difficult to find a laboratory willing to undertake it, and (b) it only proves that the animal was exposed to PAs, while death might have been due to another cause.


March 2014

Case B


In a group of 350 weaned lambs, 24 were found dead or dying. About 20% more looked weak with diarrhoea or wet faeces in the perineal wool. At necropsy, dark areas were described in the wall of the large intestine.

Example Histopathological Description

There is one section of colon and one of small intestine on the same slide. Post-mortem degeneration is minor.

In the colon, most of the crypt epithelium has been replaced by gametogenous stages of protozoa consistent with Eimeria sp. Most of the gamonts are macrogametocytes, and there are also many unsporulated oocysts. A few microgametocytes are also present, but no schizogeny is apparent. Superficial colonic epithelium is almost entirely eroded; deep ulceration is not a feature but the surface bears a thick pile of large bacilli that are apparently adherent end-on to the mucosa. The superficial lamina propria is variably diffusely infiltrated by degenerate leucocytes and high-protein oedema. Surviving crypt epithelium shows basophilia and attenuation consistent with attempted regeneration.

The small intestine also shows almost complete villous atrophy with severe attenuation of surface epithelium and severe and extensive invasion of crypt mucosa by the same sort of coccidial forms as those in the colon (although not quite as heavily or uniformly distributed). In addition, there are extensive areas of partial- to full-thickness mucosal necrosis associated with dense colonies of large bacteria of mixed morphology. These colonies are either attached to the necrotic mucosal surface, or at middle and deeper levels of necrotic mucosa. There are dense colonies at the interface with the muscularis mucosa in areas of full thickness necrosis. Throughout the lamina propria and loose tissue spaces of the submucosa there is extensive high-protein oedema and infiltration by scattered inflammatory cells, predominantly degenerate polymorphs.

Morphological Diagnosis

Colitis; coccidial, extensive, severe, subacute with secondary mixed bacterial superficial sub-acute colitis

Necrotic enteritis of the small intestine; coccidial, extensive, severe, sub-acute, with mixed bacterial colonies.

Aetiological Diagnosis

Coccidial enteritis and colitis


This is probably a primary Eimeria infection (the most common species in Australia are E. crandallis, E. ovinoidalis, and E.weybridgensis) with secondary infection by mixed bacteria, most probably Clostridia sp. among others, which is most severe in the small intestine.

Combined coccidiosis and bacterial necrotic enteritis is unusual in sheep, so confirmation of the association in this outbreak would be facilitated by additional necropsies, which would provide fresh material to enable coccidial identification to be made and bacterial culture for better definition of this unusual condition.


Yang R et al ‘Longitudinal prevalence, oocyst shedding and molecular characterisation of Eimeria species in sheep across four states in Australia’  Exp Parasitol. 2014 Oct;145:14-21