March 2010

Case A

open slide in the AHA AAPSP Digital Slide Server


An 18 month old Brahman steer with a history of weight loss and onset of neurological signs.

Example histopathological description

Throughout this liver section, hepatocytes are very large with large nuclei (megalocytosis). There are 3 – 4 small round nodules that are composed of uniformly smaller hepatocytes than those within the matrix of larger hepatocytes (nodular hyperplasia). There is extensive periportal proliferation of stem cells (bile ductular hyperplasia) which extends diffusely throughout the acini. Associated with the stem cell proliferation there is a mild increase in fibrous tissue, forming delicate bridging between portal triads. Scattered foci of lymphocyte infiltration are also present, particularly in periportal areas. Periportal lymphatics in larger triads are dilated, with a low amount of protein and small numbers of erythrocytes in the lumen. There is some oedema surrounding some bile ducts. The cytoplasm of some hepatocytes is expanded by large pale homogenous accumulations, and in others there are densely eosinophilic globular bodies (cytosegrosomes), while others appear to have a granular cytoplasm and some contain pigment deposits consistent with bile retention. Some also have small clefts in their cytoplasm. There are a few small foci of hepatocytes with fatty vacuolation present in some areas. There is possibly some cuboidal metaplasia of the mesothelium of the capsule, but it is slightly out of focus and difficult to be certain. At one edge of the section there is a large hepatic vein whose intima bears bulky loose accumulations of fibrous tissue within which are some multinucleate forms.

Morphological diagnosis

Hepatopathy; chronic, diffuse, severe, characterised by condensation-type fibrosis, stem cell hyperplasia, megalocytosis and mild nodular hyperplasia.  There is also possible venular intimal fibrosis (so-called veno-occlusive disease).


This is chronic hepato-intoxication, with pyrrolizidine alkaloidosis being more likely than aflatoxicosis or MAM (methylazoxymethanol in zamia) intoxication.  Chronic phomopsin poisoning is discounted by the absence of corrupted mitoses.  Lantana sp poisoning is not likely to cause hepato-encephalopathy, nor would one expect such severe variation in hepatocyte size with nodular regeneration.  Chronic sporidesmin poisoning would cause much more severe portal fibrosis and little or no megalocytosis.

Case B

open slide in the AHA AAPSP Digital Slide Server


A group of grower pigs with a few that are anorexic, listless, collapsing and dying.

Example histological description

These two sections are of cardiac muscle, one of which has a section of valve leaflet attached. In both there is moderate to marked, diffuse, interstitial infiltration of leucocytes with moderate to marked oedema separating the cardiac myocytes. The infiltrate consists predominantly of macrophages, with some lymphocytes, plasma cells and lesser numbers of neutrophils and eosinophils. Scattered nuclear debris is occasionally present with this cellular infiltration. There is also some early interstitial fibrosis in some areas, and moderate epicardial oedema. There are widespread degenerative changes in the myocardium; these are characterised by loss of cross striations, sarcoplasmic vacuolation, pallor, and fragmentation. There are a few necrotic cardiac myocytes and a little associated dystrophic mineralisation. Minimal inflammation is associated with these areas of mineralisation.

Morphological diagnosis

Myocarditis, non-suppurative interstitial, subacute, diffuse, severe, with multifocal myocardial degeneration.

Aetiological diagnosis

Encephalomyocarditis virus infection.