Domestic rabbit (Oryctolagus cuniculus) with a brief history of sneezing, coughing, serous conjunctivitis and neurological signs, followed by death.
Example histopathological description
This is a triangular section (13 x 21 x 22 mm) from the edge of the liver, with serosal capsule on 2 sides and one cut surface. There is a widespread but poorly defined pattern of acute hepatocyte degeneration and necrosis. In some areas changes are more severe in midzonal to periportal locations; in other areas the pattern appears random. Affected hepatocytes exhibit a range of changes from mild swelling, vesiculation and vacuolation, to hypereosinophilia, separation, karyorrhexis and karyolysis. Necrosis ranges from single cell to multiple foci of small clusters of cells (coagulative necrosis) with disruption of hepatic cords. Occasional heterophils are associated with areas of necrosis. Portal areas are sparsely infiltrated with lymphocytes and macrophages but the biliary system is largely spared. Dark brown, fine to coarse granular pigment is present in scattered hepatocytes and Kupffer cells throughout the section (indicating haemosiderin, bile, acid haematin). There are modest numbers of binucleate hepatocytes, which is normal for this species. In two large vessels there are irregular sheets of hepatocytes, many of which are degenerate or necrotic. The presence of sparse microthrombi and vascular wall degeneration is equivocal.
Hepatocellular necrosis, coagulative; acute, diffuse, moderate to severe.
Rabbit calicivirus disease
A range of toxic hepatopathies is possible including aflatoxins, cyanobacterial toxins, copper, fluoride, paracetamol, and some hepatotoxic plants (including gossypol toxicity (cottonseed)). Heat stress and a range of bacterial hepatopathies must also be considered including salmonellosis, pasteurellosis, Tyzzer’s disease, tularaemia, listeriosis and bubonic plague.
Toxic hepatopathies are considered less likely due to the pattern of individual cell necrosis. Similarly, bacterial hepatopathies are less likely due to the very limited inflammatory cell response and the absence of liquefactive necrosis. It should be noted that myxomatosis can occasionally be associated with small foci of hepatic necrosis and or periacinar ischaemic changes. Antigen detection of the calicivirus using ELISA, PCR or immunohistochemistry is required to confirm the diagnosis.
Multifocal haemorrhagic ulcers on a Jade perch or Barcoo grunter (Scortum barcoo)
Example histopathological description
Four sections of skin, subcutis and skeletal muscle are present. The skin has multiple areas of ulceration with loss of scales and locally extensive inflammation and granuloma formation. The lesion extends along connective tissue tracts deep into the subcutis and skeletal muscle. Adjacent intact epidermis shows hyperplasia, oedema and infiltration with granulocytes and mononuclear cells. The subcutis contains areas of extensive oedema, scattered haemorrhages and mixed inflammatory cell infiltrates with granulocytes and macrophages prominent. Fibrosis and vascular proliferation are prominently associated with multifocal granuloma formation. Skeletal muscle has variable degrees of inflammation including granular (flocculated) degeneration, and sarcolemmal oedema extending to necrosis and phagocytosis in places. Granuloma formation is prominent in the dermis and subdermis. There is a central core of hypereosinophilic degenerate cells, often with one or more round to irregular shaped central clear areas. Around the central core is a prominent zone of viable mononuclear cells (presumed to be macrophages) with lesser numbers of granulocytes and lymphocytes. Indistinct fungal hyphae are present in the centre of some granulomas. Fungi are branching and thin walled. The diameter and the presence of septae are difficult to determine in this H&E preparation.
Dermatitis, panniculitis and myositis; granulomatous, chronic, locally extensive, severe, with intralesional fungal elements.
Aphanomyces invadans infection (Red Spot Disease, Epizootic Ulcerative Syndrome)
Other fungi (including other Aphanomyces spp) and other oomycetes are possible. Also, a range of bacterial agents, including Aeromonas salmonicida and mycobacteria, might be considered. However, most other fungi do not usually cause this type of severe, deeply penetrating lesion and the absence of bacterial colonies and parasites make their involvement less likely. Special stains (fungal silver, PAS, ZN) and antigen identification, using PCR or other techniques, are required to confirm the diagnosis.