JPC SYSTEMIC PATHOLOGY
DIGESTIVE SYSTEM
October 2018
D-T04

Signalment (JPC #2548697):  An 8-month-old Holstein steer

SLIDE A:

HISTORY:  This animal died while being transported to a diagnostic laboratory.  The steer had suddenly stopped eating and became lethargic the day before.  The only significant gross lesion was a pale and extremely firm liver.  Groundsel (Senecio spp.) was identified in the hay that had been fed to this animal.

HISTOPATHOLOGIC DESCRIPTION:  Liver:  Diffusely, there dissociation of hepatic cords with loss of hepatic cord architecture and multifocal loss of hepatocytes with replacement by intersecting bands of fibrous connective tissue.  These fibrous bands expand and bridge centrilobular and portal zones (bridging fibrosis), extend into and replace approximately 50% of the normal hepatic cord architecture, and separate, surround, and individualize hepatocytes.  The fibrous bands are admixed with markedly increased numbers of biliary duct profiles (ductular reaction).  Multifocally, centrilobular fibrosis surrounds, compresses, and occasionally obliterates central veins (veno-occlusion).  Multifocally, hepatocytes are mildly swollen with pale, vacuolated cytoplasm (degeneration) or less frequently have abundant cytoplasm and nuclei up to twice normal size (megalocytosis) with rare intranuclear cytoplasmic invaginations.  Multifocally individual hepatocytes are shrunken with hypereosinophilic nuclei and pyknotic or karryorhectic nuclei (necrosis).

MORPHOLOGIC DIAGNOSIS:  Liver: Hepatocellular degeneration and loss, diffuse, severe, with centrilobular and portal bridging fibrosis, marked biliary ductular reaction, hepatic veno-occlusion, and megalocytosis, Holstein, bovine.

SLIDE B:

HISTORY:  This 9-month-old, male, sport horse presented with a 6-week history of lesions involving the dorsal cervical and nasal skin.

HISTOPATHOLOGIC DESCRIPTION: Liver:  Diffusely, periportal and to a lesser extend midzonal sinusoids are expanded and often effaced by a florid proliferation of bile ducts admixed with a moderate amount of mature collagen, hypertrophied fibroblasts (fibrous connective tissue), and few neutrophils and lymphocytes.  In these affected areas, there is loss of normal hepatocellular architecture; hepatocytes are separated, individualized, surrounded, and often replaced by proliferating bile ducts.  Remaining hepatocytes are often enlarged up to 2-3 times normal (megalocytosis), with cytoplasm ranging from a lacy, pink, ground glass appearance (glycogen-type vacuolar change) to microvacuolated (lipid-type vacuolar change); both changes may be seen in the same hepatocyte.  Many hepatocytes contain nuclei which are three times the size of surrounding hepatocytes and have open chromatin and a prominent nucleolus (megalocytosis); low numbers of nuclei contain entrapped, eosinophilic, intranuclear cytoplasmic invaginations.  Entrapped hepatocytes are often shrunken (atrophic) and rarely are hypereosinophilic with pyknotic nuclei (necrotic), occasionally surrounded by low numbers of neutrophils.  Some hepatocytes contain abundant cytoplasmic granular brown pigment (hemosiderin or lipofuscin), and scattered macrophages within areas of biliary reduplication contain similar pigment (hemosiderin).  There are scattered nodules of hepatocyte hyperplasia/nodular regeneration, and the overlying capsule is undulant.  Portal areas contain small numbers of lymphocytes, plasma cells, and rare hemosiderin-laden macrophages.  Portal lymphatics are moderately ectatic.

MORPHOLOGIC DIAGNOSIS:  Liver: Hepatocyte degeneration, necrosis and loss, chronic, diffuse, severe with severe biliary hyperplasia,  portal and bridging fibrosis, nodular regenerative hyperplasia, and hepatocellular megalocytosis, sport horse, equine.

ETIOLOGIC DIAGNOSIS:  Pyrrolizidine alkaloid hepatopathy

CAUSE:  Pyrrolizidine alkaloids

GENERAL DISCUSSION:

PATHOGENESIS:

CLINICAL FINDINGS:

TYPICAL GROSS FINDINGS:

TYPICAL LIGHT MICROSCOPIC FINDINGS:

ADDITIONAL DIAGNOSTIC TESTS:

DIFFERENTIAL DIAGNOSIS:

Hepatocellular megalocytosis in cattle:

Causes of end-stage liver:

COMPARATIVE PATHOLOGY: 

REFERENCES:

  1. Brown DL, Van Wettere AJV, Cullen JM. Hepatobiliary system and exocrine pancreas. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 6th ed. St. Louis, MO: Elsevier; 2017:429-430, 440, 449-450.
  2. Cullen JM, Stalker MJ. Liver and Biliary system. In: Maxie MG, ed. Jubb, Kennedy and Palmer’s Pathology of Domestic Animals. Vol 2. 6th ed. St. Louis, MO: Elsevier Ltd; 2016:336-338, 519-520.


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