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Read-Only Case Details Reviewed: Jan 2010

JPC SYSTEMIC PATHOLOGY

DIGESTIVE SYSTEM

October 2024

D-T01

 

Signalment (JPC #1617774): A pig

 

HISTORY: This animal was non-confinement raised and died acutely.

 

HISTOPATHOLOGIC DESCRIPTION: Liver: Affecting 60% of hepatic lobules, there is submassive necrosis characterized by disorganization and loss of centrilobular and midzonal hepatic cords with replacement by abundant necrotic debris and hemorrhage. Remaining hepatocytes are individualized, shrunken, and hypereosinophilic with pyknotic, karyorrhectic, or karyolytic nuclei (single cell death), and are admixed with moderate hemorrhage, fibrin, edema, and few neutrophils. Adjacent to areas of necrosis, few hepatocytes are swollen with clear, vacuolated cytoplasm (degeneration) admixed with few lymphocytes, plasma cells, rare neutrophils, and eosinophils. Centrilobular sinusoids are diffusely markedly congested. Multifocally within portal areas, there is a mild to moderate infiltrate of the previously described inflammatory cells, expansion by eosinophilic homogenous fluid (edema), increased numbers of ductular profiles (ductular reaction) and mildly dilated lymphatics.

 

MORPHOLOGIC DIAGNOSIS: 1. Liver: Necrosis, acute, centrilobular to midzonal (submassive), diffuse, with multifocal hemorrhage and congestion, breed unspecified, porcine.

2. Liver: Hepatitis, portal, lymphoplasmacytic, chronic , multifocal, mild. 

 

ETIOLOGIC DIAGNOSIS: Toxic hepatic necrosis

 

CAUSE: Xanthium strumarium 

 

CONDITION: Cocklebur intoxication

 

GENERAL DISCUSSION:

 

PATHOGENESIS:

  • Carboxyatractyloside inhibits oxidative phosphorylation by binding to ADP/ATP carrier 1 (AAC1) > inhibits the exchange of ATP from mitochondria with ADP in the cytosol > decreased ATP > mitochondrial damage > pore leakage > release of cytochrome-c > apoptosis OR necrosis with massive mitochondrial damage, ion pump failure, lipid peroxidation, and glutathione depletion

 

TYPICAL CLINICAL FINDINGS:

  

TYPICAL GROSS FINDINGS:

 

TYPICAL LIGHT MICROSCOPIC FINDINGS:

  • Severe centrilobular to massive hepatic necrosis 

 

DIFFERENTIAL DIAGNOSIS 

Microscopic:

 

COMPARATIVE PATHOLOGY:

Toxic plant causes of centrilobular necrosis in animals: 

Plant Family

Species Affected

Toxic Principle

Characteristic Injury

Miscellaneous

Compositae

Xanthium spp.

Cattle, pigs

Carboxyatractyloside

Centrilobular necrosis

Hypoglycemia and ascites occur in acute intoxication in pigs.

Myoporaceae

Myoporum spp.

Sheep, cattle, horses, pigs

Furanosesquiterpenoid oils (ngaione)

Usually centrilobular to variable zonal necrosis

Sheep also develop pulmonary injury.

Leguminosae

Cassia spp.

Cattle

Unknown

Centrilobular necrosis

Myocardial and skeletal muscle injuries predominate in Cassia occidentalis intoxication.






Ulmaceae

  Trema aspera

Trema tomentosa

Cattle, sheep, goats

Trematoxin (glycoside)

Centrilobular necrosis

Neuromuscular toxins also. Usually acute disease.

Solanaceae

 Cestrum parqui,   

 C. laevigatum 

 (not C. diurnum)

Cattle, sheep

Saponins

Centrilobular necrosis

Gallbladder edema and hemorrhage. Usually acute disease.

Asteraceae

  Tetradymia  

  glabrata

 

Wedelia glauca

 

Sheep

 

Ox, swine, goat, horse

Tetradymol

 

Wedelocide (atractyloside)

Centrilobular necrosis

Photosensitization is common.

 

(Giannitti, Vet Pathol. 2013)






Cycadales

  Zamiaceae

  Cycadaceae

  Stangeriaceae

Cattle, sheep, goats, dogs

Methylazoxymethanol

Centrilobular necrosis, megalocytosis, cholestasis

Toxin split from nontoxic glycoside. Neurotoxins also present. Chronic ingestion causes paralysis in cattle.

Fabaceae

  Indigofera 

  linnaei

Cattle, dogs

Indospicine

Centrilobular necrosis

Dogs can be intoxicated by eating meat from horses ingesting Indigofera.

Cyanophyceae (blue-green algae)

  Microcystis

 Aphanizomenon

Cattle, sheep, horses, goats, dogs

Microcystins and others

Centrilobular to massive necrosis

Blue-green algae are not considered to be plants but cyanobacteria. Multiple toxins are present and can cause death by neuromuscular injury

 

Table adapted from Pathologic Basis of Veterinary Disease, 7th ed., 2022, E Table 8-1 Common Hepatotoxic Plants of Veterinary Importance

 

REFERENCES:

  1. Brown DL, Van Wettere AJV, Cullen JM. Hepatobiliary system and exocrine pancreas. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 7th ed. St. Louis, MO: Elsevier; 2022: ETable 8-1: 512. 
  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: 330- 331.
  3. Ensley SM, Radke SL. Toxic Minerals, Chemicals, Plants and Gases. In: Zimmerman JJ, Karriker LA, Ramirez A, Schwartz KJ, Stevenson GW, Zhang J Diseases of Swine. 11th ed. Hoboken, NJ: Wiley Blackwell; 2019: 1080. 

 


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