Etiology 

• Chemical Exposure:

  • Organic solvents (e.g., CCl4)

  • Phosphorous

• Drugs:

  • Nalidixic acid (antibiotic)

• Viral Infection:

  • Infectious Canine Hepatitis (caused by canine adenovirus-1)

• Mycotoxins:

  • Aflatoxin B1

• Other causes:

  • Sepsis (reactive hepatitis)

  • Leptospirosis

  • Hemolysis (discussed separately)

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Pathogenesis

• General Signs:

  • Enzyme levels, particularly liver enzymes, are usually elevated.

  • Fever can occur due to pyrogens from necrotic tissue and impaired removal of endotoxins and bacteria from portal blood.

  • Disseminated intravascular coagulation (DIC) is common.

• Fulminant Hepatitis:

  • Severe form, characterized by massive liver cell necrosis.

  • Leads to hepatic encephalopathy, DIC, jaundice, and hypoglycemia.

  • Progresses rapidly to coma and death.

• Histopathology:

  • Necrosis typically presents as liquefactive necrosis with collapse of the liver’s structural framework.

  • Inflammatory cells include round cells and neutrophils, along with "scavenger cells" (ceroid-laden macrophages).

• Canine Adenovirus-1 Infection:

  • Characterized by confluent and bridging necrosis in the centrilobular zone.

  • Presence of intranuclear inclusions in hepatocytes and Kupffer cells.

  • Immunofluorescence can identify the virus in liver tissue sections.

• Toxin-Induced Hepatitis:

  • Toxins such as Amanita mushroom toxins, blue-green algae toxins, and acetaminophen (in dogs and cats) can cause acute hepatitis.

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Clinical Symptoms

• Common Symptoms:

  • Sudden onset of illness

  • Lethargy (apathetic)

  • Fever (occasionally)

  • Anorexia

  • Vomiting

  • Dehydration

  • Icterus (yellowing of the skin or mucous membranes)

• Severe Cases:

  • DIC and bleeding tendency may develop.

  • Disease severity can range from mild to fulminant, potentially lethal disease.

  • In moderate cases, recovery is possible.

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Diagnosis

• Blood Work:

  • Elevated liver enzymes, particularly ALT (Alanine Aminotransferase).

• Liver Biopsy:

  • Confirm diagnosis by histopathology.

  • Coagulation status should be checked first, as it is often abnormal in these cases.

• Fulminant Hepatitis:

  • Hepatic encephalopathy often present with elevated blood ammonia (NH3) levels.

  • In many cases, the exact cause may remain unidentified.

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Treatment

• Symptomatic Treatment:

  • IV fluids to correct:

    • Hypovolemia

    • Shock

    • Acidosis or alkalosis

    • Hypoglycemia

    • Electrolyte imbalances

• Corticosteroids:

  • Should not be used in acute infections; they are contraindicated.

• Liver Toxicity Treatment:

  • For phalloidine or acetaminophen toxicity (oxidative damage):

    • Silymarin (50 mg/kg/day) for 3–5 days.

    • Effectiveness decreases if given too late (i.e., after a few hours of intoxication).

  • Acetaminophen Toxicity (if applicable):

    • Treatment with N-acetylcysteine (140 mg/kg PO, every 6 hours for 3 days).

    • Vitamin C (25–35 mg/kg PO, every 6 hours for 2 days).

    • Cimetidine (5 mg/kg BID for 4 days).

    • Hemolysis may occur, requiring blood transfusion.

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Prognosis​​

• Dependent on the degree of liver damage; may range from mild (recoverable) to severe (fatal) disease.