Infectious Canine Hepatitis (ICH)
Introduction:  Infectious canine hepatitis (ICH) is a multisystemic viral disease with primary effects on the liver.  It is caused by the canine adenovirus type 1 (CAV-1), a DNA virus that is moderately resistant to environmental assault and may survive up to several months outside of a host under the proper conditions.  ICH is a disease of moderate to severe clinical illness that may progress to hemorrhage and other coagulopathies such as disseminated intravascular coagulation.  The disease is uncommon, most likely due to widespread immunity in the current canine population (population immunity).

Canine Adenovirus - 1


Pathogenesis:  Exposure to the CAV-1 virus occurs through the oronasal passages.  After entering, the virus localizes in the tonsils and cervical lymph nodes before traveling to the circulation through the thoracic duct.  Viremia occurs by day 5, when the virus has distributed to the eyes, liver, kidney and to other endothelial tissues located in the brain, lungs, and lymph nodes in limited quantities.  After distribution, the virus is found in the feces, saliva, and urine, making contamination a concern in litter situations or multi-dog households.  In animals that survive the viremia which lasts 4-8 days, the virus localizes to the kidneys and continues to be shed in the urine.  Viral replication in the tissues results in the majority of clinical signs.  In the ocular tissues, immune complexes and severe uveitis lead to corneal edema, glaucoma, and phthisis bulbi.  In the liver, the virus localizes to the Kupffer cells and hepatocytes, causing either acute hepatic necrosis and hepatitis or (uncommonly) chronic hepatitis.   In the kidney, the glomerular epithelium is subjected to multiple immune complexes leading to glomerulonephritis.  Death is usually due to poor humoral immunity, and centrilobular to panlobular hepatic necrosis.  In dogs, which exhibit partial humoral immunity, liver disease may progress to chronic hepatitis and fibrosis.  Common sequelae to infections with CAV-1 include a predisposition to polynephritis, disseminated intravascular coagulation secondary to vasculitis, hepatic insufficiency, and glaucoma.

Gross Pathology:  

  • Subcutaneous edema due to the effects of the virus on endothelial cells.
  • Diffuse hemorrhage of serosal surfaces and superficial lymph nodes due to the effects of the virus on endothelial cells.  
  • The liver may be enlarged, dark, mottled in appearance and coated with a fibrinous exudate.  It may also have white spots corresponding to multiple, often coalescing foci of necrosis.  In cases of chronic infection producing chronic hepatitis, the liver is generally small, firm and nodular.   
  • Serosanguinous fluid and fibrin tags are often found in the abdomen.  
  • Splenomegaly is a common finding. 
  • Intraluminal gastrointestinal hemorrhage is a common finding.   
  • Multifocal hemorrhagic renal cortical infarcts 
  • Multiple areas of pulmonary consolidation.

ICH-gross_thumbnail.jpg (16550 bytes)

Careful examination of the liver may reveal coalescing white foci that represent acute hepatic necrosis.

Click on the image for a larger view and more information.

 

Histopathology:  The main pathologic change noted on histopathology is centrilobular to panlobular necrosis in cases of acute hepatitis.  In chronic disease, sporadic foci of necrosis containing neutrophils, lymphocytes, and plasma cells are seen.  Fibrosis may also be a prominent feature.

ICH-histo_thumbnail.jpg (24328 bytes)

Click on the image for a larger view and more information.

Species affected:  Dogs of any age, breed or sex may become infected.  Clinical cases are most frequently observed in dogs less than one year of age. 


Clinical Signs:  Onset of disease may be peracute or acute.  


Clinical Pathology:  There are multiple parameters altered with this disease.  These are listed in the table below.

Hematology Neutropenia, Lymphopenia, and Thrombocytopenia. These are followed by Neutrophilia and Lymphocytosis in the recovery phase.
Coagulation Parameters Increased APTT, OSPT, PT, and increased fibrin degradation products due to DIC.
Biochemical Panel Elevated ALT and AP.  Hypoglycemia in terminal cases.  Transient increases in globulins.
Urinalysis Bilirubinuria
Cerebrospinal Fluid Increased protein levels.  Mononuclear pleocytosis.