Canine Viral Hepatitis

Canine viral hepatitis, also called infectious canine hepatitis (ICH), is a severe disease with the mortality rate of 25% in puppies. The disease is caused by canine adenovirus-1 (CAV-1) that infects bears, coyotes, wolves, mink, ferrets, striped skunks, raccoons, but not humans. The virus is a medium sized DNA virus that resists environmental inactivation with chemicals such as chloroform, ether, acid, and formalin, but chemical disinfection with iodine, phenol and sodium hydroxide is effective. The virus is able to survive for days at room temperature and remain viable for months at temperatures below freezing, but is inactivated after 5 minutes at 500°C to 600°C. Vaccination has greatly reduced the incidence of the disease and it is now rare in many countries; however, it is not eradicated and outbreaks occur. Most infections with ICH are mild, but occasionally the virus causes acute fatal disease that clinically resembles canine distemper and other canine virus infections. There is also a form of the disease in which the animals are found dead after an illness of only a few hours.

Some of these cases have been associated with midbrain bleeding. The cause of death in ICH is uncertain, although the liver is the primary site of viral injury. Some dogs die suddenly. Death in these dogs may be as the result of damage to the brain, lungs, and other vital organs. During the recovery period and 8-12 days after vaccination, corneal edema ("blue eye") is occasionally observed, which disappears after a few days without consequence. The edema is due to the virus-antibody complexes deposited in the small blood vessels that interfere with the normal fluid exchange within the cornea.10

Infectious canine hepatitis is highly contagious. Natural infection with CAV-1 probably occurs via the oral route.4 The time from the moment of exposure to the virus until signs of the disease appear (incubation period) is from 4 to 7 days. The virus multiplication occurs first in the tonsils leading to tonsillitis and inflammation of one or more lymph nodes. It then reaches the blood via the main duct of the lymphatic system (thoracic duct). Within the first week after infection it can be detected in the bloodstream from where it spreads to other tissues and body secretions, including saliva, urine, and feces. The virus persists in the kidneys and may be shed in the urine for up to 6 months after recovery.9 Early signs are fever, depression, lethargy, and respiratory disease. Later signs include reluctance to move, abdominal tenderness, pale mucous membranes, vomiting, diarrhea, and loss of appetite. Inflammation of the throat and lymph nodes of the neck are common. In severe cases, bleeding around teeth may occur, which may be prolonged. The liver becomes enlarged and may be palpated. Although central nervous system involvement is uncommon, dogs affected severely may convulse.10

Vaccination with a live modified vaccine produces life-long immunity, although most vaccines contain weakened, less vigorous viruses (CAV-1 or CAV-2). Recommended vaccination schedules usually begin at about 6 weeks of age and may continue up to 4 months of age. Most dogs are exposed to the disease either in the form of the vaccine as young dogs, or in the form of the disease-causing virus as adults, and therefore most adult dogs will have serum antibodies. Most female dogs will transfer antibodies against ICH in their colostrum to their pups shortly after parturition, giving them early protection from the disease. Annual vaccination has been recommended, but is probably not essential due to the persisting immunity produced by the vaccine.


  1. An acute virus disease with liver lesions in dogs (hepatitis contagiosa canis): a pathologico-anatomical and etiological investigation. S. Rubarth. In: Acta. Pathol. Microbiol. Scand. Suppl. 69: 1-207, 1947.
  2. Cross-protective immunity to canine adenovirus type-2 by canine adenovirus type-1 vaccination. Emery, J.B., House, J.A. and Brown, W.R. In: Am. J. Vet. Res. 39: 1778-1783, 1978.
  3. Infectious canine hepatitis and canine acidophil cell hepatitis. Greene, C.E. (1999).
  4. Canine viral diseases. In: Ettinger, S.J. (ED.): Textbook of Veterinary Internal Medicine. W.B. Saunders Co. Philadelphia. pp. 303-305, 1989.
  5. Persistence of virus in urine as a factor in spread of infectious canine hepatitis. Poppensiek, G.G. and Baker, J.A. Proc. Soc. Exp. Biol. Med. 77: 279-281, 1951.
  6. Carmichael, L.E.: The pathogenesis of ocular lesions of infectious canine hepatitis. II. Experimental ocular hypersensitivity produced by the virus. Vet. Pathol. 2: 344-359, 1965.
  7. The liver and biliary system. In: Jubb, K.V.F., Kennedy, P.C. and Palmer, N. (Eds.): Pathology of Domestic Animals. Vol. 2. Academic Press, Inc. San Diego. pp. 364-366, 2000
  8. Canine viral diseases. Hoskins, J.D. In: Ettinger, S.J. and Feldman, E.C. (Eds.): Textbook of Veterinary Internal Medicine. W.B. Saunders Co. Philadelphia. pp. 418-419, 2000.
  9. Infectious diseases of wild mammals. Elizabeth S. Williams, Ian K. Barker
  10. Veterinary virology. Frederick A. Murphy, E. Paul J. Gibbs (1999)

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