Infectious canine hepatitis

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Canine adenovirus 1

Infectious canine hepatitis (ICH) is a contagious viral disease of dogs worldwide.

ICH is caused by canine adenovirus type 1, which is antigenically related only to CAV-2 (one of the causes of infectious canine tracheobronchitis, Infectious Tracheobronchitis of Dogs). CAV-1 is resistant to lipid solvents and survives outside the host for weeks or months, but a 1-3% solution of sodium hypochlorite (household bleach) is an effective disinfectant.

Ingestion of urine, feces, or saliva of infected dogs is the main route of infection. Recovered dogs shed virus in their urine for ≥6 mo. Initial infection occurs in the tonsillar crypts and Peyer’s patches, followed by viremia and infection of endothelial cells in many tissues. Liver, kidneys, spleen, and lungs are the main target organs. Chronic kidney lesions and corneal clouding (“blue eye”) result from immune-complex reactions after recovery from acute or subclinical disease.

Clinical signs

Signs vary from a slight fever to death. The mortality rate is highest in very young dogs. The incubation period is 4-9 days. The first sign is a fever of >104°F (40°C), which lasts 1-6 days and is usually biphasic. If the fever is of short duration, leukopenia may be the only other sign, but if it persists for >1 day, acute illness develops. Tachycardia out of proportion to the fever may occur. On the day after the initial temperature rise, leukopenia develops and persists throughout the febrile period. The degree of leukopenia varies and seems to be correlated with the severity of illness.

Signs are apathy, anorexia, thirst, conjunctivitis, serous discharge from the eyes and nose, and occasionally abdominal pain and vomiting. Intense hyperemia or petechiae of the oral mucosa, as well as enlarged tonsils, may be seen. There may be subcutaneous edema of the head, neck, and trunk.

Clotting time is directly correlated with the severity of illness. It may be difficult to control hemorrhage, which is manifest by bleeding around deciduous teeth and by spontaneous hematomas, because of underlying disseminated intravascular coagulation. Respiratory signs usually are not seen in dogs with ICH; however, CAV-1 has been recovered from dogs with signs of infectious tracheobronchitis and from dogs with respiratory signs induced by exposure to the nebulated virus. Although CNS involvement is unusual, severely infected dogs may develop convulsions from forebrain damage; brain stem hemorrhages, resulting in paresis, are common. Foxes more consistently have CNS signs and intermittent convulsions during the course of illness, and paralysis may involve one or more limbs or the entire body.

On recovery, dogs eat well but regain weight slowly. Bilateral corneal opacity develops 7-10 days after the acute signs disappear in ~25% of recovered dogs and usually disappears spontaneously. In mild cases, transient corneal opacity may be the only sign of disease. Chronic hepatitis may develop in dogs having low levels of passive antibody when exposed. Simultaneous infection with CAV-1 and distemper virus is sometimes seen.

Lesions: Endothelial damage results in “paint brush” hemorrhages on the gastric serosa, lymph nodes, thymus, pancreas, and subcutaneous tissues. Hepatic cell necrosis produces a variegated color change in the liver, which may be normal in size or swollen. The gallbladder wall may be edematous and thickened; edema of the thymus may be found. Grayish white foci may be seen in the kidney cortex.


Usually, the abrupt onset and bleeding suggest ICH. Clinical evidence is not always sufficient to differentiate ICH from distemper, although the gross changes in the liver and gallbladder are more conclusive. Diagnosis is confirmed by virus isolation, immunofluorescence, or characteristic intranuclear inclusion bodies in the liver.


Blood transfusions may be necessary in severely ill dogs. In addition, 5% dextrose in isotonic saline should be given, preferably IV. In dogs with prolonged clotting time, SC administration of fluids may be dangerous. A broad-spectrum antibiotic should be given. Because tetracyclines may cause discoloration of the teeth during tooth development, they should not be used in puppies before their permanent teeth erupt. Although the transient corneal opacity (that may be seen during the course of ICH or be associated with vaccination with attenuated CAV-1 vaccines) usually requires no treatment, atropine ophthalmic ointment may alleviate the painful ciliary spasm that is sometimes associated with it. Dogs with corneal clouding should be protected against bright light. Systemic corticosteroids are generally contraindicated for treatment of corneal opacity associated with ICH.

Modified-live virus vaccines are available and are often combined with other vaccines. Vaccination against ICH is recommended at the time of canine distemper vaccinations. Attenuated CAV-1 vaccines have produced transient unilateral or bilateral opacities of the cornea, and the virus may be shed in urine. CAV-2 attenuated live virus strains, which provide cross protection against CAV-1, are preferentially used because they have very little tendency to produce corneal opacities or uveitis, and the virus is not shed in urine. Annual revaccination against ICH is often practiced. Maternal antibody from immune bitches interferes with active immunization in puppies until they are 9-12 wk old.