Synonyms: Rubarth’s disease,Hepatitis contagiosa canis,Contagious hepatitis,Fox encephalitis.

It is an acute contagious viral disease of dogs irrespective of their ages and is characterized by high rise of temperature, vomition, culars and convulsion. Distribution

It was Rubaith who for the first time recorded the disease in 1947 in Sweden where the disease was widely prevalent. The disease is prevalent in many countries of the world. The disease is prevalent in epizootic proportions in India.


The disease is caused by a D.N.A. containing virus which belongs to adenovirus group. Three adenoviruses are recognized, two of which produce typical canine hepatitis and the other produce respiratory disease. It is, therefore, suggested that the diseases may flare up as complex and the respiratory symptom may lead the clinician to confuse the disease with distemper.

Sources of virus

  • Saliva
  • Urine
  • Faeces The virus can resist either, chloroform, and alcohol. Lysol and Iodine can kill the virus and thus can be used as de contaminant

Susceptible hosts

The canine family is affected with canine hepatitis virus infection. Amongst canine family, dogs and foxes are the important species to suffer from this infection. In fox, the disease is manifested with neurological disturbances (encephalitis). The dog and fox may remain as reservoirs of infection. Younger dogs under one year of age show acute form of the disease and afler’ which the dogs are inapparently infected with periodic relapses. Experimentally the disease can be produced in pups and foxes but not in ferret and other animals. Raccoons and ferrets will develop interstitial keratitis following incoculation of the virus into the anterior eye chamber

Mode of transmission

  • The disease may be transmitted through ingestion of contaminated food and water.

The virus is not transmitted through droplets. This is in contrast to distemper virus. The most significant method of transmission is excretion of the virus through the urine for a considerably prolonged period. This is similar, to leptospiral infection. Following even after recovery for acute disease, a diJ!1 may continue to harbour virus in the kidneys and excrete it in the urine for months together or even for more than a year. The infection takes place througl. Ingestion. The disease can be transmitted by placing urine or saliva in the oral cavity of susceptible dog .The virus is shed through urine, saliva and faeces during acute illness. Recovered dogs shed virus through urine for about 6 months.


Tonsil and Peyer’s Patche’s get infected and cause viraemia. The virus has got affinity for epithelial, mesolethelial and hepatic cells. The virus damages these cells. There is haemorrhages and necrosis of hepatic cells. The liver and spleen are congested and enlarged. The superficial lymph nodes are congested, oedematous, and haemorrhagic. Mortality is about 10% but the mortality is expected to be more if it occurs with or shortly after distemper

Clinical findings

The disease may flare up as

  • Acute
  • Per acute
  • Inapparent

Acute form.

In the acute form, the disease starts with apathy, anorexia and high rise of temperature upto 105°F. There is often vomition and culars. The faeces is often blood tinged and there is abdominal pain. Leukopaenia is usually observed in the second day of temperature reaction and it persists longer than 3 or 4 days. Animal shows intense thirst and the buccal mucous membrane turn fiery red or even haemorrhagic. There is sign of cularsis. There is abdominal tenderness. The animal shows sign of pain on palpation of xiphoid region. This pain may be due to swelling of liver capsule. Dogs may show “tucked up” condition of the abdomen.

At the initial phase of convalescence after 1-3 weeks following disappearance of clinical signs, a transient corneal opacity may develop. This condition _ ascribed as “Hepatitis blue eye”. This is due to iridocyclitis and corneal oedema. Small haemorrhagic spots may be noted over the skin of the abdomen. It may be a hard job to control the haemorrhage as the clotting mechanism of the blood may be impaired. The prognosis is grave if the animal shows profuse bleeding.

Following a period of 4-7 days, many dogs may recover and their appetite returns to normal.

Per-acute form.

In this form animal dies within 12 to 24 hours. The clinical signs mentioned above in the acute form of the disease may not be appreciated by the owner or the clinician. The dog which remains apparently normal in the night would die the next morning.

Inapparent form.

This is the most common form. The dog shows a very mild or subclinical attack with a passing temperature, mild photophobia, enlarged tonsil and rapid recovery. The weight lost during illness is very slow in the affected dog.


  • Liver – Enlarged, mottled, friable with fibrinous exudation. Large number of intra nuclear inclusion bodies in the hepatic cells and kupffer cells. Hepatic cell degeneration and in the centre lobular necrosis.
  • Gall bladder – Enlarged, oedematous and thickened.
  • Lymph glands – Swollen and haemorrhagic.
  • Spleen – Enlarged, blood filled.
  • Kidneys – Interstitial nephritis and cortical culars.
  • Skin – Petechiae and ecchymoses.
  • Stomach & Intestine - Inflammed, haemorrhage of gastric mucosa “Paint brush” haemorrhage of gastric mucosa.
  • Brain - Haemorrhage; Inclusion bodies.
  • Eyes - Iris and cilliary body inflammation. Inclusion bodies in the corneal cells and iridal endothelial cells


It is based on the following criteria:

  • Microscopic changes – Demonstration of intranuclear inclusion bodies in the liver, gall bladder, brain and cornea.
  • Gel diffusion test. – This test helps to diagnose this disease even when decomposition of the animal has occurred.
  • Complement fixation test. – This test may be used to diagnose the virus.
  • Neutralization test. – This test is also used for the identification of the virus.
  • Animal inoculation test. When ferrets are inoculated with suspected materials, production of the disease will indicate canine distemper and resistance will indicate infectious hepatitis virus.
  • Liver function test. Tests for liver functions will indicate about the functional activity of the liver. Transaminase enzyme elevation will be noted in severely ill dogs.

Differential diagnosis

  • Warfarin poisoning.
  • Tonsilitis. Caused by Strepto or Staphylococcus
  • Leptospirosis.
  • Distemper.


There is no specific treatment. Symptomatic treatments are to be rendered. Antiserum may be tried. Severely affected case may require blood transfusion. Dose is 5-8 ml / lb of body weight, by slow intravenous infusion. More than one transfusion will be required.

Broad spectrum antibiotics are to be given to control secondary bacterial infection. Fluid and electrolytes are to be extended to restore the fluid and electrolyte deficits. Protein hydrolysate is required to restore vitality. Careful nursing is of great importance.


Combined vaccine as made against distemper may be used to prevent this disease. Single vaccine against this disease is not available. Live virus vaccine occasionally cause allergic corneal and iridial reaction, 1 to 3 weeks after injection. This eye reaction may disappear spontaneously and may not require any treatment.