Synonyms. Canine influenza; Carres; Hard pad disease.

It is an acute highly infectious viral disease of carnivorous animals characterized by diphasic fever, ocular and nasal catarrh and frequent cutaneous eruptions. This infection is often manifested by bronchopneumonia, gastro enteritis and encephalitis.


The disease is caused by R.N.A. virus belonging to paramyxo group. The virus is closely related to measles and rinderpest viruses. Several strains of the virus differ in virulence but there is only one antigenic type.

Type A virus is prevalent In 14%,

Type B virus in 20% and

Type C virus in 55% of the dog population.

The types A and B of the virus are more pathogenic whereas type C is of low virulence in nature.

Resistance to physical and chemical action

  • The virus is sensitive to ether and is fragile in nature.
  • The virus is easily destroyed at 50°C in 60 minutes, 55°C for 10 minutes, 25°C in 7 to 8 days and at 4°C in 7-8 weeks.
  • The virus remains viable at pH ranging from 4.5 to 9.
  • The virus is destroyed by 0.1% formalin in 1 to 2 hours, 0.57% phenol in 48.72 hours and 0.3% chloroform in 10 minutes.

The disease is enzootic in almost all the countries of the world.

Indigenous breeds are quite resistant. The disease may be noted in all age group, but the young ones between age group of 3 to 6 months are more susceptible and case fatality rate in them are maximum.


  • In nature, the transmission of the virus takes place by inhalation (droplet or aerosol). This is an air borne disease.
  • The disease may indirectly be transmitted through ingestion of contaminated food and water.

Sources of virus

  • The virus is discharged through secretions and excretions. The virus is present in all the excretions during the systemic reaction phase of the disease.


The virus has got affinity for epithelial cells of the respiratory and alimentary tract. Lymphoid cells and nerve cells are prone to get the attack. The pathogenesis is as follows:

Virus – inhalation – Pharynx – Palatine tonsil –Macrophages–Lymphoid vessels – Blood vessels – Bone + marrow –Spleen – Lymphoid tissues – Leukopaenia – Leukocytosis.

Respiratory epithelial cells are mostly affected and virus gain entry through the cells. On entry, the virus is carried to the regional lymph nodes and thus the lymphatic system gets affected. 9 days post infection some dogs may develop neutralizing antibody and recover rapidly-while others may fail to develop antibody and ultimately die. The virus multiplies in the lymph nodes and spreads to other lympho proliferative organs. In about 7 days, the virus begins to settle in and proliferate in the epithelial cells of the skin, respiratory, alimentary, urinary and biliary tracts. The virus then culars in the vascular endothelium of the brain and thus spreads to the nervous tissues. The virus afterwards, get settled and proliferate in the nuclei and cytoplasm of neurons. There is always super imposed- secondary infections. They are bacteria, mycoplasma, toxoplasma and culars

Clinical findings

The animal is dull and depressed and is indifferent to its surroundings.

There is high rise of temperature. This temperature reaction is characteristic and is known as diphasic reaction. The temperature rises upto 103 to 104°F. In this stage, the nose of the animal will turn dry and hot and eyes will turn congested. The animal is markedly depressed and refuses to take food. Within few days yellowish green discharge is voided from the eyes and nose. This temperature usually come down in 96 hours to normal level and remains so till 11 to 12 days. Afterwards, temperature rises to a second peak which remains continuous during the course of the systemic infection. The second rise of temperature is accompanied by rhinitis, conjunctivitis, gastroenteritis and broncho­pneumonia.

The clinical manifestations vary in respect to severity and involvement of the system concerned.

Pulmonary form.

A coryza like syndrome characterized by oculonasal discharge, pharyngitis, bronchitis is seen. Bronchopneumonia is the common feature. The pulmonary form is more prevalent than digestive form. The pneumonic condition may persist for a long period.

Digestive form.

This is characterized by loss of appetite, vomiting and abdominal pain. The faeces are semisolid or loose and foul smelling leading to dehydration. The diarrhoic faeces may contain blood. The haemorrhagic enteritis is commonly seen in young pup.

Occular form.

This is manifested as swollen eye lids, congestion of conjunctival mucosa (conjunctivitis), purulent discharge from the eyes. The pus may lead to ulceration of the cornea. Transient keratitis may also be located

Nervous form.

The affection of the nerve cells lead to neurological disorders. These are characterized by restlessness, excitement, chewing movements, excessive salivation and convulsion. The dog may fall and show epilepticform fits. The nervous manifestations are noted when the animal can resist the primary infection and suffer from secondary complication. Lymphopaenia is the distinct feature of distemper but this may not occur in dogs with delayed encephalitis. A condition known as “Old dog encephalitis” characterized by mental disorders, motor deteriotion and death as clinical features has also been described. The nervous form may be characterized by chorea. Chorea indicates jerky movements of group of muscles. The muscular spasms may be observed in the lips, alae nasii, cheeks, jaws, head, neck or limb muscles.

Cutaneous form

There is appearance of rash, vesicles and pustules, In some cases, the skin of the foot pads and nose may become hard due to hyper keratitis and the condition is ascribed as “hard pad disease”. When the foot pads are thickened, the I dog may experience some difficulty in walking on hard objects. There is obvious pain characterized by lameness. There may be vesicopustular eruptions on the ventral aspect of the abdomen and on the inner parts of the thighs of skin. This type of distemper eruptions are known as distemper exanthema.


Brain & Meninges

There is congestion of the brain and meninges. The microscopic changes in the brain are characterized by mild inflammation to severe meningo encephalomyelitis with demyelination. Perivascular cuffing may be noted in the meninges and brain. There is neuronal degeneration and neuronophagia. Cellular infiltra­tions may be noted. The inflammatory cells are lymphocytes, plasma cells, mononuclear cells and astrocytes. These cells are found to be deposited in the myelinated zones. Eosinophilic intracytoplasmic inclusion bodies are noted in the glial cells, neurons, ependymal and meningeal cells.

Thymus & Lymph glands

Reduction in the size of thymus and depletion of lymphocytes.


Diffuse interstitial pneumonic changes. The changes are comprised of thickening of alveolar walls, hyperplasia, proliferation of alveolar epithelium and presence of macrophages. Cytoplasmic inclusion bodies are noted in the bronchial epithelium.


Signs of catarrhal or haemorrhagic enteritis. Haemorrhagic enteritis may set in due to secondary bacterial invasion. Degenerative changes and inclusion bodies may be recorded in intestinal epithelium.

Kidney & Urinary bladder:

There is degenerative changes in the renal and bladder epithelium. The epithelium of the organs may contain number of inclusion bodies.

Foot pad & Nose

There is sign of hyperkeratitis




  • Animal inoculation
  • Detection of inclusion bodies.
  • Fluorescent antibody technique.
  • Isolation of the virus.
  • Serum neutralization test.


  • Anticanine distemper serum may be tried to safeguard the life of the patient. Antidistemper serum (Homoserum) 1-5 ml per kg. body weight I/V, I/M or S/C is to be administered as quickly as possible. Massive dose 5-10 ml per kg. body weight is also indicated in severe cases.
  • Treatment is mostly symptomatic
  • Symptomatic treatments are to be rendered. To check respiratory complications broad spectrum antibiotics may be tried. In order to combat B. bronchiseptica antibiotics should be given in aerosol methods. For better expectoration, steam inhalation, bronchodilator, mucinolytics may be tried. To check culars, antidiarrhoeal preparations, low residue diet and fluid and electrolytes therapy shoulo be rendered.
  • To control neurological derangement sedatives and anticonvulsants should be given. To inhibit chorea, drugs used for human parkinsonism may be tried, e.g. Lardopa (500 mg) ½ tab once daily followed by ½ tab. Every week or Pacitane (2 mg) 1 tab b.i.d. orally. Anticonvulsants may be helpful in reducing epileptic seizure.
  • For restoration of vitality water soluble B-vitamins, protein hydrolysate and vitamin-C are to be given.
  • All care should be made to make the animal free from ectoparasitic and endoparasitic burdens by rendering specific acaricide or anthelmintic drugs.


  • A dog after recovery from an attack of distemper generally acquire a long lasting immunity
  • Vaccinations