Canine Distemper Virus

Also known as:

Canine Distemper CDV

Description

Canine distemper is a contagious, febrile disease of canids and other carnivores caused by Canine Distemper Virus. Canine distemper virus is a member of the Paramyxoviridae family and the morbillivirus genus. The Paramyxoviridae have a helical nucleocapsid surrounded by an envelope which possesses spiked glycoproteins responsible for haemagglutinin, neuraminidase and haemolytic activities. The genome of the Paramyxoviridae is single-stranded, negative-sense RNA which is used as a template for the production of messenger (positive-sense) RNA and further genomic material. Paramyxoviridae are sensitive to heat, dessication and most disinfectants, and so are not resistant in the environment. The Paramyxovididae family is divided to two sub-families, the Paramyxovirinae and the Pneumovirinae. It is within the Paramyxovirinae sub-family that morbilliviruses fall, along with respiroviruses, henipaviruses, rubulaviruses and avulaviruses. As well as canine distemper virus (CDV), the morbilliviruses include rinderpest, peste de petits ruminants, measles, phocine distemper and dolphin distemper.

Canine distemper virus is spread by direct and indirect contact via ingestion or inhalation of aerosolised droplets. Initial infection of the nasal cavity, pharynx and lungs is followed by a macrophage-associated viraemia to local lymph nodes where the virus replicates. Within one week, all lymphoid tissue is infected, causing lymphopenia. A second viraemic stage then distributes the virus to the surface epithelium of the respiratory, gastrointestinal and urogenital tracts, endocrine tissue and the grey and white matter of the CNS. A biphasic pyrexia is typical of distemper infection: the first fever occurs 3-6 days post-infection and is associated with lymphopenia, and the second peak coincides with widespread viraemia. Further signs depend on both the virus strain and the immune response mounted. In the event of a strong humoral and cellular response, disease may remain subclinicals, and if a weak immune response is mounted infection is generally subacute. If the immune response fails, acute death occurs 2-4 weeks post-infection, commonly due to convulsions or other CNS disturbances. When clinical disease manifests, this is initially characterised by lethargy, dehydration, anorexia, and weight loss followed by more specific signs depending on the principally affected organ.

Signalment

Although canine distemper virus is found worldwide, outbreaks in dogs are sporadic due to effective vaccination protocols. However, many other wildlife species may be affected by the virus, and some examples are listed in the table below. Large cats in Tanzania and in some US zoos have also been found to have CDV. Although young animals are more susceptible than adults and, clearly, unvaccinated animals are at a higher risk of infection, there are no breeed or sex predilections for canine distemper.

Canidae	Procyonidae	Mustelidae
Coyote Dingo Fox Jackal Wolf	Lesser panda Racoon Coati Bassariscus	Ferret Marten Mink Otter Sable Wolverine Badger Skunk

Diagnosis

Although a presumptive diagnosis is frequently made on the basis of clinical signs in a young unvaccinated dog, there are several methods of investigating and confirming canine distemper.

Clinical Signs

Canine distemper is characterised by a biphasic fever, with the first peak 3-6 days post-infection and the second peak several days later and intermittently thereafter. The second peak of pyrexia is usually associated with the onset of other clinical signs. These initially include conjested conjunctiva and nasal mucosa leading to serous ocular and nasal discharges that become mucopurulent. The animal is depressed and anorexic, and vomiting, diarrhoea and pneumonia commonly follow. These gastrointestinal and respiratory signs are often complicated by secondary bacterial infections. Lesions may occur on the retina and optic neuritis can develop. Some strains of CDV cause hyperkeratosis of the footpads and the nose, and retinal lesions and optic neuritis can occur. In neonates, hypoplasia of the tooth enamal is common following infection, causing "distemper rings". Pustular dermatitis may also be seen on the abdomen of infected puppies.

Many, but not all, infected dogs develop CNS signs after systemic disease but this is dependent on the strain of the virus. Either the white matter or the grey matter may be affected. Grey matter disease affects the cerebral coretx, brainstem and spinal cord, and may give a non-suppurative meningitis, seizures, stupor, hysteria or ataxia. Dogs with grey matter disease may die within 2-3 weeks, recover, or alterntatively progress to white matter disease. In this, mutlifocal lesions mean that the signs are variable: cerebellovestibular signs are common, as well as spinal cord paresis, ataxia and occasionaly myoclonus. Once white matter disease has developed, some dogs die with a non-inflammatory, demyelinating disease 4-5 weeks after intial systemic infection. Other animals may recover with minimal injury to the CNS but may still suffer neuromuscular tics or "chewing gum" seizures.

Although canine distemper is often fatal, in some cases an increased production of virus-neutralising antibodies promotes the recovery of the animal. However, CDV can persist in the uvea, CNS, lymphoid organs and footpads despite elimination from most organs and the blood. This can result in "old dog encephalitis" in dogs that recovered from acute canine distemper years previously. In this, several neurological episodes occur over weeks to months, and end in the death of the dog.

Laboratory Tests

• A reliable way to diagnose canine distemper is the demonstration of viral infected cells by immunofluorescence. Examination of conjunctival scrapings and blood smears is useful during early stages of the illness, but false negative results are likely to occur as the disease progresses. Tests are accurate when performed on appropriate necropsy tissues.

   * Clinical specimens: Conjunctival scrapings, blood (buffy coat) smears, lung, urinary bladder, stomach, and brain.

Diagnostic Imaging

Thoracic radiographs may be taken to determine the extent of pneumonia for use in planning treatment and determining prognosis. CT or MRI may or may not disclose lesions in the CNS.

Pathology

On post-mortem examination, the thymus is often found to be greatly reduced in size and gelatinous in young dogs. There is patchy consolidation of the lungs due to interstitial pneumonia, and signs of catarrhal enteritis may be present. Mucopurlent discharges are commonly seen from the eyed and nose and bronchopneumonis is sometimes present. Skin pustules and hyperkeratosis of the footpads and nose are seen occasionally.

Microscopic lesions are widespread in organs and the brain. Characteristic viral inclusion bodies are commonly found in brain, lung, stomach, and urinary bladder.

• May present as series of infections
• Immunocytochemistry of inclusion bodies
  • Intracytoplasmic inclusions may be found in most affected tissues
  • Inclusions persist longest in the brain (may be intranuclear) and the alveolar macrophages
  • Sections of fixed bronchial tissue, lung, macrophages, bladder may be used or nasal or conjunctival epithelium from live animals
• Giant cells may be seen in the alveol
• Microscopic lesions of demyelination in the cerebellum and characteristic inclusion bodies in various tissues are diagnostically significant. The inclusions are primarily intranuclear in the brain and intracytoplasmic in other tissues.

   * The prognosis is poor for dogs with CNS involvement.

• Rhinitis
• Although many organs can be affected by CDV, a relatively constant feature is the respiratory signs which occur in varying severity
• A syndrome of catharral oculonasal discharge, pharyngitis and bronchitis is relatively common in the initial stages
• Since one of the primary sites of action of this virus is lymphoid tissue, the resultant immunosuppression -> predisposition to secondary bacterial infection
• May cause interstitial pneumonia where inclusions are found within alveolar macrophages
• Gross pathology:
  • Oedematous lungs, diffuse interstitial pneumonia
• Micro pathology:
  • Necrosis of pneumocytes, necrotising bronchiolitis, alveolar oedema, thickening of alveolar walls and type II pneumocyte hyperplasia

Treatment

• Live attenuated virus vaccines given at 10 and 12 weeks of age
  • Some now given at 7 and 10 weeks to allow socialisation
• Homeopathic vaccines do not work
• Live attenuated vaccines may kill some wildlife therefore Iscom vaccine is used in seal sanctuaries

Treatment

   * Supportive treatment, and antimicrobial therapy to cope with secondary bacterial respiratory infection.

Prevention

   * Modified live vaccines are administered to dogs between six and 16 weeks of age, usually at 2 - 3 week intervals. This multiple dose regimen is necessary because the maternal antibody in puppies greatly hampers the efficacy of vaccination by neutralizing viral antigen.
   * Dogs older than three months with unknown immune status should be vaccinated twice, 2 - 4 weeks apart, all dogs should receive periodic (one to two years-interval ) boosters.
   * Pregnant bitches should not be vaccinated with modified live vaccines.

References

1. Carter, GR and Wise, DJ (2005) A Concise Review of Veterinary Virology, International Veterinary Information Service.