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 comprised of host cell membrance spiked with viral 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 shed in all excretions and secretions, and 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, as CDV is highly immunosuppressive. 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. In pregnant animals, transplacental infection can result in abortions, stillbirths, or the birth of persistent excretors of virus, depending on the stage of gestation.

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

With the exception of lymphopenia during early infection, routine haematology and biochemistry do not show any typical changes. Serology is also of limited value for several reasons. Firstly, a patient may die before an antibody response is mounted; secondly, a positive antibody titre does not discriminate between infected and vaccinated animals; and thirdly, IgM may remain high for up to three weeks following vaccination and three months after infection. Detection of canine distemper virus antibody in the cerebrospinal fluid is, however, indicative (although not diagnostic) of distemper encephalitis.

There are a number of tests available to confirm the diagnosis of canine distemper. Immunohistochemistry can be used to detect viral antigen in samples of skin, nasal mucosa or footpad epithelium, and viral antigen or inclusions may be demonstrated in buffy coat cells, urine sediment and conjunctival or vaginal imprints. However, negative results do not rule out a diagnosis of distemper. RT-PCR can also be performed on buffy coat, urine sediment, conjuncival swabs or cerebrospinal fluid. A retrospective diagnosis can be made post-mortem on the basis of histopathology, immunofluorescence or immunohistochemistry, virus isolation or RT-PCR. The preferred tissues for these techniques are lung, stomach, urinary bladder, lymph nodes 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 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.

Microscopically, eosinophilic intracytoplasmic inclusion bodies are often found in the bronchial, gastric and urinary epithelium. They may also be seen in leukocytes and lymphoid tissue. In the CNS, inclusion bodies are frequently intra-nuclear in neurons and glial cells. Demyelination may also be seen. When inclusion bodies are not seen, immunofluorescence or immunohistochemistry may be used to detect canine distemper virus antigen. Virus isolation or RT-PCR can also be carried out post-mortem using lung, stomach, urinary bladder, lymph nodes or brain.

Treatment

Dogs suffering distemper should be treated in isolation with barrier nursing to prevent spread to other dogs. Treatment is supportive, including intravenous fluid therapy to correct the deficit cause by vomiting and diarrhoea and antiobiotics to reduce secondary infections. Anticonvulsants such as phenobarbital and potassium bromide may be necessary to control seizures. Although corticosteroids may alleviate clinical signs in the short term, they should be used with caution as they augment the immunosuppression caused by CDV and may enhance viral dissemination. Animals should be rested and fed a diet appropriate to the severity of their gastrointestinal signs.

Vaccination is key to controlling canine distemper. Modified live vaccines are available, and are considered a "core" vaccination for dogs. Puppies can receive their first vaccination between 6 and 8 weeks of age, and must be given at least two doses of CDV vaccine with the final does being adminstered after 12 weeks of age. This multiple dose regimen is necessary because the maternal antibody in puppies greatly hampers the efficacy of vaccination by neutralising viral antigen. Modified live vaccines should not be used in pregnant bitches, and may cause fatal disease in certain wildlife species. Therefore a killed vaccine is available for use in, for example, red pandas.

Prognosis

The prognosis for CDV infection is dependent on the strain of the virus and the host immune response, as infection may be subclinical, subacute or acute. Overall, the mortality rate is around 50%, with death occuring 2 weeks to 3 months post-infection. Animals that appear to recover from early systemic signs may go on to develop CNS involvement which can vary in severity. Euthanasia may be considered with the onset of neurological signs, and is indicated when seizuring is uncontrollable. Dogs that fully recover do not shed the virus.

Links

• The Merck Veterinary Manual - Canine Distemper
• AVMA Brochure - Canine Distemper

References

1. Tilley, L.P. and Smith, F.W.K.(2004)The 5-minute Veterinary Consult (Fourth Edition) Blackwell Publishing.
2. Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition) Merial.
3. Carter, GR and Wise, DJ (2005) A Concise Review of Veterinary Virology, International Veterinary Information Service.
4. Vandevelde, M and Zurbriggen, A (1995) The neurobiology of canine distemper virus infection. Veterinary Microbiology 44, 271-280.
5. Chappuis, G (1995) Control of canine distemper. Veterinary Microbiology, 44, 351-358.
6. Beineke, A, Puff, C, Seehusen, F, Baumgartner, W (2009) Pathogenesis and immunopathology of systemic and nervous canine distemper. Veterinary Immunology and Immunopathology, 127, 1-18.