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

• 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

Clinical Signs

5.2. Clinical manifestations According to clinical features a catarrhal and nervous form or a combination of both, also termed acute systemic form, and a chronic nervous manifestation can be distinguished. In addition, various unusual manifestations, including old dog encephalitis and hard pad disease are recognized (Krakowka et al., 1985; Baumga¨ rtner, 1993; Moritz et al., 1998, 2000, 2003). At the acute stage, virus is found in every secretion and excretion of the body. This phase is accompanied by various dramatic clinical signs including onset of a cutaneous rash, serous nasal and ocular discharge, conjunctivitis and anorexia, followed by gastrointestinal and respiratory signs, which are often complicated by secondary bacterial infections and neurological disturbances (Krakowka et al., 1985). Nervous signs are diverse and progressive (Parker, 1978; Greene and Appel, 1998) and include myoclonus, nystagmus, ataxia, postural reaction deficits and tetraparesis or plegia (Koutinas et al., 2002; Vandevelde and Zurbriggen, 2005; Amude et al., 2007). In some cases, an improved immune response especially an increased production of virus-specific neutralizing antibodies can promote the recovery of the animal. However, despite elimination of the virus from several organs and the peripheral blood, CDV can persist in certain tissues including uvea, CNS, lymphoid organs and footpads (Appel, 1970, 1987; Zurbriggen et al., 1995a,b; Greene and Appel, 1998; Gro¨ne et al., 2003a; Schobesberger et al., 2005). Moreover, some infected animals display a delayed progression of the disease and a moderate immune response with subtle early clinical signs. Later, as a consequence of viral persistence in the CNS, overt CNS disturbances can be observed resulting in the nervous form of canine distemper. Dogs with nervous signs usually die, but some recover, and may display lifelong residual signs such as a persistent myoclonus.

Canine distemper is usually an acute, febrile disease, especially of young dogs, although older unprotected dogs are also susceptible. The first clinical manifestation of distemper is a diphasic febrile response. The first response may be overlooked, but the second generally occurs 2 - 3 days later in conjunction with other clinical signs, which initially include congested conjunctiva and nasal mucosa with subsequent serous to mucopurulent discharges. Pneumonia, depression, anorexia, vomiting, and diarrhea usually follow. Neurologic disturbances, such as neuromuscular tics, "chewing gum" seizures, and paresis are frequent sequelae in dogs that recover from acute disease. Hyperkeratosis of the nose and digital pads ("hard pad") develops in some cases. Pustular dermatitis may be seen affecting the abdomen of puppies. Gross necropsy lesions characteristic of pneumonia and enteritis may be present. Thymic atrophy may be noted in young dogs. Microscopic lesions are widespread in visceral organs and the brain and characteristic viral inclusion bodies are commonly found in brain, lung, stomach, and urinary bladder. Dogs that recover may years later develop what has been called "old dog encephalitis" as a result of a persistent infection. This manifestation is usually recurrent, with a few to several episodes of neurological manifestations within weeks to months that usually end with death of the dog.

   * Clinical specimens: Conjunctival scrapings, blood (buffy coat) smears, lung, urinary bladder, stomach, and brain.
   * A laboratory diagnosis may not be feasible. A presumptive diagnosis is frequently made on the basis of clinical signs in a young unvaccinated dog. Nonetheless, the vaccinated status does not assure protection since many cases of distemper have been reported in well vaccinated dogs.
   * 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.
   * 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.

• Clinical signs:
  • Mucopurulent oculonasal discharge
  • Keratitis
  • Interstitial pneumonia
  • Severe clinical pneumonia follows secondary infection with Bordetella bronchiseptica
  • Smelly sometimes bloody diarrhoea
  • Eruptions on the skin including hyperkeratosis of the nose and pads (hardpad)
  • Demyelination (especially in cerebellum) -> incoordination or muscle tremors -> paralysis and coma or convulsions -> death
  • Encephalitis
  • Secondary pyogenic infections associated with immunosuppression and damage to epithelia
  • Recovered animals may have persistent or spasmodic chorea
  • The severity of the disease may vary; if enough neutralising antibody develops in the early stages, the virus maybe kept restricted largely to the lymph nodes
• Variable mortality depending on virulence
• May occur subclinically
• Involvement of central nervous system generally results in death

• Can contribute to Infectious Canine Tracheitis
• May be involved in chronic interstitial pancreatitis
• May cause growth retardation lattice
• May also trigger latent Toxoplasmosis due to suppressing effect on lymphoid tissue

Pathology

• 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.