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Canine Distemper Virus

Canine distemper virus (CDV) is a relatively large (150– 250 nm) single-stranded RNA virus with a lipoprotein envelope. It is a morbillivirus in the family Paramyxoviridae and is related to the measles virus, phocine distemper virus, and rinderpest virus (Deem et al, 2000; Elia et al, 2006). It's RNA encodes six structural proteins: two membrane glycoproteins, the fusion (F), the hemagglutinin (H), the envelope-associated matrix protein (M), the phosphoprotein (P), the large polymerase (L), and the nucleocapsid protein (N) (Elia et al, 2006). CDV is highly contagious and has a fatality rate that is second only to that of rabies (Ek-Kommonen et al, 1997; Deem et al, 2000). Canine distemper virus can affect a wide range a hosts and infection has been reported in all families of terrestrial carnivores: Canidae, Felidae, Hyaenidae, Mustelidae, Procyonidae, Ursidae, and Viverridae. It also infects the red or lesser panda (Ailurus fulgens) and giant panda (Ailuropoda melanoleuca) (Deem et al, 2000).      

Pathogenesis of

Canine Distemper Virus

The initial infection occurs in epithelial cells and lymphoid tissue in the nasopharynx, and within 24 hours of entering the respiratory tracts, the virus spreads in macrophages via local lymphatics to tonsils and bronchial lymph nodes (Deem et al, 2000; Messling et al, 2003). Replication of the virus occurs in the tonsils and bronchial lymph nodes 2–4 days post infection; while, low numbers of CDV-infected mononuclear cells are found in other lymphoid organs. A transient fever as well as the onset of lymphopenia can be observed between 3 and 6 days after infection, which coincides with the first viremia 

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The spread of CDV. 

Canine distemper virus is highly contagious and is  transmitted by aerosol (Messling et al, 2003; Deem et al, 2000). Aerosolization of respiratory exudate and other body excretions and secretions (e.g., urine) containing the virus can result in infection in susceptible hosts (Deem et al, 2000). Transplacental infection has also been documented in domestic dogs (Deem et al, 2000). Though the occurence of canine distemper virus has decreased since the use of vaccination in the 1960's, there have still been outbreaks among vaccinated dogs (Ek-Kommonen et al, 1997). On the other hand, 50–70% of infected domestic dogs may remain asymptomatic carriers (Deem et al, 2000). This could make domestic dogs the reservoir of CDV for free-ranging wildlife (Deem et al, 2000).  

that results in the infection of all lymphatic tissue (Deem et al, 2000; Messling et al, 2003). Within 4–6 days, the virus proliferates widely in lymphoid organs (e.g., spleen, mesenteric lymph nodes, Kupffer’s cells in the liver, and the lamina propria of the stomach and small intestine). This second viremia coincides with a high fever. Within 8–9 days of infection, the virus spreads to epithelial and CNS tissues. This is accompanied by the onset of rash, and marks the beginning of the symptomatic phase, characterized by serious nasal discharge, conjunctivitis, and anorexia (Messling et al, 2003). Gastrointestinal and respiratory signs may follow and are often complicated by secondary bacterial infections. An acute encephalomyelitis may occur in association with or immediately after, the systemic disease but the involvement of the central nervous system (CNS) is variable and dependent on the host’s immune response and the individual strain of the virus (Deem et al, 2000; Messling et al, 2003). If acute encephalomyelitis occurs, around 10% of dogs die from the damage to the CNS and the resulting complications, such as seizures, while their immune system fails to control the infection (Rudd et al, 2006). Hyperkeratosis of footpads and epithelium of the nasal plane are often observed if the virus persists in uveal, neural, and integumental tissues (Deem et al, 2000). The pathogenesis within 9–14 days depends on the humoral and cell mediated host immune response. Dogs with adequate antibody titers and cell-mediated cytotoxicity will clear the virus from most tissues with no clinical signs. Whereas, dogs, with a poor immune response, experience viral spread to many tissues (Deem et al, 2000; Messling et al, 2003).

 

For information on the prevention and treatment of Canine Distemper Virus, click here.

 

References:

  1. Deem SL, Spelman LH, Yates RA, Montali RJ. CANINE DISTEMPER IN TERRESTRIAL CARNIVORES: A REVIEW. Journal of Zoo and Wildlife Medicine. 2000; 31(4): 441-451.

  2. Elia G, Decaro N, Martella V, Cirone F, Lucente MS, Lorusso E, Trani LD, Buonovogkia C. Detection of Canine Distemper Virus in Dogs by Real-time RT-PCR. Journal of Virological Methods. 2006; 136: 171-176.

  3. Er-Kommonen C, Sihvonen L, PekkanenK, Rikula U, Nuotio L. Outbreak ofcanine distemper in vaccinated dogs in Finland. The Vetinary Record. 1997; 141: 380-383.

  4. Messling VV, Springfield C, Devaux P, Cattanoe R. A Ferret Model of Canine Distemper Virus Virulence and Immunosuppression. Journal of Virology. 2003; 77(23): 12579-12591.

  5. Rudd PA, Cattaneo R, Messling VV. Canine Distemper Virus Uses both the Anterograde and the Hematogenous Pathway for Neuroinvasion. Journal of Virology. 2006; 80(19):9361-9370.

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