Transmision of CDV

CDV is most often shed through the air from respiratory secretions, but the virus can also be shed via urine and other body secretions. Once outside the host the virus is unstable in the environment and deteriorates rapidly (1).


                                    Spread of CDV thoughout the host                                                                                      

    Following oral or nasal entry into the host, the virus is engulfed by macrophages of the respiratory tract epithelium (see diagram to the right). Infected macrophages then spread the virus throughout the host, arriving first (within 24 hours) to local the lymph nodes of the lung.  Within a week, the virus may become well dispersed in the blood stream (viraemia) and migrate to the spleen, stomach, small intestine, liver, and CNS (1). During this period of post infection fever develops alongside interferons in the circulation. Disease is the result of replication of the virus in infected cells (3).  

  Progression of CDV and host immunity

    One week following infection the host mounts an immune response in which the outcome depends on the magnitude of the response. A strong immune response may clear the virus within two weeks and recover without presenting any further symptoms. On the other hand, a weak immune response enables the virus to infect surface epithelium of the host. Macrophages carry the virus to epithelium of the alimentary, respiratory, and urogenital tracts and to the central nervous system (1). Clinical signs follow the local infection are these areas. However, as the virus spreads and the host’s immune system may mount and the symptoms may wane. Occasionally, symptoms may appear long after the infection was thought to be cleared as the virus remains latent for long periods in the nervous system and skin (REF B). Otherwise, most dogs that recover from CDV infection are immune for life. They are not persistently infected and they do not shed virus (2).

    Lethal presentation of the disease may occur within a few weeks or be more delayed for 2 or 3 months. In acute fatal infections the virus strains mostly affect the grey matter, causing neuronal destruction. In more delayed disease fatalities affects, virus strains affect white matter and cause demyelination (2).