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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 and a secondary viraemia distributes the virus to the surface epithelium of the respiratory, gastrointestinal and urogenital tracts, and the grey and white matter of the CNS. In early infection, a fever of 1-2 days duration and lymphopenia (due to replication in lymphoid tissue) may be the only clinical findings, and 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.
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 and a secondary viraemia distributes the virus to the surface epithelium of the respiratory, gastrointestinal and urogenital tracts, and the grey and white matter of the CNS. In early infection, a fever of 1-2 days duration and lymphopenia (due to replication in lymphoid tissue) may be the only clinical findings, and 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.
First clinical signs are characterized by lethargy,
dehydration, anorexia, and weight loss followed by a more
pronounced clinical manifestation depending on the predominantly
affected organ. Development of a biphasic fever
represents another characteristic clinical finding (Wright
et al., 1974). A transient fever and the onset of lymphopenia
can be observed 3–6 days pi (Krakowka et al., 1980) and
coincide with the first viremia that results in a generalized
infection of all lymphoid tissues including spleen, thymus,
lymph nodes, bone marrow, mucosa-associated lymphatic
tissues(MALT) and macrophages in the lamina propria of the
gastrointestinal tract (Appel, 1970; Wright et al., 1974), as
well as hepatic Kupffer cells (Appel, 1987). Viremia occurs
by spread of cell free virus as well as leukocyte and
thrombocyte associated infectious pathogens. The second
viremia follows several days later, frequently associated
with high fever, and results in infection of parenchymal and
tissue cells throughout the body (Appel, 1969; Appel and
Gillespie, 1972; Blixenkrone-Møller, 1989; Blixenkrone-
Møller et al., 1989; Okita et al., 1997). Thus, CDV can be
found in cells of the respiratory, gastrointestinal and urinary
tract, endocrine system, lymphoid tissues, central nervous
systemand vasculature including keratinocytes, fibroblasts,
thrombocytes and different lymphoid cell subsets, aswell as
bronchial, endothelial, epithelial and neuroectodermal cells
(Baumga¨ rtner et al., 1989; Gro¨ne et al., 2004a,b; Koutinas
et al., 2004).
==Signalment==
==Signalment==