CDV is an enveloped, non-segmented, single-stranded RNA virus and is a member of the Morbilliviruses, thus closely related to measles virus (LAMBandKOLAKOFSKY 2001; VANDEVELDE and ZURBRIGGEN 2005). CDV possesses a nucleocapsid containing the viral genome, which consists of the nucleoprotein (N) and the polymerase complex including the (P) and (L) proteins (DEMETER et al., 2007). The membrane protein (M) is located at the inner surface of the envelope, which exhibits two surface glycoproteins: the attachment protein (H) and the fusion protein (F; VANDEVELDE and ZURBRIGGEN 2005). CDV belongs to the Morbillivirus genus, which also includes other important viruses like measles virus (MV) and rinderpest virus (CARVALHO et al., 2012). Antigenic differences
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The virus can be detected at high titers in secretions and excretions, including urine (ELIA et al.. 2006). The initial infection occurs in epithelial cells and lymphoid tissue in the nasopharynx and replication takes place primarily in the lymphoid tissue of the respiratory tract (VON MESSLING et al.. 2003). The virus replicates within tissue macrophages and spread locally followed by disseminated distribution by lymphatics and blood (APPEL 1970; BEINEKE et al.. 2009). This widespread dissemination of the virus is accompanied byan increase in body temperature and leukopenia (BEINEKE et al.. 2009). The virus multiplies within lymphoid tissues including spleen, thymus, lymph nodes, bone marrow, mucosa-associated lymphoid tissues and macrophages in the lamina propria of the gastrointestinal tract and hepatic Kupffer cells (APPEL 1970; WRIGHT et al.. 1974). The second phase results in spread of the virus intomultiple parenchymal organs throughout the body, including respiratory, gastrointestinal and urinary tract, endocrine and central nervous system (BEINEKE et al.. 2009). The disease occurs as an acute systemic disease, a chronic nervous disorder or a combination of both. The main manifestations include respiratory and gastrointestinal signs, immunosuppression, demyelinating leukoencephalomyelitis and unusual clinical signs such as enamel defects and hard pad disease (LAPP et al.. 2014). Therefore clinical changes include anorexia, depression, conjunctivitis, hyperkeratosis of digital pads, catarrhal inflammation of bronchi and
The virus can be detected at high titers in secretions and excretions, including urine (ELIA et al.. 2006). The initial infection occurs in epithelial cells and lymphoid tissue in the nasopharynx and replication takes place primarily in the lymphoid tissue of the respiratory tract (VON MESSLING et al.. 2003). The virus replicates within tissue macrophages and spread locally followed by disseminated distribution by lymphatics and blood (APPEL 1970; BEINEKE et al.. 2009). This widespread dissemination of the virus is accompanied byan increase in body temperature and leukopenia (BEINEKE et al.. 2009). The virus multiplies within lymphoid tissues including spleen, thymus, lymph nodes, bone marrow, mucosa-associated lymphoid tissues and macrophages in the lamina propria of the gastrointestinal tract and hepatic Kupffer cells (APPEL 1970; WRIGHT et al.. 1974). The second phase results in spread of the virus intomultiple parenchymal organs throughout the body, including respiratory, gastrointestinal and urinary tract, endocrine and central nervous system (BEINEKE et al.. 2009). The disease occurs as an acute systemic disease, a chronic nervous disorder or a combination of both. The main manifestations include respiratory and gastrointestinal signs, immunosuppression, demyelinating leukoencephalomyelitis and unusual clinical signs such as enamel defects and hard pad disease (LAPP et al.. 2014). Therefore clinical changes include anorexia, depression, conjunctivitis, hyperkeratosis of digital pads, catarrhal inflammation of bronchi and