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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 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 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 (3-6 days post-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. A biphasic pyrexia is typical of distemper infection, and the 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. A biphasic fever is a typical of distemper: a transient pyrexia is associated with the onset of virus dissemination to lymphoid tissue lymphopenia at 3-6 days post-infection represents another characteristic clinical finding (Wright
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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, 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 spread to the lymphoid tissue and 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.
et al., 1974). A transient fever and the onset of lymphopenia
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can be observed 3–6 days pi (Krakowka et al., 1980) and
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coincide with the first viremia that results in a generalized
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infection of all lymphoid tissues including spleen, thymus,
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lymph nodes, bone marrow, mucosa-associated lymphatic
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tissues(MALT) and macrophages in the lamina propria of the
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gastrointestinal tract (Appel, 1970; Wright et al., 1974), as
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well as hepatic Kupffer cells (Appel, 1987). Viremia occurs
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by spread of cell free virus as well as leukocyte and
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thrombocyte associated infectious pathogens. The second
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viremia follows several days later, frequently associated
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with high fever, and results in infection of parenchymal and
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tissue cells throughout the body (Appel, 1969; Appel and
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Gillespie, 1972; Blixenkrone-Møller, 1989; Blixenkrone-
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Møller et al., 1989; Okita et al., 1997). Thus, CDV can be
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found in cells of the respiratory, gastrointestinal and urinary
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tract, endocrine system, lymphoid tissues, central nervous
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systemand vasculature including keratinocytes, fibroblasts,
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thrombocytes and different lymphoid cell subsets, aswell as
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bronchial, endothelial, epithelial and neuroectodermal cells
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(Baumga¨ rtner et al., 1989; Gro¨ne et al., 2004a,b; Koutinas
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et al., 2004).
      
==Signalment==
 
==Signalment==
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