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→Transmission and Pathogenesis
==Transmission and Pathogenesis==
==Transmission and Pathogenesis==
In field cases of CSFV, transmission is mainly oronasal by direct or indirect contact with infected pigs. Infected feed or pork products may also cause spread of disease, and transmission in semen can occur. Once the virus gains entry to the host an incubation period of around 7 days occurs prior to the onset of clinical signs, but this may vary from 4-10 days. Initially, virus infects the epithelial cells of the tonsillar crypts before spreading via the lymphatics to regional lymph nodes. From here, the virus enters the blood stream and then replicates in the spleen, bone marrow and lymph nodes before spreading to other tissues. Replication in the endothelial cells of blood vessels leads to apoptosis, causing superficial and internal haemorrhages. CSFV also induces a [[thrombocytopenia]] which contributes to haemorrhage by impairing primary [[Normal Mechanisms of Haemostatic Control|haemostasis]]. In acute CSF this angiopathy, in association with shock and pyrexia, leads to death. Surviving swine go on to develop a chronic form of the disease where tissue infarction results in joint and enteric lesions.
In field cases of CSFV, transmission is mainly oronasal by direct or indirect contact with infected pigs. Infected feed or pork products may also cause spread of disease, and transmission in semen can occur. Once the virus gains entry to the host an incubation period of around 7 days occurs prior to the onset of clinical signs, but this may vary from 4-10 days. Initially, virus infects the epithelial cells of the tonsillar crypts before spreading via the lymphatics to regional lymph nodes. From here, the virus enters the blood stream and then replicates in the spleen, bone marrow and lymph nodes before spreading to other tissues. Replication in the endothelial cells of blood vessels leads to apoptosis, causing superficial and internal haemorrhages. CSFV also induces a [[thrombocytopenia]] which contributes to haemorrhage by impairing primary [[Normal_Mechanisms_of_Haemostatic_Control#Introduction|haemostasis]]. In acute CSF this angiopathy, in association with shock and pyrexia, leads to death. Surviving swine go on to develop a chronic form of the disease where tissue infarction results in joint and enteric lesions.
The outcome of transplacental infection depends largely on the point of gestation and may result in abortions, stillbirths, mummifications, malformations or the birth of weak or persistently viraemic piglets. Although persistently infected piglets may be clinically normal at birth, they grow poorly, excrete virus over long periods and invariably die eventually from full blown CSF.
The outcome of transplacental infection depends largely on the point of gestation and may result in abortions, stillbirths, mummifications, malformations or the birth of weak or persistently viraemic piglets. Although persistently infected piglets may be clinically normal at birth, they grow poorly, excrete virus over long periods and invariably die eventually from full blown CSF.