Primary viremia refers to the initial spread of virus in the blood from the first site of infection.
Secondary viremia occurs when primary viremia has resulted in infection of additional tissues via bloodstream, in which the virus has replicated and once more entered the circulation.
Usually secondary viremia results in higher viral shedding and viral loads within the bloodstream due to the possibility that the virus is able to reach its natural host cell from the bloodstream and replicate more efficiently than the initial site. An excellent example to profile this distinction is the rabies virus. Usually the virus will replicate briefly within the first site of say the bite of a rabid dog, within the muscle tissues. Viral replication then leads to viremia and the virus spreads to its secondary site of infection, the CNS. Upon infection of the CNS, secondary viremia results and symptoms usually begin. Vaccination at this point is useless, as the spread to the brain, leading to death, is unstoppable (the only clinical exception is Jeanna Giese). Hence vaccination must be done before secondary viremia takes place for the individual to be saved.
Active viremia is caused by the replication of viruses which results in viruses being introduced into the bloodstream. Examples include the measles, in which primary viremia occurs in the epithelial lining of the respiratory tract before replicating and budding out the cell basal layer, resulting in viruses budding into capillaries and blood vessels .
Passive viremia is the introduction of viruses in the bloodstream without the need of active viral replication. Examples include direct inoculation from mosquitoes, through physical breaches or via blood transfusions.