Vaccinia is introduced into the skin by means of multiple punctures of a bifurcated needle. The virus replicates in the basal layer and disseminates from cell to cell, causing necrosis and the formation of fluid-filled vesicles. Nonetheless, the initial spread of the virus is slowed by innate antiviral mechanisms, and, by the second week, the cell-mediated immune response begins to eliminate infected cells. Neutrophils, macrophages, and lymphocytes infiltrate the inoculation site, forming a confluent pustule and releasing cytokines and chemokines that cause hyperemia and edema in surrounding tissues. This may initially manifest into complaints of malaise and other mild constitutional symptoms, fever, vomiting, and tender enlarged axillary lymph nodes. Some vaccinees develop additional local “satellite” pustules that resolve along with the primary lesion. The virus may gain access to the blood at an early stage, and secondary skin lesions, which follow the same evolution as the inoculation site, may appear across the body. Bacteria, like Staphylococcus aureus, may infect the ulcerated, and necrotic lesions. Coalescent lesions may cover large portions of the body with extensive tissue destruction. Although some vaccinia viruses commonly disseminate through the bloodstream, the NYCBOH strain reportedly causes only limited viremia in a small percentage of recipients during the period of pustule formation. The inflammatory process reaches its peak by days 10–12 after vaccination and begins to resolve by day 14, with the shedding of the scab and other pustules by day 21. This sequence of events, which simulates the development of smallpox "pock", is known as a “take” reaction. A successful "take" is required for the development of antivaccinia antibody and cell-mediated responses.
Progressive vaccinia
Generalized vaccinia
Chickenpox
Sealpox
Cowpox
Smallpox
Farmyard pox
Mumps