One of the most economically important diseases of maize in Canada is gibberella ear rot caused by Fusarium graminearum Schwabe (teleomorph = Gibberella zeae (Schw.) Petch). Understanding how the fungus becomes established will help in developing effective strategies to reduce the incidence of this disease. This study investigates the infection process of F. graminearum on maize silks using both a wild-type F. graminearum as well as a strain transformed with a gene from jellyfish to constitutively express green fluorescent protein. Immature ears of maize were inoculated in the field with wild-type F. graminearum and harvested at specific times post infection, and the silks were stained with Chlorazol Black E for examination. In addition, uninoculated ears were excised, placed on water agar in large Petri dishes, and the silks inoculated with a suspension of macroconidia of the transformed fungus. The progress of fungal growth was then monitored using microscopy. Germination of conidia was observed 4–6 h after inoculation. A variable period of random growth often followed, after which some of the hyphae would grow in more or less straight lines down the silk towards the cob (rachis), and ultimately infect the developing kernels. Access to the cob occurred in 7–9 d in susceptible genotypes and 12–15 d in resistant genotypes. The fungus could penetrate the ovary directly through the silk attachment point or, when the silk was growing over other kernels, the fungus could traverse from the silk to colonize interkernel spaces. Entry into the cob was either through the rachis surface via exterior growth between kernels, or into the rachis via the pedicel.